Endocrine Abstracts

Introduction: Anti-phospholipid syndrome is characterised by the presence of arterial or venous thrombosis, it is autoimmune in nature and manifests as a systemic disease. Adrenal vein haemorrhagic infarction which is a sequel of adrenal vein thrombosis ultimately leads to loss of adrenal function, it is one of the presentations of anti-phospholipid syndrome especially with catastrophic type. In one analysis adrenal involvement was reported in only 13% of the reported cases of a catastrophic type of anti-phospholipid syndrome.

Case report: A 64-year-old man presented with generalised fatigue, dizzy spells nausea, vomiting, and vague abdominal pain. His past medical history includes previous admission with pneumonia complicated with right leg deep venous thrombosis. At that time a thrombophilia screen was performedand revealed positive anticardiolipin (serum level of >120 U/ml) and anti-B-2 glycoprotein antibodies (268 RU/ml). Hence the patient was diagnosed with antiphospholipid syndrome secondary to pneumonia. At the time of admission, he looked plethoric, his blood pressure was 90/45 mmHg, and no significant systolic drop in blood pressure was noted. The blood sugar level was 4.0 mmol/l. Initial investigations revealed serum sodium 129 mmol/l (136–145 mmol/l) potassium t 5.7 mmol/l (3.6–5.1). APTT of 72 seconds (28–40). ESR 73 mm/hr (1–14). Given the clinical presentation, the low sodium, and the high potassium, synacthen test was performed. Pre synacthen serum cortisol was 41 nmol/l (119–618 nmol/l) and post synacthen cortisolwas 43 nmol/l (> 450 nmol/l), indicating no significant response to ACTH. Adrenal antibodies were negative. Abdominal ultrasound revealed a left kidney cyst measuring 3 cm in maximum diameter. This led to a CT scan of the abdomen that showed enlarged adrenal glands bilaterally. Urinary catecholamines and VMA were requested and werewithin the normal range. A PET CT was done to rule out malignant enlarged adrenal gland and showed no FDG avid macroscopic disease. Serum QuantiFERON sample was requested as TB remains an important cause and revealed strongly positive result. Anti-tuberculosis treatment was started in view of evidence at hand. Regular follow up plan put in place. Five months after the initial scan, a repeat scan showed a significantly reduced size of adrenal glands to 1.3 cm .After reviewing the serial scans at MDT discussion the initial diagnosis was revised and the MDT Consensus washaemorrhagic infarcts secondary to anti-phospholipid syndromeas the final diagnosis.

Conclusion: APS should be considered as a cause of hypoadrenalism even though it is a very rare cause.