bluuebunny/crossref_metadata_2025_split huggingface dataset:
FRI512 Thyrotoxic Periodic Paralysis With Extreme Hypokalemia Precipitated By Acute Alcohol Intoxication In A Patient With Graves’ Disease
Authors: Batra Jaskaran , Reddy Ankireddypalli Anvitha , Kaur Jasleen 
Published: October 2023

Abstract
Disclosure: J. Batra: None. A.R. Ankireddypalli: None. J. Kaur: None.
Introduction: Thyrotoxic periodic paralysis (TPP) is a muscle and electrolyte disorder, mostly seen in the setting of hyperthyroidism. It is characterized by reversible painless muscle weakness and hypokalemia. Prevalence is highest in East Asian populations, approximately 2%, and 0.1-0.2% in other populations. Males are much more likely to be affected. Common provoking factors include exercise, fasting, and changes in diet. Clinical case: A 29-year-old male of East Asian ethnicity presented to the hospital with the complaint of multiple bouts of inability to lift his extremities for 1 day. He also complained of generalized weakness. He did not have any changes in his mental status and was fully oriented at the time of the presentation. No breathing difficulty was reported. He had been drinking the night before with his friends and drank 1 L of vodka. His past medical history was significant for hyperthyroidism secondary to Graves’ disease, which was diagnosed a year ago. He had been prescribed methimazole but had not been adherent to the medication. The basic metabolic panel revealed undetectable serum potassium of &lt;1.5 (3.4 to 5.3 mmol/L). The rest of the electrolytes and renal function were unremarkable. TSH was suppressed at &lt;0.01 (0.3 to 4.20 uIU/L) and free T4 levels were significantly elevated at 7.77 (0.9 to 1.70 ng/dL). The thyrotropin receptor antibody was 33 (0.00 to 1.75 IU/L). EKG showed sinus tachycardia with nonspecific T-wave abnormalities. Thyroid ultrasound showed diffusely heterogenous parenchyma with diffusely increased blood flow throughout the thyroid on doppler. Echocardiogram showed a normal ejection fraction of 55-60% with mild concentric left ventricular wall thickening consistent with left ventricular hypertrophy. He was initially treated with intravenous potassium replacement and high doses of propylthiouracil, hydrocortisone, and propranolol, leading to the resolution of his symptoms. He was discharged on methimazole and propranolol therapies. Learning points: • Patients with Graves’ disease are routinely counseled against tobacco use to avoid worsening of orbitopathy. Hyperthyroid patients should also be counseled regarding avoidance or moderation of alcohol intake to avoid this rare but potentially life-threatening complication of thyrotoxic periodic paralysis. • The incidence of TPP is significantly higher in the East Asian populations, especially among males (8.7-13%). Counseling regarding provoking factors, the importance of adherence to medications, and the maintenance of euthyroidism to avoid TPP is essential.
Presentation: Friday, June 16, 2023
FRI561 The Thyroid Trifecta
Authors: Kachhadia Palak , Khan Shaza , Abu Limon Ahmad , Aldasouqi Saleh 
Published: October 2023

Abstract
Disclosure: P. Kachhadia: None. S. Khan: None. A. Abu Limon: None. S. Aldasouqi: None.
Introduction: Autoimmune Hashimoto’s Thyroiditis (HT) and Graves’ Disease (GD) may co-exist or may occur alternatingly, known in many case reports as Graves’s Alternans. Hyperfunctioning (Toxic, hot) thyroid nodules (TN) may also co-exist with GD, a rare condition called Marine-Lenhart syndrome. However, the co-existence of HT, GD and TN is perceivably rarer. Case Presentation: The patient is a 45 year old female with a prior history of HT for 20 years, who presented to the clinic with symptoms of minimal eye pain, tremors, fatigue, diarrhea and anxiety. She was not on thyroid replacement, with normal thyroid function tests (TFTs). Physical exam showed bilateral proptosis, a moderate goiter, hand tremors, mild anxiety and tachycardia. Labs showed high TPO (3995.0 IU/mL, n &lt;18 IU/mL), Thyrotropin receptor antibody (5.25 IU/L, n&lt;1.75 IU/L), and Thyroid-stimulating immunoglobulins (1.8 TSI index, n&lt;1.3 TSI index) with low-normal TSH of 0.42 uIU/mL (0.35-4.01 uIU/mL) , mid-range free triiodothyronine (FT3) at 3.6 pg/mL (2.8-4.4 pg/mL) and normal free thyroxine (FT4) at 0.80 NG/dL (0.61-1.37 NG/dL). Thyroid US showed a 2.4 cm left lobe inferior nodule classified as TI-RADS 3. Fine needle aspiration of this nodule was benign. Radioactive Iodine-123 Uptake Scan showed a hot nodule in the left inferior lobe and with visible uptake in the rest of the gland (uptake was mid-normal). She was started on methimazole 5mg once daily and propranolol 10mg BID with improvement in her symptoms. Subsequent TFTs showed stable T4 and T3 and normalization of TSH to 1.78 uIU/mL (0.35-4.01 uIU/mL). Discussion: Marine-Lenhart syndrome was described in 1911 by surgeons David Marine and Carl Lenhart. Graves’ Alternans has been described in the literature, with variable time separation. Though thyroid nodules occur in up to 35% of those with GD, only 1-4.1% are deemed functional nodules. Nuclear medicine imaging via Tc-99m pertechnetate or I-123 iodine at diagnosis of GD generally shows such nodules as cold nodules lacking uptake, while the rest of the gland has diffuse uptake. However, with normalization of TSH through treatment, these cold nodules may alternate uptake and present as hot nodules. Conclusion: In conclusion, this case presents the co-existence of HT, GD and HN, a term we are calling “Thyroid Trifecta”. It is imperative that HNs should be identified if RAI treatment is planned in such patients. Literature review portrays cases in which if thyrotoxicosis persists post RAI treatment for GD, careful examination and repeat RAIU may show a hot nodule consistent with Marine-Lenhart Syndrome. These patients may benefit instead from thyroidectomy. In the case of our patient, definitive treatment options have been discussed and she has been referred for thyroidectomy due to the presence of the TN. RAI ablation will be avoided in view of mild but active thyroid eye disease.
Presentation: Friday, June 16, 2023
SAT549 False Alarm: Profoundly High Thyroglobulin Level Without Evidence Of Thyroid Malignancy
Authors: Thelmo Franklin L , Watari Jessica , Miller Jeffrey L 
Published: October 2023

Abstract
Disclosure: F.L. Thelmo: None. J. Watari: None. J.L. Miller: None.
Thyroglobulin (TG) remains a clinical mainstay for monitoring of disease burden and recurrence in patients with differentiated thyroid cancer. TG levels are expected to be low to undetectable in patients who undergo total thyroidectomy and less than 30 ng/mL in patients who undergo thyroid lobectomy. We describe a case of a 52-year-old patient who underwent thyroid lobectomy for a 16 mm minimally invasive follicular thyroid carcinoma (single vessel angioinvasion) who was later found to have a TG level in excess of 2,000 despite no signs of metastatic disease. A 52-year-old male with past medical history of prediabetes and minimally invasive follicular thyroid cancer presented for follow-up after right lobectomy five years prior. The patient was lost to follow-up after his lobectomy. During work-up of paresthesias, a cervical spine MRI incidentally noted a 41 mm enhancing mass in the left thyroid lobe. The patient had a TSH of 1.1 mIU/L. A dedicated thyroid ultrasound was performed which found a left 2.9 cm TI-RADS 3 nodule which was biopsied and found to be benign (Bethesda II). TG level was obtained and found to be significantly elevated at 2,479.9 ng/mL with negative thyroglobulin antibodies. This was repeated twice with subsequent levels being 1,857.5 ng/mL and 2,555.1 ng/mL. TG antibodies remained undetectable throughout the clinical course. The patient had a CT chest, abdomen, and pelvis exam for which no signs of metastatic disease were detected. A skeletal survey was performed which showed no evidence of metastatic disease. The patient elected for a completion thyroidectomy to ensure there was no undetected malignancy. The patient underwent successful completion thyroidectomy. Surgical pathology showed benign nodular hyperplasia. The patient was started on replacement levothyroxine and one month later the TG level became undetectable. We would like to draw attention to this patient’s profoundly high TG levels which are normally associated with recurrence of thyroid malignancy or large goiter. After comprehensive evaluation this patient was found to have no underlying disease recurrence. A completion thyroidectomy showed no malignancy within remnant thyroid tissue or adjacent lymph nodes and repeat TG level was undetectable after completion showing that native thyroid tissue had significantly high TG production without underlying disease. We believe his remaining relatively normal thyroid lobe was a super producer of thyroglobulin. Despite TG being a sensitive marker for residual thyroid tissue and disease, the standard cut-off for lobectomy must be used with caution and may not apply to every patient.
Presentation Date: Saturday, June 17, 2023
SAT557 Unexpected Whole Body Scan Finding
Authors: Gastelum Alheli Arce , Liu Catherine Y , McCowen Karen 
Published: October 2023

Abstract
Disclosure: A. Arce Gastelum: None. C.Y. Liu: None. K. McCowen: None.
A 41-year-old man presented with a neck mass. Following total thyroidectomy with central and bilateral lateral neck node dissection, he received a diagnosis of stage I T2N1bMx multifocal papillary thyroid cancer with extensive extrathyroidal extension, angioinvasion and 14/65 positive lymph nodes. Surgery was complicated by temporary post operative hypoparathyroidism. Lab testing one week post thyroidectomy, before radioiodine ablation showed a serum TSH 23 uIU/mL, thyroglobulin: 34.1 ng/mL, with thyroglobulin antibody: &lt;0.9 [IU]/mL.Post RAIA Whole Body Scan revealed increased uptake in the right orbit, concerning for metastatic disease. Confirmatory MRI of the brain showed a right superior intraorbital cystic lesion. Although orbital metastases are infrequent, a metastatic lesion was suspected due to the aggressiveness of his thyroid cancer. The patient was referred to ophthalmology several months after surgery and underwent right orbitotomy with excision and biopsy of the mass. The pathology was consistent with a multilocular cystic tumor lined by bland cuboidal epithelium, containing proteinaceous concretions and entirely negative for metastasis. Extensive thyroid cancer is treated with surgery followed by radioactive iodine (I-131) in case of tissue remnants or extra nodal metastases. Although unusual, false-positive scans exhibiting the presence of 131I uptake in the absence of residual thyroid tissue can occur.Fibrotic lung conditions, pleural effusions and bronchiectatic lesions have been reported to concentrate iodine in the absence of thyroid cancer metastasis. One prior report of a conjunctival inclusion cyst also resulted in radioiodine uptake in the orbit. Unless identified as a false positive, radioiodine uptake may result in a diagnostic fallacy. The correlation of clinical signs and serum thyroglobulin trends with imaging techniques should be emphasized to prevent unnecessary additional therapy.
Presentation Date: Saturday, June 17, 2023
SAT564 Metastatic Malignant Pleural Effusion In A Patient With Remote History Of FTC
Authors: Lee David M , Gong Michael , Czerlanis Cheryl , Arif Ayesha , Arceo-Mendoza Rod Marianne 
Published: October 2023

Abstract
Disclosure: D.M. Lee: None. M. Gong: None. C. Czerlanis: None. A. Arif: None. R. Arceo-Mendoza: None.
Introduction: Differentiated thyroid follicular epithelial-derived cancers include Papillary (PTC) and Follicular Thyroid Cancer (FTC). FTC is less common, accounting for only 5-15% of all thyroid cancers. It is more common in older patients and spreads via hematogenous route, with distant metastases in 10-15% of patients, commonly in the lungs and bone. We describe an unusual case of a patient with a remote history of FTC who presents with recurrence more than 50 years later in the form of a malignant pleural effusion. Clinical Case: A 79/M with a remote history of FTC that was diagnosed in the 1960s presents with one week of L sided pleuritic chest pain and dyspnea. CXR on admission showed opacification of the L hemidiaphragm. A chest CT confirmed the L sided pleural effusion. Thyroid US showed surgically absent thyroid and a 1.1cm solid nodule in the L surgical bed. PET/CT demonstrated hypermetabolic rim of L pleural effusion with no uptake in the neck. Thoracentesis was done which showed exudative pleural fluid concerning for malignancy. Immunohistochemical stains were positive for TTF-1 and thyroglobulin, consistent with metastatic thyroid cancer. He also underwent L supraclavicular lymph node FNA with findings suspicious for metastatic thyroid cancer with follicular features, with NO nuclear features of PTC. On further history, the patient reports having radiation therapy for acne around age 17 and was then diagnosed with FTC in his 20s. He underwent total thyroidectomy and RAI treatment. He recalls being told that he had a few weeks to live, and an “experimental treatment” was offered at the time, which we suspect was cobalt radiation. The patient unfortunately was eventually lost to endocrine follow up but denies any known recurrence prior to this admission. Upon discharge, an I-123 WBS was performed showing multiple foci in the R neck. Uptake is also noted in bilateral lung base, greater on the left. He was treated with 250 mCi I-131. He is currently doing well overall, asymptomatic, and with stable surveillance imaging. He is on levothyroxine suppression therapy with Tg level on a downward trend. Clinical Lesson/Conclusion: Involvement of pleural fluid by metastatic thyroid cancer though reported, is relatively rare, accounting for only less than 1% in all the patients with malignant pleural effusion. To our knowledge, there are no reported cases of malignant pleural effusions from metastatic FTC presenting remotely so many years after the initial diagnosis. The diagnosis of metastatic thyroid cancer in pleural fluid can be challenging and knowledge of the clinical context, even with remote history dating back 50 years ago just like in our case, and supporting immunohistochemical stains is essential for making the right diagnosis.
Presentation Date: Saturday, June 17, 2023
SAT569 Papillary Thyroid Carcinoma With Renal Metastasis Treated With Radioactive Iodine: A Case Report
Authors: Apa-Ap Archimedes Almasol , Sedurante Myrna Buenaluz , Lacuata Jan Alexeis , Gacula John Kenneth V , Lee Vannah Marjolaine , Hernandez Melfred L 
Published: October 2023

Abstract
Disclosure: A.A. Apa-ap: None. M.B. Sedurante: None. J. Lacuata: None. J. Gacula: None. V. Lee: None. M.L. Hernandez: None.
INTRODUCTION. Papillary thyroid cancer (PTC) is one of the most treatable cancers in comparison to undifferentiated thyroid malignancies. It advances slowly, and there is only 1-4 percent of cases of distant metastases. Renal involvement from PTC is very rare with an incidence of 0.47 percent.
CASE DESCRIPTION. This paper describes a 34-year-old Filipino female presenting with an 8-year history of hoarseness and a gradually enlarging anterior neck mass. Metastatic workup revealed innumerable bilateral pulmonary nodules bilateral cervical lymphadenopathy, and bilateral renal mass on CT scan. The right pole of the kidney shows a solid heterogeneously enhancing partially-exophytic focus measuring 4.9 x 4.2 x 4.3cm likely a primary renal cell carcinoma versus metastasis. The left renal mass shows a hypodense non-enhancing partially-exophytic focus measuring 3.9 x 3.6 x 3.6cm probably a renal cyst. Clinically, the patient did not show any urinary symptoms and creatine clearance was normal. The patient underwent total thyroidectomy and neck dissection and histopathology revealed PTC. The patient underwent simultaneous ultrasound right renal mass biopsy which revealed few fragments of thyroid tissues with atypia most likely representative of metastasis of PTC. Since the radiographic finding was suggestive of a renal cyst, the left renal mass was not biopsied. Patient refused nephrectomy and underwent 1 cycle of Radioactive Iodine (RAI) Therapy. Post therapy whole body scan showed mildly increased and diffuse tracer uptake activity in bilateral lungs and large avid focus, approximately 5.0 x 4.4 cm, seen in the inferior pole of the right kidney. Surveillance showed increased thyroglobulin. To date, the patient still refused surgery and is contemplating undergoing another cycle of RAI therapy.
DISCUSSION. Due to the rarity of the metastatic site, the ideal course of treatment for this illness is unknown. To our knowledge, there are only approximate of 30 case reports on WDTC with renal metastasis in the literature.
Presentation: Saturday, June 17, 2023
SAT311 A Time And Place For Metyrosine: Successful Treatment Of A Pheochromocytoma Presenting With Hypotension And Multisystem Organ Failure
Authors: Shafiq Ramsha , Giordano Jennifer 
Published: October 2023

Abstract
Disclosure: R. Shafiq: None. J. Giordano: None.
Pheochromocytomas are rare neuroendocrine catecholamine-secreting tumors. The surgical excision of pheochromocytoma is definitive management which requires presurgical preparation with an alpha blocker, beta blocker, and sometimes metyrosine to reduce perioperative hemodynamic instability. We present a case of pheochromocytoma complicated with acute on chronic renal failure and acute on chronic heart failure with hypotension requiring metyrosine in presurgical preparation due to hypotension and intolerance to alpha-blocker with successful surgical excision of the tumor. Case: 67 yo M admitted for acute on chronic heart failure and acute on chronic renal failure. He was noted to have an incidental right adrenal mass of 4.3 x 4.5 cm on the CT chest. He denied any prior history of hypertension, episodes of flushing, sweating, palpitations, headaches, or any family history of adrenal malignancies. His labs were consistent with significantly elevated plasma metanephrines to 4.5 nmol/L (normal range &lt; 0.5 nmol/L) and normetanephrine 36 nmol/L (normal range &lt; 0.9 nmol/L). Levels were repeated with slight worsening of metanephrines to 5.6 and normetanephrine to 42. He was hypotensive on presentation initially on milrinone drip that was slowly tapered off. His echo on admission showed left ventricle global hypokinesis with EF 25-30%. He had a worsening renal function on admission and required a few dialysis sessions before being referred to our hospital. He had an MRI adrenal done w/o contrast in the setting of renal failure with a heterogenous mass concerning for pheochromocytoma. PET CT was done which was negative for metastatic disease. Due to strong suspicion of uncontrolled pheochromocytoma as a cause of his heart failure and acute on chronic renal failure, the team and patient opted for unilateral adrenalectomy. He was started on metyrosine pre-surgically as he could not tolerate alpha blockade due to hypotension. His metanephrine levels improved from 5.6 to 1.8 and normetanephrine from 43 to 15 with metyrosine prior to surgery. He had a successful right adrenalectomy and pathology confirmed pheochromocytoma. Of note, he had a history of diabetes with uncontrolled hyperglycemia during admission. Hyperglycemia resolved after adrenalectomy. His plasma metanephrine levels normalized post-adrenalectomy and remained normal on the follow-up visit. Conclusion: Preoperative medical stabilization is a crucial step before surgical resection of pheochromocytoma that traditionally includes an alpha blocker followed by a beta-blocking agent to reduce intra-operative hypertensive crisis. Metyrosine is an often-overlooked agent due to cost, however, should remain in our armamentarium for pheochromocytoma crisis complicated with hypotension when the patient is unable to tolerate an alpha-blocking agent.
Presentation: Saturday, June 17, 2023
SAT331 A Case Of Iatrogenic Cushing’s Syndrome Due To The Concomitant Use Of Cobicistat With An Inhaled Glucocorticoid Followed By Adrenal Insufficiency Upon Discontinuation Of Cobicistat
Authors: Noor Laila , Mullally Jamie , Glassman Rebecca 
Published: October 2023

Abstract
Disclosure: L. Noor: None. J. Mullally: None. R. Glassman: None.
Cobicistat is an inhibitor of cytochrome P4503A (CYP3A) used to increase the systemic exposure of antiretroviral drugs for treatment of HIV, and because of it’s mechanism of action, can have significant drug interactions. A similar “pharmacologic booster” ritonavir has now been widely reported to cause cases of iatrogenic Cushing’s syndrome when used in combination with glucocorticoids, but the data on this risk with cobicistat is much more limited. This case describes a patient who developed florid Cushing’s syndrome while on cobicistat and inhaled glucocorticoids followed by secondary adrenal insufficiency upon discontinuation of cobicistat.
A 60 year old male with past medical history of well-controlled HIV on elvitegravir, cobicistat, emtricitabine and tenofovir, asthma on chronic inhaled fluticasone/salmeterol, presented with several months of progressive abdominal distention, back pain, irritability, easy bruising, proximal muscle weakness and weight gain. On physical exam, he appeared Cushingoid with central obesity, supraclavicular fullness, dorsocervical fat pad, wide violaceous striae on his abdomen and multiple ecchymoses. Iatrogenic Cushing's syndrome was suspected and labs showed undetectable morning serum cortisol and 24 hour urine free cortisol as well as newly elevated A1C of 5.7%. DEXA scan showed osteopenia. CT abdomen pelvis showed small adrenal glands. His HIV medication was switched to a combination of bictegravir, emtricitabine and tenofovir and he subsequently developed significant fatigue, nausea, abdominal discomfort and headaches. He was started on replacement doses of prednisone and his symptoms improved significantly. The prednisone dose is being gradually tapered, with ongoing recovery of the hypothalamic-pituitary-adrenal(HPA) axis, with now low, but detectable cortisol and ACTH levels.
We present a unique case of iatrogenic Cushing’s syndrome due to concomitant use of cobicistat with inhaled fluticasone and the subsequent development of secondary adrenal insufficiency upon discontinuation of cobicistat. Cobicistat is an inhibitor of CYP3A which can cause decreased metabolism of exogenous glucocorticoids resulting in HPA axis suppression and exogenous Cushing’s syndrome. Fluticasone causes more cortisol suppression than other inhaled steroids because of it’s long half-life, higher binding affinity for glucocorticoid receptors and high lipophilicity. Concomitant use of cobicistat and glucocorticoids, including inhaled fluticasone, should be avoided and clinicians should be aware of the potential for iatrogenic Cushing’s syndrome and consequent adrenal insufficiency upon discontinuation of cobicistat after use with concomitant glucocorticoids.
Presentation: Saturday, June 17, 2023