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Endocrine Abstracts (2022) 82 WD3 | DOI: 10.1530/endoabs.82.WD3

Watford General Hospital, West Hertfordshire NHS Trust, Watford, United Kingdom


We report a case of 39-year-old woman presenting with sudden severe abdominal pain and vomiting. She had a past medical history of anti-phospholipid antibody syndrome (APLS) diagnosed in the United States (US) 20 years ago. She had multiple episodes of vomiting over the last 10 years and was diagnosed with cyclical vomiting as investigations including CT abdomen and endoscopy did not reveal a structural cause. She was taking warfarin for APLS. She was haemodynamically stable and clinical examination was unremarkable. Investigations showed normal electrolytes, subtherapeutic international normalised ratio (INR), raised cardiolipin antibody and raised activated partial thromboplastin time (APTT). CT abdomen showed enlarged bilateral adrenal glands with heterogenous parenchyma suggestive of adrenal haemorrhage and warfarin was stopped. A morning cortisol level was 171 nmol/l and short synacthen test showed inadequate cortisol response rising from 166 mmol/l only to 179 nmol/l at 30 minutes confirming the diagnosis of primary adrenal insufficiency. She was commenced on oral hydrocortisone. Subsequent MRI adrenals confirmed stable bilateral adrenal haemorrhage with cystic area of peripheral methaemoglobin and central haemosiderin. As the adrenal haemorrhage was non-progressive, anticoagulation was restarted due to high risk of thrombosis in the future. She is being followed up in the endocrine clinic with full adrenal work up including renin and aldosterone awaited. Adrenal infarction or haemorrhage is a rare complication of APLS, and hypercoagulable state may lead to adrenal vein thrombosis with haemorrhagic transformation of adrenal glands. The presenting features of adrenal thrombosis and haemorrhage include localised pain and / or adrenal insufficiency but often such patients do not have any symptoms. Patients with APLS and adrenal insufficiency may not present with hypotension as patients with APLS are commonly hypertensive, therefore masking hypotension. Unless promptly treated with intravenous glucocorticoids, complete adrenal insufficiency associated with vascular phenomenon of APLS can potentially be fatal. Therefore, physicians should have a high index of suspicion in such cases. Decision about anticoagulation should be individualised but most patients need anticoagulation as they remain at high risk of thrombotic phenomenon elsewhere.

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