Unusual case of antiphospholipid syndrome presenting as adrenal insufficiency.

A 64-year-old man presented to the emergency department with generalised fatigue and dizzy spells. His background history includes a previous admission with right leg deep vein thrombosis, provoked by pneumonia. Laboratory results showed evidence of hyponatremia and hyperkalaemia. A synacthen test was performed that indicated hypoadrenalism. CT of his abdomen revealed enlarged adrenal glands bilaterally. Adrenal antibodies and positron emission tomography (PET) scan were performed to assess the cause of enlarged adrenals. PET scan showed no evidence of increased uptake. Adrenal antibodies were found to be negative. Tuberculous (TB) adrenalitis was the principle differential diagnosis. TB QuantiFERON was strongly positive. Following 9 months of TB treatment, surveillance CT scan indicated a significant reduction in adrenal gland size. However, subsequent events culminated in a retrospective review of CT scans questioning the initial clinical diagnosis and suggesting that the observed adrenal gland enlargement was secondary to bilateral adrenal infarction and haemorrhage. Equally, the subsequently observed marked reduction in adrenal gland size was not secondary to an assumed response to TB therapy, but rather the sequela of infracted atrophied adrenal glands, as a manifestation of the underlying antiphospholipid syndrome (APS). The case highlights the importance of recognising adrenal insufficiency in patients with a history of APS. It also illustrates the role of multidisciplinary meetings in the management of such complex cases.

Rare case: paraneoplastic syndrome affecting peripheral nerves, associated with anti-collapsin-response mediator protein-5 (anti-CRMP5) antibodies, as early manifestation of small cell lung cancer confined to a solitary lymph node without evidence of lung mass on routine CT thorax.

A 69-year-old woman presented with 9 months history of progressively worsening upper and lower limb weakness leading to reduced functional status. She was diagnosed with peripheral neuropathy (predominantly sensory) initially and had received immunoglobulins and pulsed steroid therapy with no benefit. She was following up with respiratory team for surveillance of hamartoma in left lower lobe. Investigations included a battery of serum samples and tissue samples on two different occasions. Anti-HU and anti-CV2 antibodies were found positive in serum. Sural nerve biopsy raised suspicion of paraneoplastic phenomenon. CT thorax abdomen and pelvis was carried out to identify a primary neoplastic source; however no lesion was identified except for the previously documented hamartoma in the left lower lobe. Positron emission tomography (PET) scan was carried out that identified a single fluorodeoxyglucose (FDG)-avid focus either in the mid oesophagus or in the left para oesophageal region below the left main bronchus. Gastroscopy showed evidence of inflammation only. Bronchoscopy/endobronchial ultrasound (EBUS)-guided lymph node biopsy turned out be small cell lung carcinoma on histological analysis. She was then referred to oncology services, and received 4 cycles of carboplatin/etoposide chemotherapy followed by 30 fractions of radiotherapy. She finished chemotherapeutic treatment without any complications. So far her symptoms have not settled, but not worsening anymore and she continues physiotherapy to regain limb function.