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A 25-year-old primigravida with a history of pre-eclampsia was brought to the emergency department with sudden onset of severe headache. The headache started two days after delivery. It was followed by confusion and loss of consciousness over a few hours. On initial evaluation, the patient was confused with a Glasgow Coma Scale (GCS) of 12/15, blood pressure of 130/90 mmHg, pulse rate of 82 beats/min, respiratory rate of 30/min, temperature 98°C, and oxygen saturation of 97 mmHg at room temperature. On physical examination, bilateral equivocal planters were noted with no other significant findings, and bilateral papillary edema on fundoscopy was seen. The rest of the review system was unremarkable. She underwent an urgent MRI with magnetic resonance venography (MRV) of the brain, which showed right transverse sinus thrombosis with an element of SAH (Figure ).\nCoagulation profile, including thrombin time (TT), prothrombin time (PT), partial thromboplastin time (PTT), antithrombin III, fibrinogen, proteins C and S, antiphospholipid antibody titers, and homocysteine levels, were normal. She was started on a half dosage of low molecular weight heparin (LMWH) (60 mg subcutaneously once a day) with regular monitoring of her blood pressure and GCS. Her GCS started improving; therefore, she was continued on a half dose of LMWH for 10 days, and brain MRI was repeated after 10 days, which showed the gradual resolution of SAH (Figure ). The quantity of LMWH was doubled, and warfarin was started after a full dose of LMWH. After improving her GCS and achievement of international normalized ratio (INR) of two to three, she was discharged with the advice of regular INR monitoring and follow-up to the outpatient department. On follow-up at six weeks, MRI with MRV was repeated, which showed thrombosis had resolved, although a mild filling defect was noted. She was kept on anticoagulants for one year, and on further follow-up at six months, she was doing well.

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 25-year-old primigravida with a history of pre-eclampsia was brought to the emergency department with sudden onset of severe headache. The headache started two days after delivery. It was followed by confusion and loss of consciousness over a few hours. On initial evaluation, the patient was confused with a Glasgow Coma Scale (GCS) of 12/15, blood pressure of 130/90 mmHg, pulse rate of 82 beats/min, respiratory rate of 30/min, temperature 98°C, and oxygen saturation of 97 mmHg at room temperature. On physical examination, bilateral equivocal planters were noted with no other significant findings, and bilateral papillary edema on fundoscopy was seen. The rest of the review system was unremarkable. She underwent an urgent MRI with magnetic resonance venography (MRV) of the brain, which showed right transverse sinus thrombosis with an element of SAH (Figure ).\nCoagulation profile, including thrombin time (TT), prothrombin time (PT), partial thromboplastin time (PTT), antithrombin III, fibrinogen, proteins C and S, antiphospholipid antibody titers, and homocysteine levels, were normal. She was started on a half dosage of low molecular weight heparin (LMWH) (60 mg subcutaneously once a day) with regular monitoring of her blood pressure and GCS. Her GCS started improving; therefore, she was continued on a half dose of LMWH for 10 days, and brain MRI was repeated after 10 days, which showed the gradual resolution of SAH (Figure ). The quantity of LMWH was doubled, and warfarin was started after a full dose of LMWH. After improving her GCS and achievement of international normalized ratio (INR) of two to three, she was discharged with the advice of regular INR monitoring and follow-up to the outpatient department. On follow-up at six weeks, MRI with MRV was repeated, which showed thrombosis had resolved, although a mild filling defect was noted. She was kept on anticoagulants for one year, and on further follow-up at six months, she was doing well.

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().

A 58-year-old right-handed postmenopausal woman presented to the emergency with progressively increasing holocephalic headache for 3 days. She did not have fever, nausea, and vomiting. The headache gradually worsened in severity and on the day of presentation, she developed a generalized tonic clonic seizure. Apart from the history of well-controlled diabetes mellitus, she did not have significant past medical, personal, and family history. She had not received any vaccines in the recent past. On examination, she was ill-looking, but her vital signs were stable. She had Wernicke's aphasia. She did not have disc edema; cranial nerve examination was normal, and she did not have any focal deficits.\nAn urgent CT scan of the head without contrast showed left temporal hematoma with surrounding vasogenic edema (Figure ). Hemorrhagic picture was noted in the insular cistern (Figure ), left fronto-temporal subdural space (Figure ), the perimesencephalic, ambient and suprasellar cisterns (Figures and ), and the sulci of the left temporo-parietal lobes (Figures and ). There was a subtle dense clot sign in the left transverse sinus (Figure ). She was diagnosed as having left transverse sinus thrombosis leading to left temporal hematoma, SAH and SDH. She was treated with low molecular weight heparin, levetiracetam, and 3% hypertonic saline. The magnetic resonance venography (MRV) done the following day confirmed the presence of left transverse sinus thrombosis (Figure ). CT angiography of the brain did not reveal any vascular malformations. Her complete blood counts, coagulation profiles, routine blood chemistry, and C-reactive protein were within normal limits. Antinuclear antibody and SARS-CoV-2 RNA polymerase chain reaction tests were negative. She underwent CT scan of neck, chest, abdomen and pelvis, mammogram, stool occult blood, carcinoembryonic antigen, CA-125, and Ca 19–9 tests, all of which were non-contributory to any occult malignancy. Thrombophilia screening was not done at this acute stage. We decided to get those done after the completion of anticoagulant treatment. She showed good clinical improvement over the course of the next few days. A repeat CT scan of the head done on day seven, revealed decreasing edema and stable hematoma volume with no new bleeding. The cause of her CVST was deemed undermined at this stage and she was discharged home on dabigatran 150 mg twice daily, as she could not get PT/INR done reliably due to the current lockdown imposed by the government. She has been doing well on follow up.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 77-year-old male with a recent syncope-related fall and closed head injury presented with gradually worsening isolated right upper extremity monoparesis. The fall occurred 1 month before presentation. On examination, the patient demonstrated 4/5 strength in his right upper extremity, with no additional neurologic deficits. Noncontrast head CT demonstrated bilateral mixed density convexity subdural hematomas [22 mm on the left and 14 mm on the right; and ]. The patient underwent a left craniotomy for evacuation of the larger hematoma, in conjunction with bilateral MMA embolization as primary treatment for the right convexity subdural hematoma in addition to limiting potential recurrence along the left convexity. Intraprocedural digital subtraction angiogram revealed two Cognard Grade III DAVFs, one arising from the parietal branch of the right MMA draining into an occipital cortical vein, and the second arising from the temporal branch of the left MMA draining into the vein of Labbe [-]. Given the presence of cortical venous reflux and associated risk of future intracranial hemorrhage, treatment of the fistulae was indicated. This was approached in two staged procedures. Following an uncomplicated left MMA embolization (frontoparietal branch), the incidental findings were discussed with the patient and he underwent a second stage embolization for the DAVF on a later date. During the second stage, a more prolonged infusion of liquid embolic was employed to ensure penetration into the recipient cortical venous outflow, resulting in nonopacification of the aforementioned fistulae. The postoperative course was complicated by seizures which resolved with uptitration in antiepileptic medications. At 6-month follow-up, there was complete resolution of the patient’s presenting symptoms and surveillance CT demonstrated no residual SDH.

This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).

This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().

A 59-year-old male with a recent fall and closed head injury presented with progressively worsening headaches. The fall occurred 9 days before presentation. On examination, no neurologic deficits were found. Noncontrast head CT demonstrated a 5 mm left convexity CSDH []. He underwent burr hole evacuation and was discharged on the subsequent day. He presented again on postoperative day 6 with recurrence of his headaches. Noncontrast head CT demonstrated recurrence of the left convexity subdural hematoma []. He subsequently underwent a left craniotomy for evacuation. He was discharged on postoperative day 2 with no postprocedural complications. At 1-month follow-up, he continued to complain of severe headaches. Surveillance CT demonstrated a new 27 mm right convexity mixed density subdural hematoma [ and ]. He subsequently underwent right MMA embolization as primary treatment. Intraprocedural digital subtraction angiogram revealed a Cognard Grade III cribriform plate DAVF supplied by the right ophthalmic artery draining into a right frontal cortical vein [ and ]. The right MMA temporoparietal and frontal branches were embolized with n-BCA glue. Follow-up was arranged to treat the DAVF at a later date and he was discharged the following day. The patient was subsequently lost to follow-up, but presented to the emergency department 4 months later with diplopia and a right abducens nerve palsy. Noncontrast head CT demonstrated significant reduction in size of the previously embolized right convexity subdural hematoma. He was admitted and underwent attempted endovascular treatment of the DAVF. Catheterization of the arterial and venous sides of the fistula achieved suboptimal positioning for liquid embolic embolization and so he underwent a right craniotomy for surgical ligation of the fistula. The patient experienced no postprocedural complications. At 2-week follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

A 58-year-old right-handed postmenopausal woman presented to the emergency with progressively increasing holocephalic headache for 3 days. She did not have fever, nausea, and vomiting. The headache gradually worsened in severity and on the day of presentation, she developed a generalized tonic clonic seizure. Apart from the history of well-controlled diabetes mellitus, she did not have significant past medical, personal, and family history. She had not received any vaccines in the recent past. On examination, she was ill-looking, but her vital signs were stable. She had Wernicke's aphasia. She did not have disc edema; cranial nerve examination was normal, and she did not have any focal deficits.\nAn urgent CT scan of the head without contrast showed left temporal hematoma with surrounding vasogenic edema (Figure ). Hemorrhagic picture was noted in the insular cistern (Figure ), left fronto-temporal subdural space (Figure ), the perimesencephalic, ambient and suprasellar cisterns (Figures and ), and the sulci of the left temporo-parietal lobes (Figures and ). There was a subtle dense clot sign in the left transverse sinus (Figure ). She was diagnosed as having left transverse sinus thrombosis leading to left temporal hematoma, SAH and SDH. She was treated with low molecular weight heparin, levetiracetam, and 3% hypertonic saline. The magnetic resonance venography (MRV) done the following day confirmed the presence of left transverse sinus thrombosis (Figure ). CT angiography of the brain did not reveal any vascular malformations. Her complete blood counts, coagulation profiles, routine blood chemistry, and C-reactive protein were within normal limits. Antinuclear antibody and SARS-CoV-2 RNA polymerase chain reaction tests were negative. She underwent CT scan of neck, chest, abdomen and pelvis, mammogram, stool occult blood, carcinoembryonic antigen, CA-125, and Ca 19–9 tests, all of which were non-contributory to any occult malignancy. Thrombophilia screening was not done at this acute stage. We decided to get those done after the completion of anticoagulant treatment. She showed good clinical improvement over the course of the next few days. A repeat CT scan of the head done on day seven, revealed decreasing edema and stable hematoma volume with no new bleeding. The cause of her CVST was deemed undermined at this stage and she was discharged home on dabigatran 150 mg twice daily, as she could not get PT/INR done reliably due to the current lockdown imposed by the government. She has been doing well on follow up.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

A 77-year-old male with a recent syncope-related fall and closed head injury presented with gradually worsening isolated right upper extremity monoparesis. The fall occurred 1 month before presentation. On examination, the patient demonstrated 4/5 strength in his right upper extremity, with no additional neurologic deficits. Noncontrast head CT demonstrated bilateral mixed density convexity subdural hematomas [22 mm on the left and 14 mm on the right; and ]. The patient underwent a left craniotomy for evacuation of the larger hematoma, in conjunction with bilateral MMA embolization as primary treatment for the right convexity subdural hematoma in addition to limiting potential recurrence along the left convexity. Intraprocedural digital subtraction angiogram revealed two Cognard Grade III DAVFs, one arising from the parietal branch of the right MMA draining into an occipital cortical vein, and the second arising from the temporal branch of the left MMA draining into the vein of Labbe [-]. Given the presence of cortical venous reflux and associated risk of future intracranial hemorrhage, treatment of the fistulae was indicated. This was approached in two staged procedures. Following an uncomplicated left MMA embolization (frontoparietal branch), the incidental findings were discussed with the patient and he underwent a second stage embolization for the DAVF on a later date. During the second stage, a more prolonged infusion of liquid embolic was employed to ensure penetration into the recipient cortical venous outflow, resulting in nonopacification of the aforementioned fistulae. The postoperative course was complicated by seizures which resolved with uptitration in antiepileptic medications. At 6-month follow-up, there was complete resolution of the patient’s presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).

A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

A 59-year-old male with a recent fall and closed head injury presented with progressively worsening headaches. The fall occurred 9 days before presentation. On examination, no neurologic deficits were found. Noncontrast head CT demonstrated a 5 mm left convexity CSDH []. He underwent burr hole evacuation and was discharged on the subsequent day. He presented again on postoperative day 6 with recurrence of his headaches. Noncontrast head CT demonstrated recurrence of the left convexity subdural hematoma []. He subsequently underwent a left craniotomy for evacuation. He was discharged on postoperative day 2 with no postprocedural complications. At 1-month follow-up, he continued to complain of severe headaches. Surveillance CT demonstrated a new 27 mm right convexity mixed density subdural hematoma [ and ]. He subsequently underwent right MMA embolization as primary treatment. Intraprocedural digital subtraction angiogram revealed a Cognard Grade III cribriform plate DAVF supplied by the right ophthalmic artery draining into a right frontal cortical vein [ and ]. The right MMA temporoparietal and frontal branches were embolized with n-BCA glue. Follow-up was arranged to treat the DAVF at a later date and he was discharged the following day. The patient was subsequently lost to follow-up, but presented to the emergency department 4 months later with diplopia and a right abducens nerve palsy. Noncontrast head CT demonstrated significant reduction in size of the previously embolized right convexity subdural hematoma. He was admitted and underwent attempted endovascular treatment of the DAVF. Catheterization of the arterial and venous sides of the fistula achieved suboptimal positioning for liquid embolic embolization and so he underwent a right craniotomy for surgical ligation of the fistula. The patient experienced no postprocedural complications. At 2-week follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 58-year-old right-handed postmenopausal woman presented to the emergency with progressively increasing holocephalic headache for 3 days. She did not have fever, nausea, and vomiting. The headache gradually worsened in severity and on the day of presentation, she developed a generalized tonic clonic seizure. Apart from the history of well-controlled diabetes mellitus, she did not have significant past medical, personal, and family history. She had not received any vaccines in the recent past. On examination, she was ill-looking, but her vital signs were stable. She had Wernicke's aphasia. She did not have disc edema; cranial nerve examination was normal, and she did not have any focal deficits.\nAn urgent CT scan of the head without contrast showed left temporal hematoma with surrounding vasogenic edema (Figure ). Hemorrhagic picture was noted in the insular cistern (Figure ), left fronto-temporal subdural space (Figure ), the perimesencephalic, ambient and suprasellar cisterns (Figures and ), and the sulci of the left temporo-parietal lobes (Figures and ). There was a subtle dense clot sign in the left transverse sinus (Figure ). She was diagnosed as having left transverse sinus thrombosis leading to left temporal hematoma, SAH and SDH. She was treated with low molecular weight heparin, levetiracetam, and 3% hypertonic saline. The magnetic resonance venography (MRV) done the following day confirmed the presence of left transverse sinus thrombosis (Figure ). CT angiography of the brain did not reveal any vascular malformations. Her complete blood counts, coagulation profiles, routine blood chemistry, and C-reactive protein were within normal limits. Antinuclear antibody and SARS-CoV-2 RNA polymerase chain reaction tests were negative. She underwent CT scan of neck, chest, abdomen and pelvis, mammogram, stool occult blood, carcinoembryonic antigen, CA-125, and Ca 19–9 tests, all of which were non-contributory to any occult malignancy. Thrombophilia screening was not done at this acute stage. We decided to get those done after the completion of anticoagulant treatment. She showed good clinical improvement over the course of the next few days. A repeat CT scan of the head done on day seven, revealed decreasing edema and stable hematoma volume with no new bleeding. The cause of her CVST was deemed undermined at this stage and she was discharged home on dabigatran 150 mg twice daily, as she could not get PT/INR done reliably due to the current lockdown imposed by the government. She has been doing well on follow up.

A 77-year-old male with a recent syncope-related fall and closed head injury presented with gradually worsening isolated right upper extremity monoparesis. The fall occurred 1 month before presentation. On examination, the patient demonstrated 4/5 strength in his right upper extremity, with no additional neurologic deficits. Noncontrast head CT demonstrated bilateral mixed density convexity subdural hematomas [22 mm on the left and 14 mm on the right; and ]. The patient underwent a left craniotomy for evacuation of the larger hematoma, in conjunction with bilateral MMA embolization as primary treatment for the right convexity subdural hematoma in addition to limiting potential recurrence along the left convexity. Intraprocedural digital subtraction angiogram revealed two Cognard Grade III DAVFs, one arising from the parietal branch of the right MMA draining into an occipital cortical vein, and the second arising from the temporal branch of the left MMA draining into the vein of Labbe [-]. Given the presence of cortical venous reflux and associated risk of future intracranial hemorrhage, treatment of the fistulae was indicated. This was approached in two staged procedures. Following an uncomplicated left MMA embolization (frontoparietal branch), the incidental findings were discussed with the patient and he underwent a second stage embolization for the DAVF on a later date. During the second stage, a more prolonged infusion of liquid embolic was employed to ensure penetration into the recipient cortical venous outflow, resulting in nonopacification of the aforementioned fistulae. The postoperative course was complicated by seizures which resolved with uptitration in antiepileptic medications. At 6-month follow-up, there was complete resolution of the patient’s presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).

A 58-year-old right-handed postmenopausal woman presented to the emergency with progressively increasing holocephalic headache for 3 days. She did not have fever, nausea, and vomiting. The headache gradually worsened in severity and on the day of presentation, she developed a generalized tonic clonic seizure. Apart from the history of well-controlled diabetes mellitus, she did not have significant past medical, personal, and family history. She had not received any vaccines in the recent past. On examination, she was ill-looking, but her vital signs were stable. She had Wernicke's aphasia. She did not have disc edema; cranial nerve examination was normal, and she did not have any focal deficits.\nAn urgent CT scan of the head without contrast showed left temporal hematoma with surrounding vasogenic edema (Figure ). Hemorrhagic picture was noted in the insular cistern (Figure ), left fronto-temporal subdural space (Figure ), the perimesencephalic, ambient and suprasellar cisterns (Figures and ), and the sulci of the left temporo-parietal lobes (Figures and ). There was a subtle dense clot sign in the left transverse sinus (Figure ). She was diagnosed as having left transverse sinus thrombosis leading to left temporal hematoma, SAH and SDH. She was treated with low molecular weight heparin, levetiracetam, and 3% hypertonic saline. The magnetic resonance venography (MRV) done the following day confirmed the presence of left transverse sinus thrombosis (Figure ). CT angiography of the brain did not reveal any vascular malformations. Her complete blood counts, coagulation profiles, routine blood chemistry, and C-reactive protein were within normal limits. Antinuclear antibody and SARS-CoV-2 RNA polymerase chain reaction tests were negative. She underwent CT scan of neck, chest, abdomen and pelvis, mammogram, stool occult blood, carcinoembryonic antigen, CA-125, and Ca 19–9 tests, all of which were non-contributory to any occult malignancy. Thrombophilia screening was not done at this acute stage. We decided to get those done after the completion of anticoagulant treatment. She showed good clinical improvement over the course of the next few days. A repeat CT scan of the head done on day seven, revealed decreasing edema and stable hematoma volume with no new bleeding. The cause of her CVST was deemed undermined at this stage and she was discharged home on dabigatran 150 mg twice daily, as she could not get PT/INR done reliably due to the current lockdown imposed by the government. She has been doing well on follow up.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 58-year-old right-handed postmenopausal woman presented to the emergency with progressively increasing holocephalic headache for 3 days. She did not have fever, nausea, and vomiting. The headache gradually worsened in severity and on the day of presentation, she developed a generalized tonic clonic seizure. Apart from the history of well-controlled diabetes mellitus, she did not have significant past medical, personal, and family history. She had not received any vaccines in the recent past. On examination, she was ill-looking, but her vital signs were stable. She had Wernicke's aphasia. She did not have disc edema; cranial nerve examination was normal, and she did not have any focal deficits.\nAn urgent CT scan of the head without contrast showed left temporal hematoma with surrounding vasogenic edema (Figure ). Hemorrhagic picture was noted in the insular cistern (Figure ), left fronto-temporal subdural space (Figure ), the perimesencephalic, ambient and suprasellar cisterns (Figures and ), and the sulci of the left temporo-parietal lobes (Figures and ). There was a subtle dense clot sign in the left transverse sinus (Figure ). She was diagnosed as having left transverse sinus thrombosis leading to left temporal hematoma, SAH and SDH. She was treated with low molecular weight heparin, levetiracetam, and 3% hypertonic saline. The magnetic resonance venography (MRV) done the following day confirmed the presence of left transverse sinus thrombosis (Figure ). CT angiography of the brain did not reveal any vascular malformations. Her complete blood counts, coagulation profiles, routine blood chemistry, and C-reactive protein were within normal limits. Antinuclear antibody and SARS-CoV-2 RNA polymerase chain reaction tests were negative. She underwent CT scan of neck, chest, abdomen and pelvis, mammogram, stool occult blood, carcinoembryonic antigen, CA-125, and Ca 19–9 tests, all of which were non-contributory to any occult malignancy. Thrombophilia screening was not done at this acute stage. We decided to get those done after the completion of anticoagulant treatment. She showed good clinical improvement over the course of the next few days. A repeat CT scan of the head done on day seven, revealed decreasing edema and stable hematoma volume with no new bleeding. The cause of her CVST was deemed undermined at this stage and she was discharged home on dabigatran 150 mg twice daily, as she could not get PT/INR done reliably due to the current lockdown imposed by the government. She has been doing well on follow up.

A 59-year-old male with a recent fall and closed head injury presented with progressively worsening headaches. The fall occurred 9 days before presentation. On examination, no neurologic deficits were found. Noncontrast head CT demonstrated a 5 mm left convexity CSDH []. He underwent burr hole evacuation and was discharged on the subsequent day. He presented again on postoperative day 6 with recurrence of his headaches. Noncontrast head CT demonstrated recurrence of the left convexity subdural hematoma []. He subsequently underwent a left craniotomy for evacuation. He was discharged on postoperative day 2 with no postprocedural complications. At 1-month follow-up, he continued to complain of severe headaches. Surveillance CT demonstrated a new 27 mm right convexity mixed density subdural hematoma [ and ]. He subsequently underwent right MMA embolization as primary treatment. Intraprocedural digital subtraction angiogram revealed a Cognard Grade III cribriform plate DAVF supplied by the right ophthalmic artery draining into a right frontal cortical vein [ and ]. The right MMA temporoparietal and frontal branches were embolized with n-BCA glue. Follow-up was arranged to treat the DAVF at a later date and he was discharged the following day. The patient was subsequently lost to follow-up, but presented to the emergency department 4 months later with diplopia and a right abducens nerve palsy. Noncontrast head CT demonstrated significant reduction in size of the previously embolized right convexity subdural hematoma. He was admitted and underwent attempted endovascular treatment of the DAVF. Catheterization of the arterial and venous sides of the fistula achieved suboptimal positioning for liquid embolic embolization and so he underwent a right craniotomy for surgical ligation of the fistula. The patient experienced no postprocedural complications. At 2-week follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 58-year-old right-handed postmenopausal woman presented to the emergency with progressively increasing holocephalic headache for 3 days. She did not have fever, nausea, and vomiting. The headache gradually worsened in severity and on the day of presentation, she developed a generalized tonic clonic seizure. Apart from the history of well-controlled diabetes mellitus, she did not have significant past medical, personal, and family history. She had not received any vaccines in the recent past. On examination, she was ill-looking, but her vital signs were stable. She had Wernicke's aphasia. She did not have disc edema; cranial nerve examination was normal, and she did not have any focal deficits.\nAn urgent CT scan of the head without contrast showed left temporal hematoma with surrounding vasogenic edema (Figure ). Hemorrhagic picture was noted in the insular cistern (Figure ), left fronto-temporal subdural space (Figure ), the perimesencephalic, ambient and suprasellar cisterns (Figures and ), and the sulci of the left temporo-parietal lobes (Figures and ). There was a subtle dense clot sign in the left transverse sinus (Figure ). She was diagnosed as having left transverse sinus thrombosis leading to left temporal hematoma, SAH and SDH. She was treated with low molecular weight heparin, levetiracetam, and 3% hypertonic saline. The magnetic resonance venography (MRV) done the following day confirmed the presence of left transverse sinus thrombosis (Figure ). CT angiography of the brain did not reveal any vascular malformations. Her complete blood counts, coagulation profiles, routine blood chemistry, and C-reactive protein were within normal limits. Antinuclear antibody and SARS-CoV-2 RNA polymerase chain reaction tests were negative. She underwent CT scan of neck, chest, abdomen and pelvis, mammogram, stool occult blood, carcinoembryonic antigen, CA-125, and Ca 19–9 tests, all of which were non-contributory to any occult malignancy. Thrombophilia screening was not done at this acute stage. We decided to get those done after the completion of anticoagulant treatment. She showed good clinical improvement over the course of the next few days. A repeat CT scan of the head done on day seven, revealed decreasing edema and stable hematoma volume with no new bleeding. The cause of her CVST was deemed undermined at this stage and she was discharged home on dabigatran 150 mg twice daily, as she could not get PT/INR done reliably due to the current lockdown imposed by the government. She has been doing well on follow up.

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 58-year-old right-handed postmenopausal woman presented to the emergency with progressively increasing holocephalic headache for 3 days. She did not have fever, nausea, and vomiting. The headache gradually worsened in severity and on the day of presentation, she developed a generalized tonic clonic seizure. Apart from the history of well-controlled diabetes mellitus, she did not have significant past medical, personal, and family history. She had not received any vaccines in the recent past. On examination, she was ill-looking, but her vital signs were stable. She had Wernicke's aphasia. She did not have disc edema; cranial nerve examination was normal, and she did not have any focal deficits.\nAn urgent CT scan of the head without contrast showed left temporal hematoma with surrounding vasogenic edema (Figure ). Hemorrhagic picture was noted in the insular cistern (Figure ), left fronto-temporal subdural space (Figure ), the perimesencephalic, ambient and suprasellar cisterns (Figures and ), and the sulci of the left temporo-parietal lobes (Figures and ). There was a subtle dense clot sign in the left transverse sinus (Figure ). She was diagnosed as having left transverse sinus thrombosis leading to left temporal hematoma, SAH and SDH. She was treated with low molecular weight heparin, levetiracetam, and 3% hypertonic saline. The magnetic resonance venography (MRV) done the following day confirmed the presence of left transverse sinus thrombosis (Figure ). CT angiography of the brain did not reveal any vascular malformations. Her complete blood counts, coagulation profiles, routine blood chemistry, and C-reactive protein were within normal limits. Antinuclear antibody and SARS-CoV-2 RNA polymerase chain reaction tests were negative. She underwent CT scan of neck, chest, abdomen and pelvis, mammogram, stool occult blood, carcinoembryonic antigen, CA-125, and Ca 19–9 tests, all of which were non-contributory to any occult malignancy. Thrombophilia screening was not done at this acute stage. We decided to get those done after the completion of anticoagulant treatment. She showed good clinical improvement over the course of the next few days. A repeat CT scan of the head done on day seven, revealed decreasing edema and stable hematoma volume with no new bleeding. The cause of her CVST was deemed undermined at this stage and she was discharged home on dabigatran 150 mg twice daily, as she could not get PT/INR done reliably due to the current lockdown imposed by the government. She has been doing well on follow up.

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).

A 77-year-old male with a recent syncope-related fall and closed head injury presented with gradually worsening isolated right upper extremity monoparesis. The fall occurred 1 month before presentation. On examination, the patient demonstrated 4/5 strength in his right upper extremity, with no additional neurologic deficits. Noncontrast head CT demonstrated bilateral mixed density convexity subdural hematomas [22 mm on the left and 14 mm on the right; and ]. The patient underwent a left craniotomy for evacuation of the larger hematoma, in conjunction with bilateral MMA embolization as primary treatment for the right convexity subdural hematoma in addition to limiting potential recurrence along the left convexity. Intraprocedural digital subtraction angiogram revealed two Cognard Grade III DAVFs, one arising from the parietal branch of the right MMA draining into an occipital cortical vein, and the second arising from the temporal branch of the left MMA draining into the vein of Labbe [-]. Given the presence of cortical venous reflux and associated risk of future intracranial hemorrhage, treatment of the fistulae was indicated. This was approached in two staged procedures. Following an uncomplicated left MMA embolization (frontoparietal branch), the incidental findings were discussed with the patient and he underwent a second stage embolization for the DAVF on a later date. During the second stage, a more prolonged infusion of liquid embolic was employed to ensure penetration into the recipient cortical venous outflow, resulting in nonopacification of the aforementioned fistulae. The postoperative course was complicated by seizures which resolved with uptitration in antiepileptic medications. At 6-month follow-up, there was complete resolution of the patient’s presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 77-year-old male with a recent syncope-related fall and closed head injury presented with gradually worsening isolated right upper extremity monoparesis. The fall occurred 1 month before presentation. On examination, the patient demonstrated 4/5 strength in his right upper extremity, with no additional neurologic deficits. Noncontrast head CT demonstrated bilateral mixed density convexity subdural hematomas [22 mm on the left and 14 mm on the right; and ]. The patient underwent a left craniotomy for evacuation of the larger hematoma, in conjunction with bilateral MMA embolization as primary treatment for the right convexity subdural hematoma in addition to limiting potential recurrence along the left convexity. Intraprocedural digital subtraction angiogram revealed two Cognard Grade III DAVFs, one arising from the parietal branch of the right MMA draining into an occipital cortical vein, and the second arising from the temporal branch of the left MMA draining into the vein of Labbe [-]. Given the presence of cortical venous reflux and associated risk of future intracranial hemorrhage, treatment of the fistulae was indicated. This was approached in two staged procedures. Following an uncomplicated left MMA embolization (frontoparietal branch), the incidental findings were discussed with the patient and he underwent a second stage embolization for the DAVF on a later date. During the second stage, a more prolonged infusion of liquid embolic was employed to ensure penetration into the recipient cortical venous outflow, resulting in nonopacification of the aforementioned fistulae. The postoperative course was complicated by seizures which resolved with uptitration in antiepileptic medications. At 6-month follow-up, there was complete resolution of the patient’s presenting symptoms and surveillance CT demonstrated no residual SDH.

A 59-year-old male with a recent fall and closed head injury presented with progressively worsening headaches. The fall occurred 9 days before presentation. On examination, no neurologic deficits were found. Noncontrast head CT demonstrated a 5 mm left convexity CSDH []. He underwent burr hole evacuation and was discharged on the subsequent day. He presented again on postoperative day 6 with recurrence of his headaches. Noncontrast head CT demonstrated recurrence of the left convexity subdural hematoma []. He subsequently underwent a left craniotomy for evacuation. He was discharged on postoperative day 2 with no postprocedural complications. At 1-month follow-up, he continued to complain of severe headaches. Surveillance CT demonstrated a new 27 mm right convexity mixed density subdural hematoma [ and ]. He subsequently underwent right MMA embolization as primary treatment. Intraprocedural digital subtraction angiogram revealed a Cognard Grade III cribriform plate DAVF supplied by the right ophthalmic artery draining into a right frontal cortical vein [ and ]. The right MMA temporoparietal and frontal branches were embolized with n-BCA glue. Follow-up was arranged to treat the DAVF at a later date and he was discharged the following day. The patient was subsequently lost to follow-up, but presented to the emergency department 4 months later with diplopia and a right abducens nerve palsy. Noncontrast head CT demonstrated significant reduction in size of the previously embolized right convexity subdural hematoma. He was admitted and underwent attempted endovascular treatment of the DAVF. Catheterization of the arterial and venous sides of the fistula achieved suboptimal positioning for liquid embolic embolization and so he underwent a right craniotomy for surgical ligation of the fistula. The patient experienced no postprocedural complications. At 2-week follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 77-year-old male with a recent syncope-related fall and closed head injury presented with gradually worsening isolated right upper extremity monoparesis. The fall occurred 1 month before presentation. On examination, the patient demonstrated 4/5 strength in his right upper extremity, with no additional neurologic deficits. Noncontrast head CT demonstrated bilateral mixed density convexity subdural hematomas [22 mm on the left and 14 mm on the right; and ]. The patient underwent a left craniotomy for evacuation of the larger hematoma, in conjunction with bilateral MMA embolization as primary treatment for the right convexity subdural hematoma in addition to limiting potential recurrence along the left convexity. Intraprocedural digital subtraction angiogram revealed two Cognard Grade III DAVFs, one arising from the parietal branch of the right MMA draining into an occipital cortical vein, and the second arising from the temporal branch of the left MMA draining into the vein of Labbe [-]. Given the presence of cortical venous reflux and associated risk of future intracranial hemorrhage, treatment of the fistulae was indicated. This was approached in two staged procedures. Following an uncomplicated left MMA embolization (frontoparietal branch), the incidental findings were discussed with the patient and he underwent a second stage embolization for the DAVF on a later date. During the second stage, a more prolonged infusion of liquid embolic was employed to ensure penetration into the recipient cortical venous outflow, resulting in nonopacification of the aforementioned fistulae. The postoperative course was complicated by seizures which resolved with uptitration in antiepileptic medications. At 6-month follow-up, there was complete resolution of the patient’s presenting symptoms and surveillance CT demonstrated no residual SDH.

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 77-year-old male with a recent syncope-related fall and closed head injury presented with gradually worsening isolated right upper extremity monoparesis. The fall occurred 1 month before presentation. On examination, the patient demonstrated 4/5 strength in his right upper extremity, with no additional neurologic deficits. Noncontrast head CT demonstrated bilateral mixed density convexity subdural hematomas [22 mm on the left and 14 mm on the right; and ]. The patient underwent a left craniotomy for evacuation of the larger hematoma, in conjunction with bilateral MMA embolization as primary treatment for the right convexity subdural hematoma in addition to limiting potential recurrence along the left convexity. Intraprocedural digital subtraction angiogram revealed two Cognard Grade III DAVFs, one arising from the parietal branch of the right MMA draining into an occipital cortical vein, and the second arising from the temporal branch of the left MMA draining into the vein of Labbe [-]. Given the presence of cortical venous reflux and associated risk of future intracranial hemorrhage, treatment of the fistulae was indicated. This was approached in two staged procedures. Following an uncomplicated left MMA embolization (frontoparietal branch), the incidental findings were discussed with the patient and he underwent a second stage embolization for the DAVF on a later date. During the second stage, a more prolonged infusion of liquid embolic was employed to ensure penetration into the recipient cortical venous outflow, resulting in nonopacification of the aforementioned fistulae. The postoperative course was complicated by seizures which resolved with uptitration in antiepileptic medications. At 6-month follow-up, there was complete resolution of the patient’s presenting symptoms and surveillance CT demonstrated no residual SDH.

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).

A 59-year-old male with a recent fall and closed head injury presented with progressively worsening headaches. The fall occurred 9 days before presentation. On examination, no neurologic deficits were found. Noncontrast head CT demonstrated a 5 mm left convexity CSDH []. He underwent burr hole evacuation and was discharged on the subsequent day. He presented again on postoperative day 6 with recurrence of his headaches. Noncontrast head CT demonstrated recurrence of the left convexity subdural hematoma []. He subsequently underwent a left craniotomy for evacuation. He was discharged on postoperative day 2 with no postprocedural complications. At 1-month follow-up, he continued to complain of severe headaches. Surveillance CT demonstrated a new 27 mm right convexity mixed density subdural hematoma [ and ]. He subsequently underwent right MMA embolization as primary treatment. Intraprocedural digital subtraction angiogram revealed a Cognard Grade III cribriform plate DAVF supplied by the right ophthalmic artery draining into a right frontal cortical vein [ and ]. The right MMA temporoparietal and frontal branches were embolized with n-BCA glue. Follow-up was arranged to treat the DAVF at a later date and he was discharged the following day. The patient was subsequently lost to follow-up, but presented to the emergency department 4 months later with diplopia and a right abducens nerve palsy. Noncontrast head CT demonstrated significant reduction in size of the previously embolized right convexity subdural hematoma. He was admitted and underwent attempted endovascular treatment of the DAVF. Catheterization of the arterial and venous sides of the fistula achieved suboptimal positioning for liquid embolic embolization and so he underwent a right craniotomy for surgical ligation of the fistula. The patient experienced no postprocedural complications. At 2-week follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 59-year-old male with a recent fall and closed head injury presented with progressively worsening headaches. The fall occurred 9 days before presentation. On examination, no neurologic deficits were found. Noncontrast head CT demonstrated a 5 mm left convexity CSDH []. He underwent burr hole evacuation and was discharged on the subsequent day. He presented again on postoperative day 6 with recurrence of his headaches. Noncontrast head CT demonstrated recurrence of the left convexity subdural hematoma []. He subsequently underwent a left craniotomy for evacuation. He was discharged on postoperative day 2 with no postprocedural complications. At 1-month follow-up, he continued to complain of severe headaches. Surveillance CT demonstrated a new 27 mm right convexity mixed density subdural hematoma [ and ]. He subsequently underwent right MMA embolization as primary treatment. Intraprocedural digital subtraction angiogram revealed a Cognard Grade III cribriform plate DAVF supplied by the right ophthalmic artery draining into a right frontal cortical vein [ and ]. The right MMA temporoparietal and frontal branches were embolized with n-BCA glue. Follow-up was arranged to treat the DAVF at a later date and he was discharged the following day. The patient was subsequently lost to follow-up, but presented to the emergency department 4 months later with diplopia and a right abducens nerve palsy. Noncontrast head CT demonstrated significant reduction in size of the previously embolized right convexity subdural hematoma. He was admitted and underwent attempted endovascular treatment of the DAVF. Catheterization of the arterial and venous sides of the fistula achieved suboptimal positioning for liquid embolic embolization and so he underwent a right craniotomy for surgical ligation of the fistula. The patient experienced no postprocedural complications. At 2-week follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 59-year-old male with a recent fall and closed head injury presented with progressively worsening headaches. The fall occurred 9 days before presentation. On examination, no neurologic deficits were found. Noncontrast head CT demonstrated a 5 mm left convexity CSDH []. He underwent burr hole evacuation and was discharged on the subsequent day. He presented again on postoperative day 6 with recurrence of his headaches. Noncontrast head CT demonstrated recurrence of the left convexity subdural hematoma []. He subsequently underwent a left craniotomy for evacuation. He was discharged on postoperative day 2 with no postprocedural complications. At 1-month follow-up, he continued to complain of severe headaches. Surveillance CT demonstrated a new 27 mm right convexity mixed density subdural hematoma [ and ]. He subsequently underwent right MMA embolization as primary treatment. Intraprocedural digital subtraction angiogram revealed a Cognard Grade III cribriform plate DAVF supplied by the right ophthalmic artery draining into a right frontal cortical vein [ and ]. The right MMA temporoparietal and frontal branches were embolized with n-BCA glue. Follow-up was arranged to treat the DAVF at a later date and he was discharged the following day. The patient was subsequently lost to follow-up, but presented to the emergency department 4 months later with diplopia and a right abducens nerve palsy. Noncontrast head CT demonstrated significant reduction in size of the previously embolized right convexity subdural hematoma. He was admitted and underwent attempted endovascular treatment of the DAVF. Catheterization of the arterial and venous sides of the fistula achieved suboptimal positioning for liquid embolic embolization and so he underwent a right craniotomy for surgical ligation of the fistula. The patient experienced no postprocedural complications. At 2-week follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).

A 59-year-old male patient suffered from rapidly progressive and pulsatile headache over the right parietal region characterized as thunderclap and nausea. He had no fever. These symptoms were followed by generalized seizure. Neurological examination showed a normal level of consciousness. On examination, meningism was seen. The rest of the physical examination was unremarkable. CT scan head was normal. MRI revealed right parasagittal high fronto-parietal subarachnoid hemorrhage with mild gyral edema. MRV showed superior sagittal sinus and bilateral transverse sinus thrombosis [Figures and ]. DSA confirmed [Figures and ] the diagnosis of DST without any potential cause of SAH. Coagulation testing, including prothrombin time, activated prothrombin time, anticardiolipin antibody titer, antiphospholipid antibody titer, homocysteine titer, and levels of protein C and S, antithrombin III, and fibrinogen were all within normal limits and done simultaneously with MRI, MR Venography, DSA within one to two days of admission. Subcutaneous LMW heparin therapy was given. The patient's condition stabilized after nine days of treatment. Oral warfarin maintained an INR of 2.0-3.0. Patient's improvement was clinically satisfactory within six weeks, Repeat DSA done after six weeks was normal, except minimal filling defect. Patient was followed up at two-weeks intervals for three months

Write a detailed clinical case vignette based on the following key phrases: Subdural Hematoma, Cerebral Venous Thrombosis, Dural Arteriovenous Fistula

A 52-year-old woman presented at our hospital with heat intolerance, palpitation, and chest discomfort persisting for 2 months. Physical examination revealed thyroid gland enlargement but no exophthalmos. Thyroid function test indicated hyperthyroidism with thyroid stimulating hormone (TSH) <0.05 µIU/mL (normal range, 0.4 to 4.1), free thyroxine (free T4) 5.71 ng/dL (normal range, 0.70 to 1.80), and triiodothyronine (T3) 375 ng/dL (normal range, 87 to 184). The level of thyroid stimulating immunoglobulin was 60.8% (normal range, 0 to 15). A thyroid scan demonstrated an increase of 20-minute thyroid uptake of 99mTc. A diagnosis of Graves' disease was made and the patient was started on methimazole 30 mg/day. Four weeks after beginning methimazole treatment, she suffered general weakness and sweating that disappeared with food intake. The patient visited the emergency room because of confusion, irritability, and inappropriate verbal responses. She had no history of diabetes mellitus or exposure to insulin or oral antidiabetic agents. The patient's younger brother had a medical history of hyperthyroidism; however, there was no family history of diabetes mellitus. The patient's initial serum glucose level was 34 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. Thyroid function study revealed TSH <0.05 µIU/mL, free T4 0.77 ng/dL, and T3 146 ng/dL. Hemoglobin A1c (HbA1c) was 5.8%. The total serum insulin concentration was 119 µIU/mL (normal range, 2 to 25) and serum C-peptide was 14.7 ng/mL (normal range, 0.8 to 4.0). Insulin autoantibody was measured by radioimmunoassay at 84.7% (normal range, 0 to 7). Percent 125I-insulin binding was not measured. A computed tomography (CT) scan revealed a small cyst of the pancreas tail, which had no contrast enhancement. There was no evidence of insulinoma or extrapancreatic neoplasm. The result of 75-g oral glucose tolerance test showed an abnormal increase of total serum insulin levels with delayed hypoglycemia developing after 240 minutes with symptoms of sweating and dizziness (). A diagnosis of methimazole-induced insulin autoimmune syndrome was made based on the high serum concentration of total insulin, fasting hypoglycemia, and the presence of insulin autoantibodies. Methimazole was discontinued, and consumption of six or more small meals throughout the day with low carbohydrate was recommended. Hypoglycemic attacks subsided within 1 week and there were no further hypoglycemic episodes after discharge. Total serum insulin, titer of insulin autoantibody, and level of serum C-peptide decreased gradually after 5 months (). Treatment with 131I 20 mCi was performed to address Graves' disease in the patient.

This patient was a 71-year-old man who was admitted because of polydipsia and polyuria that had persisted for 8 years, as well as recurrent episodes of unconsciousness throughout this period. He was diagnosed with type 2 diabetes mellitus 8 years before admission. Acarbose was initially prescribed, but was switched to insulin aspart 30 (8–12 units twice a day) because of poor glucose control 5 years previously. Three months previously, the dose of insulin aspart 30 was gradually reduced to 4–10 units because of hypoglycemia. However, he had unexpected episodes of unconsciousness due to hypoglycemia 12 days before admission. Moreover, his symptoms were obviously relieved after food intake. He was subsequently treated with voglibose instead of insulin injections. However, the hypoglycemic symptoms continued to appear between 02:00 am and 03:00 am, despite the absence of other treatments. A laboratory examination showed the following: C-peptide values were 15.22/17.59/19.73/15.22 nmol/L at 0/1/2/3 h, and insulin concentrations were > 2089.5/> 2089.5/> 2089.5/> 2089.5 pmol/L at 0/1/2/3 h during the OGTT, respectively. The anti-insulin antibody test was also positive. His treatment regimen was changed to prednisone (5 mg three times a day), acarbose (50 mg three times a day), metformin (0.5 g twice a day), and glargine (12–18 units twice a day) for glucose control. Insulin injections were also gradually discontinued. Following this treatment, he showed improved glucose control. Laboratory tests during a recent follow-up showed the following: C-peptide levels of 0.77/2.40 nmol/L at 0/2 h and insulin levels of 430.13/1350.21 pmol/L at 0/2 h during the OGTT, respectively.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

A 52-year-old woman presented at our hospital with heat intolerance, palpitation, and chest discomfort persisting for 2 months. Physical examination revealed thyroid gland enlargement but no exophthalmos. Thyroid function test indicated hyperthyroidism with thyroid stimulating hormone (TSH) <0.05 µIU/mL (normal range, 0.4 to 4.1), free thyroxine (free T4) 5.71 ng/dL (normal range, 0.70 to 1.80), and triiodothyronine (T3) 375 ng/dL (normal range, 87 to 184). The level of thyroid stimulating immunoglobulin was 60.8% (normal range, 0 to 15). A thyroid scan demonstrated an increase of 20-minute thyroid uptake of 99mTc. A diagnosis of Graves' disease was made and the patient was started on methimazole 30 mg/day. Four weeks after beginning methimazole treatment, she suffered general weakness and sweating that disappeared with food intake. The patient visited the emergency room because of confusion, irritability, and inappropriate verbal responses. She had no history of diabetes mellitus or exposure to insulin or oral antidiabetic agents. The patient's younger brother had a medical history of hyperthyroidism; however, there was no family history of diabetes mellitus. The patient's initial serum glucose level was 34 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. Thyroid function study revealed TSH <0.05 µIU/mL, free T4 0.77 ng/dL, and T3 146 ng/dL. Hemoglobin A1c (HbA1c) was 5.8%. The total serum insulin concentration was 119 µIU/mL (normal range, 2 to 25) and serum C-peptide was 14.7 ng/mL (normal range, 0.8 to 4.0). Insulin autoantibody was measured by radioimmunoassay at 84.7% (normal range, 0 to 7). Percent 125I-insulin binding was not measured. A computed tomography (CT) scan revealed a small cyst of the pancreas tail, which had no contrast enhancement. There was no evidence of insulinoma or extrapancreatic neoplasm. The result of 75-g oral glucose tolerance test showed an abnormal increase of total serum insulin levels with delayed hypoglycemia developing after 240 minutes with symptoms of sweating and dizziness (). A diagnosis of methimazole-induced insulin autoimmune syndrome was made based on the high serum concentration of total insulin, fasting hypoglycemia, and the presence of insulin autoantibodies. Methimazole was discontinued, and consumption of six or more small meals throughout the day with low carbohydrate was recommended. Hypoglycemic attacks subsided within 1 week and there were no further hypoglycemic episodes after discharge. Total serum insulin, titer of insulin autoantibody, and level of serum C-peptide decreased gradually after 5 months (). Treatment with 131I 20 mCi was performed to address Graves' disease in the patient.

This patient was a 52-year-old man diagnosed with type 2 diabetes mellitus at the local hospital according to a fasting glucose test that showed a concentration of 16 mmol/L. His postprandial glucose concentration was 27 mmol/L. However, the patient was asymptomatic. He was then treated with a 50/50 Mixture Recombinant Human Insulin Injection (Gansulin 50R) of 12–16 units twice a day, and the dose had been adjusted to 6–10 units 2 months previously. During this period, his glucose was well controlled. One month previously, he developed dizziness and was flustered again. He also started sweating excessively, and at that time, his fasting plasma glucose concentration was 2.8 mmol/L. One week previously, the treatment was changed to acarbose 0.1 mg three times a day because of repeated occurrence of hypoglycemic symptoms. His insulin concentrations were 1294.01/1303.77/1456.7/2057.11/2032.41 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 1.30/1.80/2.21/2.87/2.55 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. The anti-insulin antibody test was positive. He was prescribed metformin (0.5 g twice a day), acarbose (0.05 g three times a day), aspart (6–5-5 units three times a day), and methylprednisolone (4 mg three times a day) for glucose control. After these changes, hypoglycemia syndrome did not recur (Table ).

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

A 52-year-old woman presented at our hospital with heat intolerance, palpitation, and chest discomfort persisting for 2 months. Physical examination revealed thyroid gland enlargement but no exophthalmos. Thyroid function test indicated hyperthyroidism with thyroid stimulating hormone (TSH) <0.05 µIU/mL (normal range, 0.4 to 4.1), free thyroxine (free T4) 5.71 ng/dL (normal range, 0.70 to 1.80), and triiodothyronine (T3) 375 ng/dL (normal range, 87 to 184). The level of thyroid stimulating immunoglobulin was 60.8% (normal range, 0 to 15). A thyroid scan demonstrated an increase of 20-minute thyroid uptake of 99mTc. A diagnosis of Graves' disease was made and the patient was started on methimazole 30 mg/day. Four weeks after beginning methimazole treatment, she suffered general weakness and sweating that disappeared with food intake. The patient visited the emergency room because of confusion, irritability, and inappropriate verbal responses. She had no history of diabetes mellitus or exposure to insulin or oral antidiabetic agents. The patient's younger brother had a medical history of hyperthyroidism; however, there was no family history of diabetes mellitus. The patient's initial serum glucose level was 34 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. Thyroid function study revealed TSH <0.05 µIU/mL, free T4 0.77 ng/dL, and T3 146 ng/dL. Hemoglobin A1c (HbA1c) was 5.8%. The total serum insulin concentration was 119 µIU/mL (normal range, 2 to 25) and serum C-peptide was 14.7 ng/mL (normal range, 0.8 to 4.0). Insulin autoantibody was measured by radioimmunoassay at 84.7% (normal range, 0 to 7). Percent 125I-insulin binding was not measured. A computed tomography (CT) scan revealed a small cyst of the pancreas tail, which had no contrast enhancement. There was no evidence of insulinoma or extrapancreatic neoplasm. The result of 75-g oral glucose tolerance test showed an abnormal increase of total serum insulin levels with delayed hypoglycemia developing after 240 minutes with symptoms of sweating and dizziness (). A diagnosis of methimazole-induced insulin autoimmune syndrome was made based on the high serum concentration of total insulin, fasting hypoglycemia, and the presence of insulin autoantibodies. Methimazole was discontinued, and consumption of six or more small meals throughout the day with low carbohydrate was recommended. Hypoglycemic attacks subsided within 1 week and there were no further hypoglycemic episodes after discharge. Total serum insulin, titer of insulin autoantibody, and level of serum C-peptide decreased gradually after 5 months (). Treatment with 131I 20 mCi was performed to address Graves' disease in the patient.

This patient was a 79-year-old man who had a 10-year history of hyperglycemia in addition to fluctuating glucose concentrations for more than 1 year. This was accompanied by diabetic nephropathy as well as a history of gout for more than 30 years. His glucose concentrations were initially well controlled with metformin after diagnosis of type 2 diabetes mellitus. A subcutaneous insulin pump (lispro) was recently added to his treatment regimen for renal insufficiency, and metformin was gradually changed to Humulin R (6–4-4 units, three times a day) combined with glargine 12 units a day. Thereafter, he had recurrent midnight hypoglycemia and daytime hyperglycemia, with blood glucose concentrations up to 20 mmol/L. Therefore, he was treated with acarbose (50 mg three times a day) instead of insulin injections. At this time, his C-peptide values were 5.45/6.94/6.94/7.89/7.17 nmol/L at 0/0.5/1/2/3 h, respectively (normal range: 0.27–1.28 nmol/L). His insulin concentrations were > 1000.00/> 1000.00 pmol/L at 0/2 h, respectively (normal range: 13–161 pmol/L), during an oral glucose tolerance test (OGTT), his HbA1c concentration was 10.2%, and an anti-insulin antibody test was positive (reference level: < 0.4). His glucose concentrations still fluctuated between 11 mmol/L and 22 mmol/L in the daytime, while hypoglycemia occurred at night. Subsequently, acarbose (100–100-50 mg three times a day) and sitagliptin (50 mg per day) were prescribed for symptom management, and his glucose concentrations returned to the normal range. Laboratory findings at a 1-year follow-up showed an HbA1c concentration of 7.0%, insulin concentrations of 138.53/733.40 pmol/L at 0/2 h, and C-peptide concentrations of 1.35/2.21 nmol/L at 0/2 h, respectively.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

A 52-year-old woman presented at our hospital with heat intolerance, palpitation, and chest discomfort persisting for 2 months. Physical examination revealed thyroid gland enlargement but no exophthalmos. Thyroid function test indicated hyperthyroidism with thyroid stimulating hormone (TSH) <0.05 µIU/mL (normal range, 0.4 to 4.1), free thyroxine (free T4) 5.71 ng/dL (normal range, 0.70 to 1.80), and triiodothyronine (T3) 375 ng/dL (normal range, 87 to 184). The level of thyroid stimulating immunoglobulin was 60.8% (normal range, 0 to 15). A thyroid scan demonstrated an increase of 20-minute thyroid uptake of 99mTc. A diagnosis of Graves' disease was made and the patient was started on methimazole 30 mg/day. Four weeks after beginning methimazole treatment, she suffered general weakness and sweating that disappeared with food intake. The patient visited the emergency room because of confusion, irritability, and inappropriate verbal responses. She had no history of diabetes mellitus or exposure to insulin or oral antidiabetic agents. The patient's younger brother had a medical history of hyperthyroidism; however, there was no family history of diabetes mellitus. The patient's initial serum glucose level was 34 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. Thyroid function study revealed TSH <0.05 µIU/mL, free T4 0.77 ng/dL, and T3 146 ng/dL. Hemoglobin A1c (HbA1c) was 5.8%. The total serum insulin concentration was 119 µIU/mL (normal range, 2 to 25) and serum C-peptide was 14.7 ng/mL (normal range, 0.8 to 4.0). Insulin autoantibody was measured by radioimmunoassay at 84.7% (normal range, 0 to 7). Percent 125I-insulin binding was not measured. A computed tomography (CT) scan revealed a small cyst of the pancreas tail, which had no contrast enhancement. There was no evidence of insulinoma or extrapancreatic neoplasm. The result of 75-g oral glucose tolerance test showed an abnormal increase of total serum insulin levels with delayed hypoglycemia developing after 240 minutes with symptoms of sweating and dizziness (). A diagnosis of methimazole-induced insulin autoimmune syndrome was made based on the high serum concentration of total insulin, fasting hypoglycemia, and the presence of insulin autoantibodies. Methimazole was discontinued, and consumption of six or more small meals throughout the day with low carbohydrate was recommended. Hypoglycemic attacks subsided within 1 week and there were no further hypoglycemic episodes after discharge. Total serum insulin, titer of insulin autoantibody, and level of serum C-peptide decreased gradually after 5 months (). Treatment with 131I 20 mCi was performed to address Graves' disease in the patient.

A 53-year-old woman visited the emergency room of our hospital complaining of headache, palpitation, and chest discomfort. She was diagnosed with Graves' disease at a different hospital 1 month prior to being admitted at our hospital and had been taking both methimazole 40 mg/day and β-blocker since her diagnosis. Prior to visiting our emergency room, she consumed breakfast and was measured with a serum glucose level of 294 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. The result of thyroid function tests were TSH <0.01 µIU/mL, free T4 2.74 ng/dL, and T3 184.8 ng/dL. The patient's symptoms were initially attributed to hyperthyroidism due to the lack of abnormal findings on neurologic exam and brain magnetic resonance imaging. However, 6 hours after discharge, the patient revisited our emergency room due to sweating and altered mental state, where it was noted that she had neither a history of diabetes mellitus nor previous exposure to insulin or oral antidiabetic agents. Furthermore, there was no family history of thyroid disease and diabetes mellitus. The patient's initial serum glucose level was 27 mg/dL, HbA1c was 5.8%, serum total insulin was 600 µIU/mL, and serum C-peptide was 15.3 ng/mL. The titer of insulin autoantibody was 84.8%, while detection of both insulin receptor antibody and islet cell antibody were negative. The percent of 125I-insulin binding was not measured. The titers of serum thyroid autoantibodies were high. Specifically, antithyroid peroxidase antibody was 2,876 U/mL (normal range, 0 to 100), antithyroglobulin antibody was 330 IU/mL (normal range, 0 to 115), and TSH receptor antibody was 2.95 IU/L (normal range, <1.22). A CT scan revealed no evidence of insulinoma or extrapancreatic neoplasm. The patient's fasting insulin level was more than 3,000 µIU/mL and C-peptide was 25.9 ng/mL on hospital day 7. A 75-g oral glucose tolerance test showed marked increase of total insulin level and subsequent hypoglycemia developed after 240 minutes (). HLA genotyping was performed by sequence based typing and the result was HLA-DRB1*0406 and *1501. Continuous intravenous glucose injection was needed due to recurrent fasting hypoglycemia. Methimazole-induced insulin autoimmune syndrome was diagnosed, and methimazole was subsequently discontinued. Hypoglycemic episodes disappeared after 1 month, with the patient consuming small frequent meals and a low carbohydrate diet. The concentration of serum total insulin, titer of insulin autoantibody, and serum C-peptide level decreased gradually after 5 months (). Radioactive iodine therapy with 131I 15 mCi was performed to address Graves' disease in the patient.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

A 52-year-old woman presented at our hospital with heat intolerance, palpitation, and chest discomfort persisting for 2 months. Physical examination revealed thyroid gland enlargement but no exophthalmos. Thyroid function test indicated hyperthyroidism with thyroid stimulating hormone (TSH) <0.05 µIU/mL (normal range, 0.4 to 4.1), free thyroxine (free T4) 5.71 ng/dL (normal range, 0.70 to 1.80), and triiodothyronine (T3) 375 ng/dL (normal range, 87 to 184). The level of thyroid stimulating immunoglobulin was 60.8% (normal range, 0 to 15). A thyroid scan demonstrated an increase of 20-minute thyroid uptake of 99mTc. A diagnosis of Graves' disease was made and the patient was started on methimazole 30 mg/day. Four weeks after beginning methimazole treatment, she suffered general weakness and sweating that disappeared with food intake. The patient visited the emergency room because of confusion, irritability, and inappropriate verbal responses. She had no history of diabetes mellitus or exposure to insulin or oral antidiabetic agents. The patient's younger brother had a medical history of hyperthyroidism; however, there was no family history of diabetes mellitus. The patient's initial serum glucose level was 34 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. Thyroid function study revealed TSH <0.05 µIU/mL, free T4 0.77 ng/dL, and T3 146 ng/dL. Hemoglobin A1c (HbA1c) was 5.8%. The total serum insulin concentration was 119 µIU/mL (normal range, 2 to 25) and serum C-peptide was 14.7 ng/mL (normal range, 0.8 to 4.0). Insulin autoantibody was measured by radioimmunoassay at 84.7% (normal range, 0 to 7). Percent 125I-insulin binding was not measured. A computed tomography (CT) scan revealed a small cyst of the pancreas tail, which had no contrast enhancement. There was no evidence of insulinoma or extrapancreatic neoplasm. The result of 75-g oral glucose tolerance test showed an abnormal increase of total serum insulin levels with delayed hypoglycemia developing after 240 minutes with symptoms of sweating and dizziness (). A diagnosis of methimazole-induced insulin autoimmune syndrome was made based on the high serum concentration of total insulin, fasting hypoglycemia, and the presence of insulin autoantibodies. Methimazole was discontinued, and consumption of six or more small meals throughout the day with low carbohydrate was recommended. Hypoglycemic attacks subsided within 1 week and there were no further hypoglycemic episodes after discharge. Total serum insulin, titer of insulin autoantibody, and level of serum C-peptide decreased gradually after 5 months (). Treatment with 131I 20 mCi was performed to address Graves' disease in the patient.

This patient was a 79-year-old man who presented with a 3-year history of hyperglycemia and a 1-year history of polydipsia. At the time of presentation, he had been in a hypodynamic state for 15 days. Three years previously, he was diagnosed with impaired glucose tolerance without any symptoms, but no treatment was provided. One year earlier, he developed polydipsia, hyperuresis, and cutaneous pruritus, and lost weight. His random plasma glucose concentrations increased to as high as 20 mmol/L. Consequently, he was started on aspart 30 (21 units before breakfast and 8 units before dinner) and metformin (0.5 g twice a day). One month previously, he visited our hospital because of complaints of recurrent midnight hypoglycemia, particularly at approximately 02:00 am. During that period, although an insulin injection was gradually reduced and subsequently discontinued, his glucose concentration still dropped to 3 mmol/L. Laboratory tests showed that C-peptide and insulin concentrations were above the normal range, and the insulin autoantibody test was positive. At that time, non-classical IAS was considered as the probable cause of repeated hypoglycemia, and treatment was changed to acarbose (50 mg three times a day). After 15 days, blood tests showed the following: fasting plasma glucose level, 3.71 mmol/L; anti-insulin antibody, > 45.4 U/mL; and insulin concentrations were 1567.44/1493.06/1370.20/1616.43/1812.01 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 3.41/3.68/3.95/4.56/4.51 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. For treatment of IAS, prednisone therapy was started at 12 mg daily (4 mg per dose three time daily) then reduced to 8 mg daily after 2 weeks and to 4 mg per night 1 week later. The diabetes treatment plan was changed to human biosynthetic insulin injection (16 units per day), sitagliptin (50 mg per day), and voglibose (0.3–0.2 mg twice a day). Repeated laboratory tests showed the following: C-peptide concentrations were 0.73/1.67 nmol/L at 0/2 h, respectively, and the insulin concentration was 728.14 pmol/L at 0 h during the OGTT. The glucose concentration fluctuated between 7 and 12.9 mmol/L.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 71-year-old man who was admitted because of polydipsia and polyuria that had persisted for 8 years, as well as recurrent episodes of unconsciousness throughout this period. He was diagnosed with type 2 diabetes mellitus 8 years before admission. Acarbose was initially prescribed, but was switched to insulin aspart 30 (8–12 units twice a day) because of poor glucose control 5 years previously. Three months previously, the dose of insulin aspart 30 was gradually reduced to 4–10 units because of hypoglycemia. However, he had unexpected episodes of unconsciousness due to hypoglycemia 12 days before admission. Moreover, his symptoms were obviously relieved after food intake. He was subsequently treated with voglibose instead of insulin injections. However, the hypoglycemic symptoms continued to appear between 02:00 am and 03:00 am, despite the absence of other treatments. A laboratory examination showed the following: C-peptide values were 15.22/17.59/19.73/15.22 nmol/L at 0/1/2/3 h, and insulin concentrations were > 2089.5/> 2089.5/> 2089.5/> 2089.5 pmol/L at 0/1/2/3 h during the OGTT, respectively. The anti-insulin antibody test was also positive. His treatment regimen was changed to prednisone (5 mg three times a day), acarbose (50 mg three times a day), metformin (0.5 g twice a day), and glargine (12–18 units twice a day) for glucose control. Insulin injections were also gradually discontinued. Following this treatment, he showed improved glucose control. Laboratory tests during a recent follow-up showed the following: C-peptide levels of 0.77/2.40 nmol/L at 0/2 h and insulin levels of 430.13/1350.21 pmol/L at 0/2 h during the OGTT, respectively.

This patient was a 52-year-old man diagnosed with type 2 diabetes mellitus at the local hospital according to a fasting glucose test that showed a concentration of 16 mmol/L. His postprandial glucose concentration was 27 mmol/L. However, the patient was asymptomatic. He was then treated with a 50/50 Mixture Recombinant Human Insulin Injection (Gansulin 50R) of 12–16 units twice a day, and the dose had been adjusted to 6–10 units 2 months previously. During this period, his glucose was well controlled. One month previously, he developed dizziness and was flustered again. He also started sweating excessively, and at that time, his fasting plasma glucose concentration was 2.8 mmol/L. One week previously, the treatment was changed to acarbose 0.1 mg three times a day because of repeated occurrence of hypoglycemic symptoms. His insulin concentrations were 1294.01/1303.77/1456.7/2057.11/2032.41 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 1.30/1.80/2.21/2.87/2.55 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. The anti-insulin antibody test was positive. He was prescribed metformin (0.5 g twice a day), acarbose (0.05 g three times a day), aspart (6–5-5 units three times a day), and methylprednisolone (4 mg three times a day) for glucose control. After these changes, hypoglycemia syndrome did not recur (Table ).

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 71-year-old man who was admitted because of polydipsia and polyuria that had persisted for 8 years, as well as recurrent episodes of unconsciousness throughout this period. He was diagnosed with type 2 diabetes mellitus 8 years before admission. Acarbose was initially prescribed, but was switched to insulin aspart 30 (8–12 units twice a day) because of poor glucose control 5 years previously. Three months previously, the dose of insulin aspart 30 was gradually reduced to 4–10 units because of hypoglycemia. However, he had unexpected episodes of unconsciousness due to hypoglycemia 12 days before admission. Moreover, his symptoms were obviously relieved after food intake. He was subsequently treated with voglibose instead of insulin injections. However, the hypoglycemic symptoms continued to appear between 02:00 am and 03:00 am, despite the absence of other treatments. A laboratory examination showed the following: C-peptide values were 15.22/17.59/19.73/15.22 nmol/L at 0/1/2/3 h, and insulin concentrations were > 2089.5/> 2089.5/> 2089.5/> 2089.5 pmol/L at 0/1/2/3 h during the OGTT, respectively. The anti-insulin antibody test was also positive. His treatment regimen was changed to prednisone (5 mg three times a day), acarbose (50 mg three times a day), metformin (0.5 g twice a day), and glargine (12–18 units twice a day) for glucose control. Insulin injections were also gradually discontinued. Following this treatment, he showed improved glucose control. Laboratory tests during a recent follow-up showed the following: C-peptide levels of 0.77/2.40 nmol/L at 0/2 h and insulin levels of 430.13/1350.21 pmol/L at 0/2 h during the OGTT, respectively.

This patient was a 79-year-old man who had a 10-year history of hyperglycemia in addition to fluctuating glucose concentrations for more than 1 year. This was accompanied by diabetic nephropathy as well as a history of gout for more than 30 years. His glucose concentrations were initially well controlled with metformin after diagnosis of type 2 diabetes mellitus. A subcutaneous insulin pump (lispro) was recently added to his treatment regimen for renal insufficiency, and metformin was gradually changed to Humulin R (6–4-4 units, three times a day) combined with glargine 12 units a day. Thereafter, he had recurrent midnight hypoglycemia and daytime hyperglycemia, with blood glucose concentrations up to 20 mmol/L. Therefore, he was treated with acarbose (50 mg three times a day) instead of insulin injections. At this time, his C-peptide values were 5.45/6.94/6.94/7.89/7.17 nmol/L at 0/0.5/1/2/3 h, respectively (normal range: 0.27–1.28 nmol/L). His insulin concentrations were > 1000.00/> 1000.00 pmol/L at 0/2 h, respectively (normal range: 13–161 pmol/L), during an oral glucose tolerance test (OGTT), his HbA1c concentration was 10.2%, and an anti-insulin antibody test was positive (reference level: < 0.4). His glucose concentrations still fluctuated between 11 mmol/L and 22 mmol/L in the daytime, while hypoglycemia occurred at night. Subsequently, acarbose (100–100-50 mg three times a day) and sitagliptin (50 mg per day) were prescribed for symptom management, and his glucose concentrations returned to the normal range. Laboratory findings at a 1-year follow-up showed an HbA1c concentration of 7.0%, insulin concentrations of 138.53/733.40 pmol/L at 0/2 h, and C-peptide concentrations of 1.35/2.21 nmol/L at 0/2 h, respectively.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 71-year-old man who was admitted because of polydipsia and polyuria that had persisted for 8 years, as well as recurrent episodes of unconsciousness throughout this period. He was diagnosed with type 2 diabetes mellitus 8 years before admission. Acarbose was initially prescribed, but was switched to insulin aspart 30 (8–12 units twice a day) because of poor glucose control 5 years previously. Three months previously, the dose of insulin aspart 30 was gradually reduced to 4–10 units because of hypoglycemia. However, he had unexpected episodes of unconsciousness due to hypoglycemia 12 days before admission. Moreover, his symptoms were obviously relieved after food intake. He was subsequently treated with voglibose instead of insulin injections. However, the hypoglycemic symptoms continued to appear between 02:00 am and 03:00 am, despite the absence of other treatments. A laboratory examination showed the following: C-peptide values were 15.22/17.59/19.73/15.22 nmol/L at 0/1/2/3 h, and insulin concentrations were > 2089.5/> 2089.5/> 2089.5/> 2089.5 pmol/L at 0/1/2/3 h during the OGTT, respectively. The anti-insulin antibody test was also positive. His treatment regimen was changed to prednisone (5 mg three times a day), acarbose (50 mg three times a day), metformin (0.5 g twice a day), and glargine (12–18 units twice a day) for glucose control. Insulin injections were also gradually discontinued. Following this treatment, he showed improved glucose control. Laboratory tests during a recent follow-up showed the following: C-peptide levels of 0.77/2.40 nmol/L at 0/2 h and insulin levels of 430.13/1350.21 pmol/L at 0/2 h during the OGTT, respectively.

A 53-year-old woman visited the emergency room of our hospital complaining of headache, palpitation, and chest discomfort. She was diagnosed with Graves' disease at a different hospital 1 month prior to being admitted at our hospital and had been taking both methimazole 40 mg/day and β-blocker since her diagnosis. Prior to visiting our emergency room, she consumed breakfast and was measured with a serum glucose level of 294 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. The result of thyroid function tests were TSH <0.01 µIU/mL, free T4 2.74 ng/dL, and T3 184.8 ng/dL. The patient's symptoms were initially attributed to hyperthyroidism due to the lack of abnormal findings on neurologic exam and brain magnetic resonance imaging. However, 6 hours after discharge, the patient revisited our emergency room due to sweating and altered mental state, where it was noted that she had neither a history of diabetes mellitus nor previous exposure to insulin or oral antidiabetic agents. Furthermore, there was no family history of thyroid disease and diabetes mellitus. The patient's initial serum glucose level was 27 mg/dL, HbA1c was 5.8%, serum total insulin was 600 µIU/mL, and serum C-peptide was 15.3 ng/mL. The titer of insulin autoantibody was 84.8%, while detection of both insulin receptor antibody and islet cell antibody were negative. The percent of 125I-insulin binding was not measured. The titers of serum thyroid autoantibodies were high. Specifically, antithyroid peroxidase antibody was 2,876 U/mL (normal range, 0 to 100), antithyroglobulin antibody was 330 IU/mL (normal range, 0 to 115), and TSH receptor antibody was 2.95 IU/L (normal range, <1.22). A CT scan revealed no evidence of insulinoma or extrapancreatic neoplasm. The patient's fasting insulin level was more than 3,000 µIU/mL and C-peptide was 25.9 ng/mL on hospital day 7. A 75-g oral glucose tolerance test showed marked increase of total insulin level and subsequent hypoglycemia developed after 240 minutes (). HLA genotyping was performed by sequence based typing and the result was HLA-DRB1*0406 and *1501. Continuous intravenous glucose injection was needed due to recurrent fasting hypoglycemia. Methimazole-induced insulin autoimmune syndrome was diagnosed, and methimazole was subsequently discontinued. Hypoglycemic episodes disappeared after 1 month, with the patient consuming small frequent meals and a low carbohydrate diet. The concentration of serum total insulin, titer of insulin autoantibody, and serum C-peptide level decreased gradually after 5 months (). Radioactive iodine therapy with 131I 15 mCi was performed to address Graves' disease in the patient.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 71-year-old man who was admitted because of polydipsia and polyuria that had persisted for 8 years, as well as recurrent episodes of unconsciousness throughout this period. He was diagnosed with type 2 diabetes mellitus 8 years before admission. Acarbose was initially prescribed, but was switched to insulin aspart 30 (8–12 units twice a day) because of poor glucose control 5 years previously. Three months previously, the dose of insulin aspart 30 was gradually reduced to 4–10 units because of hypoglycemia. However, he had unexpected episodes of unconsciousness due to hypoglycemia 12 days before admission. Moreover, his symptoms were obviously relieved after food intake. He was subsequently treated with voglibose instead of insulin injections. However, the hypoglycemic symptoms continued to appear between 02:00 am and 03:00 am, despite the absence of other treatments. A laboratory examination showed the following: C-peptide values were 15.22/17.59/19.73/15.22 nmol/L at 0/1/2/3 h, and insulin concentrations were > 2089.5/> 2089.5/> 2089.5/> 2089.5 pmol/L at 0/1/2/3 h during the OGTT, respectively. The anti-insulin antibody test was also positive. His treatment regimen was changed to prednisone (5 mg three times a day), acarbose (50 mg three times a day), metformin (0.5 g twice a day), and glargine (12–18 units twice a day) for glucose control. Insulin injections were also gradually discontinued. Following this treatment, he showed improved glucose control. Laboratory tests during a recent follow-up showed the following: C-peptide levels of 0.77/2.40 nmol/L at 0/2 h and insulin levels of 430.13/1350.21 pmol/L at 0/2 h during the OGTT, respectively.

This patient was a 79-year-old man who presented with a 3-year history of hyperglycemia and a 1-year history of polydipsia. At the time of presentation, he had been in a hypodynamic state for 15 days. Three years previously, he was diagnosed with impaired glucose tolerance without any symptoms, but no treatment was provided. One year earlier, he developed polydipsia, hyperuresis, and cutaneous pruritus, and lost weight. His random plasma glucose concentrations increased to as high as 20 mmol/L. Consequently, he was started on aspart 30 (21 units before breakfast and 8 units before dinner) and metformin (0.5 g twice a day). One month previously, he visited our hospital because of complaints of recurrent midnight hypoglycemia, particularly at approximately 02:00 am. During that period, although an insulin injection was gradually reduced and subsequently discontinued, his glucose concentration still dropped to 3 mmol/L. Laboratory tests showed that C-peptide and insulin concentrations were above the normal range, and the insulin autoantibody test was positive. At that time, non-classical IAS was considered as the probable cause of repeated hypoglycemia, and treatment was changed to acarbose (50 mg three times a day). After 15 days, blood tests showed the following: fasting plasma glucose level, 3.71 mmol/L; anti-insulin antibody, > 45.4 U/mL; and insulin concentrations were 1567.44/1493.06/1370.20/1616.43/1812.01 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 3.41/3.68/3.95/4.56/4.51 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. For treatment of IAS, prednisone therapy was started at 12 mg daily (4 mg per dose three time daily) then reduced to 8 mg daily after 2 weeks and to 4 mg per night 1 week later. The diabetes treatment plan was changed to human biosynthetic insulin injection (16 units per day), sitagliptin (50 mg per day), and voglibose (0.3–0.2 mg twice a day). Repeated laboratory tests showed the following: C-peptide concentrations were 0.73/1.67 nmol/L at 0/2 h, respectively, and the insulin concentration was 728.14 pmol/L at 0 h during the OGTT. The glucose concentration fluctuated between 7 and 12.9 mmol/L.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 52-year-old man diagnosed with type 2 diabetes mellitus at the local hospital according to a fasting glucose test that showed a concentration of 16 mmol/L. His postprandial glucose concentration was 27 mmol/L. However, the patient was asymptomatic. He was then treated with a 50/50 Mixture Recombinant Human Insulin Injection (Gansulin 50R) of 12–16 units twice a day, and the dose had been adjusted to 6–10 units 2 months previously. During this period, his glucose was well controlled. One month previously, he developed dizziness and was flustered again. He also started sweating excessively, and at that time, his fasting plasma glucose concentration was 2.8 mmol/L. One week previously, the treatment was changed to acarbose 0.1 mg three times a day because of repeated occurrence of hypoglycemic symptoms. His insulin concentrations were 1294.01/1303.77/1456.7/2057.11/2032.41 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 1.30/1.80/2.21/2.87/2.55 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. The anti-insulin antibody test was positive. He was prescribed metformin (0.5 g twice a day), acarbose (0.05 g three times a day), aspart (6–5-5 units three times a day), and methylprednisolone (4 mg three times a day) for glucose control. After these changes, hypoglycemia syndrome did not recur (Table ).

This patient was a 79-year-old man who had a 10-year history of hyperglycemia in addition to fluctuating glucose concentrations for more than 1 year. This was accompanied by diabetic nephropathy as well as a history of gout for more than 30 years. His glucose concentrations were initially well controlled with metformin after diagnosis of type 2 diabetes mellitus. A subcutaneous insulin pump (lispro) was recently added to his treatment regimen for renal insufficiency, and metformin was gradually changed to Humulin R (6–4-4 units, three times a day) combined with glargine 12 units a day. Thereafter, he had recurrent midnight hypoglycemia and daytime hyperglycemia, with blood glucose concentrations up to 20 mmol/L. Therefore, he was treated with acarbose (50 mg three times a day) instead of insulin injections. At this time, his C-peptide values were 5.45/6.94/6.94/7.89/7.17 nmol/L at 0/0.5/1/2/3 h, respectively (normal range: 0.27–1.28 nmol/L). His insulin concentrations were > 1000.00/> 1000.00 pmol/L at 0/2 h, respectively (normal range: 13–161 pmol/L), during an oral glucose tolerance test (OGTT), his HbA1c concentration was 10.2%, and an anti-insulin antibody test was positive (reference level: < 0.4). His glucose concentrations still fluctuated between 11 mmol/L and 22 mmol/L in the daytime, while hypoglycemia occurred at night. Subsequently, acarbose (100–100-50 mg three times a day) and sitagliptin (50 mg per day) were prescribed for symptom management, and his glucose concentrations returned to the normal range. Laboratory findings at a 1-year follow-up showed an HbA1c concentration of 7.0%, insulin concentrations of 138.53/733.40 pmol/L at 0/2 h, and C-peptide concentrations of 1.35/2.21 nmol/L at 0/2 h, respectively.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

A 53-year-old woman visited the emergency room of our hospital complaining of headache, palpitation, and chest discomfort. She was diagnosed with Graves' disease at a different hospital 1 month prior to being admitted at our hospital and had been taking both methimazole 40 mg/day and β-blocker since her diagnosis. Prior to visiting our emergency room, she consumed breakfast and was measured with a serum glucose level of 294 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. The result of thyroid function tests were TSH <0.01 µIU/mL, free T4 2.74 ng/dL, and T3 184.8 ng/dL. The patient's symptoms were initially attributed to hyperthyroidism due to the lack of abnormal findings on neurologic exam and brain magnetic resonance imaging. However, 6 hours after discharge, the patient revisited our emergency room due to sweating and altered mental state, where it was noted that she had neither a history of diabetes mellitus nor previous exposure to insulin or oral antidiabetic agents. Furthermore, there was no family history of thyroid disease and diabetes mellitus. The patient's initial serum glucose level was 27 mg/dL, HbA1c was 5.8%, serum total insulin was 600 µIU/mL, and serum C-peptide was 15.3 ng/mL. The titer of insulin autoantibody was 84.8%, while detection of both insulin receptor antibody and islet cell antibody were negative. The percent of 125I-insulin binding was not measured. The titers of serum thyroid autoantibodies were high. Specifically, antithyroid peroxidase antibody was 2,876 U/mL (normal range, 0 to 100), antithyroglobulin antibody was 330 IU/mL (normal range, 0 to 115), and TSH receptor antibody was 2.95 IU/L (normal range, <1.22). A CT scan revealed no evidence of insulinoma or extrapancreatic neoplasm. The patient's fasting insulin level was more than 3,000 µIU/mL and C-peptide was 25.9 ng/mL on hospital day 7. A 75-g oral glucose tolerance test showed marked increase of total insulin level and subsequent hypoglycemia developed after 240 minutes (). HLA genotyping was performed by sequence based typing and the result was HLA-DRB1*0406 and *1501. Continuous intravenous glucose injection was needed due to recurrent fasting hypoglycemia. Methimazole-induced insulin autoimmune syndrome was diagnosed, and methimazole was subsequently discontinued. Hypoglycemic episodes disappeared after 1 month, with the patient consuming small frequent meals and a low carbohydrate diet. The concentration of serum total insulin, titer of insulin autoantibody, and serum C-peptide level decreased gradually after 5 months (). Radioactive iodine therapy with 131I 15 mCi was performed to address Graves' disease in the patient.

This patient was a 52-year-old man diagnosed with type 2 diabetes mellitus at the local hospital according to a fasting glucose test that showed a concentration of 16 mmol/L. His postprandial glucose concentration was 27 mmol/L. However, the patient was asymptomatic. He was then treated with a 50/50 Mixture Recombinant Human Insulin Injection (Gansulin 50R) of 12–16 units twice a day, and the dose had been adjusted to 6–10 units 2 months previously. During this period, his glucose was well controlled. One month previously, he developed dizziness and was flustered again. He also started sweating excessively, and at that time, his fasting plasma glucose concentration was 2.8 mmol/L. One week previously, the treatment was changed to acarbose 0.1 mg three times a day because of repeated occurrence of hypoglycemic symptoms. His insulin concentrations were 1294.01/1303.77/1456.7/2057.11/2032.41 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 1.30/1.80/2.21/2.87/2.55 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. The anti-insulin antibody test was positive. He was prescribed metformin (0.5 g twice a day), acarbose (0.05 g three times a day), aspart (6–5-5 units three times a day), and methylprednisolone (4 mg three times a day) for glucose control. After these changes, hypoglycemia syndrome did not recur (Table ).

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 52-year-old man diagnosed with type 2 diabetes mellitus at the local hospital according to a fasting glucose test that showed a concentration of 16 mmol/L. His postprandial glucose concentration was 27 mmol/L. However, the patient was asymptomatic. He was then treated with a 50/50 Mixture Recombinant Human Insulin Injection (Gansulin 50R) of 12–16 units twice a day, and the dose had been adjusted to 6–10 units 2 months previously. During this period, his glucose was well controlled. One month previously, he developed dizziness and was flustered again. He also started sweating excessively, and at that time, his fasting plasma glucose concentration was 2.8 mmol/L. One week previously, the treatment was changed to acarbose 0.1 mg three times a day because of repeated occurrence of hypoglycemic symptoms. His insulin concentrations were 1294.01/1303.77/1456.7/2057.11/2032.41 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 1.30/1.80/2.21/2.87/2.55 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. The anti-insulin antibody test was positive. He was prescribed metformin (0.5 g twice a day), acarbose (0.05 g three times a day), aspart (6–5-5 units three times a day), and methylprednisolone (4 mg three times a day) for glucose control. After these changes, hypoglycemia syndrome did not recur (Table ).

This patient was a 79-year-old man who presented with a 3-year history of hyperglycemia and a 1-year history of polydipsia. At the time of presentation, he had been in a hypodynamic state for 15 days. Three years previously, he was diagnosed with impaired glucose tolerance without any symptoms, but no treatment was provided. One year earlier, he developed polydipsia, hyperuresis, and cutaneous pruritus, and lost weight. His random plasma glucose concentrations increased to as high as 20 mmol/L. Consequently, he was started on aspart 30 (21 units before breakfast and 8 units before dinner) and metformin (0.5 g twice a day). One month previously, he visited our hospital because of complaints of recurrent midnight hypoglycemia, particularly at approximately 02:00 am. During that period, although an insulin injection was gradually reduced and subsequently discontinued, his glucose concentration still dropped to 3 mmol/L. Laboratory tests showed that C-peptide and insulin concentrations were above the normal range, and the insulin autoantibody test was positive. At that time, non-classical IAS was considered as the probable cause of repeated hypoglycemia, and treatment was changed to acarbose (50 mg three times a day). After 15 days, blood tests showed the following: fasting plasma glucose level, 3.71 mmol/L; anti-insulin antibody, > 45.4 U/mL; and insulin concentrations were 1567.44/1493.06/1370.20/1616.43/1812.01 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 3.41/3.68/3.95/4.56/4.51 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. For treatment of IAS, prednisone therapy was started at 12 mg daily (4 mg per dose three time daily) then reduced to 8 mg daily after 2 weeks and to 4 mg per night 1 week later. The diabetes treatment plan was changed to human biosynthetic insulin injection (16 units per day), sitagliptin (50 mg per day), and voglibose (0.3–0.2 mg twice a day). Repeated laboratory tests showed the following: C-peptide concentrations were 0.73/1.67 nmol/L at 0/2 h, respectively, and the insulin concentration was 728.14 pmol/L at 0 h during the OGTT. The glucose concentration fluctuated between 7 and 12.9 mmol/L.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 79-year-old man who had a 10-year history of hyperglycemia in addition to fluctuating glucose concentrations for more than 1 year. This was accompanied by diabetic nephropathy as well as a history of gout for more than 30 years. His glucose concentrations were initially well controlled with metformin after diagnosis of type 2 diabetes mellitus. A subcutaneous insulin pump (lispro) was recently added to his treatment regimen for renal insufficiency, and metformin was gradually changed to Humulin R (6–4-4 units, three times a day) combined with glargine 12 units a day. Thereafter, he had recurrent midnight hypoglycemia and daytime hyperglycemia, with blood glucose concentrations up to 20 mmol/L. Therefore, he was treated with acarbose (50 mg three times a day) instead of insulin injections. At this time, his C-peptide values were 5.45/6.94/6.94/7.89/7.17 nmol/L at 0/0.5/1/2/3 h, respectively (normal range: 0.27–1.28 nmol/L). His insulin concentrations were > 1000.00/> 1000.00 pmol/L at 0/2 h, respectively (normal range: 13–161 pmol/L), during an oral glucose tolerance test (OGTT), his HbA1c concentration was 10.2%, and an anti-insulin antibody test was positive (reference level: < 0.4). His glucose concentrations still fluctuated between 11 mmol/L and 22 mmol/L in the daytime, while hypoglycemia occurred at night. Subsequently, acarbose (100–100-50 mg three times a day) and sitagliptin (50 mg per day) were prescribed for symptom management, and his glucose concentrations returned to the normal range. Laboratory findings at a 1-year follow-up showed an HbA1c concentration of 7.0%, insulin concentrations of 138.53/733.40 pmol/L at 0/2 h, and C-peptide concentrations of 1.35/2.21 nmol/L at 0/2 h, respectively.

A 53-year-old woman visited the emergency room of our hospital complaining of headache, palpitation, and chest discomfort. She was diagnosed with Graves' disease at a different hospital 1 month prior to being admitted at our hospital and had been taking both methimazole 40 mg/day and β-blocker since her diagnosis. Prior to visiting our emergency room, she consumed breakfast and was measured with a serum glucose level of 294 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. The result of thyroid function tests were TSH <0.01 µIU/mL, free T4 2.74 ng/dL, and T3 184.8 ng/dL. The patient's symptoms were initially attributed to hyperthyroidism due to the lack of abnormal findings on neurologic exam and brain magnetic resonance imaging. However, 6 hours after discharge, the patient revisited our emergency room due to sweating and altered mental state, where it was noted that she had neither a history of diabetes mellitus nor previous exposure to insulin or oral antidiabetic agents. Furthermore, there was no family history of thyroid disease and diabetes mellitus. The patient's initial serum glucose level was 27 mg/dL, HbA1c was 5.8%, serum total insulin was 600 µIU/mL, and serum C-peptide was 15.3 ng/mL. The titer of insulin autoantibody was 84.8%, while detection of both insulin receptor antibody and islet cell antibody were negative. The percent of 125I-insulin binding was not measured. The titers of serum thyroid autoantibodies were high. Specifically, antithyroid peroxidase antibody was 2,876 U/mL (normal range, 0 to 100), antithyroglobulin antibody was 330 IU/mL (normal range, 0 to 115), and TSH receptor antibody was 2.95 IU/L (normal range, <1.22). A CT scan revealed no evidence of insulinoma or extrapancreatic neoplasm. The patient's fasting insulin level was more than 3,000 µIU/mL and C-peptide was 25.9 ng/mL on hospital day 7. A 75-g oral glucose tolerance test showed marked increase of total insulin level and subsequent hypoglycemia developed after 240 minutes (). HLA genotyping was performed by sequence based typing and the result was HLA-DRB1*0406 and *1501. Continuous intravenous glucose injection was needed due to recurrent fasting hypoglycemia. Methimazole-induced insulin autoimmune syndrome was diagnosed, and methimazole was subsequently discontinued. Hypoglycemic episodes disappeared after 1 month, with the patient consuming small frequent meals and a low carbohydrate diet. The concentration of serum total insulin, titer of insulin autoantibody, and serum C-peptide level decreased gradually after 5 months (). Radioactive iodine therapy with 131I 15 mCi was performed to address Graves' disease in the patient.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

This patient was a 79-year-old man who had a 10-year history of hyperglycemia in addition to fluctuating glucose concentrations for more than 1 year. This was accompanied by diabetic nephropathy as well as a history of gout for more than 30 years. His glucose concentrations were initially well controlled with metformin after diagnosis of type 2 diabetes mellitus. A subcutaneous insulin pump (lispro) was recently added to his treatment regimen for renal insufficiency, and metformin was gradually changed to Humulin R (6–4-4 units, three times a day) combined with glargine 12 units a day. Thereafter, he had recurrent midnight hypoglycemia and daytime hyperglycemia, with blood glucose concentrations up to 20 mmol/L. Therefore, he was treated with acarbose (50 mg three times a day) instead of insulin injections. At this time, his C-peptide values were 5.45/6.94/6.94/7.89/7.17 nmol/L at 0/0.5/1/2/3 h, respectively (normal range: 0.27–1.28 nmol/L). His insulin concentrations were > 1000.00/> 1000.00 pmol/L at 0/2 h, respectively (normal range: 13–161 pmol/L), during an oral glucose tolerance test (OGTT), his HbA1c concentration was 10.2%, and an anti-insulin antibody test was positive (reference level: < 0.4). His glucose concentrations still fluctuated between 11 mmol/L and 22 mmol/L in the daytime, while hypoglycemia occurred at night. Subsequently, acarbose (100–100-50 mg three times a day) and sitagliptin (50 mg per day) were prescribed for symptom management, and his glucose concentrations returned to the normal range. Laboratory findings at a 1-year follow-up showed an HbA1c concentration of 7.0%, insulin concentrations of 138.53/733.40 pmol/L at 0/2 h, and C-peptide concentrations of 1.35/2.21 nmol/L at 0/2 h, respectively.

This patient was a 79-year-old man who presented with a 3-year history of hyperglycemia and a 1-year history of polydipsia. At the time of presentation, he had been in a hypodynamic state for 15 days. Three years previously, he was diagnosed with impaired glucose tolerance without any symptoms, but no treatment was provided. One year earlier, he developed polydipsia, hyperuresis, and cutaneous pruritus, and lost weight. His random plasma glucose concentrations increased to as high as 20 mmol/L. Consequently, he was started on aspart 30 (21 units before breakfast and 8 units before dinner) and metformin (0.5 g twice a day). One month previously, he visited our hospital because of complaints of recurrent midnight hypoglycemia, particularly at approximately 02:00 am. During that period, although an insulin injection was gradually reduced and subsequently discontinued, his glucose concentration still dropped to 3 mmol/L. Laboratory tests showed that C-peptide and insulin concentrations were above the normal range, and the insulin autoantibody test was positive. At that time, non-classical IAS was considered as the probable cause of repeated hypoglycemia, and treatment was changed to acarbose (50 mg three times a day). After 15 days, blood tests showed the following: fasting plasma glucose level, 3.71 mmol/L; anti-insulin antibody, > 45.4 U/mL; and insulin concentrations were 1567.44/1493.06/1370.20/1616.43/1812.01 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 3.41/3.68/3.95/4.56/4.51 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. For treatment of IAS, prednisone therapy was started at 12 mg daily (4 mg per dose three time daily) then reduced to 8 mg daily after 2 weeks and to 4 mg per night 1 week later. The diabetes treatment plan was changed to human biosynthetic insulin injection (16 units per day), sitagliptin (50 mg per day), and voglibose (0.3–0.2 mg twice a day). Repeated laboratory tests showed the following: C-peptide concentrations were 0.73/1.67 nmol/L at 0/2 h, respectively, and the insulin concentration was 728.14 pmol/L at 0 h during the OGTT. The glucose concentration fluctuated between 7 and 12.9 mmol/L.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

A 53-year-old woman visited the emergency room of our hospital complaining of headache, palpitation, and chest discomfort. She was diagnosed with Graves' disease at a different hospital 1 month prior to being admitted at our hospital and had been taking both methimazole 40 mg/day and β-blocker since her diagnosis. Prior to visiting our emergency room, she consumed breakfast and was measured with a serum glucose level of 294 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. The result of thyroid function tests were TSH <0.01 µIU/mL, free T4 2.74 ng/dL, and T3 184.8 ng/dL. The patient's symptoms were initially attributed to hyperthyroidism due to the lack of abnormal findings on neurologic exam and brain magnetic resonance imaging. However, 6 hours after discharge, the patient revisited our emergency room due to sweating and altered mental state, where it was noted that she had neither a history of diabetes mellitus nor previous exposure to insulin or oral antidiabetic agents. Furthermore, there was no family history of thyroid disease and diabetes mellitus. The patient's initial serum glucose level was 27 mg/dL, HbA1c was 5.8%, serum total insulin was 600 µIU/mL, and serum C-peptide was 15.3 ng/mL. The titer of insulin autoantibody was 84.8%, while detection of both insulin receptor antibody and islet cell antibody were negative. The percent of 125I-insulin binding was not measured. The titers of serum thyroid autoantibodies were high. Specifically, antithyroid peroxidase antibody was 2,876 U/mL (normal range, 0 to 100), antithyroglobulin antibody was 330 IU/mL (normal range, 0 to 115), and TSH receptor antibody was 2.95 IU/L (normal range, <1.22). A CT scan revealed no evidence of insulinoma or extrapancreatic neoplasm. The patient's fasting insulin level was more than 3,000 µIU/mL and C-peptide was 25.9 ng/mL on hospital day 7. A 75-g oral glucose tolerance test showed marked increase of total insulin level and subsequent hypoglycemia developed after 240 minutes (). HLA genotyping was performed by sequence based typing and the result was HLA-DRB1*0406 and *1501. Continuous intravenous glucose injection was needed due to recurrent fasting hypoglycemia. Methimazole-induced insulin autoimmune syndrome was diagnosed, and methimazole was subsequently discontinued. Hypoglycemic episodes disappeared after 1 month, with the patient consuming small frequent meals and a low carbohydrate diet. The concentration of serum total insulin, titer of insulin autoantibody, and serum C-peptide level decreased gradually after 5 months (). Radioactive iodine therapy with 131I 15 mCi was performed to address Graves' disease in the patient.

This patient was a 79-year-old man who presented with a 3-year history of hyperglycemia and a 1-year history of polydipsia. At the time of presentation, he had been in a hypodynamic state for 15 days. Three years previously, he was diagnosed with impaired glucose tolerance without any symptoms, but no treatment was provided. One year earlier, he developed polydipsia, hyperuresis, and cutaneous pruritus, and lost weight. His random plasma glucose concentrations increased to as high as 20 mmol/L. Consequently, he was started on aspart 30 (21 units before breakfast and 8 units before dinner) and metformin (0.5 g twice a day). One month previously, he visited our hospital because of complaints of recurrent midnight hypoglycemia, particularly at approximately 02:00 am. During that period, although an insulin injection was gradually reduced and subsequently discontinued, his glucose concentration still dropped to 3 mmol/L. Laboratory tests showed that C-peptide and insulin concentrations were above the normal range, and the insulin autoantibody test was positive. At that time, non-classical IAS was considered as the probable cause of repeated hypoglycemia, and treatment was changed to acarbose (50 mg three times a day). After 15 days, blood tests showed the following: fasting plasma glucose level, 3.71 mmol/L; anti-insulin antibody, > 45.4 U/mL; and insulin concentrations were 1567.44/1493.06/1370.20/1616.43/1812.01 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 3.41/3.68/3.95/4.56/4.51 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. For treatment of IAS, prednisone therapy was started at 12 mg daily (4 mg per dose three time daily) then reduced to 8 mg daily after 2 weeks and to 4 mg per night 1 week later. The diabetes treatment plan was changed to human biosynthetic insulin injection (16 units per day), sitagliptin (50 mg per day), and voglibose (0.3–0.2 mg twice a day). Repeated laboratory tests showed the following: C-peptide concentrations were 0.73/1.67 nmol/L at 0/2 h, respectively, and the insulin concentration was 728.14 pmol/L at 0 h during the OGTT. The glucose concentration fluctuated between 7 and 12.9 mmol/L.

Write a detailed clinical case vignette based on the following key phrases: Insulin Autoantibody, Hypoglycemia, Autoimmune Syndrome

A 27-year-old, nulliparous (0-0-0-0), married woman was referred to our institution with a huge pelvic mass and left flank pain. She had no history of surgical or medical disease. Transvaginal ultrasonography revealed a 16 cm right adnexal cyst with intramural nodules and thickened cyst wall (). Abdomino-pelvic computed tomography (CT) scan showed a 16 cm cystic mass with enhancing solid intramural nodules in the pelvic cavity (). The CT scan showed no evidence of ascites, peritoneal seeding, omental cake, or pelvic or para-aortic lymph node involvement. It looked like an epithelial ovarian cancer because the CT scan showed delayed enhancement. Her serum cancer antigen 125 (CA-125) concentration was 19.3 U/mL (reference value, <35 U/mL), and the results of other preoperative work-up tests were unremarkable.\nWe performed an exploratory laparotomy through a low midline abdominal incision, which revealed a 16 cm right paratubal cyst completely differentiated from the right ovary and fallopian tube. Paratubal cystectomy was performed without rupture of the cyst. Frozen section analysis of the specimen showed that it was a paratubal serous borderline tumor. Exploration of the entire peritoneal cavity showed no evidence of intraperitoneal tumor spread. Her fallopian tubes, ovaries and uterus were not involved. Washing cytology and multiple peritoneal biopsies were taken. Because the patient and her husband had a strong desire to preserve fertility, her uterus and both adnexae were preserved.\nGrossly, the tumor had a homogeneous, purplish white inner surface and multiple papillary projections up to 2.1 cm in greatest dimension (). The external surface of the tumor was homogeneously purplish white and smooth, with multifocal hemorrhage. However, there was no evidence of surface involvement. The final pathology results were identical to the frozen biopsy results indicating that the mass was a paratubal serous borderline tumor (). The results of the peritoneal washing cytology and multiple biopsies were negative.\nHer postoperative course was uneventful and she was discharged 5 days after surgery. Regular check-ups at the outpatient clinic include serum CA-125 measurements, transvaginal ultrasonography, and/or abdomino-pelvic CT. She delivered a healthy baby at term 13 months after surgery. Twenty months after surgery, she is doing well, without evidence of disease.

An obese 31-year-old nulliparous woman was admitted to the general emergency service with back pain that had started one week earlier and gradually become constant and increased in intensity. She was also vomiting but denied fever, dysuria, constipation, diarrhoea or anorexia. She had never been pregnant and had had amenorrhea for the past 7 years, due to polycystic ovary syndrome. Her body mass index was 39 kg/m2 (height 168 cm; weight 110 kg); she was taking no medication and had no other surgical or medical history to disclose.\nDuring her physical exam, her vital signs were normal and abdominal examination revealed only tenderness in right quadrants, without guarding or rebound. Blood tests were performed and revealed a high white blood cell count (16,700 per mm3, 72% neutrophils), normal renal function and were negative for C-reactive protein. Urine analysis and pregnancy test were also negative.\nBecause her pain worsened, despite the administration of analgesic drugs, the patient underwent an abdominal and pelvic computed tomography (CT) scan, which showed a huge central abdominal-pelvic cyst arising from the right adnexa (). The cyst measured 25 cm × 20 cm × 14 cm and there was an adjacent enlarged oedematous ovary, highly suggestive of torsion. The left ovary, uterus and the appendix were normal and no free fluid in the abdomen and pelvis was observed.\nShe was then referred to the gynaecology department. Her gynaecologic exam was apparently normal but limited due to obesity. A pelvic ultrasound revealed a 20 cm × 20 cm thin-walled mass of the right adnexa, not clearly separate from it. Doppler examination showed that the right ovary was visible and had a polycystic ovarian morphology and apparent presence of vascular flow. The left ovary had the same polycystic pattern.\nHer pain became acutely worse, which reinforced the hypothesis of adnexal torsion. Based on these findings and the increased pain, we decided to perform exploratory laparotomy. Intraoperatively, a giant (~25 cm) cystic median mass of apparent right adnexal origin was seen, occupying the entire pelvis up to the diaphragm. The cyst wall was intact, adhesion-free and swollen. Necrotic ovarian tissue was identified within the mass, but no cleavage planes were identified. The pedicle, which included the infundibulopelvic and utero-ovarian ligaments, was twisted twice around its stalk (). The left adnexa and the uterus looked normal.\nThe patient underwent resection of the mass without rupture. Frozen-section analysis was not available since the surgery was performed during the night. The final pathology report noted a paratubal serous papillary cystadenoma, an ovary with polycystic morphology and a normal fallopian tube. All fragments had congestion, oedema and haemorrhage, consistent with obstruction of the arteriovenous flow (torsion). The postoperative course was uneventful.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 27-year-old, nulliparous (0-0-0-0), married woman was referred to our institution with a huge pelvic mass and left flank pain. She had no history of surgical or medical disease. Transvaginal ultrasonography revealed a 16 cm right adnexal cyst with intramural nodules and thickened cyst wall (). Abdomino-pelvic computed tomography (CT) scan showed a 16 cm cystic mass with enhancing solid intramural nodules in the pelvic cavity (). The CT scan showed no evidence of ascites, peritoneal seeding, omental cake, or pelvic or para-aortic lymph node involvement. It looked like an epithelial ovarian cancer because the CT scan showed delayed enhancement. Her serum cancer antigen 125 (CA-125) concentration was 19.3 U/mL (reference value, <35 U/mL), and the results of other preoperative work-up tests were unremarkable.\nWe performed an exploratory laparotomy through a low midline abdominal incision, which revealed a 16 cm right paratubal cyst completely differentiated from the right ovary and fallopian tube. Paratubal cystectomy was performed without rupture of the cyst. Frozen section analysis of the specimen showed that it was a paratubal serous borderline tumor. Exploration of the entire peritoneal cavity showed no evidence of intraperitoneal tumor spread. Her fallopian tubes, ovaries and uterus were not involved. Washing cytology and multiple peritoneal biopsies were taken. Because the patient and her husband had a strong desire to preserve fertility, her uterus and both adnexae were preserved.\nGrossly, the tumor had a homogeneous, purplish white inner surface and multiple papillary projections up to 2.1 cm in greatest dimension (). The external surface of the tumor was homogeneously purplish white and smooth, with multifocal hemorrhage. However, there was no evidence of surface involvement. The final pathology results were identical to the frozen biopsy results indicating that the mass was a paratubal serous borderline tumor (). The results of the peritoneal washing cytology and multiple biopsies were negative.\nHer postoperative course was uneventful and she was discharged 5 days after surgery. Regular check-ups at the outpatient clinic include serum CA-125 measurements, transvaginal ultrasonography, and/or abdomino-pelvic CT. She delivered a healthy baby at term 13 months after surgery. Twenty months after surgery, she is doing well, without evidence of disease.

A 34-year old multigravida was found to have right adnexal mass on her routine gynecologic examination. Her previous medical history was uneventfull and Pap smear was normal. Transvaginal ultrasonography identified a cystic mass adjacent to the right ovary. Serum CA 125 was 5.1 U/ml (reference range: < 35 U/ml). At laparoscopy a dilated fallopian tube with bluish discoloration was found. The contralateral fallopian tube, ovaries and uterus were unremarkable. Exploration of the abdomino-pelvic cavity revealed smooth and shiny peritoneal surphace. Obtained peritoneal and pelvic washing were negative. Fine needle aspiration of dilated part of the fallopian tube revealed a 4 ml of bloody content. Cytological findings were consistent with hematosalpinx. Right salpingectomy was performed without using endoscopic bag. The patient was followed up by means of ultrasonography and serum CA 125 for 4.6 years. During this period she had no evidence of the disease.\nGrossly, a 7.0 cm long fallopian tube was irregularly dilated up to 4.4 cm in diameter at the ampulary region. The fimbriae were intact. The serosal surphace was smooth. Sections of the dilated part of the fallopian tube revealed a cystic tumor with focally yellow to tan, soft papillary excrescences protruding into the lumen (Fig. ) and foci of intracystic hemorrhage. On microscopic examination the papillae were covered by serous type of epithelium, displaying stratification and budding with focal nuclear atypia (Fig. ). Three types of cells were recognised; ciliated cells, hob-nail cells and mesothelium-like cells. Small foci of tumor tissue necroses and hemorrhage were noted. There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Focus of endosalpingiosis within the adjacent mesosalpinx was found. DNA analysis determined by flow cytometry paraffin technique revealed DNA diploid tumor with low S-phase fraction of 6.5 %.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 27-year-old, nulliparous (0-0-0-0), married woman was referred to our institution with a huge pelvic mass and left flank pain. She had no history of surgical or medical disease. Transvaginal ultrasonography revealed a 16 cm right adnexal cyst with intramural nodules and thickened cyst wall (). Abdomino-pelvic computed tomography (CT) scan showed a 16 cm cystic mass with enhancing solid intramural nodules in the pelvic cavity (). The CT scan showed no evidence of ascites, peritoneal seeding, omental cake, or pelvic or para-aortic lymph node involvement. It looked like an epithelial ovarian cancer because the CT scan showed delayed enhancement. Her serum cancer antigen 125 (CA-125) concentration was 19.3 U/mL (reference value, <35 U/mL), and the results of other preoperative work-up tests were unremarkable.\nWe performed an exploratory laparotomy through a low midline abdominal incision, which revealed a 16 cm right paratubal cyst completely differentiated from the right ovary and fallopian tube. Paratubal cystectomy was performed without rupture of the cyst. Frozen section analysis of the specimen showed that it was a paratubal serous borderline tumor. Exploration of the entire peritoneal cavity showed no evidence of intraperitoneal tumor spread. Her fallopian tubes, ovaries and uterus were not involved. Washing cytology and multiple peritoneal biopsies were taken. Because the patient and her husband had a strong desire to preserve fertility, her uterus and both adnexae were preserved.\nGrossly, the tumor had a homogeneous, purplish white inner surface and multiple papillary projections up to 2.1 cm in greatest dimension (). The external surface of the tumor was homogeneously purplish white and smooth, with multifocal hemorrhage. However, there was no evidence of surface involvement. The final pathology results were identical to the frozen biopsy results indicating that the mass was a paratubal serous borderline tumor (). The results of the peritoneal washing cytology and multiple biopsies were negative.\nHer postoperative course was uneventful and she was discharged 5 days after surgery. Regular check-ups at the outpatient clinic include serum CA-125 measurements, transvaginal ultrasonography, and/or abdomino-pelvic CT. She delivered a healthy baby at term 13 months after surgery. Twenty months after surgery, she is doing well, without evidence of disease.

The patient, a 41-year-old woman with a non-relevant past medical history, concluded her fourth pregnancy by cesarean delivery owing to macrosomic product (July 2013). Tubal ligation was performed on postoperative day one by the Kroener fimbriectomy method, which coursed uneventfully and without any remarkable findings. The specimens obtained were sent for routine histopathological assessment, and the patient was discharged after full recovery. To date she is healthy and without any complaints.\nBoth distal tubes and fimbriae were identified; the large tube was bulky with a nodular appearance (3.5×2×1.3 cm) (). Transverse sections taken from this dilated duct revealed an overfilled lumen with a caramel-like substance surrounding an ill-defined peripheral spot, which, when seen under a magnifying glass, showed a fractal pattern similar to a snowflake (). Histologically, this hazy frame was sketched by a slender stalk with progressively branching papillae lined by columnar non-ciliated cells with plump eosinophilic cytoplasm showing focal pseudostratification and budding (, ). The nuclei of these cells were centrally located, enlarged, and rounded or oval. The nuclei displayed a variable appearance, either dense and hyperchromatic, or vesicular with a prominent nucleolus, and sometimes having coarse chromatin, membrane foldings, pseudoinclusions or grooves. Mitotic activity was not identified.\nDespite the presence of luminal extracellular mucin, several subnuclear mucin-filled vacuoles were also identified, occasionally expanding into cyst-like structures (). Periodic acid– Schiff and Alcian blue stains highlighted the extracellular and intracellular mucin, while the intracytoplasmic vacuoles were stained with Mayer’s mucicarmine (–).\nImmunoperoxidase stains demonstrated an intensely positive reaction for cytokeratin cocktail (CK AE1/AE3) in the membrane and cytoplasm () of cells, as well as for epithelial membrane antigen (EMA) with weak cytoplasmic expression and luminal border reinforcement (). Detection of progesterone receptors (PR) was markedly positive in 95% of cells, while estrogen receptors (ER) and androgen receptors were moderately and weakly positive in 70% and 10% of cells, respectively (–). The proliferation index labeled with Ki-67 was rated in approximately 3% of cells (). Surprisingly, cyclin D1 staining was observed in nearly 90% of cells (). No reaction was detected toward a variety of factors, including carcinoembryonic antigen (CEA), human chorionic gonadotropin, human epidermal growth factor receptor 2 (HER2/Neu), or B-cell lymphoma 2 protein (Bcl-2).\nAccordingly, the proliferation was diagnosed as a metaplastic papillary tumor of the Fallopian tube, with a note to the clinician about the benign behavior of the alteration.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 27-year-old, nulliparous (0-0-0-0), married woman was referred to our institution with a huge pelvic mass and left flank pain. She had no history of surgical or medical disease. Transvaginal ultrasonography revealed a 16 cm right adnexal cyst with intramural nodules and thickened cyst wall (). Abdomino-pelvic computed tomography (CT) scan showed a 16 cm cystic mass with enhancing solid intramural nodules in the pelvic cavity (). The CT scan showed no evidence of ascites, peritoneal seeding, omental cake, or pelvic or para-aortic lymph node involvement. It looked like an epithelial ovarian cancer because the CT scan showed delayed enhancement. Her serum cancer antigen 125 (CA-125) concentration was 19.3 U/mL (reference value, <35 U/mL), and the results of other preoperative work-up tests were unremarkable.\nWe performed an exploratory laparotomy through a low midline abdominal incision, which revealed a 16 cm right paratubal cyst completely differentiated from the right ovary and fallopian tube. Paratubal cystectomy was performed without rupture of the cyst. Frozen section analysis of the specimen showed that it was a paratubal serous borderline tumor. Exploration of the entire peritoneal cavity showed no evidence of intraperitoneal tumor spread. Her fallopian tubes, ovaries and uterus were not involved. Washing cytology and multiple peritoneal biopsies were taken. Because the patient and her husband had a strong desire to preserve fertility, her uterus and both adnexae were preserved.\nGrossly, the tumor had a homogeneous, purplish white inner surface and multiple papillary projections up to 2.1 cm in greatest dimension (). The external surface of the tumor was homogeneously purplish white and smooth, with multifocal hemorrhage. However, there was no evidence of surface involvement. The final pathology results were identical to the frozen biopsy results indicating that the mass was a paratubal serous borderline tumor (). The results of the peritoneal washing cytology and multiple biopsies were negative.\nHer postoperative course was uneventful and she was discharged 5 days after surgery. Regular check-ups at the outpatient clinic include serum CA-125 measurements, transvaginal ultrasonography, and/or abdomino-pelvic CT. She delivered a healthy baby at term 13 months after surgery. Twenty months after surgery, she is doing well, without evidence of disease.

The patient is a 25-year-old woman, gravida 0, who was referred to the gynecology oncology division at Chonnam National University Hospital with lower abdominal pain and abdominal mass. Her gynecologic history was unremarkable. Physical examination was notable for abdominal mass that was near at xiphoid process. Pelvic ultrasound revealed about more than 20 cm cystic mass. Magnetic resonance imaging of the pelvis revealed about 23×21×9 cm sized serous borderline cystic tumor in the right ovary and 2.2 cm corpus luteum of the left ovary. There was no remarkable findings in the uterus and no abnormal pelvic lymphadenopathy. The tumor marker profile was as follows: CA-125 38.2 U/mL (0-35). Another tumor markers and the result of hematological analyses were within their normal ranges.\nExploration of the abdominopelvic cavity revealed about 23 cm sized brownish fluid contained cyst located within the right fallopian tube. Its surface was clear and on cut section, it had multiple papillary growing in inner surface (). The left ovary had about 1 cm sized whitish nodule. A right salpingectomy, left ovary wedge biopsy, appendectomy and cytology were performed. A frozen section of the right fallopian tube revealed a serous borderline tumor. And a frozen section of the left ovary revealed a fibroma. Exploration of the right ovary and left tube was unremarkable, and, in view of patient's age and desire for future fertility, no further surgical procedure was undertaken. Histologically, right tubal mass was serous borderline tumor and appendix uninvolved by tumor cells and cytology of peritoneal washing fluid was negative for malignant cells. Tumor had cystic change and papillary nodules. On microscopic examination the papillae were covered by serous type of epithelium (), displaying stratification and budding with focal nuclear atypia (). There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Micropapillary pattern of the tumor was absent and there was no papillary tubal hyperplasia in the fallopian tube. In general, the histology of the tumor was similar to that of an ovarian borderline serous tumor. Pathologic diagnosis was serous borderline tumor of the right fallopian tube. Close follow-up was recommended and currently, the patient's postoperative recovery was uneventful.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 27-year-old, nulliparous (0-0-0-0), married woman was referred to our institution with a huge pelvic mass and left flank pain. She had no history of surgical or medical disease. Transvaginal ultrasonography revealed a 16 cm right adnexal cyst with intramural nodules and thickened cyst wall (). Abdomino-pelvic computed tomography (CT) scan showed a 16 cm cystic mass with enhancing solid intramural nodules in the pelvic cavity (). The CT scan showed no evidence of ascites, peritoneal seeding, omental cake, or pelvic or para-aortic lymph node involvement. It looked like an epithelial ovarian cancer because the CT scan showed delayed enhancement. Her serum cancer antigen 125 (CA-125) concentration was 19.3 U/mL (reference value, <35 U/mL), and the results of other preoperative work-up tests were unremarkable.\nWe performed an exploratory laparotomy through a low midline abdominal incision, which revealed a 16 cm right paratubal cyst completely differentiated from the right ovary and fallopian tube. Paratubal cystectomy was performed without rupture of the cyst. Frozen section analysis of the specimen showed that it was a paratubal serous borderline tumor. Exploration of the entire peritoneal cavity showed no evidence of intraperitoneal tumor spread. Her fallopian tubes, ovaries and uterus were not involved. Washing cytology and multiple peritoneal biopsies were taken. Because the patient and her husband had a strong desire to preserve fertility, her uterus and both adnexae were preserved.\nGrossly, the tumor had a homogeneous, purplish white inner surface and multiple papillary projections up to 2.1 cm in greatest dimension (). The external surface of the tumor was homogeneously purplish white and smooth, with multifocal hemorrhage. However, there was no evidence of surface involvement. The final pathology results were identical to the frozen biopsy results indicating that the mass was a paratubal serous borderline tumor (). The results of the peritoneal washing cytology and multiple biopsies were negative.\nHer postoperative course was uneventful and she was discharged 5 days after surgery. Regular check-ups at the outpatient clinic include serum CA-125 measurements, transvaginal ultrasonography, and/or abdomino-pelvic CT. She delivered a healthy baby at term 13 months after surgery. Twenty months after surgery, she is doing well, without evidence of disease.

A 31-year-old woman presented with abdominal distention and discomfort worsening over the past 6 months. Concurrently, she had development overactive bladder symptoms, bloating, and dyspepsia. Her medical history was pertinent for epilepsy controlled with antiepileptic medications. Urine analysis was negative for any signs of infection, and her pregnancy test was negative. Abdominal examination was positive for a firm and distended abdomen, uniformly enlarged from the xiphoid bone to the pubic symphysis. No tenderness was reported on palpation; however, pressure was endorsed. A bedside abdominal ultrasound was performed that revealed an abdomen fully distended with fluid, initially suspected to be ascites. Computed tomography in 2.5 mm helical slices with both IV and oral contrast suggested the presence of an encapsulated cystic mass containing clear fluid (6 Hounsfield units). Dimensions reported were 36 cm in long axis, 28 cm in transverse diameter, and 15 cm in anteroposterior diameter, corresponding to 7 liters in volume, suggestive of a right ovarian cystadenoma (Figures and ). No capsular irregularities were seen or intracystic vegetations identified. Concurrently noted was right renal pelvicalyceal dilatation resulting from compression due to the proximity of the right ureter with the renal pelvis measuring 2 cm in anteroposterior diameter. No abdominal ascites or other abdominopelvic abnormalities noted. Tumor markers were in the normal ranges (CA125: 12.13 U/ml, CEA:1.51 ng/ml, and AFP: 1.46 IU/ml). While understanding her risks, the patient stressed the avoidance of excision of ovarian or fallopian tissue due to fertility concerns and preferred that the cyst be removed in a cosmetic manner including avoidance of larger laparotomy incisions.\nThe patient underwent resection of the mass. The procedure was begun by drainage of the cyst in order to identify the stalk and excise all cyst walls. A 3 cm supraumbilical incision was performed with careful dissection until reaching the peritoneal cavity. An Alexis O™ wound protector/retractor Applied Medical was introduced through the small incision permitting better visualization of the cyst (). Three hemostats were used to hold the cyst wall in place, followed by meticulous introduction of an 11 mm trocar into the cyst cavity under direct vision. This was followed by insertion of a 5 mm suction tube through the trocar to aspirate the fluid contents while avoiding spillage of fluid into the peritoneal cavity. Eight liters of serous fluid were aspirated. Following fluid evacuation, the cyst wall had collapsed. The trocar site in the cyst wall was sutured shut in a purse-string manner followed by a second closure layer. Then, the cyst was released off the hemostats, and the laparoscopic gel cap was fitted onto the Alexis retractor to convert the abdominal incision into a laparoscopic port site. This was used to insufflate the abdomen with CO2. Thereafter, 2 additional 5 mm trocars on each side of the midline were introduced.\nThe cyst borders were identified (). Using the bipolar forceps and scissors, it was completely dissected off the fallopian tube. Both the fallopian tube and ovarian tissues were noted to be intact. The cyst was removed through the supraumbilical incision and sent to pathology. The trocars were removed and all incisions approximated as per protocol. The patient was discharged soon thereafter from the observation unit.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 27-year-old, nulliparous (0-0-0-0), married woman was referred to our institution with a huge pelvic mass and left flank pain. She had no history of surgical or medical disease. Transvaginal ultrasonography revealed a 16 cm right adnexal cyst with intramural nodules and thickened cyst wall (). Abdomino-pelvic computed tomography (CT) scan showed a 16 cm cystic mass with enhancing solid intramural nodules in the pelvic cavity (). The CT scan showed no evidence of ascites, peritoneal seeding, omental cake, or pelvic or para-aortic lymph node involvement. It looked like an epithelial ovarian cancer because the CT scan showed delayed enhancement. Her serum cancer antigen 125 (CA-125) concentration was 19.3 U/mL (reference value, <35 U/mL), and the results of other preoperative work-up tests were unremarkable.\nWe performed an exploratory laparotomy through a low midline abdominal incision, which revealed a 16 cm right paratubal cyst completely differentiated from the right ovary and fallopian tube. Paratubal cystectomy was performed without rupture of the cyst. Frozen section analysis of the specimen showed that it was a paratubal serous borderline tumor. Exploration of the entire peritoneal cavity showed no evidence of intraperitoneal tumor spread. Her fallopian tubes, ovaries and uterus were not involved. Washing cytology and multiple peritoneal biopsies were taken. Because the patient and her husband had a strong desire to preserve fertility, her uterus and both adnexae were preserved.\nGrossly, the tumor had a homogeneous, purplish white inner surface and multiple papillary projections up to 2.1 cm in greatest dimension (). The external surface of the tumor was homogeneously purplish white and smooth, with multifocal hemorrhage. However, there was no evidence of surface involvement. The final pathology results were identical to the frozen biopsy results indicating that the mass was a paratubal serous borderline tumor (). The results of the peritoneal washing cytology and multiple biopsies were negative.\nHer postoperative course was uneventful and she was discharged 5 days after surgery. Regular check-ups at the outpatient clinic include serum CA-125 measurements, transvaginal ultrasonography, and/or abdomino-pelvic CT. She delivered a healthy baby at term 13 months after surgery. Twenty months after surgery, she is doing well, without evidence of disease.

A 30-year-old woman visited the outpatient clinic seeking treatment for abdominal\ndistention present since the last 4 months. She had no history of surgery. Bowel and\nbladder functions were normal. Menstruation was regular and without any pain. The\npatient was nulliparous. Computed tomography (CT) scan with contrast showed a thin\nwalled unilocular cyst arising from the left adnexa with dimensions of\n22.3 cm × 18.4 cm × 6.8 cm; no papillary projections or nodules were observed (). The Ca 125 level\nwas 13.64 U/mL.\nBecause of the large size of the cyst and the patient’s preference, a laparotomy was\nperformed. We performed a midline incision above the umbilicus, trying to\nexteriorize the cyst without any rupture. Intraoperative exploration showed a large,\nthin-walled, unilocular cyst arising from the left para-tubal tissue without any\nadhesions; the left tube and left ovary were normal (). The para tubal cyst was dissected\nto separate it from the normal ovary and tube (). The para tubal cyst was removed\nand sent for histopathological examination (). The left tube and left ovary were\npreserved (). The\nuterus and right adnexa were normal. Frozen section examination confirmed by final\nhistopathological examination revealed a benign serous cyst of size\n22 cm × 17 cm × 6 cm.\nWritten, informed consent was obtained from the patient for the publication of this\nreport and its accompanying images ().

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

An obese 31-year-old nulliparous woman was admitted to the general emergency service with back pain that had started one week earlier and gradually become constant and increased in intensity. She was also vomiting but denied fever, dysuria, constipation, diarrhoea or anorexia. She had never been pregnant and had had amenorrhea for the past 7 years, due to polycystic ovary syndrome. Her body mass index was 39 kg/m2 (height 168 cm; weight 110 kg); she was taking no medication and had no other surgical or medical history to disclose.\nDuring her physical exam, her vital signs were normal and abdominal examination revealed only tenderness in right quadrants, without guarding or rebound. Blood tests were performed and revealed a high white blood cell count (16,700 per mm3, 72% neutrophils), normal renal function and were negative for C-reactive protein. Urine analysis and pregnancy test were also negative.\nBecause her pain worsened, despite the administration of analgesic drugs, the patient underwent an abdominal and pelvic computed tomography (CT) scan, which showed a huge central abdominal-pelvic cyst arising from the right adnexa (). The cyst measured 25 cm × 20 cm × 14 cm and there was an adjacent enlarged oedematous ovary, highly suggestive of torsion. The left ovary, uterus and the appendix were normal and no free fluid in the abdomen and pelvis was observed.\nShe was then referred to the gynaecology department. Her gynaecologic exam was apparently normal but limited due to obesity. A pelvic ultrasound revealed a 20 cm × 20 cm thin-walled mass of the right adnexa, not clearly separate from it. Doppler examination showed that the right ovary was visible and had a polycystic ovarian morphology and apparent presence of vascular flow. The left ovary had the same polycystic pattern.\nHer pain became acutely worse, which reinforced the hypothesis of adnexal torsion. Based on these findings and the increased pain, we decided to perform exploratory laparotomy. Intraoperatively, a giant (~25 cm) cystic median mass of apparent right adnexal origin was seen, occupying the entire pelvis up to the diaphragm. The cyst wall was intact, adhesion-free and swollen. Necrotic ovarian tissue was identified within the mass, but no cleavage planes were identified. The pedicle, which included the infundibulopelvic and utero-ovarian ligaments, was twisted twice around its stalk (). The left adnexa and the uterus looked normal.\nThe patient underwent resection of the mass without rupture. Frozen-section analysis was not available since the surgery was performed during the night. The final pathology report noted a paratubal serous papillary cystadenoma, an ovary with polycystic morphology and a normal fallopian tube. All fragments had congestion, oedema and haemorrhage, consistent with obstruction of the arteriovenous flow (torsion). The postoperative course was uneventful.

A 34-year old multigravida was found to have right adnexal mass on her routine gynecologic examination. Her previous medical history was uneventfull and Pap smear was normal. Transvaginal ultrasonography identified a cystic mass adjacent to the right ovary. Serum CA 125 was 5.1 U/ml (reference range: < 35 U/ml). At laparoscopy a dilated fallopian tube with bluish discoloration was found. The contralateral fallopian tube, ovaries and uterus were unremarkable. Exploration of the abdomino-pelvic cavity revealed smooth and shiny peritoneal surphace. Obtained peritoneal and pelvic washing were negative. Fine needle aspiration of dilated part of the fallopian tube revealed a 4 ml of bloody content. Cytological findings were consistent with hematosalpinx. Right salpingectomy was performed without using endoscopic bag. The patient was followed up by means of ultrasonography and serum CA 125 for 4.6 years. During this period she had no evidence of the disease.\nGrossly, a 7.0 cm long fallopian tube was irregularly dilated up to 4.4 cm in diameter at the ampulary region. The fimbriae were intact. The serosal surphace was smooth. Sections of the dilated part of the fallopian tube revealed a cystic tumor with focally yellow to tan, soft papillary excrescences protruding into the lumen (Fig. ) and foci of intracystic hemorrhage. On microscopic examination the papillae were covered by serous type of epithelium, displaying stratification and budding with focal nuclear atypia (Fig. ). Three types of cells were recognised; ciliated cells, hob-nail cells and mesothelium-like cells. Small foci of tumor tissue necroses and hemorrhage were noted. There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Focus of endosalpingiosis within the adjacent mesosalpinx was found. DNA analysis determined by flow cytometry paraffin technique revealed DNA diploid tumor with low S-phase fraction of 6.5 %.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

An obese 31-year-old nulliparous woman was admitted to the general emergency service with back pain that had started one week earlier and gradually become constant and increased in intensity. She was also vomiting but denied fever, dysuria, constipation, diarrhoea or anorexia. She had never been pregnant and had had amenorrhea for the past 7 years, due to polycystic ovary syndrome. Her body mass index was 39 kg/m2 (height 168 cm; weight 110 kg); she was taking no medication and had no other surgical or medical history to disclose.\nDuring her physical exam, her vital signs were normal and abdominal examination revealed only tenderness in right quadrants, without guarding or rebound. Blood tests were performed and revealed a high white blood cell count (16,700 per mm3, 72% neutrophils), normal renal function and were negative for C-reactive protein. Urine analysis and pregnancy test were also negative.\nBecause her pain worsened, despite the administration of analgesic drugs, the patient underwent an abdominal and pelvic computed tomography (CT) scan, which showed a huge central abdominal-pelvic cyst arising from the right adnexa (). The cyst measured 25 cm × 20 cm × 14 cm and there was an adjacent enlarged oedematous ovary, highly suggestive of torsion. The left ovary, uterus and the appendix were normal and no free fluid in the abdomen and pelvis was observed.\nShe was then referred to the gynaecology department. Her gynaecologic exam was apparently normal but limited due to obesity. A pelvic ultrasound revealed a 20 cm × 20 cm thin-walled mass of the right adnexa, not clearly separate from it. Doppler examination showed that the right ovary was visible and had a polycystic ovarian morphology and apparent presence of vascular flow. The left ovary had the same polycystic pattern.\nHer pain became acutely worse, which reinforced the hypothesis of adnexal torsion. Based on these findings and the increased pain, we decided to perform exploratory laparotomy. Intraoperatively, a giant (~25 cm) cystic median mass of apparent right adnexal origin was seen, occupying the entire pelvis up to the diaphragm. The cyst wall was intact, adhesion-free and swollen. Necrotic ovarian tissue was identified within the mass, but no cleavage planes were identified. The pedicle, which included the infundibulopelvic and utero-ovarian ligaments, was twisted twice around its stalk (). The left adnexa and the uterus looked normal.\nThe patient underwent resection of the mass without rupture. Frozen-section analysis was not available since the surgery was performed during the night. The final pathology report noted a paratubal serous papillary cystadenoma, an ovary with polycystic morphology and a normal fallopian tube. All fragments had congestion, oedema and haemorrhage, consistent with obstruction of the arteriovenous flow (torsion). The postoperative course was uneventful.

The patient, a 41-year-old woman with a non-relevant past medical history, concluded her fourth pregnancy by cesarean delivery owing to macrosomic product (July 2013). Tubal ligation was performed on postoperative day one by the Kroener fimbriectomy method, which coursed uneventfully and without any remarkable findings. The specimens obtained were sent for routine histopathological assessment, and the patient was discharged after full recovery. To date she is healthy and without any complaints.\nBoth distal tubes and fimbriae were identified; the large tube was bulky with a nodular appearance (3.5×2×1.3 cm) (). Transverse sections taken from this dilated duct revealed an overfilled lumen with a caramel-like substance surrounding an ill-defined peripheral spot, which, when seen under a magnifying glass, showed a fractal pattern similar to a snowflake (). Histologically, this hazy frame was sketched by a slender stalk with progressively branching papillae lined by columnar non-ciliated cells with plump eosinophilic cytoplasm showing focal pseudostratification and budding (, ). The nuclei of these cells were centrally located, enlarged, and rounded or oval. The nuclei displayed a variable appearance, either dense and hyperchromatic, or vesicular with a prominent nucleolus, and sometimes having coarse chromatin, membrane foldings, pseudoinclusions or grooves. Mitotic activity was not identified.\nDespite the presence of luminal extracellular mucin, several subnuclear mucin-filled vacuoles were also identified, occasionally expanding into cyst-like structures (). Periodic acid– Schiff and Alcian blue stains highlighted the extracellular and intracellular mucin, while the intracytoplasmic vacuoles were stained with Mayer’s mucicarmine (–).\nImmunoperoxidase stains demonstrated an intensely positive reaction for cytokeratin cocktail (CK AE1/AE3) in the membrane and cytoplasm () of cells, as well as for epithelial membrane antigen (EMA) with weak cytoplasmic expression and luminal border reinforcement (). Detection of progesterone receptors (PR) was markedly positive in 95% of cells, while estrogen receptors (ER) and androgen receptors were moderately and weakly positive in 70% and 10% of cells, respectively (–). The proliferation index labeled with Ki-67 was rated in approximately 3% of cells (). Surprisingly, cyclin D1 staining was observed in nearly 90% of cells (). No reaction was detected toward a variety of factors, including carcinoembryonic antigen (CEA), human chorionic gonadotropin, human epidermal growth factor receptor 2 (HER2/Neu), or B-cell lymphoma 2 protein (Bcl-2).\nAccordingly, the proliferation was diagnosed as a metaplastic papillary tumor of the Fallopian tube, with a note to the clinician about the benign behavior of the alteration.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

An obese 31-year-old nulliparous woman was admitted to the general emergency service with back pain that had started one week earlier and gradually become constant and increased in intensity. She was also vomiting but denied fever, dysuria, constipation, diarrhoea or anorexia. She had never been pregnant and had had amenorrhea for the past 7 years, due to polycystic ovary syndrome. Her body mass index was 39 kg/m2 (height 168 cm; weight 110 kg); she was taking no medication and had no other surgical or medical history to disclose.\nDuring her physical exam, her vital signs were normal and abdominal examination revealed only tenderness in right quadrants, without guarding or rebound. Blood tests were performed and revealed a high white blood cell count (16,700 per mm3, 72% neutrophils), normal renal function and were negative for C-reactive protein. Urine analysis and pregnancy test were also negative.\nBecause her pain worsened, despite the administration of analgesic drugs, the patient underwent an abdominal and pelvic computed tomography (CT) scan, which showed a huge central abdominal-pelvic cyst arising from the right adnexa (). The cyst measured 25 cm × 20 cm × 14 cm and there was an adjacent enlarged oedematous ovary, highly suggestive of torsion. The left ovary, uterus and the appendix were normal and no free fluid in the abdomen and pelvis was observed.\nShe was then referred to the gynaecology department. Her gynaecologic exam was apparently normal but limited due to obesity. A pelvic ultrasound revealed a 20 cm × 20 cm thin-walled mass of the right adnexa, not clearly separate from it. Doppler examination showed that the right ovary was visible and had a polycystic ovarian morphology and apparent presence of vascular flow. The left ovary had the same polycystic pattern.\nHer pain became acutely worse, which reinforced the hypothesis of adnexal torsion. Based on these findings and the increased pain, we decided to perform exploratory laparotomy. Intraoperatively, a giant (~25 cm) cystic median mass of apparent right adnexal origin was seen, occupying the entire pelvis up to the diaphragm. The cyst wall was intact, adhesion-free and swollen. Necrotic ovarian tissue was identified within the mass, but no cleavage planes were identified. The pedicle, which included the infundibulopelvic and utero-ovarian ligaments, was twisted twice around its stalk (). The left adnexa and the uterus looked normal.\nThe patient underwent resection of the mass without rupture. Frozen-section analysis was not available since the surgery was performed during the night. The final pathology report noted a paratubal serous papillary cystadenoma, an ovary with polycystic morphology and a normal fallopian tube. All fragments had congestion, oedema and haemorrhage, consistent with obstruction of the arteriovenous flow (torsion). The postoperative course was uneventful.

The patient is a 25-year-old woman, gravida 0, who was referred to the gynecology oncology division at Chonnam National University Hospital with lower abdominal pain and abdominal mass. Her gynecologic history was unremarkable. Physical examination was notable for abdominal mass that was near at xiphoid process. Pelvic ultrasound revealed about more than 20 cm cystic mass. Magnetic resonance imaging of the pelvis revealed about 23×21×9 cm sized serous borderline cystic tumor in the right ovary and 2.2 cm corpus luteum of the left ovary. There was no remarkable findings in the uterus and no abnormal pelvic lymphadenopathy. The tumor marker profile was as follows: CA-125 38.2 U/mL (0-35). Another tumor markers and the result of hematological analyses were within their normal ranges.\nExploration of the abdominopelvic cavity revealed about 23 cm sized brownish fluid contained cyst located within the right fallopian tube. Its surface was clear and on cut section, it had multiple papillary growing in inner surface (). The left ovary had about 1 cm sized whitish nodule. A right salpingectomy, left ovary wedge biopsy, appendectomy and cytology were performed. A frozen section of the right fallopian tube revealed a serous borderline tumor. And a frozen section of the left ovary revealed a fibroma. Exploration of the right ovary and left tube was unremarkable, and, in view of patient's age and desire for future fertility, no further surgical procedure was undertaken. Histologically, right tubal mass was serous borderline tumor and appendix uninvolved by tumor cells and cytology of peritoneal washing fluid was negative for malignant cells. Tumor had cystic change and papillary nodules. On microscopic examination the papillae were covered by serous type of epithelium (), displaying stratification and budding with focal nuclear atypia (). There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Micropapillary pattern of the tumor was absent and there was no papillary tubal hyperplasia in the fallopian tube. In general, the histology of the tumor was similar to that of an ovarian borderline serous tumor. Pathologic diagnosis was serous borderline tumor of the right fallopian tube. Close follow-up was recommended and currently, the patient's postoperative recovery was uneventful.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

An obese 31-year-old nulliparous woman was admitted to the general emergency service with back pain that had started one week earlier and gradually become constant and increased in intensity. She was also vomiting but denied fever, dysuria, constipation, diarrhoea or anorexia. She had never been pregnant and had had amenorrhea for the past 7 years, due to polycystic ovary syndrome. Her body mass index was 39 kg/m2 (height 168 cm; weight 110 kg); she was taking no medication and had no other surgical or medical history to disclose.\nDuring her physical exam, her vital signs were normal and abdominal examination revealed only tenderness in right quadrants, without guarding or rebound. Blood tests were performed and revealed a high white blood cell count (16,700 per mm3, 72% neutrophils), normal renal function and were negative for C-reactive protein. Urine analysis and pregnancy test were also negative.\nBecause her pain worsened, despite the administration of analgesic drugs, the patient underwent an abdominal and pelvic computed tomography (CT) scan, which showed a huge central abdominal-pelvic cyst arising from the right adnexa (). The cyst measured 25 cm × 20 cm × 14 cm and there was an adjacent enlarged oedematous ovary, highly suggestive of torsion. The left ovary, uterus and the appendix were normal and no free fluid in the abdomen and pelvis was observed.\nShe was then referred to the gynaecology department. Her gynaecologic exam was apparently normal but limited due to obesity. A pelvic ultrasound revealed a 20 cm × 20 cm thin-walled mass of the right adnexa, not clearly separate from it. Doppler examination showed that the right ovary was visible and had a polycystic ovarian morphology and apparent presence of vascular flow. The left ovary had the same polycystic pattern.\nHer pain became acutely worse, which reinforced the hypothesis of adnexal torsion. Based on these findings and the increased pain, we decided to perform exploratory laparotomy. Intraoperatively, a giant (~25 cm) cystic median mass of apparent right adnexal origin was seen, occupying the entire pelvis up to the diaphragm. The cyst wall was intact, adhesion-free and swollen. Necrotic ovarian tissue was identified within the mass, but no cleavage planes were identified. The pedicle, which included the infundibulopelvic and utero-ovarian ligaments, was twisted twice around its stalk (). The left adnexa and the uterus looked normal.\nThe patient underwent resection of the mass without rupture. Frozen-section analysis was not available since the surgery was performed during the night. The final pathology report noted a paratubal serous papillary cystadenoma, an ovary with polycystic morphology and a normal fallopian tube. All fragments had congestion, oedema and haemorrhage, consistent with obstruction of the arteriovenous flow (torsion). The postoperative course was uneventful.

A 31-year-old woman presented with abdominal distention and discomfort worsening over the past 6 months. Concurrently, she had development overactive bladder symptoms, bloating, and dyspepsia. Her medical history was pertinent for epilepsy controlled with antiepileptic medications. Urine analysis was negative for any signs of infection, and her pregnancy test was negative. Abdominal examination was positive for a firm and distended abdomen, uniformly enlarged from the xiphoid bone to the pubic symphysis. No tenderness was reported on palpation; however, pressure was endorsed. A bedside abdominal ultrasound was performed that revealed an abdomen fully distended with fluid, initially suspected to be ascites. Computed tomography in 2.5 mm helical slices with both IV and oral contrast suggested the presence of an encapsulated cystic mass containing clear fluid (6 Hounsfield units). Dimensions reported were 36 cm in long axis, 28 cm in transverse diameter, and 15 cm in anteroposterior diameter, corresponding to 7 liters in volume, suggestive of a right ovarian cystadenoma (Figures and ). No capsular irregularities were seen or intracystic vegetations identified. Concurrently noted was right renal pelvicalyceal dilatation resulting from compression due to the proximity of the right ureter with the renal pelvis measuring 2 cm in anteroposterior diameter. No abdominal ascites or other abdominopelvic abnormalities noted. Tumor markers were in the normal ranges (CA125: 12.13 U/ml, CEA:1.51 ng/ml, and AFP: 1.46 IU/ml). While understanding her risks, the patient stressed the avoidance of excision of ovarian or fallopian tissue due to fertility concerns and preferred that the cyst be removed in a cosmetic manner including avoidance of larger laparotomy incisions.\nThe patient underwent resection of the mass. The procedure was begun by drainage of the cyst in order to identify the stalk and excise all cyst walls. A 3 cm supraumbilical incision was performed with careful dissection until reaching the peritoneal cavity. An Alexis O™ wound protector/retractor Applied Medical was introduced through the small incision permitting better visualization of the cyst (). Three hemostats were used to hold the cyst wall in place, followed by meticulous introduction of an 11 mm trocar into the cyst cavity under direct vision. This was followed by insertion of a 5 mm suction tube through the trocar to aspirate the fluid contents while avoiding spillage of fluid into the peritoneal cavity. Eight liters of serous fluid were aspirated. Following fluid evacuation, the cyst wall had collapsed. The trocar site in the cyst wall was sutured shut in a purse-string manner followed by a second closure layer. Then, the cyst was released off the hemostats, and the laparoscopic gel cap was fitted onto the Alexis retractor to convert the abdominal incision into a laparoscopic port site. This was used to insufflate the abdomen with CO2. Thereafter, 2 additional 5 mm trocars on each side of the midline were introduced.\nThe cyst borders were identified (). Using the bipolar forceps and scissors, it was completely dissected off the fallopian tube. Both the fallopian tube and ovarian tissues were noted to be intact. The cyst was removed through the supraumbilical incision and sent to pathology. The trocars were removed and all incisions approximated as per protocol. The patient was discharged soon thereafter from the observation unit.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

An obese 31-year-old nulliparous woman was admitted to the general emergency service with back pain that had started one week earlier and gradually become constant and increased in intensity. She was also vomiting but denied fever, dysuria, constipation, diarrhoea or anorexia. She had never been pregnant and had had amenorrhea for the past 7 years, due to polycystic ovary syndrome. Her body mass index was 39 kg/m2 (height 168 cm; weight 110 kg); she was taking no medication and had no other surgical or medical history to disclose.\nDuring her physical exam, her vital signs were normal and abdominal examination revealed only tenderness in right quadrants, without guarding or rebound. Blood tests were performed and revealed a high white blood cell count (16,700 per mm3, 72% neutrophils), normal renal function and were negative for C-reactive protein. Urine analysis and pregnancy test were also negative.\nBecause her pain worsened, despite the administration of analgesic drugs, the patient underwent an abdominal and pelvic computed tomography (CT) scan, which showed a huge central abdominal-pelvic cyst arising from the right adnexa (). The cyst measured 25 cm × 20 cm × 14 cm and there was an adjacent enlarged oedematous ovary, highly suggestive of torsion. The left ovary, uterus and the appendix were normal and no free fluid in the abdomen and pelvis was observed.\nShe was then referred to the gynaecology department. Her gynaecologic exam was apparently normal but limited due to obesity. A pelvic ultrasound revealed a 20 cm × 20 cm thin-walled mass of the right adnexa, not clearly separate from it. Doppler examination showed that the right ovary was visible and had a polycystic ovarian morphology and apparent presence of vascular flow. The left ovary had the same polycystic pattern.\nHer pain became acutely worse, which reinforced the hypothesis of adnexal torsion. Based on these findings and the increased pain, we decided to perform exploratory laparotomy. Intraoperatively, a giant (~25 cm) cystic median mass of apparent right adnexal origin was seen, occupying the entire pelvis up to the diaphragm. The cyst wall was intact, adhesion-free and swollen. Necrotic ovarian tissue was identified within the mass, but no cleavage planes were identified. The pedicle, which included the infundibulopelvic and utero-ovarian ligaments, was twisted twice around its stalk (). The left adnexa and the uterus looked normal.\nThe patient underwent resection of the mass without rupture. Frozen-section analysis was not available since the surgery was performed during the night. The final pathology report noted a paratubal serous papillary cystadenoma, an ovary with polycystic morphology and a normal fallopian tube. All fragments had congestion, oedema and haemorrhage, consistent with obstruction of the arteriovenous flow (torsion). The postoperative course was uneventful.

A 30-year-old woman visited the outpatient clinic seeking treatment for abdominal\ndistention present since the last 4 months. She had no history of surgery. Bowel and\nbladder functions were normal. Menstruation was regular and without any pain. The\npatient was nulliparous. Computed tomography (CT) scan with contrast showed a thin\nwalled unilocular cyst arising from the left adnexa with dimensions of\n22.3 cm × 18.4 cm × 6.8 cm; no papillary projections or nodules were observed (). The Ca 125 level\nwas 13.64 U/mL.\nBecause of the large size of the cyst and the patient’s preference, a laparotomy was\nperformed. We performed a midline incision above the umbilicus, trying to\nexteriorize the cyst without any rupture. Intraoperative exploration showed a large,\nthin-walled, unilocular cyst arising from the left para-tubal tissue without any\nadhesions; the left tube and left ovary were normal (). The para tubal cyst was dissected\nto separate it from the normal ovary and tube (). The para tubal cyst was removed\nand sent for histopathological examination (). The left tube and left ovary were\npreserved (). The\nuterus and right adnexa were normal. Frozen section examination confirmed by final\nhistopathological examination revealed a benign serous cyst of size\n22 cm × 17 cm × 6 cm.\nWritten, informed consent was obtained from the patient for the publication of this\nreport and its accompanying images ().

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

The patient, a 41-year-old woman with a non-relevant past medical history, concluded her fourth pregnancy by cesarean delivery owing to macrosomic product (July 2013). Tubal ligation was performed on postoperative day one by the Kroener fimbriectomy method, which coursed uneventfully and without any remarkable findings. The specimens obtained were sent for routine histopathological assessment, and the patient was discharged after full recovery. To date she is healthy and without any complaints.\nBoth distal tubes and fimbriae were identified; the large tube was bulky with a nodular appearance (3.5×2×1.3 cm) (). Transverse sections taken from this dilated duct revealed an overfilled lumen with a caramel-like substance surrounding an ill-defined peripheral spot, which, when seen under a magnifying glass, showed a fractal pattern similar to a snowflake (). Histologically, this hazy frame was sketched by a slender stalk with progressively branching papillae lined by columnar non-ciliated cells with plump eosinophilic cytoplasm showing focal pseudostratification and budding (, ). The nuclei of these cells were centrally located, enlarged, and rounded or oval. The nuclei displayed a variable appearance, either dense and hyperchromatic, or vesicular with a prominent nucleolus, and sometimes having coarse chromatin, membrane foldings, pseudoinclusions or grooves. Mitotic activity was not identified.\nDespite the presence of luminal extracellular mucin, several subnuclear mucin-filled vacuoles were also identified, occasionally expanding into cyst-like structures (). Periodic acid– Schiff and Alcian blue stains highlighted the extracellular and intracellular mucin, while the intracytoplasmic vacuoles were stained with Mayer’s mucicarmine (–).\nImmunoperoxidase stains demonstrated an intensely positive reaction for cytokeratin cocktail (CK AE1/AE3) in the membrane and cytoplasm () of cells, as well as for epithelial membrane antigen (EMA) with weak cytoplasmic expression and luminal border reinforcement (). Detection of progesterone receptors (PR) was markedly positive in 95% of cells, while estrogen receptors (ER) and androgen receptors were moderately and weakly positive in 70% and 10% of cells, respectively (–). The proliferation index labeled with Ki-67 was rated in approximately 3% of cells (). Surprisingly, cyclin D1 staining was observed in nearly 90% of cells (). No reaction was detected toward a variety of factors, including carcinoembryonic antigen (CEA), human chorionic gonadotropin, human epidermal growth factor receptor 2 (HER2/Neu), or B-cell lymphoma 2 protein (Bcl-2).\nAccordingly, the proliferation was diagnosed as a metaplastic papillary tumor of the Fallopian tube, with a note to the clinician about the benign behavior of the alteration.

A 34-year old multigravida was found to have right adnexal mass on her routine gynecologic examination. Her previous medical history was uneventfull and Pap smear was normal. Transvaginal ultrasonography identified a cystic mass adjacent to the right ovary. Serum CA 125 was 5.1 U/ml (reference range: < 35 U/ml). At laparoscopy a dilated fallopian tube with bluish discoloration was found. The contralateral fallopian tube, ovaries and uterus were unremarkable. Exploration of the abdomino-pelvic cavity revealed smooth and shiny peritoneal surphace. Obtained peritoneal and pelvic washing were negative. Fine needle aspiration of dilated part of the fallopian tube revealed a 4 ml of bloody content. Cytological findings were consistent with hematosalpinx. Right salpingectomy was performed without using endoscopic bag. The patient was followed up by means of ultrasonography and serum CA 125 for 4.6 years. During this period she had no evidence of the disease.\nGrossly, a 7.0 cm long fallopian tube was irregularly dilated up to 4.4 cm in diameter at the ampulary region. The fimbriae were intact. The serosal surphace was smooth. Sections of the dilated part of the fallopian tube revealed a cystic tumor with focally yellow to tan, soft papillary excrescences protruding into the lumen (Fig. ) and foci of intracystic hemorrhage. On microscopic examination the papillae were covered by serous type of epithelium, displaying stratification and budding with focal nuclear atypia (Fig. ). Three types of cells were recognised; ciliated cells, hob-nail cells and mesothelium-like cells. Small foci of tumor tissue necroses and hemorrhage were noted. There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Focus of endosalpingiosis within the adjacent mesosalpinx was found. DNA analysis determined by flow cytometry paraffin technique revealed DNA diploid tumor with low S-phase fraction of 6.5 %.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

The patient is a 25-year-old woman, gravida 0, who was referred to the gynecology oncology division at Chonnam National University Hospital with lower abdominal pain and abdominal mass. Her gynecologic history was unremarkable. Physical examination was notable for abdominal mass that was near at xiphoid process. Pelvic ultrasound revealed about more than 20 cm cystic mass. Magnetic resonance imaging of the pelvis revealed about 23×21×9 cm sized serous borderline cystic tumor in the right ovary and 2.2 cm corpus luteum of the left ovary. There was no remarkable findings in the uterus and no abnormal pelvic lymphadenopathy. The tumor marker profile was as follows: CA-125 38.2 U/mL (0-35). Another tumor markers and the result of hematological analyses were within their normal ranges.\nExploration of the abdominopelvic cavity revealed about 23 cm sized brownish fluid contained cyst located within the right fallopian tube. Its surface was clear and on cut section, it had multiple papillary growing in inner surface (). The left ovary had about 1 cm sized whitish nodule. A right salpingectomy, left ovary wedge biopsy, appendectomy and cytology were performed. A frozen section of the right fallopian tube revealed a serous borderline tumor. And a frozen section of the left ovary revealed a fibroma. Exploration of the right ovary and left tube was unremarkable, and, in view of patient's age and desire for future fertility, no further surgical procedure was undertaken. Histologically, right tubal mass was serous borderline tumor and appendix uninvolved by tumor cells and cytology of peritoneal washing fluid was negative for malignant cells. Tumor had cystic change and papillary nodules. On microscopic examination the papillae were covered by serous type of epithelium (), displaying stratification and budding with focal nuclear atypia (). There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Micropapillary pattern of the tumor was absent and there was no papillary tubal hyperplasia in the fallopian tube. In general, the histology of the tumor was similar to that of an ovarian borderline serous tumor. Pathologic diagnosis was serous borderline tumor of the right fallopian tube. Close follow-up was recommended and currently, the patient's postoperative recovery was uneventful.

A 34-year old multigravida was found to have right adnexal mass on her routine gynecologic examination. Her previous medical history was uneventfull and Pap smear was normal. Transvaginal ultrasonography identified a cystic mass adjacent to the right ovary. Serum CA 125 was 5.1 U/ml (reference range: < 35 U/ml). At laparoscopy a dilated fallopian tube with bluish discoloration was found. The contralateral fallopian tube, ovaries and uterus were unremarkable. Exploration of the abdomino-pelvic cavity revealed smooth and shiny peritoneal surphace. Obtained peritoneal and pelvic washing were negative. Fine needle aspiration of dilated part of the fallopian tube revealed a 4 ml of bloody content. Cytological findings were consistent with hematosalpinx. Right salpingectomy was performed without using endoscopic bag. The patient was followed up by means of ultrasonography and serum CA 125 for 4.6 years. During this period she had no evidence of the disease.\nGrossly, a 7.0 cm long fallopian tube was irregularly dilated up to 4.4 cm in diameter at the ampulary region. The fimbriae were intact. The serosal surphace was smooth. Sections of the dilated part of the fallopian tube revealed a cystic tumor with focally yellow to tan, soft papillary excrescences protruding into the lumen (Fig. ) and foci of intracystic hemorrhage. On microscopic examination the papillae were covered by serous type of epithelium, displaying stratification and budding with focal nuclear atypia (Fig. ). Three types of cells were recognised; ciliated cells, hob-nail cells and mesothelium-like cells. Small foci of tumor tissue necroses and hemorrhage were noted. There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Focus of endosalpingiosis within the adjacent mesosalpinx was found. DNA analysis determined by flow cytometry paraffin technique revealed DNA diploid tumor with low S-phase fraction of 6.5 %.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 31-year-old woman presented with abdominal distention and discomfort worsening over the past 6 months. Concurrently, she had development overactive bladder symptoms, bloating, and dyspepsia. Her medical history was pertinent for epilepsy controlled with antiepileptic medications. Urine analysis was negative for any signs of infection, and her pregnancy test was negative. Abdominal examination was positive for a firm and distended abdomen, uniformly enlarged from the xiphoid bone to the pubic symphysis. No tenderness was reported on palpation; however, pressure was endorsed. A bedside abdominal ultrasound was performed that revealed an abdomen fully distended with fluid, initially suspected to be ascites. Computed tomography in 2.5 mm helical slices with both IV and oral contrast suggested the presence of an encapsulated cystic mass containing clear fluid (6 Hounsfield units). Dimensions reported were 36 cm in long axis, 28 cm in transverse diameter, and 15 cm in anteroposterior diameter, corresponding to 7 liters in volume, suggestive of a right ovarian cystadenoma (Figures and ). No capsular irregularities were seen or intracystic vegetations identified. Concurrently noted was right renal pelvicalyceal dilatation resulting from compression due to the proximity of the right ureter with the renal pelvis measuring 2 cm in anteroposterior diameter. No abdominal ascites or other abdominopelvic abnormalities noted. Tumor markers were in the normal ranges (CA125: 12.13 U/ml, CEA:1.51 ng/ml, and AFP: 1.46 IU/ml). While understanding her risks, the patient stressed the avoidance of excision of ovarian or fallopian tissue due to fertility concerns and preferred that the cyst be removed in a cosmetic manner including avoidance of larger laparotomy incisions.\nThe patient underwent resection of the mass. The procedure was begun by drainage of the cyst in order to identify the stalk and excise all cyst walls. A 3 cm supraumbilical incision was performed with careful dissection until reaching the peritoneal cavity. An Alexis O™ wound protector/retractor Applied Medical was introduced through the small incision permitting better visualization of the cyst (). Three hemostats were used to hold the cyst wall in place, followed by meticulous introduction of an 11 mm trocar into the cyst cavity under direct vision. This was followed by insertion of a 5 mm suction tube through the trocar to aspirate the fluid contents while avoiding spillage of fluid into the peritoneal cavity. Eight liters of serous fluid were aspirated. Following fluid evacuation, the cyst wall had collapsed. The trocar site in the cyst wall was sutured shut in a purse-string manner followed by a second closure layer. Then, the cyst was released off the hemostats, and the laparoscopic gel cap was fitted onto the Alexis retractor to convert the abdominal incision into a laparoscopic port site. This was used to insufflate the abdomen with CO2. Thereafter, 2 additional 5 mm trocars on each side of the midline were introduced.\nThe cyst borders were identified (). Using the bipolar forceps and scissors, it was completely dissected off the fallopian tube. Both the fallopian tube and ovarian tissues were noted to be intact. The cyst was removed through the supraumbilical incision and sent to pathology. The trocars were removed and all incisions approximated as per protocol. The patient was discharged soon thereafter from the observation unit.

A 34-year old multigravida was found to have right adnexal mass on her routine gynecologic examination. Her previous medical history was uneventfull and Pap smear was normal. Transvaginal ultrasonography identified a cystic mass adjacent to the right ovary. Serum CA 125 was 5.1 U/ml (reference range: < 35 U/ml). At laparoscopy a dilated fallopian tube with bluish discoloration was found. The contralateral fallopian tube, ovaries and uterus were unremarkable. Exploration of the abdomino-pelvic cavity revealed smooth and shiny peritoneal surphace. Obtained peritoneal and pelvic washing were negative. Fine needle aspiration of dilated part of the fallopian tube revealed a 4 ml of bloody content. Cytological findings were consistent with hematosalpinx. Right salpingectomy was performed without using endoscopic bag. The patient was followed up by means of ultrasonography and serum CA 125 for 4.6 years. During this period she had no evidence of the disease.\nGrossly, a 7.0 cm long fallopian tube was irregularly dilated up to 4.4 cm in diameter at the ampulary region. The fimbriae were intact. The serosal surphace was smooth. Sections of the dilated part of the fallopian tube revealed a cystic tumor with focally yellow to tan, soft papillary excrescences protruding into the lumen (Fig. ) and foci of intracystic hemorrhage. On microscopic examination the papillae were covered by serous type of epithelium, displaying stratification and budding with focal nuclear atypia (Fig. ). Three types of cells were recognised; ciliated cells, hob-nail cells and mesothelium-like cells. Small foci of tumor tissue necroses and hemorrhage were noted. There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Focus of endosalpingiosis within the adjacent mesosalpinx was found. DNA analysis determined by flow cytometry paraffin technique revealed DNA diploid tumor with low S-phase fraction of 6.5 %.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 30-year-old woman visited the outpatient clinic seeking treatment for abdominal\ndistention present since the last 4 months. She had no history of surgery. Bowel and\nbladder functions were normal. Menstruation was regular and without any pain. The\npatient was nulliparous. Computed tomography (CT) scan with contrast showed a thin\nwalled unilocular cyst arising from the left adnexa with dimensions of\n22.3 cm × 18.4 cm × 6.8 cm; no papillary projections or nodules were observed (). The Ca 125 level\nwas 13.64 U/mL.\nBecause of the large size of the cyst and the patient’s preference, a laparotomy was\nperformed. We performed a midline incision above the umbilicus, trying to\nexteriorize the cyst without any rupture. Intraoperative exploration showed a large,\nthin-walled, unilocular cyst arising from the left para-tubal tissue without any\nadhesions; the left tube and left ovary were normal (). The para tubal cyst was dissected\nto separate it from the normal ovary and tube (). The para tubal cyst was removed\nand sent for histopathological examination (). The left tube and left ovary were\npreserved (). The\nuterus and right adnexa were normal. Frozen section examination confirmed by final\nhistopathological examination revealed a benign serous cyst of size\n22 cm × 17 cm × 6 cm.\nWritten, informed consent was obtained from the patient for the publication of this\nreport and its accompanying images ().

A 34-year old multigravida was found to have right adnexal mass on her routine gynecologic examination. Her previous medical history was uneventfull and Pap smear was normal. Transvaginal ultrasonography identified a cystic mass adjacent to the right ovary. Serum CA 125 was 5.1 U/ml (reference range: < 35 U/ml). At laparoscopy a dilated fallopian tube with bluish discoloration was found. The contralateral fallopian tube, ovaries and uterus were unremarkable. Exploration of the abdomino-pelvic cavity revealed smooth and shiny peritoneal surphace. Obtained peritoneal and pelvic washing were negative. Fine needle aspiration of dilated part of the fallopian tube revealed a 4 ml of bloody content. Cytological findings were consistent with hematosalpinx. Right salpingectomy was performed without using endoscopic bag. The patient was followed up by means of ultrasonography and serum CA 125 for 4.6 years. During this period she had no evidence of the disease.\nGrossly, a 7.0 cm long fallopian tube was irregularly dilated up to 4.4 cm in diameter at the ampulary region. The fimbriae were intact. The serosal surphace was smooth. Sections of the dilated part of the fallopian tube revealed a cystic tumor with focally yellow to tan, soft papillary excrescences protruding into the lumen (Fig. ) and foci of intracystic hemorrhage. On microscopic examination the papillae were covered by serous type of epithelium, displaying stratification and budding with focal nuclear atypia (Fig. ). Three types of cells were recognised; ciliated cells, hob-nail cells and mesothelium-like cells. Small foci of tumor tissue necroses and hemorrhage were noted. There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Focus of endosalpingiosis within the adjacent mesosalpinx was found. DNA analysis determined by flow cytometry paraffin technique revealed DNA diploid tumor with low S-phase fraction of 6.5 %.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

The patient, a 41-year-old woman with a non-relevant past medical history, concluded her fourth pregnancy by cesarean delivery owing to macrosomic product (July 2013). Tubal ligation was performed on postoperative day one by the Kroener fimbriectomy method, which coursed uneventfully and without any remarkable findings. The specimens obtained were sent for routine histopathological assessment, and the patient was discharged after full recovery. To date she is healthy and without any complaints.\nBoth distal tubes and fimbriae were identified; the large tube was bulky with a nodular appearance (3.5×2×1.3 cm) (). Transverse sections taken from this dilated duct revealed an overfilled lumen with a caramel-like substance surrounding an ill-defined peripheral spot, which, when seen under a magnifying glass, showed a fractal pattern similar to a snowflake (). Histologically, this hazy frame was sketched by a slender stalk with progressively branching papillae lined by columnar non-ciliated cells with plump eosinophilic cytoplasm showing focal pseudostratification and budding (, ). The nuclei of these cells were centrally located, enlarged, and rounded or oval. The nuclei displayed a variable appearance, either dense and hyperchromatic, or vesicular with a prominent nucleolus, and sometimes having coarse chromatin, membrane foldings, pseudoinclusions or grooves. Mitotic activity was not identified.\nDespite the presence of luminal extracellular mucin, several subnuclear mucin-filled vacuoles were also identified, occasionally expanding into cyst-like structures (). Periodic acid– Schiff and Alcian blue stains highlighted the extracellular and intracellular mucin, while the intracytoplasmic vacuoles were stained with Mayer’s mucicarmine (–).\nImmunoperoxidase stains demonstrated an intensely positive reaction for cytokeratin cocktail (CK AE1/AE3) in the membrane and cytoplasm () of cells, as well as for epithelial membrane antigen (EMA) with weak cytoplasmic expression and luminal border reinforcement (). Detection of progesterone receptors (PR) was markedly positive in 95% of cells, while estrogen receptors (ER) and androgen receptors were moderately and weakly positive in 70% and 10% of cells, respectively (–). The proliferation index labeled with Ki-67 was rated in approximately 3% of cells (). Surprisingly, cyclin D1 staining was observed in nearly 90% of cells (). No reaction was detected toward a variety of factors, including carcinoembryonic antigen (CEA), human chorionic gonadotropin, human epidermal growth factor receptor 2 (HER2/Neu), or B-cell lymphoma 2 protein (Bcl-2).\nAccordingly, the proliferation was diagnosed as a metaplastic papillary tumor of the Fallopian tube, with a note to the clinician about the benign behavior of the alteration.

The patient is a 25-year-old woman, gravida 0, who was referred to the gynecology oncology division at Chonnam National University Hospital with lower abdominal pain and abdominal mass. Her gynecologic history was unremarkable. Physical examination was notable for abdominal mass that was near at xiphoid process. Pelvic ultrasound revealed about more than 20 cm cystic mass. Magnetic resonance imaging of the pelvis revealed about 23×21×9 cm sized serous borderline cystic tumor in the right ovary and 2.2 cm corpus luteum of the left ovary. There was no remarkable findings in the uterus and no abnormal pelvic lymphadenopathy. The tumor marker profile was as follows: CA-125 38.2 U/mL (0-35). Another tumor markers and the result of hematological analyses were within their normal ranges.\nExploration of the abdominopelvic cavity revealed about 23 cm sized brownish fluid contained cyst located within the right fallopian tube. Its surface was clear and on cut section, it had multiple papillary growing in inner surface (). The left ovary had about 1 cm sized whitish nodule. A right salpingectomy, left ovary wedge biopsy, appendectomy and cytology were performed. A frozen section of the right fallopian tube revealed a serous borderline tumor. And a frozen section of the left ovary revealed a fibroma. Exploration of the right ovary and left tube was unremarkable, and, in view of patient's age and desire for future fertility, no further surgical procedure was undertaken. Histologically, right tubal mass was serous borderline tumor and appendix uninvolved by tumor cells and cytology of peritoneal washing fluid was negative for malignant cells. Tumor had cystic change and papillary nodules. On microscopic examination the papillae were covered by serous type of epithelium (), displaying stratification and budding with focal nuclear atypia (). There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Micropapillary pattern of the tumor was absent and there was no papillary tubal hyperplasia in the fallopian tube. In general, the histology of the tumor was similar to that of an ovarian borderline serous tumor. Pathologic diagnosis was serous borderline tumor of the right fallopian tube. Close follow-up was recommended and currently, the patient's postoperative recovery was uneventful.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

The patient, a 41-year-old woman with a non-relevant past medical history, concluded her fourth pregnancy by cesarean delivery owing to macrosomic product (July 2013). Tubal ligation was performed on postoperative day one by the Kroener fimbriectomy method, which coursed uneventfully and without any remarkable findings. The specimens obtained were sent for routine histopathological assessment, and the patient was discharged after full recovery. To date she is healthy and without any complaints.\nBoth distal tubes and fimbriae were identified; the large tube was bulky with a nodular appearance (3.5×2×1.3 cm) (). Transverse sections taken from this dilated duct revealed an overfilled lumen with a caramel-like substance surrounding an ill-defined peripheral spot, which, when seen under a magnifying glass, showed a fractal pattern similar to a snowflake (). Histologically, this hazy frame was sketched by a slender stalk with progressively branching papillae lined by columnar non-ciliated cells with plump eosinophilic cytoplasm showing focal pseudostratification and budding (, ). The nuclei of these cells were centrally located, enlarged, and rounded or oval. The nuclei displayed a variable appearance, either dense and hyperchromatic, or vesicular with a prominent nucleolus, and sometimes having coarse chromatin, membrane foldings, pseudoinclusions or grooves. Mitotic activity was not identified.\nDespite the presence of luminal extracellular mucin, several subnuclear mucin-filled vacuoles were also identified, occasionally expanding into cyst-like structures (). Periodic acid– Schiff and Alcian blue stains highlighted the extracellular and intracellular mucin, while the intracytoplasmic vacuoles were stained with Mayer’s mucicarmine (–).\nImmunoperoxidase stains demonstrated an intensely positive reaction for cytokeratin cocktail (CK AE1/AE3) in the membrane and cytoplasm () of cells, as well as for epithelial membrane antigen (EMA) with weak cytoplasmic expression and luminal border reinforcement (). Detection of progesterone receptors (PR) was markedly positive in 95% of cells, while estrogen receptors (ER) and androgen receptors were moderately and weakly positive in 70% and 10% of cells, respectively (–). The proliferation index labeled with Ki-67 was rated in approximately 3% of cells (). Surprisingly, cyclin D1 staining was observed in nearly 90% of cells (). No reaction was detected toward a variety of factors, including carcinoembryonic antigen (CEA), human chorionic gonadotropin, human epidermal growth factor receptor 2 (HER2/Neu), or B-cell lymphoma 2 protein (Bcl-2).\nAccordingly, the proliferation was diagnosed as a metaplastic papillary tumor of the Fallopian tube, with a note to the clinician about the benign behavior of the alteration.

A 31-year-old woman presented with abdominal distention and discomfort worsening over the past 6 months. Concurrently, she had development overactive bladder symptoms, bloating, and dyspepsia. Her medical history was pertinent for epilepsy controlled with antiepileptic medications. Urine analysis was negative for any signs of infection, and her pregnancy test was negative. Abdominal examination was positive for a firm and distended abdomen, uniformly enlarged from the xiphoid bone to the pubic symphysis. No tenderness was reported on palpation; however, pressure was endorsed. A bedside abdominal ultrasound was performed that revealed an abdomen fully distended with fluid, initially suspected to be ascites. Computed tomography in 2.5 mm helical slices with both IV and oral contrast suggested the presence of an encapsulated cystic mass containing clear fluid (6 Hounsfield units). Dimensions reported were 36 cm in long axis, 28 cm in transverse diameter, and 15 cm in anteroposterior diameter, corresponding to 7 liters in volume, suggestive of a right ovarian cystadenoma (Figures and ). No capsular irregularities were seen or intracystic vegetations identified. Concurrently noted was right renal pelvicalyceal dilatation resulting from compression due to the proximity of the right ureter with the renal pelvis measuring 2 cm in anteroposterior diameter. No abdominal ascites or other abdominopelvic abnormalities noted. Tumor markers were in the normal ranges (CA125: 12.13 U/ml, CEA:1.51 ng/ml, and AFP: 1.46 IU/ml). While understanding her risks, the patient stressed the avoidance of excision of ovarian or fallopian tissue due to fertility concerns and preferred that the cyst be removed in a cosmetic manner including avoidance of larger laparotomy incisions.\nThe patient underwent resection of the mass. The procedure was begun by drainage of the cyst in order to identify the stalk and excise all cyst walls. A 3 cm supraumbilical incision was performed with careful dissection until reaching the peritoneal cavity. An Alexis O™ wound protector/retractor Applied Medical was introduced through the small incision permitting better visualization of the cyst (). Three hemostats were used to hold the cyst wall in place, followed by meticulous introduction of an 11 mm trocar into the cyst cavity under direct vision. This was followed by insertion of a 5 mm suction tube through the trocar to aspirate the fluid contents while avoiding spillage of fluid into the peritoneal cavity. Eight liters of serous fluid were aspirated. Following fluid evacuation, the cyst wall had collapsed. The trocar site in the cyst wall was sutured shut in a purse-string manner followed by a second closure layer. Then, the cyst was released off the hemostats, and the laparoscopic gel cap was fitted onto the Alexis retractor to convert the abdominal incision into a laparoscopic port site. This was used to insufflate the abdomen with CO2. Thereafter, 2 additional 5 mm trocars on each side of the midline were introduced.\nThe cyst borders were identified (). Using the bipolar forceps and scissors, it was completely dissected off the fallopian tube. Both the fallopian tube and ovarian tissues were noted to be intact. The cyst was removed through the supraumbilical incision and sent to pathology. The trocars were removed and all incisions approximated as per protocol. The patient was discharged soon thereafter from the observation unit.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

The patient, a 41-year-old woman with a non-relevant past medical history, concluded her fourth pregnancy by cesarean delivery owing to macrosomic product (July 2013). Tubal ligation was performed on postoperative day one by the Kroener fimbriectomy method, which coursed uneventfully and without any remarkable findings. The specimens obtained were sent for routine histopathological assessment, and the patient was discharged after full recovery. To date she is healthy and without any complaints.\nBoth distal tubes and fimbriae were identified; the large tube was bulky with a nodular appearance (3.5×2×1.3 cm) (). Transverse sections taken from this dilated duct revealed an overfilled lumen with a caramel-like substance surrounding an ill-defined peripheral spot, which, when seen under a magnifying glass, showed a fractal pattern similar to a snowflake (). Histologically, this hazy frame was sketched by a slender stalk with progressively branching papillae lined by columnar non-ciliated cells with plump eosinophilic cytoplasm showing focal pseudostratification and budding (, ). The nuclei of these cells were centrally located, enlarged, and rounded or oval. The nuclei displayed a variable appearance, either dense and hyperchromatic, or vesicular with a prominent nucleolus, and sometimes having coarse chromatin, membrane foldings, pseudoinclusions or grooves. Mitotic activity was not identified.\nDespite the presence of luminal extracellular mucin, several subnuclear mucin-filled vacuoles were also identified, occasionally expanding into cyst-like structures (). Periodic acid– Schiff and Alcian blue stains highlighted the extracellular and intracellular mucin, while the intracytoplasmic vacuoles were stained with Mayer’s mucicarmine (–).\nImmunoperoxidase stains demonstrated an intensely positive reaction for cytokeratin cocktail (CK AE1/AE3) in the membrane and cytoplasm () of cells, as well as for epithelial membrane antigen (EMA) with weak cytoplasmic expression and luminal border reinforcement (). Detection of progesterone receptors (PR) was markedly positive in 95% of cells, while estrogen receptors (ER) and androgen receptors were moderately and weakly positive in 70% and 10% of cells, respectively (–). The proliferation index labeled with Ki-67 was rated in approximately 3% of cells (). Surprisingly, cyclin D1 staining was observed in nearly 90% of cells (). No reaction was detected toward a variety of factors, including carcinoembryonic antigen (CEA), human chorionic gonadotropin, human epidermal growth factor receptor 2 (HER2/Neu), or B-cell lymphoma 2 protein (Bcl-2).\nAccordingly, the proliferation was diagnosed as a metaplastic papillary tumor of the Fallopian tube, with a note to the clinician about the benign behavior of the alteration.

A 30-year-old woman visited the outpatient clinic seeking treatment for abdominal\ndistention present since the last 4 months. She had no history of surgery. Bowel and\nbladder functions were normal. Menstruation was regular and without any pain. The\npatient was nulliparous. Computed tomography (CT) scan with contrast showed a thin\nwalled unilocular cyst arising from the left adnexa with dimensions of\n22.3 cm × 18.4 cm × 6.8 cm; no papillary projections or nodules were observed (). The Ca 125 level\nwas 13.64 U/mL.\nBecause of the large size of the cyst and the patient’s preference, a laparotomy was\nperformed. We performed a midline incision above the umbilicus, trying to\nexteriorize the cyst without any rupture. Intraoperative exploration showed a large,\nthin-walled, unilocular cyst arising from the left para-tubal tissue without any\nadhesions; the left tube and left ovary were normal (). The para tubal cyst was dissected\nto separate it from the normal ovary and tube (). The para tubal cyst was removed\nand sent for histopathological examination (). The left tube and left ovary were\npreserved (). The\nuterus and right adnexa were normal. Frozen section examination confirmed by final\nhistopathological examination revealed a benign serous cyst of size\n22 cm × 17 cm × 6 cm.\nWritten, informed consent was obtained from the patient for the publication of this\nreport and its accompanying images ().

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

The patient is a 25-year-old woman, gravida 0, who was referred to the gynecology oncology division at Chonnam National University Hospital with lower abdominal pain and abdominal mass. Her gynecologic history was unremarkable. Physical examination was notable for abdominal mass that was near at xiphoid process. Pelvic ultrasound revealed about more than 20 cm cystic mass. Magnetic resonance imaging of the pelvis revealed about 23×21×9 cm sized serous borderline cystic tumor in the right ovary and 2.2 cm corpus luteum of the left ovary. There was no remarkable findings in the uterus and no abnormal pelvic lymphadenopathy. The tumor marker profile was as follows: CA-125 38.2 U/mL (0-35). Another tumor markers and the result of hematological analyses were within their normal ranges.\nExploration of the abdominopelvic cavity revealed about 23 cm sized brownish fluid contained cyst located within the right fallopian tube. Its surface was clear and on cut section, it had multiple papillary growing in inner surface (). The left ovary had about 1 cm sized whitish nodule. A right salpingectomy, left ovary wedge biopsy, appendectomy and cytology were performed. A frozen section of the right fallopian tube revealed a serous borderline tumor. And a frozen section of the left ovary revealed a fibroma. Exploration of the right ovary and left tube was unremarkable, and, in view of patient's age and desire for future fertility, no further surgical procedure was undertaken. Histologically, right tubal mass was serous borderline tumor and appendix uninvolved by tumor cells and cytology of peritoneal washing fluid was negative for malignant cells. Tumor had cystic change and papillary nodules. On microscopic examination the papillae were covered by serous type of epithelium (), displaying stratification and budding with focal nuclear atypia (). There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Micropapillary pattern of the tumor was absent and there was no papillary tubal hyperplasia in the fallopian tube. In general, the histology of the tumor was similar to that of an ovarian borderline serous tumor. Pathologic diagnosis was serous borderline tumor of the right fallopian tube. Close follow-up was recommended and currently, the patient's postoperative recovery was uneventful.

A 31-year-old woman presented with abdominal distention and discomfort worsening over the past 6 months. Concurrently, she had development overactive bladder symptoms, bloating, and dyspepsia. Her medical history was pertinent for epilepsy controlled with antiepileptic medications. Urine analysis was negative for any signs of infection, and her pregnancy test was negative. Abdominal examination was positive for a firm and distended abdomen, uniformly enlarged from the xiphoid bone to the pubic symphysis. No tenderness was reported on palpation; however, pressure was endorsed. A bedside abdominal ultrasound was performed that revealed an abdomen fully distended with fluid, initially suspected to be ascites. Computed tomography in 2.5 mm helical slices with both IV and oral contrast suggested the presence of an encapsulated cystic mass containing clear fluid (6 Hounsfield units). Dimensions reported were 36 cm in long axis, 28 cm in transverse diameter, and 15 cm in anteroposterior diameter, corresponding to 7 liters in volume, suggestive of a right ovarian cystadenoma (Figures and ). No capsular irregularities were seen or intracystic vegetations identified. Concurrently noted was right renal pelvicalyceal dilatation resulting from compression due to the proximity of the right ureter with the renal pelvis measuring 2 cm in anteroposterior diameter. No abdominal ascites or other abdominopelvic abnormalities noted. Tumor markers were in the normal ranges (CA125: 12.13 U/ml, CEA:1.51 ng/ml, and AFP: 1.46 IU/ml). While understanding her risks, the patient stressed the avoidance of excision of ovarian or fallopian tissue due to fertility concerns and preferred that the cyst be removed in a cosmetic manner including avoidance of larger laparotomy incisions.\nThe patient underwent resection of the mass. The procedure was begun by drainage of the cyst in order to identify the stalk and excise all cyst walls. A 3 cm supraumbilical incision was performed with careful dissection until reaching the peritoneal cavity. An Alexis O™ wound protector/retractor Applied Medical was introduced through the small incision permitting better visualization of the cyst (). Three hemostats were used to hold the cyst wall in place, followed by meticulous introduction of an 11 mm trocar into the cyst cavity under direct vision. This was followed by insertion of a 5 mm suction tube through the trocar to aspirate the fluid contents while avoiding spillage of fluid into the peritoneal cavity. Eight liters of serous fluid were aspirated. Following fluid evacuation, the cyst wall had collapsed. The trocar site in the cyst wall was sutured shut in a purse-string manner followed by a second closure layer. Then, the cyst was released off the hemostats, and the laparoscopic gel cap was fitted onto the Alexis retractor to convert the abdominal incision into a laparoscopic port site. This was used to insufflate the abdomen with CO2. Thereafter, 2 additional 5 mm trocars on each side of the midline were introduced.\nThe cyst borders were identified (). Using the bipolar forceps and scissors, it was completely dissected off the fallopian tube. Both the fallopian tube and ovarian tissues were noted to be intact. The cyst was removed through the supraumbilical incision and sent to pathology. The trocars were removed and all incisions approximated as per protocol. The patient was discharged soon thereafter from the observation unit.

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

The patient is a 25-year-old woman, gravida 0, who was referred to the gynecology oncology division at Chonnam National University Hospital with lower abdominal pain and abdominal mass. Her gynecologic history was unremarkable. Physical examination was notable for abdominal mass that was near at xiphoid process. Pelvic ultrasound revealed about more than 20 cm cystic mass. Magnetic resonance imaging of the pelvis revealed about 23×21×9 cm sized serous borderline cystic tumor in the right ovary and 2.2 cm corpus luteum of the left ovary. There was no remarkable findings in the uterus and no abnormal pelvic lymphadenopathy. The tumor marker profile was as follows: CA-125 38.2 U/mL (0-35). Another tumor markers and the result of hematological analyses were within their normal ranges.\nExploration of the abdominopelvic cavity revealed about 23 cm sized brownish fluid contained cyst located within the right fallopian tube. Its surface was clear and on cut section, it had multiple papillary growing in inner surface (). The left ovary had about 1 cm sized whitish nodule. A right salpingectomy, left ovary wedge biopsy, appendectomy and cytology were performed. A frozen section of the right fallopian tube revealed a serous borderline tumor. And a frozen section of the left ovary revealed a fibroma. Exploration of the right ovary and left tube was unremarkable, and, in view of patient's age and desire for future fertility, no further surgical procedure was undertaken. Histologically, right tubal mass was serous borderline tumor and appendix uninvolved by tumor cells and cytology of peritoneal washing fluid was negative for malignant cells. Tumor had cystic change and papillary nodules. On microscopic examination the papillae were covered by serous type of epithelium (), displaying stratification and budding with focal nuclear atypia (). There was no invasion of the supportive stroma of the papillae or into the fallopian tube wall. Micropapillary pattern of the tumor was absent and there was no papillary tubal hyperplasia in the fallopian tube. In general, the histology of the tumor was similar to that of an ovarian borderline serous tumor. Pathologic diagnosis was serous borderline tumor of the right fallopian tube. Close follow-up was recommended and currently, the patient's postoperative recovery was uneventful.

A 30-year-old woman visited the outpatient clinic seeking treatment for abdominal\ndistention present since the last 4 months. She had no history of surgery. Bowel and\nbladder functions were normal. Menstruation was regular and without any pain. The\npatient was nulliparous. Computed tomography (CT) scan with contrast showed a thin\nwalled unilocular cyst arising from the left adnexa with dimensions of\n22.3 cm × 18.4 cm × 6.8 cm; no papillary projections or nodules were observed (). The Ca 125 level\nwas 13.64 U/mL.\nBecause of the large size of the cyst and the patient’s preference, a laparotomy was\nperformed. We performed a midline incision above the umbilicus, trying to\nexteriorize the cyst without any rupture. Intraoperative exploration showed a large,\nthin-walled, unilocular cyst arising from the left para-tubal tissue without any\nadhesions; the left tube and left ovary were normal (). The para tubal cyst was dissected\nto separate it from the normal ovary and tube (). The para tubal cyst was removed\nand sent for histopathological examination (). The left tube and left ovary were\npreserved (). The\nuterus and right adnexa were normal. Frozen section examination confirmed by final\nhistopathological examination revealed a benign serous cyst of size\n22 cm × 17 cm × 6 cm.\nWritten, informed consent was obtained from the patient for the publication of this\nreport and its accompanying images ().

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 31-year-old woman presented with abdominal distention and discomfort worsening over the past 6 months. Concurrently, she had development overactive bladder symptoms, bloating, and dyspepsia. Her medical history was pertinent for epilepsy controlled with antiepileptic medications. Urine analysis was negative for any signs of infection, and her pregnancy test was negative. Abdominal examination was positive for a firm and distended abdomen, uniformly enlarged from the xiphoid bone to the pubic symphysis. No tenderness was reported on palpation; however, pressure was endorsed. A bedside abdominal ultrasound was performed that revealed an abdomen fully distended with fluid, initially suspected to be ascites. Computed tomography in 2.5 mm helical slices with both IV and oral contrast suggested the presence of an encapsulated cystic mass containing clear fluid (6 Hounsfield units). Dimensions reported were 36 cm in long axis, 28 cm in transverse diameter, and 15 cm in anteroposterior diameter, corresponding to 7 liters in volume, suggestive of a right ovarian cystadenoma (Figures and ). No capsular irregularities were seen or intracystic vegetations identified. Concurrently noted was right renal pelvicalyceal dilatation resulting from compression due to the proximity of the right ureter with the renal pelvis measuring 2 cm in anteroposterior diameter. No abdominal ascites or other abdominopelvic abnormalities noted. Tumor markers were in the normal ranges (CA125: 12.13 U/ml, CEA:1.51 ng/ml, and AFP: 1.46 IU/ml). While understanding her risks, the patient stressed the avoidance of excision of ovarian or fallopian tissue due to fertility concerns and preferred that the cyst be removed in a cosmetic manner including avoidance of larger laparotomy incisions.\nThe patient underwent resection of the mass. The procedure was begun by drainage of the cyst in order to identify the stalk and excise all cyst walls. A 3 cm supraumbilical incision was performed with careful dissection until reaching the peritoneal cavity. An Alexis O™ wound protector/retractor Applied Medical was introduced through the small incision permitting better visualization of the cyst (). Three hemostats were used to hold the cyst wall in place, followed by meticulous introduction of an 11 mm trocar into the cyst cavity under direct vision. This was followed by insertion of a 5 mm suction tube through the trocar to aspirate the fluid contents while avoiding spillage of fluid into the peritoneal cavity. Eight liters of serous fluid were aspirated. Following fluid evacuation, the cyst wall had collapsed. The trocar site in the cyst wall was sutured shut in a purse-string manner followed by a second closure layer. Then, the cyst was released off the hemostats, and the laparoscopic gel cap was fitted onto the Alexis retractor to convert the abdominal incision into a laparoscopic port site. This was used to insufflate the abdomen with CO2. Thereafter, 2 additional 5 mm trocars on each side of the midline were introduced.\nThe cyst borders were identified (). Using the bipolar forceps and scissors, it was completely dissected off the fallopian tube. Both the fallopian tube and ovarian tissues were noted to be intact. The cyst was removed through the supraumbilical incision and sent to pathology. The trocars were removed and all incisions approximated as per protocol. The patient was discharged soon thereafter from the observation unit.

A 30-year-old woman visited the outpatient clinic seeking treatment for abdominal\ndistention present since the last 4 months. She had no history of surgery. Bowel and\nbladder functions were normal. Menstruation was regular and without any pain. The\npatient was nulliparous. Computed tomography (CT) scan with contrast showed a thin\nwalled unilocular cyst arising from the left adnexa with dimensions of\n22.3 cm × 18.4 cm × 6.8 cm; no papillary projections or nodules were observed (). The Ca 125 level\nwas 13.64 U/mL.\nBecause of the large size of the cyst and the patient’s preference, a laparotomy was\nperformed. We performed a midline incision above the umbilicus, trying to\nexteriorize the cyst without any rupture. Intraoperative exploration showed a large,\nthin-walled, unilocular cyst arising from the left para-tubal tissue without any\nadhesions; the left tube and left ovary were normal (). The para tubal cyst was dissected\nto separate it from the normal ovary and tube (). The para tubal cyst was removed\nand sent for histopathological examination (). The left tube and left ovary were\npreserved (). The\nuterus and right adnexa were normal. Frozen section examination confirmed by final\nhistopathological examination revealed a benign serous cyst of size\n22 cm × 17 cm × 6 cm.\nWritten, informed consent was obtained from the patient for the publication of this\nreport and its accompanying images ().

Write a detailed clinical case vignette based on the following key phrases: Female reproductive system, Cystic tumors, Gynecologic surgery

A 49-year-old female presented to her primary care physician with fever and pruritic rash for four days. She denied symptoms of conjunctivitis and joint pain. Three days before the onset of symptoms, she returned with her husband (see Case 6 above) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA was positive in urine. Serum was not tested for ZIKV (RNA or IgM) nor was serologic testing done for chikungunya or dengue viruses. ZIKV test results for all cases can be seen in Table .

A 56-year-old female presented to her primary care physician with fever, conjunctivitis, arthralgia, and a rash on her chest, arms, and neck. She reported recent travel to Jamaica. History regarding trip duration and timing relative to symptom onset is not available. Body fluid samples were collected, and RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serum RT-PCR RNA for dengue virus was negative. Serology for dengue virus was negative for IgM and positive for IgG. Serum RT-PCR for chikungunya virus RNA was negative.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 48-year-old male presented to his primary care physician with fever, pruritic rash, conjunctivitis, and joint pain for four days. Three days before the onset of symptoms, he returned with his wife (see Case 7 below) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA in serum and urine as well as Zika IgM ELISA in serum were all positive. The patient was not tested for dengue or chikungunya virus.

A 56-year-old female presented to her primary care physician with fever, conjunctivitis, arthralgia, and a rash on her chest, arms, and neck. She reported recent travel to Jamaica. History regarding trip duration and timing relative to symptom onset is not available. Body fluid samples were collected, and RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serum RT-PCR RNA for dengue virus was negative. Serology for dengue virus was negative for IgM and positive for IgG. Serum RT-PCR for chikungunya virus RNA was negative.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 56-year-old male presented to the emergency department complaining of fever, joint pain, and a generalized rash for three days. He denied headache or ocular complaints. He denied any recent travel. The patient works outdoors at a hotel in the South Beach neighborhood of Miami Beach, Florida, an area known to have active vector-borne transmission of ZIKV at the time of the patient’s presentation []. On physical exam, the patient was afebrile and hemodynamically stable. He had a generalized erythematous maculopapular rash and no other relevant physical findings, including ocular manifestations. Blood urea nitrogen (BUN) and creatinine were elevated (BUN: 23 mg/dL, normal range: 6–22 mg/dL; creatinine: 1.32 mg/dL, normal range: 0.43–1.13 mg/dL). Otherwise, blood chemistry tests were within normal limits. Hematologic tests were all within normal limits. RT-PCR for ZIKV RNA was positive in urine, though the results were not available until after discharge, as the sample was analyzed at an offsite laboratory. Serum was not tested for ZIKV, chikungunya, or dengue viruses. The patient was treated with one dose of ketorolac 30 mg IV. On discharge, the patient was instructed to follow up with his primary care physician.

A 56-year-old female presented to her primary care physician with fever, conjunctivitis, arthralgia, and a rash on her chest, arms, and neck. She reported recent travel to Jamaica. History regarding trip duration and timing relative to symptom onset is not available. Body fluid samples were collected, and RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serum RT-PCR RNA for dengue virus was negative. Serology for dengue virus was negative for IgM and positive for IgG. Serum RT-PCR for chikungunya virus RNA was negative.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 33-year old female presented to the emergency department complaining of a gradually worsening rash localized to her chest, neck, and right side of her face for two days. Associated symptoms were fatigue, sore throat, nasal congestion, “itchy, red, watery eyes,” and myalgia. She denied fever, chills, and arthralgia. She had returned to the United States from the Dominican Republic one week prior, but she did not recall being bitten by a mosquito. She reported that her son had a positive test for ZIKV. On physical exam, the patient was afebrile and hemodynamically stable. She had an erythematous posterior pharynx and a trace fine papular rash on the chest, neck, and right face. Blood chemistry tests were all within normal limits. Hematologic tests showed mild anemia (hemoglobin 11.9 g/dL, normal range: 12.0–16.0 g/dL), mildly increased lymphocyte percentage (44.0%, normal range: 23.0–43.0%), and mildly increased monocyte percentage (10.7%, normal range: 0.0–10.0%). RT-PCR for ZIKV RNA was positive in urine and negative in serum. The patient was not tested for chikungunya or dengue virus infections. The ZIKV blood and urine samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: diphenhydramine 25 mg IV, acetaminophen 975 mg IV, and ondansetron 4 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 56-year-old female presented to her primary care physician with fever, conjunctivitis, arthralgia, and a rash on her chest, arms, and neck. She reported recent travel to Jamaica. History regarding trip duration and timing relative to symptom onset is not available. Body fluid samples were collected, and RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serum RT-PCR RNA for dengue virus was negative. Serology for dengue virus was negative for IgM and positive for IgG. Serum RT-PCR for chikungunya virus RNA was negative.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 28-year-old female presented to the emergency department complaining of fever, generalized rash, arthralgia, and myalgia. She denied any headache or ocular complaints. She recently traveled to the Dominican Republic where she described having been bitten by mosquitos. History regarding trip duration and timing relative to symptom onset is not available. On physical exam, the patient was afebrile and hemodynamically stable. She had a generalized maculopapular rash and no other relevant physical exam findings, including ocular manifestations. Blood chemistry tests were all within normal limits. Hematologic tests showed very mildly increased monocyte percentage (10.8%, normal range: 0.0–10.0%) with a normal white blood cell count. Laboratory findings were positive for RT-PCR for ZIKV RNA in urine and negative in serum. Chikungunya (IgM and Immunoglobulin G [IgG]) and dengue (IgM) virus serology were negative. Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available until after discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: morphine 2 mg IV, ondansetron 4 mg IV, and methylprednisolone 80 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 56-year-old female presented to her primary care physician with fever, conjunctivitis, arthralgia, and a rash on her chest, arms, and neck. She reported recent travel to Jamaica. History regarding trip duration and timing relative to symptom onset is not available. Body fluid samples were collected, and RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serum RT-PCR RNA for dengue virus was negative. Serology for dengue virus was negative for IgM and positive for IgG. Serum RT-PCR for chikungunya virus RNA was negative.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 17-year-old male presented to the emergency department due to his father’s concern that the patient was infected with ZIKV. He had no complaints or symptoms at the time of the visit. The patient reported experiencing joint pain, pruritic generalized rash, headache, and fever on the previous day. He denied any ocular complaints. He had returned from Puerto Rico on the previous day. While in Puerto Rico, he was in contact with a friend who experienced the same symptoms. Per the patient, the friend’s physician told him he had a viral condition. On physical exam, he was afebrile and hemodynamically stable. There were no positive relevant findings on physical exam. Blood chemistry tests were all within normal limits. Hematologic tests showed a mildly decreased white blood cell count (3.1 × 103/mL, normal range: 4.5–13.5 × 103/mL) and a mildly increased hemoglobin (15.3 g/dL, normal range: 11.0–15.0 g/dL) and hematocrit (43.7%, 33.0–43.0%). Lymphocyte percentage was decreased (0.9 × 103/µL, normal range: 1.2–6.4 × 103/µL). RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serology was positive for dengue virus (IgM positive, IgG negative) and negative for chikungunya virus (IgM and IgG negative). Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. The patient received no treatment during this visit. On discharge, the patient was instructed to follow up with his primary care physician and to avoid sexual contact.

A 56-year-old female presented to her primary care physician with fever, conjunctivitis, arthralgia, and a rash on her chest, arms, and neck. She reported recent travel to Jamaica. History regarding trip duration and timing relative to symptom onset is not available. Body fluid samples were collected, and RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serum RT-PCR RNA for dengue virus was negative. Serology for dengue virus was negative for IgM and positive for IgG. Serum RT-PCR for chikungunya virus RNA was negative.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 48-year-old male presented to his primary care physician with fever, pruritic rash, conjunctivitis, and joint pain for four days. Three days before the onset of symptoms, he returned with his wife (see Case 7 below) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA in serum and urine as well as Zika IgM ELISA in serum were all positive. The patient was not tested for dengue or chikungunya virus.

A 49-year-old female presented to her primary care physician with fever and pruritic rash for four days. She denied symptoms of conjunctivitis and joint pain. Three days before the onset of symptoms, she returned with her husband (see Case 6 above) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA was positive in urine. Serum was not tested for ZIKV (RNA or IgM) nor was serologic testing done for chikungunya or dengue viruses. ZIKV test results for all cases can be seen in Table .

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 56-year-old male presented to the emergency department complaining of fever, joint pain, and a generalized rash for three days. He denied headache or ocular complaints. He denied any recent travel. The patient works outdoors at a hotel in the South Beach neighborhood of Miami Beach, Florida, an area known to have active vector-borne transmission of ZIKV at the time of the patient’s presentation []. On physical exam, the patient was afebrile and hemodynamically stable. He had a generalized erythematous maculopapular rash and no other relevant physical findings, including ocular manifestations. Blood urea nitrogen (BUN) and creatinine were elevated (BUN: 23 mg/dL, normal range: 6–22 mg/dL; creatinine: 1.32 mg/dL, normal range: 0.43–1.13 mg/dL). Otherwise, blood chemistry tests were within normal limits. Hematologic tests were all within normal limits. RT-PCR for ZIKV RNA was positive in urine, though the results were not available until after discharge, as the sample was analyzed at an offsite laboratory. Serum was not tested for ZIKV, chikungunya, or dengue viruses. The patient was treated with one dose of ketorolac 30 mg IV. On discharge, the patient was instructed to follow up with his primary care physician.

A 49-year-old female presented to her primary care physician with fever and pruritic rash for four days. She denied symptoms of conjunctivitis and joint pain. Three days before the onset of symptoms, she returned with her husband (see Case 6 above) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA was positive in urine. Serum was not tested for ZIKV (RNA or IgM) nor was serologic testing done for chikungunya or dengue viruses. ZIKV test results for all cases can be seen in Table .

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 33-year old female presented to the emergency department complaining of a gradually worsening rash localized to her chest, neck, and right side of her face for two days. Associated symptoms were fatigue, sore throat, nasal congestion, “itchy, red, watery eyes,” and myalgia. She denied fever, chills, and arthralgia. She had returned to the United States from the Dominican Republic one week prior, but she did not recall being bitten by a mosquito. She reported that her son had a positive test for ZIKV. On physical exam, the patient was afebrile and hemodynamically stable. She had an erythematous posterior pharynx and a trace fine papular rash on the chest, neck, and right face. Blood chemistry tests were all within normal limits. Hematologic tests showed mild anemia (hemoglobin 11.9 g/dL, normal range: 12.0–16.0 g/dL), mildly increased lymphocyte percentage (44.0%, normal range: 23.0–43.0%), and mildly increased monocyte percentage (10.7%, normal range: 0.0–10.0%). RT-PCR for ZIKV RNA was positive in urine and negative in serum. The patient was not tested for chikungunya or dengue virus infections. The ZIKV blood and urine samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: diphenhydramine 25 mg IV, acetaminophen 975 mg IV, and ondansetron 4 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 49-year-old female presented to her primary care physician with fever and pruritic rash for four days. She denied symptoms of conjunctivitis and joint pain. Three days before the onset of symptoms, she returned with her husband (see Case 6 above) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA was positive in urine. Serum was not tested for ZIKV (RNA or IgM) nor was serologic testing done for chikungunya or dengue viruses. ZIKV test results for all cases can be seen in Table .

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 28-year-old female presented to the emergency department complaining of fever, generalized rash, arthralgia, and myalgia. She denied any headache or ocular complaints. She recently traveled to the Dominican Republic where she described having been bitten by mosquitos. History regarding trip duration and timing relative to symptom onset is not available. On physical exam, the patient was afebrile and hemodynamically stable. She had a generalized maculopapular rash and no other relevant physical exam findings, including ocular manifestations. Blood chemistry tests were all within normal limits. Hematologic tests showed very mildly increased monocyte percentage (10.8%, normal range: 0.0–10.0%) with a normal white blood cell count. Laboratory findings were positive for RT-PCR for ZIKV RNA in urine and negative in serum. Chikungunya (IgM and Immunoglobulin G [IgG]) and dengue (IgM) virus serology were negative. Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available until after discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: morphine 2 mg IV, ondansetron 4 mg IV, and methylprednisolone 80 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 49-year-old female presented to her primary care physician with fever and pruritic rash for four days. She denied symptoms of conjunctivitis and joint pain. Three days before the onset of symptoms, she returned with her husband (see Case 6 above) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA was positive in urine. Serum was not tested for ZIKV (RNA or IgM) nor was serologic testing done for chikungunya or dengue viruses. ZIKV test results for all cases can be seen in Table .

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 17-year-old male presented to the emergency department due to his father’s concern that the patient was infected with ZIKV. He had no complaints or symptoms at the time of the visit. The patient reported experiencing joint pain, pruritic generalized rash, headache, and fever on the previous day. He denied any ocular complaints. He had returned from Puerto Rico on the previous day. While in Puerto Rico, he was in contact with a friend who experienced the same symptoms. Per the patient, the friend’s physician told him he had a viral condition. On physical exam, he was afebrile and hemodynamically stable. There were no positive relevant findings on physical exam. Blood chemistry tests were all within normal limits. Hematologic tests showed a mildly decreased white blood cell count (3.1 × 103/mL, normal range: 4.5–13.5 × 103/mL) and a mildly increased hemoglobin (15.3 g/dL, normal range: 11.0–15.0 g/dL) and hematocrit (43.7%, 33.0–43.0%). Lymphocyte percentage was decreased (0.9 × 103/µL, normal range: 1.2–6.4 × 103/µL). RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serology was positive for dengue virus (IgM positive, IgG negative) and negative for chikungunya virus (IgM and IgG negative). Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. The patient received no treatment during this visit. On discharge, the patient was instructed to follow up with his primary care physician and to avoid sexual contact.

A 49-year-old female presented to her primary care physician with fever and pruritic rash for four days. She denied symptoms of conjunctivitis and joint pain. Three days before the onset of symptoms, she returned with her husband (see Case 6 above) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA was positive in urine. Serum was not tested for ZIKV (RNA or IgM) nor was serologic testing done for chikungunya or dengue viruses. ZIKV test results for all cases can be seen in Table .

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 56-year-old male presented to the emergency department complaining of fever, joint pain, and a generalized rash for three days. He denied headache or ocular complaints. He denied any recent travel. The patient works outdoors at a hotel in the South Beach neighborhood of Miami Beach, Florida, an area known to have active vector-borne transmission of ZIKV at the time of the patient’s presentation []. On physical exam, the patient was afebrile and hemodynamically stable. He had a generalized erythematous maculopapular rash and no other relevant physical findings, including ocular manifestations. Blood urea nitrogen (BUN) and creatinine were elevated (BUN: 23 mg/dL, normal range: 6–22 mg/dL; creatinine: 1.32 mg/dL, normal range: 0.43–1.13 mg/dL). Otherwise, blood chemistry tests were within normal limits. Hematologic tests were all within normal limits. RT-PCR for ZIKV RNA was positive in urine, though the results were not available until after discharge, as the sample was analyzed at an offsite laboratory. Serum was not tested for ZIKV, chikungunya, or dengue viruses. The patient was treated with one dose of ketorolac 30 mg IV. On discharge, the patient was instructed to follow up with his primary care physician.

A 48-year-old male presented to his primary care physician with fever, pruritic rash, conjunctivitis, and joint pain for four days. Three days before the onset of symptoms, he returned with his wife (see Case 7 below) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA in serum and urine as well as Zika IgM ELISA in serum were all positive. The patient was not tested for dengue or chikungunya virus.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 33-year old female presented to the emergency department complaining of a gradually worsening rash localized to her chest, neck, and right side of her face for two days. Associated symptoms were fatigue, sore throat, nasal congestion, “itchy, red, watery eyes,” and myalgia. She denied fever, chills, and arthralgia. She had returned to the United States from the Dominican Republic one week prior, but she did not recall being bitten by a mosquito. She reported that her son had a positive test for ZIKV. On physical exam, the patient was afebrile and hemodynamically stable. She had an erythematous posterior pharynx and a trace fine papular rash on the chest, neck, and right face. Blood chemistry tests were all within normal limits. Hematologic tests showed mild anemia (hemoglobin 11.9 g/dL, normal range: 12.0–16.0 g/dL), mildly increased lymphocyte percentage (44.0%, normal range: 23.0–43.0%), and mildly increased monocyte percentage (10.7%, normal range: 0.0–10.0%). RT-PCR for ZIKV RNA was positive in urine and negative in serum. The patient was not tested for chikungunya or dengue virus infections. The ZIKV blood and urine samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: diphenhydramine 25 mg IV, acetaminophen 975 mg IV, and ondansetron 4 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 48-year-old male presented to his primary care physician with fever, pruritic rash, conjunctivitis, and joint pain for four days. Three days before the onset of symptoms, he returned with his wife (see Case 7 below) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA in serum and urine as well as Zika IgM ELISA in serum were all positive. The patient was not tested for dengue or chikungunya virus.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 48-year-old male presented to his primary care physician with fever, pruritic rash, conjunctivitis, and joint pain for four days. Three days before the onset of symptoms, he returned with his wife (see Case 7 below) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA in serum and urine as well as Zika IgM ELISA in serum were all positive. The patient was not tested for dengue or chikungunya virus.

A 28-year-old female presented to the emergency department complaining of fever, generalized rash, arthralgia, and myalgia. She denied any headache or ocular complaints. She recently traveled to the Dominican Republic where she described having been bitten by mosquitos. History regarding trip duration and timing relative to symptom onset is not available. On physical exam, the patient was afebrile and hemodynamically stable. She had a generalized maculopapular rash and no other relevant physical exam findings, including ocular manifestations. Blood chemistry tests were all within normal limits. Hematologic tests showed very mildly increased monocyte percentage (10.8%, normal range: 0.0–10.0%) with a normal white blood cell count. Laboratory findings were positive for RT-PCR for ZIKV RNA in urine and negative in serum. Chikungunya (IgM and Immunoglobulin G [IgG]) and dengue (IgM) virus serology were negative. Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available until after discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: morphine 2 mg IV, ondansetron 4 mg IV, and methylprednisolone 80 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 48-year-old male presented to his primary care physician with fever, pruritic rash, conjunctivitis, and joint pain for four days. Three days before the onset of symptoms, he returned with his wife (see Case 7 below) from a 12-day trip to Saint Martin and Saint Barthélemy: territories with known vector-borne ZIKV transmission []. The patient denied sexual contact with anybody who had “recently returned from a country where Zika has been spreading.” RT-PCR for ZIKV RNA in serum and urine as well as Zika IgM ELISA in serum were all positive. The patient was not tested for dengue or chikungunya virus.

A 17-year-old male presented to the emergency department due to his father’s concern that the patient was infected with ZIKV. He had no complaints or symptoms at the time of the visit. The patient reported experiencing joint pain, pruritic generalized rash, headache, and fever on the previous day. He denied any ocular complaints. He had returned from Puerto Rico on the previous day. While in Puerto Rico, he was in contact with a friend who experienced the same symptoms. Per the patient, the friend’s physician told him he had a viral condition. On physical exam, he was afebrile and hemodynamically stable. There were no positive relevant findings on physical exam. Blood chemistry tests were all within normal limits. Hematologic tests showed a mildly decreased white blood cell count (3.1 × 103/mL, normal range: 4.5–13.5 × 103/mL) and a mildly increased hemoglobin (15.3 g/dL, normal range: 11.0–15.0 g/dL) and hematocrit (43.7%, 33.0–43.0%). Lymphocyte percentage was decreased (0.9 × 103/µL, normal range: 1.2–6.4 × 103/µL). RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serology was positive for dengue virus (IgM positive, IgG negative) and negative for chikungunya virus (IgM and IgG negative). Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. The patient received no treatment during this visit. On discharge, the patient was instructed to follow up with his primary care physician and to avoid sexual contact.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 56-year-old male presented to the emergency department complaining of fever, joint pain, and a generalized rash for three days. He denied headache or ocular complaints. He denied any recent travel. The patient works outdoors at a hotel in the South Beach neighborhood of Miami Beach, Florida, an area known to have active vector-borne transmission of ZIKV at the time of the patient’s presentation []. On physical exam, the patient was afebrile and hemodynamically stable. He had a generalized erythematous maculopapular rash and no other relevant physical findings, including ocular manifestations. Blood urea nitrogen (BUN) and creatinine were elevated (BUN: 23 mg/dL, normal range: 6–22 mg/dL; creatinine: 1.32 mg/dL, normal range: 0.43–1.13 mg/dL). Otherwise, blood chemistry tests were within normal limits. Hematologic tests were all within normal limits. RT-PCR for ZIKV RNA was positive in urine, though the results were not available until after discharge, as the sample was analyzed at an offsite laboratory. Serum was not tested for ZIKV, chikungunya, or dengue viruses. The patient was treated with one dose of ketorolac 30 mg IV. On discharge, the patient was instructed to follow up with his primary care physician.

A 33-year old female presented to the emergency department complaining of a gradually worsening rash localized to her chest, neck, and right side of her face for two days. Associated symptoms were fatigue, sore throat, nasal congestion, “itchy, red, watery eyes,” and myalgia. She denied fever, chills, and arthralgia. She had returned to the United States from the Dominican Republic one week prior, but she did not recall being bitten by a mosquito. She reported that her son had a positive test for ZIKV. On physical exam, the patient was afebrile and hemodynamically stable. She had an erythematous posterior pharynx and a trace fine papular rash on the chest, neck, and right face. Blood chemistry tests were all within normal limits. Hematologic tests showed mild anemia (hemoglobin 11.9 g/dL, normal range: 12.0–16.0 g/dL), mildly increased lymphocyte percentage (44.0%, normal range: 23.0–43.0%), and mildly increased monocyte percentage (10.7%, normal range: 0.0–10.0%). RT-PCR for ZIKV RNA was positive in urine and negative in serum. The patient was not tested for chikungunya or dengue virus infections. The ZIKV blood and urine samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: diphenhydramine 25 mg IV, acetaminophen 975 mg IV, and ondansetron 4 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 56-year-old male presented to the emergency department complaining of fever, joint pain, and a generalized rash for three days. He denied headache or ocular complaints. He denied any recent travel. The patient works outdoors at a hotel in the South Beach neighborhood of Miami Beach, Florida, an area known to have active vector-borne transmission of ZIKV at the time of the patient’s presentation []. On physical exam, the patient was afebrile and hemodynamically stable. He had a generalized erythematous maculopapular rash and no other relevant physical findings, including ocular manifestations. Blood urea nitrogen (BUN) and creatinine were elevated (BUN: 23 mg/dL, normal range: 6–22 mg/dL; creatinine: 1.32 mg/dL, normal range: 0.43–1.13 mg/dL). Otherwise, blood chemistry tests were within normal limits. Hematologic tests were all within normal limits. RT-PCR for ZIKV RNA was positive in urine, though the results were not available until after discharge, as the sample was analyzed at an offsite laboratory. Serum was not tested for ZIKV, chikungunya, or dengue viruses. The patient was treated with one dose of ketorolac 30 mg IV. On discharge, the patient was instructed to follow up with his primary care physician.

A 28-year-old female presented to the emergency department complaining of fever, generalized rash, arthralgia, and myalgia. She denied any headache or ocular complaints. She recently traveled to the Dominican Republic where she described having been bitten by mosquitos. History regarding trip duration and timing relative to symptom onset is not available. On physical exam, the patient was afebrile and hemodynamically stable. She had a generalized maculopapular rash and no other relevant physical exam findings, including ocular manifestations. Blood chemistry tests were all within normal limits. Hematologic tests showed very mildly increased monocyte percentage (10.8%, normal range: 0.0–10.0%) with a normal white blood cell count. Laboratory findings were positive for RT-PCR for ZIKV RNA in urine and negative in serum. Chikungunya (IgM and Immunoglobulin G [IgG]) and dengue (IgM) virus serology were negative. Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available until after discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: morphine 2 mg IV, ondansetron 4 mg IV, and methylprednisolone 80 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 56-year-old male presented to the emergency department complaining of fever, joint pain, and a generalized rash for three days. He denied headache or ocular complaints. He denied any recent travel. The patient works outdoors at a hotel in the South Beach neighborhood of Miami Beach, Florida, an area known to have active vector-borne transmission of ZIKV at the time of the patient’s presentation []. On physical exam, the patient was afebrile and hemodynamically stable. He had a generalized erythematous maculopapular rash and no other relevant physical findings, including ocular manifestations. Blood urea nitrogen (BUN) and creatinine were elevated (BUN: 23 mg/dL, normal range: 6–22 mg/dL; creatinine: 1.32 mg/dL, normal range: 0.43–1.13 mg/dL). Otherwise, blood chemistry tests were within normal limits. Hematologic tests were all within normal limits. RT-PCR for ZIKV RNA was positive in urine, though the results were not available until after discharge, as the sample was analyzed at an offsite laboratory. Serum was not tested for ZIKV, chikungunya, or dengue viruses. The patient was treated with one dose of ketorolac 30 mg IV. On discharge, the patient was instructed to follow up with his primary care physician.

A 17-year-old male presented to the emergency department due to his father’s concern that the patient was infected with ZIKV. He had no complaints or symptoms at the time of the visit. The patient reported experiencing joint pain, pruritic generalized rash, headache, and fever on the previous day. He denied any ocular complaints. He had returned from Puerto Rico on the previous day. While in Puerto Rico, he was in contact with a friend who experienced the same symptoms. Per the patient, the friend’s physician told him he had a viral condition. On physical exam, he was afebrile and hemodynamically stable. There were no positive relevant findings on physical exam. Blood chemistry tests were all within normal limits. Hematologic tests showed a mildly decreased white blood cell count (3.1 × 103/mL, normal range: 4.5–13.5 × 103/mL) and a mildly increased hemoglobin (15.3 g/dL, normal range: 11.0–15.0 g/dL) and hematocrit (43.7%, 33.0–43.0%). Lymphocyte percentage was decreased (0.9 × 103/µL, normal range: 1.2–6.4 × 103/µL). RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serology was positive for dengue virus (IgM positive, IgG negative) and negative for chikungunya virus (IgM and IgG negative). Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. The patient received no treatment during this visit. On discharge, the patient was instructed to follow up with his primary care physician and to avoid sexual contact.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 33-year old female presented to the emergency department complaining of a gradually worsening rash localized to her chest, neck, and right side of her face for two days. Associated symptoms were fatigue, sore throat, nasal congestion, “itchy, red, watery eyes,” and myalgia. She denied fever, chills, and arthralgia. She had returned to the United States from the Dominican Republic one week prior, but she did not recall being bitten by a mosquito. She reported that her son had a positive test for ZIKV. On physical exam, the patient was afebrile and hemodynamically stable. She had an erythematous posterior pharynx and a trace fine papular rash on the chest, neck, and right face. Blood chemistry tests were all within normal limits. Hematologic tests showed mild anemia (hemoglobin 11.9 g/dL, normal range: 12.0–16.0 g/dL), mildly increased lymphocyte percentage (44.0%, normal range: 23.0–43.0%), and mildly increased monocyte percentage (10.7%, normal range: 0.0–10.0%). RT-PCR for ZIKV RNA was positive in urine and negative in serum. The patient was not tested for chikungunya or dengue virus infections. The ZIKV blood and urine samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: diphenhydramine 25 mg IV, acetaminophen 975 mg IV, and ondansetron 4 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 28-year-old female presented to the emergency department complaining of fever, generalized rash, arthralgia, and myalgia. She denied any headache or ocular complaints. She recently traveled to the Dominican Republic where she described having been bitten by mosquitos. History regarding trip duration and timing relative to symptom onset is not available. On physical exam, the patient was afebrile and hemodynamically stable. She had a generalized maculopapular rash and no other relevant physical exam findings, including ocular manifestations. Blood chemistry tests were all within normal limits. Hematologic tests showed very mildly increased monocyte percentage (10.8%, normal range: 0.0–10.0%) with a normal white blood cell count. Laboratory findings were positive for RT-PCR for ZIKV RNA in urine and negative in serum. Chikungunya (IgM and Immunoglobulin G [IgG]) and dengue (IgM) virus serology were negative. Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available until after discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: morphine 2 mg IV, ondansetron 4 mg IV, and methylprednisolone 80 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 33-year old female presented to the emergency department complaining of a gradually worsening rash localized to her chest, neck, and right side of her face for two days. Associated symptoms were fatigue, sore throat, nasal congestion, “itchy, red, watery eyes,” and myalgia. She denied fever, chills, and arthralgia. She had returned to the United States from the Dominican Republic one week prior, but she did not recall being bitten by a mosquito. She reported that her son had a positive test for ZIKV. On physical exam, the patient was afebrile and hemodynamically stable. She had an erythematous posterior pharynx and a trace fine papular rash on the chest, neck, and right face. Blood chemistry tests were all within normal limits. Hematologic tests showed mild anemia (hemoglobin 11.9 g/dL, normal range: 12.0–16.0 g/dL), mildly increased lymphocyte percentage (44.0%, normal range: 23.0–43.0%), and mildly increased monocyte percentage (10.7%, normal range: 0.0–10.0%). RT-PCR for ZIKV RNA was positive in urine and negative in serum. The patient was not tested for chikungunya or dengue virus infections. The ZIKV blood and urine samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: diphenhydramine 25 mg IV, acetaminophen 975 mg IV, and ondansetron 4 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 17-year-old male presented to the emergency department due to his father’s concern that the patient was infected with ZIKV. He had no complaints or symptoms at the time of the visit. The patient reported experiencing joint pain, pruritic generalized rash, headache, and fever on the previous day. He denied any ocular complaints. He had returned from Puerto Rico on the previous day. While in Puerto Rico, he was in contact with a friend who experienced the same symptoms. Per the patient, the friend’s physician told him he had a viral condition. On physical exam, he was afebrile and hemodynamically stable. There were no positive relevant findings on physical exam. Blood chemistry tests were all within normal limits. Hematologic tests showed a mildly decreased white blood cell count (3.1 × 103/mL, normal range: 4.5–13.5 × 103/mL) and a mildly increased hemoglobin (15.3 g/dL, normal range: 11.0–15.0 g/dL) and hematocrit (43.7%, 33.0–43.0%). Lymphocyte percentage was decreased (0.9 × 103/µL, normal range: 1.2–6.4 × 103/µL). RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serology was positive for dengue virus (IgM positive, IgG negative) and negative for chikungunya virus (IgM and IgG negative). Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. The patient received no treatment during this visit. On discharge, the patient was instructed to follow up with his primary care physician and to avoid sexual contact.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 28-year-old female presented to the emergency department complaining of fever, generalized rash, arthralgia, and myalgia. She denied any headache or ocular complaints. She recently traveled to the Dominican Republic where she described having been bitten by mosquitos. History regarding trip duration and timing relative to symptom onset is not available. On physical exam, the patient was afebrile and hemodynamically stable. She had a generalized maculopapular rash and no other relevant physical exam findings, including ocular manifestations. Blood chemistry tests were all within normal limits. Hematologic tests showed very mildly increased monocyte percentage (10.8%, normal range: 0.0–10.0%) with a normal white blood cell count. Laboratory findings were positive for RT-PCR for ZIKV RNA in urine and negative in serum. Chikungunya (IgM and Immunoglobulin G [IgG]) and dengue (IgM) virus serology were negative. Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available until after discharge. A pregnancy test was negative. The patient was treated with one dose of each of the following medications: morphine 2 mg IV, ondansetron 4 mg IV, and methylprednisolone 80 mg IV. She was also given 1 L of normal saline IV. On discharge, the patient was instructed to follow up with her primary care physician.

A 17-year-old male presented to the emergency department due to his father’s concern that the patient was infected with ZIKV. He had no complaints or symptoms at the time of the visit. The patient reported experiencing joint pain, pruritic generalized rash, headache, and fever on the previous day. He denied any ocular complaints. He had returned from Puerto Rico on the previous day. While in Puerto Rico, he was in contact with a friend who experienced the same symptoms. Per the patient, the friend’s physician told him he had a viral condition. On physical exam, he was afebrile and hemodynamically stable. There were no positive relevant findings on physical exam. Blood chemistry tests were all within normal limits. Hematologic tests showed a mildly decreased white blood cell count (3.1 × 103/mL, normal range: 4.5–13.5 × 103/mL) and a mildly increased hemoglobin (15.3 g/dL, normal range: 11.0–15.0 g/dL) and hematocrit (43.7%, 33.0–43.0%). Lymphocyte percentage was decreased (0.9 × 103/µL, normal range: 1.2–6.4 × 103/µL). RT-PCR for ZIKV RNA was positive in urine and negative in serum. Serology was positive for dengue virus (IgM positive, IgG negative) and negative for chikungunya virus (IgM and IgG negative). Body fluid samples were analyzed at an offsite laboratory; therefore, the results were not available at the time of discharge. The patient received no treatment during this visit. On discharge, the patient was instructed to follow up with his primary care physician and to avoid sexual contact.

Write a detailed clinical case vignette based on the following key phrases: Zika virus, travel history, rash and fever

A 79-year-old Taiwanese woman came to the otolaryngologic clinic of our hospital due to an enlarging painless mass over the right neck region in the past 3 months. She denied fever, night sweats, dyspnea, hoarseness, dysphagia, dysphasia, or stridor. On physical examination, the right thyroid lobe was noted to be enlarged and firm. There was a palpable mass in the front of her neck, which moved during swallowing. She had no history of Hashimoto's thyroiditis or cervical irradiation, and her thyroid function test was within the normal range (thyroid-stimulating hormone: 2.01 nIU/mL; free T4: 1.24 ng/dL; thyroglobulin: 1.62 ng/mL; anti-thyroperoxidase: 1.03 IU/mL; and thyroglobulin antibody: 1.81 IU/mL).\nThe patient had received computed tomography (CT) at hospital outside, which revealed a hypodense nodule with minimal enhancement on the right lobe of thyroid gland []. Its size was approximately 4.1 cm × 3.6 cm, with a longitudinal dimension of 4.5 cm. The trachea, vessels, and soft tissues in the right neck were under pressure and displaced toward the left side. She underwent fine-needle aspiration (FNA) at that hospital, and the cytologic results were suspicious of lymphoma.\nIn order to obtain more definite results, this woman was referred to the radiological department of our hospital for core needle biopsy. During core needle biopsy, the neck color Doppler ultrasound showed a large heterogeneous hypoechoic mass with an irregular border in the right lobe of thyroid gland. There were twisted and chaotic intranodular vessels, but no defined calcification, hemorrhage, or necrotic portion was observed within the mass, which exhibited indistinct margins and posterior acoustic enhancement [Figure and ]. The pathology revealed diffuse large B-cell lymphoma (DLBCL). For staging the disease, a fluorodeoxyglucose (FDG) positron emission tomography (PET) scan was performed, revealing high-grade hypermetabolic lymphomatous disease, confined in the right thyroid gland, suggesting PTL Ann Arbor stage I [].\nAfter consulting oncology specialists, she started rituximab-based chemotherapy and received serial sonographic follow-up. After three cycles of rituximab plus bendamustine – rituximab (375 mg/m2) and bendamustine (Innomustine®, 90 mg/m2) by intravenous administration on day 1 were administered every 3 weeks for each cycle – neck color Doppler ultrasound showed a significant reduction of twisted blood flow signals in the PTL but no significant decrease (<25% extent) of the tumor size []. Therefore, chemotherapy regimen was adjusted to rituximab, cyclophosphamide, vincristine, prednisone (R–COP). After three cycles of R–COP, i.e., rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), and vincristine (2 mg/m2) by intravenous administration on day 1 and prednisone (100 mg/m2) by oral administration on day 1–5 were administered every 3 weeks for each cycle, the PTL disappeared on the color Doppler and gray-scale ultrasonography []. The patient was treated with R–COP regimen until complete remission of the disease, confirmed on the following FDG PET-CT and whole-body PET examination [].

A 14-year-old white British Caucasian boy presented with a 3-month history of malaise, lethargy, and weight loss. There was no history of fever or any other thyroid related symptoms. Past and family history were noncontributory and there was no recent foreign travel. On examination he was found to have a large predominantly left-sided firm thyroid swelling. Clinical examination was otherwise unremarkable with no lymphadenopathy or hepatosplenomegaly or signs of hypo/hyperthyroidism. Baseline haematological and biochemical investigations on admission were within normal limits (Hb 136 g/L, WCC 9.1 109/L, CRP <4 mg/dL). Levels of thyroxine, TSH, and calcitonin were normal. Lactase dehydrogenase (LDH) was slightly elevated at 352 U/L. Thyroperoxidase was elevated (1277 IU/mL) and thyroid stimulating hormone receptor antibodies (TRAb) of <5 U/L. CSF analysis showed no tumour cells. EBV PCR was negative as was HIV-I and HIV-II.\nA fine needle aspiration biopsy was carried out and was suspicious of NHL. The diagnosis of Burkitt type NHL (BL) was made following an open wedge biopsy. On microscopic examination, the tumour was composed of diffuse sheets of lymphoid cells () having round nuclei with coarse chromatin and conspicuous single to multiple nucleoli and scanty amphophilic cytoplasm. Numerous mitotic figures, apoptosis, and scattered tingible body type macrophages were also present. Tumour cells were positive for CD79A, CD20, and CD10 and negative for TdT and T cell markers (CD3, CD4, and CD8). Ki 67 showed proliferation index approaching 100%. Immunohistochemistry for EBV was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t(8; 14) translocation.\nStaging CT () showed a large (6.7 cm × 5.8 cm × 6.1 cm) heterogeneous mass in the left lobe and isthmus of the thyroid which extended craniocaudally from level of C4/5 to T1/2, with some evidence of intratumoural necrosis. There was significant mass effect with displacement and compression of the trachea along with compression of the left carotid artery and lateral displacement of the left jugular vein. There were two small indeterminate lung nodules. Abdominally there were two focal cortical abnormalities in the right kidney and an ill-defined attenuation in the pancreatic head. There was no evidence of bone marrow involvement.\nHe was treated according to the Children's Cancer and Leukaemia Group guidelines for BL—Group B protocol. This consisted of initial induction chemotherapy with COP (cyclophosphamide [300 mg/m2], vincristine [1 mg/m2], and prednisolone [60 mg/m2—7 days]) followed by 2 courses of COPADM (doxorubicin 60 mg/m2, methotrexate 3 g/m2, cyclophosphamide 500 mg/m2/day—5 days, vincristine [2 mg/m2], and prednisolone [60 mg/m2—5 days]) and two courses of CYM (cytarabine 100 mg/m2/day—5 days and methotrexate 3 g/m2) chemotherapy. This was accompanied by intrathecal chemotherapy (the CSF contained no tumour cells at diagnosis). The patient had a good response to treatment with a rapid decrease in the size of the thyroid mass and resolution of the lung, kidney, and pancreas metastases. Reassessment after the first course of CYM showed a residual thyroid mass of 15 mm × 30 mm but with resolution of the lung, kidney, and pancreas metastases.\nBecause of residual radiological abnormality, and in accordance with the CCLG NHL protocol, a hemithyroidectomy was performed with the residual lesion showing no evidence of tumour cells on histological examination. Chemotherapy was then completed and he is now disease-free 3 years after end of treatment.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 79-year-old Taiwanese woman came to the otolaryngologic clinic of our hospital due to an enlarging painless mass over the right neck region in the past 3 months. She denied fever, night sweats, dyspnea, hoarseness, dysphagia, dysphasia, or stridor. On physical examination, the right thyroid lobe was noted to be enlarged and firm. There was a palpable mass in the front of her neck, which moved during swallowing. She had no history of Hashimoto's thyroiditis or cervical irradiation, and her thyroid function test was within the normal range (thyroid-stimulating hormone: 2.01 nIU/mL; free T4: 1.24 ng/dL; thyroglobulin: 1.62 ng/mL; anti-thyroperoxidase: 1.03 IU/mL; and thyroglobulin antibody: 1.81 IU/mL).\nThe patient had received computed tomography (CT) at hospital outside, which revealed a hypodense nodule with minimal enhancement on the right lobe of thyroid gland []. Its size was approximately 4.1 cm × 3.6 cm, with a longitudinal dimension of 4.5 cm. The trachea, vessels, and soft tissues in the right neck were under pressure and displaced toward the left side. She underwent fine-needle aspiration (FNA) at that hospital, and the cytologic results were suspicious of lymphoma.\nIn order to obtain more definite results, this woman was referred to the radiological department of our hospital for core needle biopsy. During core needle biopsy, the neck color Doppler ultrasound showed a large heterogeneous hypoechoic mass with an irregular border in the right lobe of thyroid gland. There were twisted and chaotic intranodular vessels, but no defined calcification, hemorrhage, or necrotic portion was observed within the mass, which exhibited indistinct margins and posterior acoustic enhancement [Figure and ]. The pathology revealed diffuse large B-cell lymphoma (DLBCL). For staging the disease, a fluorodeoxyglucose (FDG) positron emission tomography (PET) scan was performed, revealing high-grade hypermetabolic lymphomatous disease, confined in the right thyroid gland, suggesting PTL Ann Arbor stage I [].\nAfter consulting oncology specialists, she started rituximab-based chemotherapy and received serial sonographic follow-up. After three cycles of rituximab plus bendamustine – rituximab (375 mg/m2) and bendamustine (Innomustine®, 90 mg/m2) by intravenous administration on day 1 were administered every 3 weeks for each cycle – neck color Doppler ultrasound showed a significant reduction of twisted blood flow signals in the PTL but no significant decrease (<25% extent) of the tumor size []. Therefore, chemotherapy regimen was adjusted to rituximab, cyclophosphamide, vincristine, prednisone (R–COP). After three cycles of R–COP, i.e., rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), and vincristine (2 mg/m2) by intravenous administration on day 1 and prednisone (100 mg/m2) by oral administration on day 1–5 were administered every 3 weeks for each cycle, the PTL disappeared on the color Doppler and gray-scale ultrasonography []. The patient was treated with R–COP regimen until complete remission of the disease, confirmed on the following FDG PET-CT and whole-body PET examination [].

An eight-year-old male presented with a mass in the right anterior neck that had been apparent for one week. Upon physical examination, blood pressure was recorded as 100/65 mmHg, heart rate was 80 beats per min, respiratory rate was 20 breaths per min and temperature was 36.1°C. A mass measuring ~4.0 cm in size, which caused difficulty in swallowing, was identified in the right anterior neck. The laboratory test results demonstrated a normal blood count and serum biochemistry, as well as normal levels of electrolytes and carcinoembryonic antigen. In addition, the test results for Epstein-Barr virus (EBV) viral capsid antigens immunoglobulin (Ig)M and IgG, human immunodeficiency virus (HIV) and hepatitis C virus antibodies, hepatitis B antigen and syphilis were negative. Furthermore, the thyroid hormone test results were as follows: Free thyroxine (FT) 4 levels of 11.8 pmol/l (normal range, 9–25 pmol/l); FT3 levels of 4.2 pmol/l (normal range, 3–9 pmol/l); thyroid-stimulating hormone levels of 0.720 μIU/ml (normal range, 0.34–5.60 μIU/ml); anti-thyroglobulin levels of 20 IU/ml (normal range, <115 IU/ml); and anti-thyroid peroxidase levels of 25 IU/ml (normal range, <34 IU/ml). The patient had no significant past medical or family history of disease. A B-mode ultrasound examination revealed a mass measuring 4.0×3.0×2.5 cm in the right lobe of the thyroid (), however, the lymph nodes surrounding the mass were normal (). The patient underwent a right lobe and isthmus thyroidectomy whereby two lymph nodes were excised simultaneously. Following the surgery, positron emission tomography-computed tomography scans showed normal metabolism in the left lobe of the thyroid and other parts of the body (). The patient’s bone marrow cytology was also normal, however, histological examination revealed diffuse infiltration of atypical lymphocytes and the observation of residual thyroid follicles and necrosis (). In addition, under low magnification, the ‘starry sky’ histology was observed in certain areas (). The atypical lymphocytes were medium-sized and consistent, with centrally located nuclei of irregular shape, displaying dispersed and deep basophilic chromatin and scanty cytoplasm. Additionally, certain neoplastic cells were visible, while varying numbers of nucleoli and apoptosis and mitosis were observed. Benign tissue cells engulfing apoptotic bodies were also observed under high magnification (), however, the isthmus of the thyroid was not infiltrated by the neoplastic cells. No reactive lymphocyte infiltration or fibrosis was identified in the stroma of the thyroid, and no oxyphilic change or squamous metaplasia was observed in the epithelial cells of the background thyroid tissues (). The only change in the two lymph nodes that were simultaneously excised, was the presence of reactive hyperplasia of the lymphoid follicles (). Immunohistochemical staining was then performed with the primary antibodies shown in (Zymed Corporation, Inc., San Francisco, CA, USA; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). The results showed that the neoplastic cells were diffusely positive for cluster of differentiation (CD)20 () and CD10 (), marginally positive for CD38, CD43 and B-cell lymphoma (Bcl)-6, but negative for Bcl-2 and terminal deoxynucleotidyl transferase (TDT). In addition, CD3 and CD5 stained the background T cells, and the Ki-67 proliferation index was >95% (). Analysis using an EBV-encoded small RNA (EBER) digoxin-labeled probe (PanPath B.V., Budel, Netherlands) was performed and revealed a negative result (), however, positive nuclei were observed in the nasopharyngeal carcinoma tissue, which was used as the positive control (). Analysis using the C-MYC break-apart detection probe (Guangzhou LBP Medical Science Technology Co., Ltd., Guangzhou, China) was also performed and the results revealed that ~90% of the neoplastic cells exhibited red and green signal separation, which indicated that chromosome breakage and translocation of the MYC gene had occurred in the neoplastic cells (). Immunoglobulin gene rearrangement assays were performed according to instructions of the Biomed-2 Polymerase Chain Reaction kit (Invivoscribe technologies, Inc., San Diego, CA, USA), followed by capillary electrophoresis, which was analyzed using Genemarker® v1.5. software (SoftGenetics, LLC, State College, PA, USA). Positive gene arrangements of IgH and IgK were observed in the tumor tissues, however, no positive gene rearrangements were observed for IgL (). Consequently, the patient was diagnosed with primary BL of the thyroid and underwent alternate R-B-NHL-BFM-90-A and R-B-NHL-BFM-90-B treatment, for four cycles each. The two regimens, including the dose and duration of chemotherapy, are described in . After almost four years of follow-up, the patient appears well and remains free of disease.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 79-year-old Taiwanese woman came to the otolaryngologic clinic of our hospital due to an enlarging painless mass over the right neck region in the past 3 months. She denied fever, night sweats, dyspnea, hoarseness, dysphagia, dysphasia, or stridor. On physical examination, the right thyroid lobe was noted to be enlarged and firm. There was a palpable mass in the front of her neck, which moved during swallowing. She had no history of Hashimoto's thyroiditis or cervical irradiation, and her thyroid function test was within the normal range (thyroid-stimulating hormone: 2.01 nIU/mL; free T4: 1.24 ng/dL; thyroglobulin: 1.62 ng/mL; anti-thyroperoxidase: 1.03 IU/mL; and thyroglobulin antibody: 1.81 IU/mL).\nThe patient had received computed tomography (CT) at hospital outside, which revealed a hypodense nodule with minimal enhancement on the right lobe of thyroid gland []. Its size was approximately 4.1 cm × 3.6 cm, with a longitudinal dimension of 4.5 cm. The trachea, vessels, and soft tissues in the right neck were under pressure and displaced toward the left side. She underwent fine-needle aspiration (FNA) at that hospital, and the cytologic results were suspicious of lymphoma.\nIn order to obtain more definite results, this woman was referred to the radiological department of our hospital for core needle biopsy. During core needle biopsy, the neck color Doppler ultrasound showed a large heterogeneous hypoechoic mass with an irregular border in the right lobe of thyroid gland. There were twisted and chaotic intranodular vessels, but no defined calcification, hemorrhage, or necrotic portion was observed within the mass, which exhibited indistinct margins and posterior acoustic enhancement [Figure and ]. The pathology revealed diffuse large B-cell lymphoma (DLBCL). For staging the disease, a fluorodeoxyglucose (FDG) positron emission tomography (PET) scan was performed, revealing high-grade hypermetabolic lymphomatous disease, confined in the right thyroid gland, suggesting PTL Ann Arbor stage I [].\nAfter consulting oncology specialists, she started rituximab-based chemotherapy and received serial sonographic follow-up. After three cycles of rituximab plus bendamustine – rituximab (375 mg/m2) and bendamustine (Innomustine®, 90 mg/m2) by intravenous administration on day 1 were administered every 3 weeks for each cycle – neck color Doppler ultrasound showed a significant reduction of twisted blood flow signals in the PTL but no significant decrease (<25% extent) of the tumor size []. Therefore, chemotherapy regimen was adjusted to rituximab, cyclophosphamide, vincristine, prednisone (R–COP). After three cycles of R–COP, i.e., rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), and vincristine (2 mg/m2) by intravenous administration on day 1 and prednisone (100 mg/m2) by oral administration on day 1–5 were administered every 3 weeks for each cycle, the PTL disappeared on the color Doppler and gray-scale ultrasonography []. The patient was treated with R–COP regimen until complete remission of the disease, confirmed on the following FDG PET-CT and whole-body PET examination [].

A 49-year-old woman with a history of Hashimoto’s thyroiditis presented with a rapidly growing neck mass and upper airway compression symptoms. No B symptoms were present. The hematological test showed a white blood cell count within the normal range (51.5 × 102/μL). Interleukin-2 receptor (801 U/mL) and lactate dehydrogenase (228 U/L) levels were elevated, although serum thyroxine and thyroid-stimulating hormone levels were within their normal ranges. An elevated thyroid peroxidase antibody of 271.4 IU/mL was detected. Ultrasonography revealed a mass measuring 2.0 × 1.0 × 1.0 cm in the right lobe of the thyroid; the border of the nodule was indistinct. The patient underwent a right thyroidectomy after a core needle biopsy revealed a diffuse large B-cell lymphoma. Following the final histological diagnosis of primary thyroid BL, the patient received rituximab, cyclosphosphamide, doxorubicin, vincristine, and prednisone for 2 weeks, as well as rituximab, hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone including prophylactic intrathecal methotrexate for 3 months. Adjuvant treatments involving 22 cycles of linear accelerator (LINAC) therapy, 40 Gy each, were administered after the chemotherapy. Thirty months after the initial diagnosis, the patient had no evidence of recurrent disease.\nThe tumor cells were composed of round, intermediate-sized lymphoid cells admixed with scattered tingible body macrophages imparting a “starry sky” appearance (Fig. ). The nuclei were uniform and round-to-oval-shaped. The chromatin was coarsely clumped and had medium-sized paracentral nucleoli, while the cytoplasm was basophilic. Mitotic figures (12 per high-power field) were identified; there was no coagulative necrosis, although extrathyroidal extension was observed. Hashimoto’s thyroiditis was identified in the non-tumoral thyroid tissue.\nDiffuse membranous immunostaining for CD10, CD20, and CD79α, as well as diffuse nuclear staining for MUM-1 (Fig. a) and p16 (Fig. b), were noted in the tumor cells. The expression of MDM2 was focal and confined to the tumor cell nuclei (Fig. c), although the cells were negative for Bcl-2, Bcl-6, and p53. The Ki-67 labeling index exceeded 90% (Fig. ). The EBER in situ hybridization test was negative (Fig. ). Ninety-six percent of the tumor cells were found to have MYC/IgH gene fusion as determined by FISH (Fig. ).\nThe clinicopathological features of 21 thyroid BLs are summarized in Table . The median age at diagnosis was 39.3 years with a male-to-female ratio of 13/8. The majority (94.4%) of these patients presented with a thyroid mass; patients also presented with a rapidly growing nodule (66.7%), dyspnea (61.1%), dysphagia (16.7%), and thyrotoxicosis (5.6%). Four of the 14 described patients (28.6%) showed B symptoms (e.g., systematic symptoms of fever, night sweats, or weight loss). None of the reported patients presented with immunosuppressive conditions or the endemic form of BL. Regarding the treatment modalities, all of the 20 patients for whom data were available (data for 1 were missing) received multidrug chemotherapy regimens; 12 received chemotherapy only, 7 received chemotherapy with combined surgery, and 1 was administered chemotherapy combined with surgery and adjuvant radiotherapy (LINAC).\nFive of 7 patients with thyroid BL (71.4%) had morphologic evidence of Hashimoto’s thyroiditis. Regarding immunohistochemical features, all patients who were tested for CD10 (n = 14), CD20 (n = 18), and CD79a (n = 5) were positive for these respective proteins. IgM was positive in the lone patient who was tested. Additional factors measured are shown in Table . The Ki-67 labeling index exceeded 90% in all 19 patients for whom such staining was performed. We demonstrated that our patient had focal immunoreactivity for MDM2, but none of the other patients had been tested for this protein. All 12 patients who were tested for EBER in situ hybridization showed negative results, and flow cytometry immunophenotyping demonstrated CD10-positive monotypic B-cell populations in all 5 tested patients; moreover, MYC gene translocation was detected using FISH in all 12 patients whose samples were tested.\nOf 19 patients with available clinical outcome data, 14 (73.7%) were alive with complete remission, 1 (5.3%) was alive with persistent disease, and 4 (21.1%) died of the disease. Three of the 19 patients lacked follow-up data; hence, the median follow-up of the 16 remaining patients was 46.5 months (range, 0.5–361 months). Kaplan-Meier survival analysis showed that the 12- and 60-month overall survival rates were 87.5 and 70.7%, respectively (Fig. ).

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 79-year-old Taiwanese woman came to the otolaryngologic clinic of our hospital due to an enlarging painless mass over the right neck region in the past 3 months. She denied fever, night sweats, dyspnea, hoarseness, dysphagia, dysphasia, or stridor. On physical examination, the right thyroid lobe was noted to be enlarged and firm. There was a palpable mass in the front of her neck, which moved during swallowing. She had no history of Hashimoto's thyroiditis or cervical irradiation, and her thyroid function test was within the normal range (thyroid-stimulating hormone: 2.01 nIU/mL; free T4: 1.24 ng/dL; thyroglobulin: 1.62 ng/mL; anti-thyroperoxidase: 1.03 IU/mL; and thyroglobulin antibody: 1.81 IU/mL).\nThe patient had received computed tomography (CT) at hospital outside, which revealed a hypodense nodule with minimal enhancement on the right lobe of thyroid gland []. Its size was approximately 4.1 cm × 3.6 cm, with a longitudinal dimension of 4.5 cm. The trachea, vessels, and soft tissues in the right neck were under pressure and displaced toward the left side. She underwent fine-needle aspiration (FNA) at that hospital, and the cytologic results were suspicious of lymphoma.\nIn order to obtain more definite results, this woman was referred to the radiological department of our hospital for core needle biopsy. During core needle biopsy, the neck color Doppler ultrasound showed a large heterogeneous hypoechoic mass with an irregular border in the right lobe of thyroid gland. There were twisted and chaotic intranodular vessels, but no defined calcification, hemorrhage, or necrotic portion was observed within the mass, which exhibited indistinct margins and posterior acoustic enhancement [Figure and ]. The pathology revealed diffuse large B-cell lymphoma (DLBCL). For staging the disease, a fluorodeoxyglucose (FDG) positron emission tomography (PET) scan was performed, revealing high-grade hypermetabolic lymphomatous disease, confined in the right thyroid gland, suggesting PTL Ann Arbor stage I [].\nAfter consulting oncology specialists, she started rituximab-based chemotherapy and received serial sonographic follow-up. After three cycles of rituximab plus bendamustine – rituximab (375 mg/m2) and bendamustine (Innomustine®, 90 mg/m2) by intravenous administration on day 1 were administered every 3 weeks for each cycle – neck color Doppler ultrasound showed a significant reduction of twisted blood flow signals in the PTL but no significant decrease (<25% extent) of the tumor size []. Therefore, chemotherapy regimen was adjusted to rituximab, cyclophosphamide, vincristine, prednisone (R–COP). After three cycles of R–COP, i.e., rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), and vincristine (2 mg/m2) by intravenous administration on day 1 and prednisone (100 mg/m2) by oral administration on day 1–5 were administered every 3 weeks for each cycle, the PTL disappeared on the color Doppler and gray-scale ultrasonography []. The patient was treated with R–COP regimen until complete remission of the disease, confirmed on the following FDG PET-CT and whole-body PET examination [].

A 52-year-old woman presented to our Endocrinology Unit with a growing thyroid mass, which had enlarged so rapidly she had become unable to wear her motorcycle helmet in the weeks prior to her visit. She suffered from Hashimoto’s thyroiditis for which she was taking levothyroxine. There was no history of neck irradiation or family history of thyroid cancer. On examination, there was a large, firm thyroid nodule on the right side of the neck, without palpable cervical lymphadenopathy. TSH was 4.79 μU/mL with FT3 and FT4 within the reference range. Otherwise, there was only a mild thrombocytopenia. Thyroid ultrasonography showed a solid hypoechoic nodule in the right lobe of the gland, with significant internal vascularity and absence of calcifications (Figure ). FNA cytology with rapid on-site evaluation of the material adequacy showed that there were only atypical lymphoid cells with no thyrocytes and the specimens were considered suggestive of a lymphoproliferative disorder but insufficient to make a diagnosis, such that a CNB was scheduled for the following day.\nAfter checking the blood coagulation profile, the patient underwent a CNB, which allowed histological/morphological tissue analysis. This showed that normal thyrocytes were virtually all replaced by homogeneous medium-sized lymphocytes with scanty blue cytoplasm, round nuclei, coarse chromatin, and multiple small nucleoli. There were frequent mitotic figures and scattered macrophages ingesting apoptotic cells, giving to the tissue section the so-called ‘starry sky’ appearance (Fig. ). Overall, these features were consistent with the presence of a thyroid Burkitt’s lymphoma, and further investigations were ordered to confirm the diagnosis and evaluate the disease extent. A CT of chest and abdomen showed the 44x43x87 mm thyroid nodule with left tracheal deviation (Figure ) without other visible masses or lymph nodes. Bone marrow biopsy showed almost 100% lymphoid infiltration, consisting of a population of intermediate-sized blast-like cells, with prominent nucleoli, which were replacing all normal cells. These cells expressed CD10, CD20, and were negative for Bcl2, CD34, and TdT. Altogether these results led us to the final diagnosis of stage IV Burkitt’s lymphoma [].\nThe patient was admitted to our hospital’s Haematology Unit and was successfully treated with 3 cycles of Hyper-CVAD chemotherapy (cyclophosphamide, vincristine, doxorubicin and dexamethasone) completed in five months. The thyroid mass disappeared (Fig. ) and the platelets returned to baseline levels. At 60 months after diagnosis the patient is alive, and remains disease-free at regular follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 79-year-old Taiwanese woman came to the otolaryngologic clinic of our hospital due to an enlarging painless mass over the right neck region in the past 3 months. She denied fever, night sweats, dyspnea, hoarseness, dysphagia, dysphasia, or stridor. On physical examination, the right thyroid lobe was noted to be enlarged and firm. There was a palpable mass in the front of her neck, which moved during swallowing. She had no history of Hashimoto's thyroiditis or cervical irradiation, and her thyroid function test was within the normal range (thyroid-stimulating hormone: 2.01 nIU/mL; free T4: 1.24 ng/dL; thyroglobulin: 1.62 ng/mL; anti-thyroperoxidase: 1.03 IU/mL; and thyroglobulin antibody: 1.81 IU/mL).\nThe patient had received computed tomography (CT) at hospital outside, which revealed a hypodense nodule with minimal enhancement on the right lobe of thyroid gland []. Its size was approximately 4.1 cm × 3.6 cm, with a longitudinal dimension of 4.5 cm. The trachea, vessels, and soft tissues in the right neck were under pressure and displaced toward the left side. She underwent fine-needle aspiration (FNA) at that hospital, and the cytologic results were suspicious of lymphoma.\nIn order to obtain more definite results, this woman was referred to the radiological department of our hospital for core needle biopsy. During core needle biopsy, the neck color Doppler ultrasound showed a large heterogeneous hypoechoic mass with an irregular border in the right lobe of thyroid gland. There were twisted and chaotic intranodular vessels, but no defined calcification, hemorrhage, or necrotic portion was observed within the mass, which exhibited indistinct margins and posterior acoustic enhancement [Figure and ]. The pathology revealed diffuse large B-cell lymphoma (DLBCL). For staging the disease, a fluorodeoxyglucose (FDG) positron emission tomography (PET) scan was performed, revealing high-grade hypermetabolic lymphomatous disease, confined in the right thyroid gland, suggesting PTL Ann Arbor stage I [].\nAfter consulting oncology specialists, she started rituximab-based chemotherapy and received serial sonographic follow-up. After three cycles of rituximab plus bendamustine – rituximab (375 mg/m2) and bendamustine (Innomustine®, 90 mg/m2) by intravenous administration on day 1 were administered every 3 weeks for each cycle – neck color Doppler ultrasound showed a significant reduction of twisted blood flow signals in the PTL but no significant decrease (<25% extent) of the tumor size []. Therefore, chemotherapy regimen was adjusted to rituximab, cyclophosphamide, vincristine, prednisone (R–COP). After three cycles of R–COP, i.e., rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), and vincristine (2 mg/m2) by intravenous administration on day 1 and prednisone (100 mg/m2) by oral administration on day 1–5 were administered every 3 weeks for each cycle, the PTL disappeared on the color Doppler and gray-scale ultrasonography []. The patient was treated with R–COP regimen until complete remission of the disease, confirmed on the following FDG PET-CT and whole-body PET examination [].

A 64-year-old man with a history of hypothyroidism and proven Hashimoto's thyroiditis presented with painless progressive asymmetric enlargement of the thyroid gland. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR), elevated thyroid peroxidase antibody titer of 850 U/mL (normal <30 U/mL), free triiodothyronine (FT3) 2.34, free thyroxine (FT4) 0.97, and thyroid stimulating hormone (TSH) level of 22.11. A contrast enhanced CT (CECT) exam of the neck revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe. A needle biopsy from the thyroid mass revealed features of non-Hodgkin's lymphoma (DLBCL) with the tumor cells staining positive for CD20, negative for cytokeratin (CK) and having a high proliferative index (MIB-1) of 35-40%. 18F-FDG PET/CT was performed for staging. It revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe with intense radiotracer uptake in the thyroid mass (SUVmax-18.7) with no other abnormal identifiable areas [Figure –]. The patient underwent four cycles of combination chemotherapy (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone) and was reevaluated with 18F-FDG PET/CT. Post therapy 18F-FDG PET/CT [Figure –] done 6 weeks after completion of chemotherapy revealed significant decrease in the size of the enlarged thyroid gland associated with no significant FDG avidity (SUVmax-2.0) of the residual thyroid mass (arrow), suggestive of complete metabolic response. The patient is in complete remission at 18 month follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 79-year-old Taiwanese woman came to the otolaryngologic clinic of our hospital due to an enlarging painless mass over the right neck region in the past 3 months. She denied fever, night sweats, dyspnea, hoarseness, dysphagia, dysphasia, or stridor. On physical examination, the right thyroid lobe was noted to be enlarged and firm. There was a palpable mass in the front of her neck, which moved during swallowing. She had no history of Hashimoto's thyroiditis or cervical irradiation, and her thyroid function test was within the normal range (thyroid-stimulating hormone: 2.01 nIU/mL; free T4: 1.24 ng/dL; thyroglobulin: 1.62 ng/mL; anti-thyroperoxidase: 1.03 IU/mL; and thyroglobulin antibody: 1.81 IU/mL).\nThe patient had received computed tomography (CT) at hospital outside, which revealed a hypodense nodule with minimal enhancement on the right lobe of thyroid gland []. Its size was approximately 4.1 cm × 3.6 cm, with a longitudinal dimension of 4.5 cm. The trachea, vessels, and soft tissues in the right neck were under pressure and displaced toward the left side. She underwent fine-needle aspiration (FNA) at that hospital, and the cytologic results were suspicious of lymphoma.\nIn order to obtain more definite results, this woman was referred to the radiological department of our hospital for core needle biopsy. During core needle biopsy, the neck color Doppler ultrasound showed a large heterogeneous hypoechoic mass with an irregular border in the right lobe of thyroid gland. There were twisted and chaotic intranodular vessels, but no defined calcification, hemorrhage, or necrotic portion was observed within the mass, which exhibited indistinct margins and posterior acoustic enhancement [Figure and ]. The pathology revealed diffuse large B-cell lymphoma (DLBCL). For staging the disease, a fluorodeoxyglucose (FDG) positron emission tomography (PET) scan was performed, revealing high-grade hypermetabolic lymphomatous disease, confined in the right thyroid gland, suggesting PTL Ann Arbor stage I [].\nAfter consulting oncology specialists, she started rituximab-based chemotherapy and received serial sonographic follow-up. After three cycles of rituximab plus bendamustine – rituximab (375 mg/m2) and bendamustine (Innomustine®, 90 mg/m2) by intravenous administration on day 1 were administered every 3 weeks for each cycle – neck color Doppler ultrasound showed a significant reduction of twisted blood flow signals in the PTL but no significant decrease (<25% extent) of the tumor size []. Therefore, chemotherapy regimen was adjusted to rituximab, cyclophosphamide, vincristine, prednisone (R–COP). After three cycles of R–COP, i.e., rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), and vincristine (2 mg/m2) by intravenous administration on day 1 and prednisone (100 mg/m2) by oral administration on day 1–5 were administered every 3 weeks for each cycle, the PTL disappeared on the color Doppler and gray-scale ultrasonography []. The patient was treated with R–COP regimen until complete remission of the disease, confirmed on the following FDG PET-CT and whole-body PET examination [].

A 70-year-old male presented a rapidly expanding mass of the neck associated with history of airway compression symptoms; progressive dyspnea and dysphonia lasting for 4 weeks, in a context of apyrexia and impairment of general condition. The patient was admitted to the hospital because of increasing dyspnea and urgently received a tracheostomy.\nA biopsy of the cervical mass was carried out and the histological examination showed diffuse infiltration of the thyroid gland by a monotonous population of atypical intermediate-sized lymphoid cells (Fig. ). These last possess scanty amphophilic to basophilic cytoplasm with centrally located nuclei of irregular shape, displaying dispersed basophilic chromatin, and frequent apoptotic figures (Fig. ). Scattered tingible body type macrophages were also present. Little residual thyroid follicles and some areas of necrosis was observed.\nImmunohistochemical staining was then performed and the tumour cells were positive for CD20, CD10 and BCL6. Ki-67 showed proliferation index approaching 100 %. CD3 and CD5 stained the background T cells (Fig. ). Immunoreactivity for Epstein-Barr virus (EBV) was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t (8; 14) translocation. Bone marrow examination was normal.\nThe patient was transferred to the Clinical Haematology department. On physical examination, he was apyretic and hemodynamically stable with a cervical armouring by a huge mass of hard consistency. Neurological examination shows no sensorimotor deficits.\nOther systemic examinations were normal, without any palpable lymphadenopathy or organomegaly.\nThe computerized tomography (CT) scan showed a heterogeneous process of the thyroid gland measuring 10.5 × 8.2 × 6.5 cm in size, extending up towards the laryngeal region, infiltrating the right vocal cord and reducing the laryngeal lumen (Fig. ).\nThe thoraco-abdominal CT scan showed no other localization.\nThe examination of the cephalorachidian liquid showed no central nervous system involvement. The patient was diagnosed with thyroidal Burkitt lymphoma, stage I of Murphy [].\nAfter cardiac, renal and liver functions assessment, the patient received chemotherapy according to the LMBA02 protocol [], group A (Age > 60 years, no CNS nor bone marrow involvement), with a first course of COP (Cyclophosphamide, Vincristine and Prednisone) and intrathecal Methotrexate, followed a week after by a course of R-COPADEM (Rituximab at day 0 and day 6, Cyclophosphamide day 2,3 and 4, Prednisone from day 1 to 5, Doxorubicineat day 2, high dose Methotrexate at day 1 with folic acid rescue from day 2 to day 6 and intrathecal chemotherapy at day 2 and day 6).\nAt day 15 of chemotherapy, the patient developed febrile neutropenia, refractory to broad-spectrum antibiotics and antifungals. The evolution was marked by the installation of a septic shock with acute respiratory distress syndrome that led to his transfer to intensive care unit where he was intubated and ventilated. The patient died 2 days after.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 14-year-old white British Caucasian boy presented with a 3-month history of malaise, lethargy, and weight loss. There was no history of fever or any other thyroid related symptoms. Past and family history were noncontributory and there was no recent foreign travel. On examination he was found to have a large predominantly left-sided firm thyroid swelling. Clinical examination was otherwise unremarkable with no lymphadenopathy or hepatosplenomegaly or signs of hypo/hyperthyroidism. Baseline haematological and biochemical investigations on admission were within normal limits (Hb 136 g/L, WCC 9.1 109/L, CRP <4 mg/dL). Levels of thyroxine, TSH, and calcitonin were normal. Lactase dehydrogenase (LDH) was slightly elevated at 352 U/L. Thyroperoxidase was elevated (1277 IU/mL) and thyroid stimulating hormone receptor antibodies (TRAb) of <5 U/L. CSF analysis showed no tumour cells. EBV PCR was negative as was HIV-I and HIV-II.\nA fine needle aspiration biopsy was carried out and was suspicious of NHL. The diagnosis of Burkitt type NHL (BL) was made following an open wedge biopsy. On microscopic examination, the tumour was composed of diffuse sheets of lymphoid cells () having round nuclei with coarse chromatin and conspicuous single to multiple nucleoli and scanty amphophilic cytoplasm. Numerous mitotic figures, apoptosis, and scattered tingible body type macrophages were also present. Tumour cells were positive for CD79A, CD20, and CD10 and negative for TdT and T cell markers (CD3, CD4, and CD8). Ki 67 showed proliferation index approaching 100%. Immunohistochemistry for EBV was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t(8; 14) translocation.\nStaging CT () showed a large (6.7 cm × 5.8 cm × 6.1 cm) heterogeneous mass in the left lobe and isthmus of the thyroid which extended craniocaudally from level of C4/5 to T1/2, with some evidence of intratumoural necrosis. There was significant mass effect with displacement and compression of the trachea along with compression of the left carotid artery and lateral displacement of the left jugular vein. There were two small indeterminate lung nodules. Abdominally there were two focal cortical abnormalities in the right kidney and an ill-defined attenuation in the pancreatic head. There was no evidence of bone marrow involvement.\nHe was treated according to the Children's Cancer and Leukaemia Group guidelines for BL—Group B protocol. This consisted of initial induction chemotherapy with COP (cyclophosphamide [300 mg/m2], vincristine [1 mg/m2], and prednisolone [60 mg/m2—7 days]) followed by 2 courses of COPADM (doxorubicin 60 mg/m2, methotrexate 3 g/m2, cyclophosphamide 500 mg/m2/day—5 days, vincristine [2 mg/m2], and prednisolone [60 mg/m2—5 days]) and two courses of CYM (cytarabine 100 mg/m2/day—5 days and methotrexate 3 g/m2) chemotherapy. This was accompanied by intrathecal chemotherapy (the CSF contained no tumour cells at diagnosis). The patient had a good response to treatment with a rapid decrease in the size of the thyroid mass and resolution of the lung, kidney, and pancreas metastases. Reassessment after the first course of CYM showed a residual thyroid mass of 15 mm × 30 mm but with resolution of the lung, kidney, and pancreas metastases.\nBecause of residual radiological abnormality, and in accordance with the CCLG NHL protocol, a hemithyroidectomy was performed with the residual lesion showing no evidence of tumour cells on histological examination. Chemotherapy was then completed and he is now disease-free 3 years after end of treatment.

An eight-year-old male presented with a mass in the right anterior neck that had been apparent for one week. Upon physical examination, blood pressure was recorded as 100/65 mmHg, heart rate was 80 beats per min, respiratory rate was 20 breaths per min and temperature was 36.1°C. A mass measuring ~4.0 cm in size, which caused difficulty in swallowing, was identified in the right anterior neck. The laboratory test results demonstrated a normal blood count and serum biochemistry, as well as normal levels of electrolytes and carcinoembryonic antigen. In addition, the test results for Epstein-Barr virus (EBV) viral capsid antigens immunoglobulin (Ig)M and IgG, human immunodeficiency virus (HIV) and hepatitis C virus antibodies, hepatitis B antigen and syphilis were negative. Furthermore, the thyroid hormone test results were as follows: Free thyroxine (FT) 4 levels of 11.8 pmol/l (normal range, 9–25 pmol/l); FT3 levels of 4.2 pmol/l (normal range, 3–9 pmol/l); thyroid-stimulating hormone levels of 0.720 μIU/ml (normal range, 0.34–5.60 μIU/ml); anti-thyroglobulin levels of 20 IU/ml (normal range, <115 IU/ml); and anti-thyroid peroxidase levels of 25 IU/ml (normal range, <34 IU/ml). The patient had no significant past medical or family history of disease. A B-mode ultrasound examination revealed a mass measuring 4.0×3.0×2.5 cm in the right lobe of the thyroid (), however, the lymph nodes surrounding the mass were normal (). The patient underwent a right lobe and isthmus thyroidectomy whereby two lymph nodes were excised simultaneously. Following the surgery, positron emission tomography-computed tomography scans showed normal metabolism in the left lobe of the thyroid and other parts of the body (). The patient’s bone marrow cytology was also normal, however, histological examination revealed diffuse infiltration of atypical lymphocytes and the observation of residual thyroid follicles and necrosis (). In addition, under low magnification, the ‘starry sky’ histology was observed in certain areas (). The atypical lymphocytes were medium-sized and consistent, with centrally located nuclei of irregular shape, displaying dispersed and deep basophilic chromatin and scanty cytoplasm. Additionally, certain neoplastic cells were visible, while varying numbers of nucleoli and apoptosis and mitosis were observed. Benign tissue cells engulfing apoptotic bodies were also observed under high magnification (), however, the isthmus of the thyroid was not infiltrated by the neoplastic cells. No reactive lymphocyte infiltration or fibrosis was identified in the stroma of the thyroid, and no oxyphilic change or squamous metaplasia was observed in the epithelial cells of the background thyroid tissues (). The only change in the two lymph nodes that were simultaneously excised, was the presence of reactive hyperplasia of the lymphoid follicles (). Immunohistochemical staining was then performed with the primary antibodies shown in (Zymed Corporation, Inc., San Francisco, CA, USA; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). The results showed that the neoplastic cells were diffusely positive for cluster of differentiation (CD)20 () and CD10 (), marginally positive for CD38, CD43 and B-cell lymphoma (Bcl)-6, but negative for Bcl-2 and terminal deoxynucleotidyl transferase (TDT). In addition, CD3 and CD5 stained the background T cells, and the Ki-67 proliferation index was >95% (). Analysis using an EBV-encoded small RNA (EBER) digoxin-labeled probe (PanPath B.V., Budel, Netherlands) was performed and revealed a negative result (), however, positive nuclei were observed in the nasopharyngeal carcinoma tissue, which was used as the positive control (). Analysis using the C-MYC break-apart detection probe (Guangzhou LBP Medical Science Technology Co., Ltd., Guangzhou, China) was also performed and the results revealed that ~90% of the neoplastic cells exhibited red and green signal separation, which indicated that chromosome breakage and translocation of the MYC gene had occurred in the neoplastic cells (). Immunoglobulin gene rearrangement assays were performed according to instructions of the Biomed-2 Polymerase Chain Reaction kit (Invivoscribe technologies, Inc., San Diego, CA, USA), followed by capillary electrophoresis, which was analyzed using Genemarker® v1.5. software (SoftGenetics, LLC, State College, PA, USA). Positive gene arrangements of IgH and IgK were observed in the tumor tissues, however, no positive gene rearrangements were observed for IgL (). Consequently, the patient was diagnosed with primary BL of the thyroid and underwent alternate R-B-NHL-BFM-90-A and R-B-NHL-BFM-90-B treatment, for four cycles each. The two regimens, including the dose and duration of chemotherapy, are described in . After almost four years of follow-up, the patient appears well and remains free of disease.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 14-year-old white British Caucasian boy presented with a 3-month history of malaise, lethargy, and weight loss. There was no history of fever or any other thyroid related symptoms. Past and family history were noncontributory and there was no recent foreign travel. On examination he was found to have a large predominantly left-sided firm thyroid swelling. Clinical examination was otherwise unremarkable with no lymphadenopathy or hepatosplenomegaly or signs of hypo/hyperthyroidism. Baseline haematological and biochemical investigations on admission were within normal limits (Hb 136 g/L, WCC 9.1 109/L, CRP <4 mg/dL). Levels of thyroxine, TSH, and calcitonin were normal. Lactase dehydrogenase (LDH) was slightly elevated at 352 U/L. Thyroperoxidase was elevated (1277 IU/mL) and thyroid stimulating hormone receptor antibodies (TRAb) of <5 U/L. CSF analysis showed no tumour cells. EBV PCR was negative as was HIV-I and HIV-II.\nA fine needle aspiration biopsy was carried out and was suspicious of NHL. The diagnosis of Burkitt type NHL (BL) was made following an open wedge biopsy. On microscopic examination, the tumour was composed of diffuse sheets of lymphoid cells () having round nuclei with coarse chromatin and conspicuous single to multiple nucleoli and scanty amphophilic cytoplasm. Numerous mitotic figures, apoptosis, and scattered tingible body type macrophages were also present. Tumour cells were positive for CD79A, CD20, and CD10 and negative for TdT and T cell markers (CD3, CD4, and CD8). Ki 67 showed proliferation index approaching 100%. Immunohistochemistry for EBV was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t(8; 14) translocation.\nStaging CT () showed a large (6.7 cm × 5.8 cm × 6.1 cm) heterogeneous mass in the left lobe and isthmus of the thyroid which extended craniocaudally from level of C4/5 to T1/2, with some evidence of intratumoural necrosis. There was significant mass effect with displacement and compression of the trachea along with compression of the left carotid artery and lateral displacement of the left jugular vein. There were two small indeterminate lung nodules. Abdominally there were two focal cortical abnormalities in the right kidney and an ill-defined attenuation in the pancreatic head. There was no evidence of bone marrow involvement.\nHe was treated according to the Children's Cancer and Leukaemia Group guidelines for BL—Group B protocol. This consisted of initial induction chemotherapy with COP (cyclophosphamide [300 mg/m2], vincristine [1 mg/m2], and prednisolone [60 mg/m2—7 days]) followed by 2 courses of COPADM (doxorubicin 60 mg/m2, methotrexate 3 g/m2, cyclophosphamide 500 mg/m2/day—5 days, vincristine [2 mg/m2], and prednisolone [60 mg/m2—5 days]) and two courses of CYM (cytarabine 100 mg/m2/day—5 days and methotrexate 3 g/m2) chemotherapy. This was accompanied by intrathecal chemotherapy (the CSF contained no tumour cells at diagnosis). The patient had a good response to treatment with a rapid decrease in the size of the thyroid mass and resolution of the lung, kidney, and pancreas metastases. Reassessment after the first course of CYM showed a residual thyroid mass of 15 mm × 30 mm but with resolution of the lung, kidney, and pancreas metastases.\nBecause of residual radiological abnormality, and in accordance with the CCLG NHL protocol, a hemithyroidectomy was performed with the residual lesion showing no evidence of tumour cells on histological examination. Chemotherapy was then completed and he is now disease-free 3 years after end of treatment.

A 49-year-old woman with a history of Hashimoto’s thyroiditis presented with a rapidly growing neck mass and upper airway compression symptoms. No B symptoms were present. The hematological test showed a white blood cell count within the normal range (51.5 × 102/μL). Interleukin-2 receptor (801 U/mL) and lactate dehydrogenase (228 U/L) levels were elevated, although serum thyroxine and thyroid-stimulating hormone levels were within their normal ranges. An elevated thyroid peroxidase antibody of 271.4 IU/mL was detected. Ultrasonography revealed a mass measuring 2.0 × 1.0 × 1.0 cm in the right lobe of the thyroid; the border of the nodule was indistinct. The patient underwent a right thyroidectomy after a core needle biopsy revealed a diffuse large B-cell lymphoma. Following the final histological diagnosis of primary thyroid BL, the patient received rituximab, cyclosphosphamide, doxorubicin, vincristine, and prednisone for 2 weeks, as well as rituximab, hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone including prophylactic intrathecal methotrexate for 3 months. Adjuvant treatments involving 22 cycles of linear accelerator (LINAC) therapy, 40 Gy each, were administered after the chemotherapy. Thirty months after the initial diagnosis, the patient had no evidence of recurrent disease.\nThe tumor cells were composed of round, intermediate-sized lymphoid cells admixed with scattered tingible body macrophages imparting a “starry sky” appearance (Fig. ). The nuclei were uniform and round-to-oval-shaped. The chromatin was coarsely clumped and had medium-sized paracentral nucleoli, while the cytoplasm was basophilic. Mitotic figures (12 per high-power field) were identified; there was no coagulative necrosis, although extrathyroidal extension was observed. Hashimoto’s thyroiditis was identified in the non-tumoral thyroid tissue.\nDiffuse membranous immunostaining for CD10, CD20, and CD79α, as well as diffuse nuclear staining for MUM-1 (Fig. a) and p16 (Fig. b), were noted in the tumor cells. The expression of MDM2 was focal and confined to the tumor cell nuclei (Fig. c), although the cells were negative for Bcl-2, Bcl-6, and p53. The Ki-67 labeling index exceeded 90% (Fig. ). The EBER in situ hybridization test was negative (Fig. ). Ninety-six percent of the tumor cells were found to have MYC/IgH gene fusion as determined by FISH (Fig. ).\nThe clinicopathological features of 21 thyroid BLs are summarized in Table . The median age at diagnosis was 39.3 years with a male-to-female ratio of 13/8. The majority (94.4%) of these patients presented with a thyroid mass; patients also presented with a rapidly growing nodule (66.7%), dyspnea (61.1%), dysphagia (16.7%), and thyrotoxicosis (5.6%). Four of the 14 described patients (28.6%) showed B symptoms (e.g., systematic symptoms of fever, night sweats, or weight loss). None of the reported patients presented with immunosuppressive conditions or the endemic form of BL. Regarding the treatment modalities, all of the 20 patients for whom data were available (data for 1 were missing) received multidrug chemotherapy regimens; 12 received chemotherapy only, 7 received chemotherapy with combined surgery, and 1 was administered chemotherapy combined with surgery and adjuvant radiotherapy (LINAC).\nFive of 7 patients with thyroid BL (71.4%) had morphologic evidence of Hashimoto’s thyroiditis. Regarding immunohistochemical features, all patients who were tested for CD10 (n = 14), CD20 (n = 18), and CD79a (n = 5) were positive for these respective proteins. IgM was positive in the lone patient who was tested. Additional factors measured are shown in Table . The Ki-67 labeling index exceeded 90% in all 19 patients for whom such staining was performed. We demonstrated that our patient had focal immunoreactivity for MDM2, but none of the other patients had been tested for this protein. All 12 patients who were tested for EBER in situ hybridization showed negative results, and flow cytometry immunophenotyping demonstrated CD10-positive monotypic B-cell populations in all 5 tested patients; moreover, MYC gene translocation was detected using FISH in all 12 patients whose samples were tested.\nOf 19 patients with available clinical outcome data, 14 (73.7%) were alive with complete remission, 1 (5.3%) was alive with persistent disease, and 4 (21.1%) died of the disease. Three of the 19 patients lacked follow-up data; hence, the median follow-up of the 16 remaining patients was 46.5 months (range, 0.5–361 months). Kaplan-Meier survival analysis showed that the 12- and 60-month overall survival rates were 87.5 and 70.7%, respectively (Fig. ).

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 14-year-old white British Caucasian boy presented with a 3-month history of malaise, lethargy, and weight loss. There was no history of fever or any other thyroid related symptoms. Past and family history were noncontributory and there was no recent foreign travel. On examination he was found to have a large predominantly left-sided firm thyroid swelling. Clinical examination was otherwise unremarkable with no lymphadenopathy or hepatosplenomegaly or signs of hypo/hyperthyroidism. Baseline haematological and biochemical investigations on admission were within normal limits (Hb 136 g/L, WCC 9.1 109/L, CRP <4 mg/dL). Levels of thyroxine, TSH, and calcitonin were normal. Lactase dehydrogenase (LDH) was slightly elevated at 352 U/L. Thyroperoxidase was elevated (1277 IU/mL) and thyroid stimulating hormone receptor antibodies (TRAb) of <5 U/L. CSF analysis showed no tumour cells. EBV PCR was negative as was HIV-I and HIV-II.\nA fine needle aspiration biopsy was carried out and was suspicious of NHL. The diagnosis of Burkitt type NHL (BL) was made following an open wedge biopsy. On microscopic examination, the tumour was composed of diffuse sheets of lymphoid cells () having round nuclei with coarse chromatin and conspicuous single to multiple nucleoli and scanty amphophilic cytoplasm. Numerous mitotic figures, apoptosis, and scattered tingible body type macrophages were also present. Tumour cells were positive for CD79A, CD20, and CD10 and negative for TdT and T cell markers (CD3, CD4, and CD8). Ki 67 showed proliferation index approaching 100%. Immunohistochemistry for EBV was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t(8; 14) translocation.\nStaging CT () showed a large (6.7 cm × 5.8 cm × 6.1 cm) heterogeneous mass in the left lobe and isthmus of the thyroid which extended craniocaudally from level of C4/5 to T1/2, with some evidence of intratumoural necrosis. There was significant mass effect with displacement and compression of the trachea along with compression of the left carotid artery and lateral displacement of the left jugular vein. There were two small indeterminate lung nodules. Abdominally there were two focal cortical abnormalities in the right kidney and an ill-defined attenuation in the pancreatic head. There was no evidence of bone marrow involvement.\nHe was treated according to the Children's Cancer and Leukaemia Group guidelines for BL—Group B protocol. This consisted of initial induction chemotherapy with COP (cyclophosphamide [300 mg/m2], vincristine [1 mg/m2], and prednisolone [60 mg/m2—7 days]) followed by 2 courses of COPADM (doxorubicin 60 mg/m2, methotrexate 3 g/m2, cyclophosphamide 500 mg/m2/day—5 days, vincristine [2 mg/m2], and prednisolone [60 mg/m2—5 days]) and two courses of CYM (cytarabine 100 mg/m2/day—5 days and methotrexate 3 g/m2) chemotherapy. This was accompanied by intrathecal chemotherapy (the CSF contained no tumour cells at diagnosis). The patient had a good response to treatment with a rapid decrease in the size of the thyroid mass and resolution of the lung, kidney, and pancreas metastases. Reassessment after the first course of CYM showed a residual thyroid mass of 15 mm × 30 mm but with resolution of the lung, kidney, and pancreas metastases.\nBecause of residual radiological abnormality, and in accordance with the CCLG NHL protocol, a hemithyroidectomy was performed with the residual lesion showing no evidence of tumour cells on histological examination. Chemotherapy was then completed and he is now disease-free 3 years after end of treatment.

A 52-year-old woman presented to our Endocrinology Unit with a growing thyroid mass, which had enlarged so rapidly she had become unable to wear her motorcycle helmet in the weeks prior to her visit. She suffered from Hashimoto’s thyroiditis for which she was taking levothyroxine. There was no history of neck irradiation or family history of thyroid cancer. On examination, there was a large, firm thyroid nodule on the right side of the neck, without palpable cervical lymphadenopathy. TSH was 4.79 μU/mL with FT3 and FT4 within the reference range. Otherwise, there was only a mild thrombocytopenia. Thyroid ultrasonography showed a solid hypoechoic nodule in the right lobe of the gland, with significant internal vascularity and absence of calcifications (Figure ). FNA cytology with rapid on-site evaluation of the material adequacy showed that there were only atypical lymphoid cells with no thyrocytes and the specimens were considered suggestive of a lymphoproliferative disorder but insufficient to make a diagnosis, such that a CNB was scheduled for the following day.\nAfter checking the blood coagulation profile, the patient underwent a CNB, which allowed histological/morphological tissue analysis. This showed that normal thyrocytes were virtually all replaced by homogeneous medium-sized lymphocytes with scanty blue cytoplasm, round nuclei, coarse chromatin, and multiple small nucleoli. There were frequent mitotic figures and scattered macrophages ingesting apoptotic cells, giving to the tissue section the so-called ‘starry sky’ appearance (Fig. ). Overall, these features were consistent with the presence of a thyroid Burkitt’s lymphoma, and further investigations were ordered to confirm the diagnosis and evaluate the disease extent. A CT of chest and abdomen showed the 44x43x87 mm thyroid nodule with left tracheal deviation (Figure ) without other visible masses or lymph nodes. Bone marrow biopsy showed almost 100% lymphoid infiltration, consisting of a population of intermediate-sized blast-like cells, with prominent nucleoli, which were replacing all normal cells. These cells expressed CD10, CD20, and were negative for Bcl2, CD34, and TdT. Altogether these results led us to the final diagnosis of stage IV Burkitt’s lymphoma [].\nThe patient was admitted to our hospital’s Haematology Unit and was successfully treated with 3 cycles of Hyper-CVAD chemotherapy (cyclophosphamide, vincristine, doxorubicin and dexamethasone) completed in five months. The thyroid mass disappeared (Fig. ) and the platelets returned to baseline levels. At 60 months after diagnosis the patient is alive, and remains disease-free at regular follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 14-year-old white British Caucasian boy presented with a 3-month history of malaise, lethargy, and weight loss. There was no history of fever or any other thyroid related symptoms. Past and family history were noncontributory and there was no recent foreign travel. On examination he was found to have a large predominantly left-sided firm thyroid swelling. Clinical examination was otherwise unremarkable with no lymphadenopathy or hepatosplenomegaly or signs of hypo/hyperthyroidism. Baseline haematological and biochemical investigations on admission were within normal limits (Hb 136 g/L, WCC 9.1 109/L, CRP <4 mg/dL). Levels of thyroxine, TSH, and calcitonin were normal. Lactase dehydrogenase (LDH) was slightly elevated at 352 U/L. Thyroperoxidase was elevated (1277 IU/mL) and thyroid stimulating hormone receptor antibodies (TRAb) of <5 U/L. CSF analysis showed no tumour cells. EBV PCR was negative as was HIV-I and HIV-II.\nA fine needle aspiration biopsy was carried out and was suspicious of NHL. The diagnosis of Burkitt type NHL (BL) was made following an open wedge biopsy. On microscopic examination, the tumour was composed of diffuse sheets of lymphoid cells () having round nuclei with coarse chromatin and conspicuous single to multiple nucleoli and scanty amphophilic cytoplasm. Numerous mitotic figures, apoptosis, and scattered tingible body type macrophages were also present. Tumour cells were positive for CD79A, CD20, and CD10 and negative for TdT and T cell markers (CD3, CD4, and CD8). Ki 67 showed proliferation index approaching 100%. Immunohistochemistry for EBV was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t(8; 14) translocation.\nStaging CT () showed a large (6.7 cm × 5.8 cm × 6.1 cm) heterogeneous mass in the left lobe and isthmus of the thyroid which extended craniocaudally from level of C4/5 to T1/2, with some evidence of intratumoural necrosis. There was significant mass effect with displacement and compression of the trachea along with compression of the left carotid artery and lateral displacement of the left jugular vein. There were two small indeterminate lung nodules. Abdominally there were two focal cortical abnormalities in the right kidney and an ill-defined attenuation in the pancreatic head. There was no evidence of bone marrow involvement.\nHe was treated according to the Children's Cancer and Leukaemia Group guidelines for BL—Group B protocol. This consisted of initial induction chemotherapy with COP (cyclophosphamide [300 mg/m2], vincristine [1 mg/m2], and prednisolone [60 mg/m2—7 days]) followed by 2 courses of COPADM (doxorubicin 60 mg/m2, methotrexate 3 g/m2, cyclophosphamide 500 mg/m2/day—5 days, vincristine [2 mg/m2], and prednisolone [60 mg/m2—5 days]) and two courses of CYM (cytarabine 100 mg/m2/day—5 days and methotrexate 3 g/m2) chemotherapy. This was accompanied by intrathecal chemotherapy (the CSF contained no tumour cells at diagnosis). The patient had a good response to treatment with a rapid decrease in the size of the thyroid mass and resolution of the lung, kidney, and pancreas metastases. Reassessment after the first course of CYM showed a residual thyroid mass of 15 mm × 30 mm but with resolution of the lung, kidney, and pancreas metastases.\nBecause of residual radiological abnormality, and in accordance with the CCLG NHL protocol, a hemithyroidectomy was performed with the residual lesion showing no evidence of tumour cells on histological examination. Chemotherapy was then completed and he is now disease-free 3 years after end of treatment.

A 64-year-old man with a history of hypothyroidism and proven Hashimoto's thyroiditis presented with painless progressive asymmetric enlargement of the thyroid gland. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR), elevated thyroid peroxidase antibody titer of 850 U/mL (normal <30 U/mL), free triiodothyronine (FT3) 2.34, free thyroxine (FT4) 0.97, and thyroid stimulating hormone (TSH) level of 22.11. A contrast enhanced CT (CECT) exam of the neck revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe. A needle biopsy from the thyroid mass revealed features of non-Hodgkin's lymphoma (DLBCL) with the tumor cells staining positive for CD20, negative for cytokeratin (CK) and having a high proliferative index (MIB-1) of 35-40%. 18F-FDG PET/CT was performed for staging. It revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe with intense radiotracer uptake in the thyroid mass (SUVmax-18.7) with no other abnormal identifiable areas [Figure –]. The patient underwent four cycles of combination chemotherapy (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone) and was reevaluated with 18F-FDG PET/CT. Post therapy 18F-FDG PET/CT [Figure –] done 6 weeks after completion of chemotherapy revealed significant decrease in the size of the enlarged thyroid gland associated with no significant FDG avidity (SUVmax-2.0) of the residual thyroid mass (arrow), suggestive of complete metabolic response. The patient is in complete remission at 18 month follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 14-year-old white British Caucasian boy presented with a 3-month history of malaise, lethargy, and weight loss. There was no history of fever or any other thyroid related symptoms. Past and family history were noncontributory and there was no recent foreign travel. On examination he was found to have a large predominantly left-sided firm thyroid swelling. Clinical examination was otherwise unremarkable with no lymphadenopathy or hepatosplenomegaly or signs of hypo/hyperthyroidism. Baseline haematological and biochemical investigations on admission were within normal limits (Hb 136 g/L, WCC 9.1 109/L, CRP <4 mg/dL). Levels of thyroxine, TSH, and calcitonin were normal. Lactase dehydrogenase (LDH) was slightly elevated at 352 U/L. Thyroperoxidase was elevated (1277 IU/mL) and thyroid stimulating hormone receptor antibodies (TRAb) of <5 U/L. CSF analysis showed no tumour cells. EBV PCR was negative as was HIV-I and HIV-II.\nA fine needle aspiration biopsy was carried out and was suspicious of NHL. The diagnosis of Burkitt type NHL (BL) was made following an open wedge biopsy. On microscopic examination, the tumour was composed of diffuse sheets of lymphoid cells () having round nuclei with coarse chromatin and conspicuous single to multiple nucleoli and scanty amphophilic cytoplasm. Numerous mitotic figures, apoptosis, and scattered tingible body type macrophages were also present. Tumour cells were positive for CD79A, CD20, and CD10 and negative for TdT and T cell markers (CD3, CD4, and CD8). Ki 67 showed proliferation index approaching 100%. Immunohistochemistry for EBV was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t(8; 14) translocation.\nStaging CT () showed a large (6.7 cm × 5.8 cm × 6.1 cm) heterogeneous mass in the left lobe and isthmus of the thyroid which extended craniocaudally from level of C4/5 to T1/2, with some evidence of intratumoural necrosis. There was significant mass effect with displacement and compression of the trachea along with compression of the left carotid artery and lateral displacement of the left jugular vein. There were two small indeterminate lung nodules. Abdominally there were two focal cortical abnormalities in the right kidney and an ill-defined attenuation in the pancreatic head. There was no evidence of bone marrow involvement.\nHe was treated according to the Children's Cancer and Leukaemia Group guidelines for BL—Group B protocol. This consisted of initial induction chemotherapy with COP (cyclophosphamide [300 mg/m2], vincristine [1 mg/m2], and prednisolone [60 mg/m2—7 days]) followed by 2 courses of COPADM (doxorubicin 60 mg/m2, methotrexate 3 g/m2, cyclophosphamide 500 mg/m2/day—5 days, vincristine [2 mg/m2], and prednisolone [60 mg/m2—5 days]) and two courses of CYM (cytarabine 100 mg/m2/day—5 days and methotrexate 3 g/m2) chemotherapy. This was accompanied by intrathecal chemotherapy (the CSF contained no tumour cells at diagnosis). The patient had a good response to treatment with a rapid decrease in the size of the thyroid mass and resolution of the lung, kidney, and pancreas metastases. Reassessment after the first course of CYM showed a residual thyroid mass of 15 mm × 30 mm but with resolution of the lung, kidney, and pancreas metastases.\nBecause of residual radiological abnormality, and in accordance with the CCLG NHL protocol, a hemithyroidectomy was performed with the residual lesion showing no evidence of tumour cells on histological examination. Chemotherapy was then completed and he is now disease-free 3 years after end of treatment.

A 70-year-old male presented a rapidly expanding mass of the neck associated with history of airway compression symptoms; progressive dyspnea and dysphonia lasting for 4 weeks, in a context of apyrexia and impairment of general condition. The patient was admitted to the hospital because of increasing dyspnea and urgently received a tracheostomy.\nA biopsy of the cervical mass was carried out and the histological examination showed diffuse infiltration of the thyroid gland by a monotonous population of atypical intermediate-sized lymphoid cells (Fig. ). These last possess scanty amphophilic to basophilic cytoplasm with centrally located nuclei of irregular shape, displaying dispersed basophilic chromatin, and frequent apoptotic figures (Fig. ). Scattered tingible body type macrophages were also present. Little residual thyroid follicles and some areas of necrosis was observed.\nImmunohistochemical staining was then performed and the tumour cells were positive for CD20, CD10 and BCL6. Ki-67 showed proliferation index approaching 100 %. CD3 and CD5 stained the background T cells (Fig. ). Immunoreactivity for Epstein-Barr virus (EBV) was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t (8; 14) translocation. Bone marrow examination was normal.\nThe patient was transferred to the Clinical Haematology department. On physical examination, he was apyretic and hemodynamically stable with a cervical armouring by a huge mass of hard consistency. Neurological examination shows no sensorimotor deficits.\nOther systemic examinations were normal, without any palpable lymphadenopathy or organomegaly.\nThe computerized tomography (CT) scan showed a heterogeneous process of the thyroid gland measuring 10.5 × 8.2 × 6.5 cm in size, extending up towards the laryngeal region, infiltrating the right vocal cord and reducing the laryngeal lumen (Fig. ).\nThe thoraco-abdominal CT scan showed no other localization.\nThe examination of the cephalorachidian liquid showed no central nervous system involvement. The patient was diagnosed with thyroidal Burkitt lymphoma, stage I of Murphy [].\nAfter cardiac, renal and liver functions assessment, the patient received chemotherapy according to the LMBA02 protocol [], group A (Age > 60 years, no CNS nor bone marrow involvement), with a first course of COP (Cyclophosphamide, Vincristine and Prednisone) and intrathecal Methotrexate, followed a week after by a course of R-COPADEM (Rituximab at day 0 and day 6, Cyclophosphamide day 2,3 and 4, Prednisone from day 1 to 5, Doxorubicineat day 2, high dose Methotrexate at day 1 with folic acid rescue from day 2 to day 6 and intrathecal chemotherapy at day 2 and day 6).\nAt day 15 of chemotherapy, the patient developed febrile neutropenia, refractory to broad-spectrum antibiotics and antifungals. The evolution was marked by the installation of a septic shock with acute respiratory distress syndrome that led to his transfer to intensive care unit where he was intubated and ventilated. The patient died 2 days after.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

An eight-year-old male presented with a mass in the right anterior neck that had been apparent for one week. Upon physical examination, blood pressure was recorded as 100/65 mmHg, heart rate was 80 beats per min, respiratory rate was 20 breaths per min and temperature was 36.1°C. A mass measuring ~4.0 cm in size, which caused difficulty in swallowing, was identified in the right anterior neck. The laboratory test results demonstrated a normal blood count and serum biochemistry, as well as normal levels of electrolytes and carcinoembryonic antigen. In addition, the test results for Epstein-Barr virus (EBV) viral capsid antigens immunoglobulin (Ig)M and IgG, human immunodeficiency virus (HIV) and hepatitis C virus antibodies, hepatitis B antigen and syphilis were negative. Furthermore, the thyroid hormone test results were as follows: Free thyroxine (FT) 4 levels of 11.8 pmol/l (normal range, 9–25 pmol/l); FT3 levels of 4.2 pmol/l (normal range, 3–9 pmol/l); thyroid-stimulating hormone levels of 0.720 μIU/ml (normal range, 0.34–5.60 μIU/ml); anti-thyroglobulin levels of 20 IU/ml (normal range, <115 IU/ml); and anti-thyroid peroxidase levels of 25 IU/ml (normal range, <34 IU/ml). The patient had no significant past medical or family history of disease. A B-mode ultrasound examination revealed a mass measuring 4.0×3.0×2.5 cm in the right lobe of the thyroid (), however, the lymph nodes surrounding the mass were normal (). The patient underwent a right lobe and isthmus thyroidectomy whereby two lymph nodes were excised simultaneously. Following the surgery, positron emission tomography-computed tomography scans showed normal metabolism in the left lobe of the thyroid and other parts of the body (). The patient’s bone marrow cytology was also normal, however, histological examination revealed diffuse infiltration of atypical lymphocytes and the observation of residual thyroid follicles and necrosis (). In addition, under low magnification, the ‘starry sky’ histology was observed in certain areas (). The atypical lymphocytes were medium-sized and consistent, with centrally located nuclei of irregular shape, displaying dispersed and deep basophilic chromatin and scanty cytoplasm. Additionally, certain neoplastic cells were visible, while varying numbers of nucleoli and apoptosis and mitosis were observed. Benign tissue cells engulfing apoptotic bodies were also observed under high magnification (), however, the isthmus of the thyroid was not infiltrated by the neoplastic cells. No reactive lymphocyte infiltration or fibrosis was identified in the stroma of the thyroid, and no oxyphilic change or squamous metaplasia was observed in the epithelial cells of the background thyroid tissues (). The only change in the two lymph nodes that were simultaneously excised, was the presence of reactive hyperplasia of the lymphoid follicles (). Immunohistochemical staining was then performed with the primary antibodies shown in (Zymed Corporation, Inc., San Francisco, CA, USA; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). The results showed that the neoplastic cells were diffusely positive for cluster of differentiation (CD)20 () and CD10 (), marginally positive for CD38, CD43 and B-cell lymphoma (Bcl)-6, but negative for Bcl-2 and terminal deoxynucleotidyl transferase (TDT). In addition, CD3 and CD5 stained the background T cells, and the Ki-67 proliferation index was >95% (). Analysis using an EBV-encoded small RNA (EBER) digoxin-labeled probe (PanPath B.V., Budel, Netherlands) was performed and revealed a negative result (), however, positive nuclei were observed in the nasopharyngeal carcinoma tissue, which was used as the positive control (). Analysis using the C-MYC break-apart detection probe (Guangzhou LBP Medical Science Technology Co., Ltd., Guangzhou, China) was also performed and the results revealed that ~90% of the neoplastic cells exhibited red and green signal separation, which indicated that chromosome breakage and translocation of the MYC gene had occurred in the neoplastic cells (). Immunoglobulin gene rearrangement assays were performed according to instructions of the Biomed-2 Polymerase Chain Reaction kit (Invivoscribe technologies, Inc., San Diego, CA, USA), followed by capillary electrophoresis, which was analyzed using Genemarker® v1.5. software (SoftGenetics, LLC, State College, PA, USA). Positive gene arrangements of IgH and IgK were observed in the tumor tissues, however, no positive gene rearrangements were observed for IgL (). Consequently, the patient was diagnosed with primary BL of the thyroid and underwent alternate R-B-NHL-BFM-90-A and R-B-NHL-BFM-90-B treatment, for four cycles each. The two regimens, including the dose and duration of chemotherapy, are described in . After almost four years of follow-up, the patient appears well and remains free of disease.

A 49-year-old woman with a history of Hashimoto’s thyroiditis presented with a rapidly growing neck mass and upper airway compression symptoms. No B symptoms were present. The hematological test showed a white blood cell count within the normal range (51.5 × 102/μL). Interleukin-2 receptor (801 U/mL) and lactate dehydrogenase (228 U/L) levels were elevated, although serum thyroxine and thyroid-stimulating hormone levels were within their normal ranges. An elevated thyroid peroxidase antibody of 271.4 IU/mL was detected. Ultrasonography revealed a mass measuring 2.0 × 1.0 × 1.0 cm in the right lobe of the thyroid; the border of the nodule was indistinct. The patient underwent a right thyroidectomy after a core needle biopsy revealed a diffuse large B-cell lymphoma. Following the final histological diagnosis of primary thyroid BL, the patient received rituximab, cyclosphosphamide, doxorubicin, vincristine, and prednisone for 2 weeks, as well as rituximab, hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone including prophylactic intrathecal methotrexate for 3 months. Adjuvant treatments involving 22 cycles of linear accelerator (LINAC) therapy, 40 Gy each, were administered after the chemotherapy. Thirty months after the initial diagnosis, the patient had no evidence of recurrent disease.\nThe tumor cells were composed of round, intermediate-sized lymphoid cells admixed with scattered tingible body macrophages imparting a “starry sky” appearance (Fig. ). The nuclei were uniform and round-to-oval-shaped. The chromatin was coarsely clumped and had medium-sized paracentral nucleoli, while the cytoplasm was basophilic. Mitotic figures (12 per high-power field) were identified; there was no coagulative necrosis, although extrathyroidal extension was observed. Hashimoto’s thyroiditis was identified in the non-tumoral thyroid tissue.\nDiffuse membranous immunostaining for CD10, CD20, and CD79α, as well as diffuse nuclear staining for MUM-1 (Fig. a) and p16 (Fig. b), were noted in the tumor cells. The expression of MDM2 was focal and confined to the tumor cell nuclei (Fig. c), although the cells were negative for Bcl-2, Bcl-6, and p53. The Ki-67 labeling index exceeded 90% (Fig. ). The EBER in situ hybridization test was negative (Fig. ). Ninety-six percent of the tumor cells were found to have MYC/IgH gene fusion as determined by FISH (Fig. ).\nThe clinicopathological features of 21 thyroid BLs are summarized in Table . The median age at diagnosis was 39.3 years with a male-to-female ratio of 13/8. The majority (94.4%) of these patients presented with a thyroid mass; patients also presented with a rapidly growing nodule (66.7%), dyspnea (61.1%), dysphagia (16.7%), and thyrotoxicosis (5.6%). Four of the 14 described patients (28.6%) showed B symptoms (e.g., systematic symptoms of fever, night sweats, or weight loss). None of the reported patients presented with immunosuppressive conditions or the endemic form of BL. Regarding the treatment modalities, all of the 20 patients for whom data were available (data for 1 were missing) received multidrug chemotherapy regimens; 12 received chemotherapy only, 7 received chemotherapy with combined surgery, and 1 was administered chemotherapy combined with surgery and adjuvant radiotherapy (LINAC).\nFive of 7 patients with thyroid BL (71.4%) had morphologic evidence of Hashimoto’s thyroiditis. Regarding immunohistochemical features, all patients who were tested for CD10 (n = 14), CD20 (n = 18), and CD79a (n = 5) were positive for these respective proteins. IgM was positive in the lone patient who was tested. Additional factors measured are shown in Table . The Ki-67 labeling index exceeded 90% in all 19 patients for whom such staining was performed. We demonstrated that our patient had focal immunoreactivity for MDM2, but none of the other patients had been tested for this protein. All 12 patients who were tested for EBER in situ hybridization showed negative results, and flow cytometry immunophenotyping demonstrated CD10-positive monotypic B-cell populations in all 5 tested patients; moreover, MYC gene translocation was detected using FISH in all 12 patients whose samples were tested.\nOf 19 patients with available clinical outcome data, 14 (73.7%) were alive with complete remission, 1 (5.3%) was alive with persistent disease, and 4 (21.1%) died of the disease. Three of the 19 patients lacked follow-up data; hence, the median follow-up of the 16 remaining patients was 46.5 months (range, 0.5–361 months). Kaplan-Meier survival analysis showed that the 12- and 60-month overall survival rates were 87.5 and 70.7%, respectively (Fig. ).

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

An eight-year-old male presented with a mass in the right anterior neck that had been apparent for one week. Upon physical examination, blood pressure was recorded as 100/65 mmHg, heart rate was 80 beats per min, respiratory rate was 20 breaths per min and temperature was 36.1°C. A mass measuring ~4.0 cm in size, which caused difficulty in swallowing, was identified in the right anterior neck. The laboratory test results demonstrated a normal blood count and serum biochemistry, as well as normal levels of electrolytes and carcinoembryonic antigen. In addition, the test results for Epstein-Barr virus (EBV) viral capsid antigens immunoglobulin (Ig)M and IgG, human immunodeficiency virus (HIV) and hepatitis C virus antibodies, hepatitis B antigen and syphilis were negative. Furthermore, the thyroid hormone test results were as follows: Free thyroxine (FT) 4 levels of 11.8 pmol/l (normal range, 9–25 pmol/l); FT3 levels of 4.2 pmol/l (normal range, 3–9 pmol/l); thyroid-stimulating hormone levels of 0.720 μIU/ml (normal range, 0.34–5.60 μIU/ml); anti-thyroglobulin levels of 20 IU/ml (normal range, <115 IU/ml); and anti-thyroid peroxidase levels of 25 IU/ml (normal range, <34 IU/ml). The patient had no significant past medical or family history of disease. A B-mode ultrasound examination revealed a mass measuring 4.0×3.0×2.5 cm in the right lobe of the thyroid (), however, the lymph nodes surrounding the mass were normal (). The patient underwent a right lobe and isthmus thyroidectomy whereby two lymph nodes were excised simultaneously. Following the surgery, positron emission tomography-computed tomography scans showed normal metabolism in the left lobe of the thyroid and other parts of the body (). The patient’s bone marrow cytology was also normal, however, histological examination revealed diffuse infiltration of atypical lymphocytes and the observation of residual thyroid follicles and necrosis (). In addition, under low magnification, the ‘starry sky’ histology was observed in certain areas (). The atypical lymphocytes were medium-sized and consistent, with centrally located nuclei of irregular shape, displaying dispersed and deep basophilic chromatin and scanty cytoplasm. Additionally, certain neoplastic cells were visible, while varying numbers of nucleoli and apoptosis and mitosis were observed. Benign tissue cells engulfing apoptotic bodies were also observed under high magnification (), however, the isthmus of the thyroid was not infiltrated by the neoplastic cells. No reactive lymphocyte infiltration or fibrosis was identified in the stroma of the thyroid, and no oxyphilic change or squamous metaplasia was observed in the epithelial cells of the background thyroid tissues (). The only change in the two lymph nodes that were simultaneously excised, was the presence of reactive hyperplasia of the lymphoid follicles (). Immunohistochemical staining was then performed with the primary antibodies shown in (Zymed Corporation, Inc., San Francisco, CA, USA; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). The results showed that the neoplastic cells were diffusely positive for cluster of differentiation (CD)20 () and CD10 (), marginally positive for CD38, CD43 and B-cell lymphoma (Bcl)-6, but negative for Bcl-2 and terminal deoxynucleotidyl transferase (TDT). In addition, CD3 and CD5 stained the background T cells, and the Ki-67 proliferation index was >95% (). Analysis using an EBV-encoded small RNA (EBER) digoxin-labeled probe (PanPath B.V., Budel, Netherlands) was performed and revealed a negative result (), however, positive nuclei were observed in the nasopharyngeal carcinoma tissue, which was used as the positive control (). Analysis using the C-MYC break-apart detection probe (Guangzhou LBP Medical Science Technology Co., Ltd., Guangzhou, China) was also performed and the results revealed that ~90% of the neoplastic cells exhibited red and green signal separation, which indicated that chromosome breakage and translocation of the MYC gene had occurred in the neoplastic cells (). Immunoglobulin gene rearrangement assays were performed according to instructions of the Biomed-2 Polymerase Chain Reaction kit (Invivoscribe technologies, Inc., San Diego, CA, USA), followed by capillary electrophoresis, which was analyzed using Genemarker® v1.5. software (SoftGenetics, LLC, State College, PA, USA). Positive gene arrangements of IgH and IgK were observed in the tumor tissues, however, no positive gene rearrangements were observed for IgL (). Consequently, the patient was diagnosed with primary BL of the thyroid and underwent alternate R-B-NHL-BFM-90-A and R-B-NHL-BFM-90-B treatment, for four cycles each. The two regimens, including the dose and duration of chemotherapy, are described in . After almost four years of follow-up, the patient appears well and remains free of disease.

A 52-year-old woman presented to our Endocrinology Unit with a growing thyroid mass, which had enlarged so rapidly she had become unable to wear her motorcycle helmet in the weeks prior to her visit. She suffered from Hashimoto’s thyroiditis for which she was taking levothyroxine. There was no history of neck irradiation or family history of thyroid cancer. On examination, there was a large, firm thyroid nodule on the right side of the neck, without palpable cervical lymphadenopathy. TSH was 4.79 μU/mL with FT3 and FT4 within the reference range. Otherwise, there was only a mild thrombocytopenia. Thyroid ultrasonography showed a solid hypoechoic nodule in the right lobe of the gland, with significant internal vascularity and absence of calcifications (Figure ). FNA cytology with rapid on-site evaluation of the material adequacy showed that there were only atypical lymphoid cells with no thyrocytes and the specimens were considered suggestive of a lymphoproliferative disorder but insufficient to make a diagnosis, such that a CNB was scheduled for the following day.\nAfter checking the blood coagulation profile, the patient underwent a CNB, which allowed histological/morphological tissue analysis. This showed that normal thyrocytes were virtually all replaced by homogeneous medium-sized lymphocytes with scanty blue cytoplasm, round nuclei, coarse chromatin, and multiple small nucleoli. There were frequent mitotic figures and scattered macrophages ingesting apoptotic cells, giving to the tissue section the so-called ‘starry sky’ appearance (Fig. ). Overall, these features were consistent with the presence of a thyroid Burkitt’s lymphoma, and further investigations were ordered to confirm the diagnosis and evaluate the disease extent. A CT of chest and abdomen showed the 44x43x87 mm thyroid nodule with left tracheal deviation (Figure ) without other visible masses or lymph nodes. Bone marrow biopsy showed almost 100% lymphoid infiltration, consisting of a population of intermediate-sized blast-like cells, with prominent nucleoli, which were replacing all normal cells. These cells expressed CD10, CD20, and were negative for Bcl2, CD34, and TdT. Altogether these results led us to the final diagnosis of stage IV Burkitt’s lymphoma [].\nThe patient was admitted to our hospital’s Haematology Unit and was successfully treated with 3 cycles of Hyper-CVAD chemotherapy (cyclophosphamide, vincristine, doxorubicin and dexamethasone) completed in five months. The thyroid mass disappeared (Fig. ) and the platelets returned to baseline levels. At 60 months after diagnosis the patient is alive, and remains disease-free at regular follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy