bluuebunny/crossref_metadata_2025_split huggingface dataset:
Giant cell arteritis as a cause of intermittent claudication
Authors: Desmond J , Hussain ST , Colin JF 
Published: May 2014

A 57-year-old lady who works in the post office presented initially in May 1994 with a 5- month history of left calf claudication at 50 yards. Six months previously she had also complained to her GP of joint pain, tiredness, and muscle aches. Rheumatoid factor was negative and erythrocyte sedimentation rate was elevated at 102. A diagnosis of polymyalgia rheumatica was made and she commenced a course of low-dose steroids, from which she gained dramatic relief. However, the pain in her legs continued and 6 months after the onset it caused sufficient handicap to interfere with her lifestyle. At presentation to the vascular clinic, she was no longer on steroids. She smoked ten cigarettes per day and had no other atherosclerotic risk factors. On examination she had palpable femorals with no pulses distally. An arteriogram was arranged, which showed bilateral femoropopliteal occlusions with both popliteal arteries being patent above the knee, with poor run off. A diagnosis of peripheral vascular disease was made and confirmed by ankle:brachial pressure indices of 0.7 and 0.76 for the dorsalis pedis arteries on the right and left side respectively. She was advised to stop smoking and was put on an exercise regime. An outpatient review was to be carried out in 2 months time. Her joint and muscle symptoms returned, so she was referred to the rheumatologist. A temporal artery biopsy was arranged. This showed multi-nucleated histiocytes consistent with giant cell arteritis. She was subsequently started on prednisolone 60 mg and methotrexate 10 mg. Three weeks after commencement of treatment she made a dramatic improvement in her symptoms of joint pains and muscle aches. Unexpectedly, the claudication disappeared, despite the continuance of her smoking habit. Her claudication symptoms were therefore attributed entirely to large vessel vasculitis as a result of giant cell arteritis. Her ankle:brachial pressure indices improved to 0.89 and 0.92 for the right and left side respectively.
The changing face of endocarditis: report of a series of cases
Authors: Brydie Alan D , Clark Andrew L 
Published: May 2014

A 67-year-old man presented with a sudden onset right homonymous hemianopia associated with a swinging pyrexia and a new early diastolic parasternal murmur. He had had a Bjork–Shiley aortic valve replacement 2 years previously for symptomatic aortic stenosis with a transvalvular gradient of 80 mmHg and had been well thereafter. Computed tomography scan of the brain showed a left occipital infarct (Figure 1), C-reactive protein was 51 mg/litre (normal <10 mg/litre), blood cultures consistently grew Candida parafilaris, and treatment with intravenous liposomal amphotericin and flucytocine was started the day the first positive culture was obtained. Transoesophageal echocardiography did not demonstrate vegetations, but did show a periprosthetic aortic incompetent leak. On day 11 the aortic prosthesis was removed and replaced because of worsening aortic incompetence. Direct inspection of the prosthesis demonstrated a vegetation on the sewing ring. The immediate postoperative recovery period was complicated by complete heart block requiring insertion of a permanent pacemaker after an initial phase of pericardial pacing. The intravenous antifungals were discontinued after 37 days of treatment and the patient commenced on lifelong oral fluconazole. At discharge on day 42 the patient was well and apyrexial with C-reactive protein less than 10 mg/litre.
The mysterious case of the lost pituitary: amiodarone-induced hypothyroidism
Authors: Weston SN , Weston CFM 
Published: May 2014

A60-year-old man with a history of ischaemic heart disease, myocardial infarction and previous coronary bypass grafting was admitted to hospital with sustained monomorphic ventricular tachycardia. He was treated with intravenous amiodarone and was later discharged on oral amiodarone 200 mg once a day in addition to his usual antianginal therapy, angiotensin-converting enzyme inhibitor and diuretic. Approximately 6 months afterwards, he presented with profound tiredness, somnolence, weight gain constipation and fluid retention. He described fluctuating disorientation in time as well as vivid visual hallucinations of people and animals. He had also experienced auditory hallucinations of the voices of his relatives conversing with him in the second person. Transient secondary delusions were evident. In particular, on the night before his readmission he became convinced that he had lost his pituitary and enlisted his wife to help search for it in the bed. Thyroid function tests (TFTs) revealed a free thyroxine level of 2 pmol/litre (normal range 11–25 pmol/litre) and markedly raised thyroid-stimulating hormone (TSH) of more than 150 mU/litre (normal range 0.35–5.00 mU/litre). Microsomal thyroid antibodies were present — 670 IU/ml (normal range 0–200 IU/ml). Amiodarone was stopped and he was given thyroxine, with gradual dose titration up to 150 μg per day. On reviewing his medical notes it was discovered that a diagnosis of hypopituitarism was made in 1984, and he had briefly been treated with steroid, testosterone and thyroxine replacement therapy. This diagnosis had later been refuted. Of relevance is that a thyrotropinreleasing hormone test was normal at this time. Plain X-ray of the skull showed an asymmetrical sella, and a diagnosis of ‘empty sella syndrome’ was made. There was no previous psychiatric history. Interestingly his basal TFTs at the time of amiodarone initiation showed a normal thyroxine level of 16 pmol/litre but TSH was not measured. A month later his free thyroxine was still 16 pmol/litre and TSH was noted to be elevated at 8.9 mU/litre. He appeared euthyroid and no changes were made to his treatment. Following the treatment of his hypothyroidism his angina worsened, while his psychiatric symptoms settled within a matter of weeks and his TFTs showed adequate replacement after 5 months. To date there has been no recurrence of his arrhythmia.
Branch retinal artery occlusion: a case complicating acute rheumatic fever and dental abscess
Authors: Tillett A , Edelsten C 
Published: May 2014

A15-year-old boy presented with a 2-month history of lethargy, weight loss and migratory arthralgia following an episode of pharyngitis while on holiday in the Mediterranean. Examination revealed the murmurs of mitral and aortic regurgitation which were confirmed on echocardiogram. The serum C-reactive protein (CRP) was high at 124 mg/litre and the streptococcal antibody titre markedly elevated at >1440 units. A diagnosis of acute rheumatic fever was made and penicillin commenced in addition to aspirin for joint pain. Three months after diagnosis he was asymptomatic, the CRP was normal and aspirin was discontinued. Six weeks later he presented with sudden onset of blurred vision in the right eye with a visual field defect in the nasal upper quadrant. There was no history of migraine and fundoscopy revealed an embolus at the disc with severe oedema below the macula consistent with occlusion of the inferotemporal branch of the retinal artery (Figure 1). Warfarin was commenced pending further investigation. Subsequent transoesophageal echo showed mild mitral regurgitation and minimal aortic regurgitation with no vegetations or thrombus. There was no evidence of arrhythmia and brain magnetic resonance imaging was normal. His protein C activity was transiently low at 64% (normal range 70–130%) and his CRP rose to 36 mg/litre. Aspirin was therefore substituted for warfarin. Three days later he presented with two dental abscesses requiring extraction. Fourteen months after presentation the superior altitudinal scotoma has improved and the retinal oedema resolved. Mild mitral valve regurgitation persists but aortic valve function appears normal. He continues on low dose aspirin and penicillin.
Mesenteric ischaemia and peptic ulcers
Authors: Mallinson RH 
Published: May 2014

Apreviously well 66-year-old man, a lifelong non-smoker, presented with left-sided abdominal pain and diarrhoea of 7 days duration. He was admitted with a haematemesis and melaena while taking aspirin. On admission his haemoglobin was 15.2 g/dl. Gastroduodenoscopy showed a large gastric ulcer on the lesser curve, with a clot adherent to the base, which was injected with 5 ml of adrenaline 1:10 000 to achieve haemostasis. A CLO test obtained from the gastric antrum showed no evidence of Helicobacter pylori infection. The patient complained of severe constant abdominal pain radiating to his back while taking lansoprazole 30 mg once daily. After 1 week repeat endoscopy showed multiple ulcers in the oesophagus, stomach and duodenum, which were irregular with sloping edges and white sclerotic bases. No biopsies were taken from the ulcers. A computed tomography contrast examination of the abdomen showed an irregular aorta narrowed by atheroma (Figure 1) and normal-looking bowel with no apparent visceral abnormalities. An angiogram was not undertaken. Ten days after presentation the patient developed an acute abdomen requiring a laparotomy at which necrotic small bowel was found. The upper third of the small bowel was resected. Histology showed the entire small bowel mesentery to be infiltrated with angiosarcoma. The patient died 4 days later. The post-mortem revealed non-healing ulcers and a 20×7×1.5 cm angiosarcoma within the aorta. The coeliac trunk was occluded and the superior mesenteric artery was partly blocked. There was positive immunohistochemical staining with factor VIII-RAg. There were splenic and renal infarcts. The left kidney was infiltrated with tumour.
Recurrent postdural puncture headache
Authors: Kelly Brendan , McDonnell Conor 
Published: May 2014

A14-year-old female presented with a 3-day history of generalized headache, photophobia, neck stiffness and nausea. She had no history of neurological illness or trauma. Clinical examination was normal. Complete blood count, serum urea and creatinine, urine culture and throat swab culture were normal. Dural puncture was carried out under aseptic technique. A 22-gauge Sprotte spinal needle was inserted between the third and fourth lumbar vertebrae, and thirty drops of clear cerebrospinal fluid were removed. Laboratory examination of the fluid was normal, and the patient was treated with analgesics. The headache improved, but did not resolve completely. She was discharged the following day, but presented 4 weeks later, with a severe, intermittent frontotemporal headache. It was associated with nausea, aggravated by changing posture, and transiently relieved by abdominal pressure. Postdural puncture headache was diagnosed, and a blood patch relieved her symptoms completely. Four weeks later, she presented with a recurrence of headache. A second blood patch relieved her symptoms again. Four weeks later, she presented again with a recurrence of headache. Computed tomography of brain and magnetic resonance imaging of lumbar spine were normal. She was treated with amitriptyline and carbamazepine. Symptoms improved, and her pain-free intervals became longer. Three months after the dural puncture she still had headache.
A solitary pulmonary cystic mass resulting from hydatid disease mimicking a pericardial cyst
Authors: Kothari P , Aly H Safar , Makker HK 
Published: May 2014

A 28-year-old male, who was a non-smoker, presented to the accident and emergency department with right anterior sharp chest pain of 2 days' duration, which was worse on swallowing, lying on his right side and deep inspiration. He had had similar pains, but milder in intensity, for the previous 8 weeks. He gave a history of cough with sputum and a single episode of haemoptysis following a flu-like illness. He had no associated breathlessness, wheeze, indigestion or heartburn. There was no history of trauma to the chest. He was an office worker and lived in London all his life except for holidays on a farm in Ireland during childhood and a recent foreign trip to New Guinea. He was in pain but had no pallor, clubbing, cyanosis or enlargement of neck lymph nodes. His pulse was regular with a rate of 90/minute, his blood pressure was 130/70 mmHg and his jugular venous pressure was not raised. Cardiac, respiratory and abdomen examination revealed no abnormality. Haemoglobin, white cell count, differential count, platelets, erythrocyte sedimentation rate, urea and electrolytes, and liver function tests were normal. An electrocardiogram showed normal sinus rhythm. A chest radiograph showed a large, round, smooth mass of 7 cm in diameter in the right mid and lower zone adjacent to the right cardiac border (Figure 1). On a computed tomography (CT) scan of the chest, this was seen to be a smooth-walled cyst, containing fluid of water density attenuation (Figure 2). It extended from the right hilum to the anterior chest wall, causing compression of the right middle lobe bronchus and partial collapse of the right middle lobe. A CT and ultrasound scan of the liver showed no similar cysts. The appearance of the cyst was thought to be characteristic of a pericardial cyst. The possibility of hydatid disease was considered. However, hydatid serology (Echinococcus antibodies) was negative (titre 1<16). In view of the symptomatic nature of the cyst causing chest pain and partial collapse of the right middle lobe, the patient was referred for surgical removal of the cyst. During the operation, a large cystic mass was seen in the right chest, outside the pericardium, displacing and compressing the right middle lobe. The cyst was excised intact with its capsule together with the right middle lobe. The gross appearance of the cyst was thought be consistent with that of a pericardial cyst (Figure 3). However, histological examination of the cyst showed active hydatid with viable germinal membrane and scolices. The patient was given praziquantel 50 mg/kg/day plus albendazole 400 mg twice daily for 7 days to treat any remaining fragments of the hydatid cyst postoperatively. He received further treatment with albendazole 400 mg twice daily for a total of 12 weeks (three 4-week courses with two 2-week breaks) to maximize the chances of eradication.
Multilocated hydatid cysts involving the liver, the spleen and the scapula
Authors: Theodorou Daphne J , Theodorou Stavroula J , Kakitsubata Yousuke 
Published: May 2014

A 75-year-old healthy woman presented with mild, right hypochondral discomfort and heaviness present for at least 2 days before admission to the hospital. She also complained of pain in the region of her left shoulder, which was moderate in nature and of approximately 1 year's duration. Shoulder pain had led to the limited use of her left arm. The patient had a history of intimate contact with sheep and dogs. Clinical examination revealed a tender, enlarged liver (5 cm below the right costal margin), as well as a tender scapula on palpation. Laboratory tests showed the white blood cell count to be 7000/mm3 with 8% eosinophils. The erythrocyte sedimentation rate was 30 mm per hour. Serological tests for Echinococcus granulosus, which included immunoelectrophoresis and indirect immunohaemagglutination assay, were strongly positive (IHA 1/800). A plain abdominal radiograph showed the enlarged hepatic shadow and a curvilinear calcification lying within it (Figure 1). An ultrasound study was then performed to further characterize the lesion. A hyperechoic band located in the right lobe of the liver associated with an acoustical shadow representing dense calcification was found (Figure 2). Two roundish, hypoechoic areas located in the enlarged spleen were found incidentally during the ultrasound examination of the abdomen (Figure 3). The diagnosis of splenic hydatid disease was favoured because of the simultaneous presence of the cystic lesion in the liver. The roentgenographic examination of the left scapula showed multiple, variously sized, round or oval osteolytic lesions, giving a honeycomb appearance of the inferior part of the scapula (Figure 4). On the basis of clinicoradiological features and laboratory findings a diagnosis of hydatid disease was proposed. A thorough clinical, radiological and ultrasonographic search did not reveal any other sites of hydatid cysts. The patient proceeded to surgery where she underwent local hepatic resection, splenectomy and local total excision with a wide healthy margin in the scapula. Histological examination of the material excised from the liver, the spleen and the scapula confirmed the diagnosis of hydatid disease. The patient made an uneventful postoperative recovery and was discharged 1 week later. Pain subsided totally following surgery. At follow-up examination 6 and 12 months later, the patient remained asymptomatic, and had no clinical or radiological evidence of the disease in the primary sites or elsewhere.
Lipogranulomatous adenopathy: a characteristic but under-recognized presentation of Whipple's disease
Authors: Turkington P , MacDonald A , Greenstone M 
Published: May 2014

A50-year-old Caucasian male was admitted with a left popliteal vein thrombosis confirmed on Doppler ultrasound scanning. He was previously well and there was no obvious precipitating cause for his venous thrombosis. Apart from pallor and the swollen left calf there were no abnormal findings on routine examination and he was anticoagulated with heparin followed by warfarin. Investigations revealed a hypochromic microcytic anaemia (haemoglobin 8.3 g) and a marginally raised serum alkaline phosphatase. Other investigations including a myeloma screen, autoimmune profile and neutrophil cytoplasmic antibodies were negative. An intra-abdominal malignancy was suspected although faecal occult bloods were negative on three occasions and tumour markers (carcinoembryonic antigen (CEA) and CA 19.9) were normal. Upper gastrointestinal endoscopy demonstrated mild gastritis and a normal-looking duodenum only. Computed tomographic (CT) scanning of the abdomen and thorax revealed massive retroperitoneal and retrocrural adenopathy extending down to the small intestinal mesentery (Figure 1). The abdominal viscera were otherwise normal and there was no mediastinal Iymphadenopathy. Small bowel Iymphoma was suspected and he underwent first a laparoscopic biopsy of the mesenteric Iymph nodes and subsequently a laparotomy. There were no abnormal findings apart from the retroperitoneal Iymphadenopathy. On both occasions the histological appearances of the Iymph nodes were the same: the Iymph node architecture was destroyed by large lipid-containing spaces. There was also infiltration by numerous lipid containing macrophages, and occasional multinucleate giant cells (Figure 2). No cause for these changes could be recognized clinically or pathologically. Three months after his initial presentation he developed weight loss, mild diarrhoea, vague abdominal pain and a rash on his legs. A systemic vasculitis was suspected but a skin biopsy showed non-specific changes only. However, 1 week later he died suddenly at home, apparently having been markedly dyspnoeic for the preceding 48 hours. At postmortem he was found to have a severe constrictive pericarditis, which was felt to be the probable cause of his death. There was no evidence of pulmonary embolism. The liver showed congestive ‘nutmeg’ changes. There was evidence of a panserositis with inflammation of pericardium, pleura and peritoneum. Bowel histology was not performed because of autolysis. However, the histology of the mesenteric Iymph nodes was reviewed and on this occasion stained with periodic acid Schiff. This was taken up by bacilliary organisms in the macrophages found in the Iymph nodes. The features were considered diagnostic of Whipple's disease.
Mullerian duct cyst: a case history and literature review
Authors: Kiberu SW , Haray PN , Ilott J 
Published: May 2014

A mullerian duct cyst results from an abnormality of regression of the mullerian system (Yoshinori et al, 1999). The prostatic utricle is a homologue of the female uterus and is a caudal remnant of paramesonephric ducts (Morgan et al, 1979; Smith and Middleton, 1979). Mullerian cysts usually present as small mid-line masses between rectum and bladder neck or prostate (Yoshinori et al, 1999). This article presents a case report.
Spinal subdural haematoma after epidural anaesthesia: a diagnosis not to be missed
Authors: Constantoyannis Constantine , Shahidi Saheed , Kourtopoulos Harry 
Published: May 2014

A63-year-old man was admitted to the authors' department because of lower back pain and paraparesis. The patient had undergone an operation 5 weeks earlier to excise a wart on the little toe of his left leg, under epidural anaesthesia. During induction of anaesthesia, immediately after the puncture the patient developed severe back pain radiating to legs with reflex movement of both legs. After the procedure, the patient experienced difficulty in walking and bladder emptying. The pain was relieved with oral medication and the patient was discharged on the second day after surgery although he complained of difficulty with walking. His doctors reassured him that the problems would be transient. The symptoms persisted and he had to use a urinary catheter. On physical examination he was normal. Neurological examination revealed a proximal weakness of both legs (3/5), with increased tendon reflexes. There was sensory loss of L2–S1 distribution. Magnetic resonance imaging (MRI) showed a subdural mass extending dorsally to the spinal cord. On T1-weighted images, the subdural mass was mixed iso-hyperintense and showed a craniocaudal extension from T12 to L1 (Figures 1 and 2). The MRI findings were consistent with an intradural haemorrhage and clot formation. No coagulation abnormality was detected. The patient underwent a T12–L1 laminectomy. After opening the dura, a grayish membrane filled with adhesions and xanthochromic blood clot was found dorsally to the cord. The spinal cord was compressed and displaced by the haematoma towards the ventral part of the spinal cord. The degradated blood clot was removed and part of the membrane was also removed. The underlying cord seemed to be traumatized by the needle in the midline of the dorsal surface. On follow-up examination 1 and 3 months after surgery, the patient was free of pain, but only a partial motor recovery (4/5 muscle strength on the left leg) had taken place. The sensory impairment was restricted to mild paraesthesia. The bladder function did not improve.
A giant pilar tumour of the scalp
Authors: Javaid Muhammad , Morris Paul , Logan Andrew 
Published: May 2014

An 85-year-old woman presented with a slowly growing lesion on her scalp which had been present for the last 20 years. In the last 2 years the lesion had started to grow rapidly. There was no relevant family history of a similar lesion. On examination a 20x20 cm dome-shaped mass was seen which was multiloculated, consisting of solid and cystic areas (Figure 1). It was fixed to the underlying skull, the overlying skin was stretched and there were no signs of ulceration or secondary infection. There was no lymph node palpable in the neck. Plain X-rays showed thinning of the skull possibly as a result of local compression. To facilitate excision, the lesion was decompressed intraoperatively by aspirating blood-stained fluid. Excision included the pericranium as the lesion had adhered to it (Figure 2). The reconstruction was performed by bilateral transposition flaps raised from the temporal regions and the donor defects were covered by a split skin graft. Histology reported a complex cystic lesion lined by stratified squamous epithelium showing abrupt keratinization and calcification. There was no dermal invasion noticed and excision appeared complete. The histological features were consistent with a proliferative pilar tumour of the scalp. The patient was discharged home 3 days after surgery and remained recurrence free after 9 months follow up (Figure 3).