Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 P96

SFEBES2009 Poster Presentations Clinical practice/governance and case reports (96 abstracts)

Primary antiphospholipid syndrome presenting as accelerated hypertension and adrenal haemorrhage associated with elevated urinary catecholamines

Ben Thomas , Simon Wordsworth , Neera Agarwal , Steve Davies & Kieron Donovan


University of Wales Hospital, Cardiff, UK.


A 51-year-old woman with no significant past medical history presented with left flank pain, accelerated hypertension, progressive deterioration in renal function and left sided pleuritic chest pain. CTPA revealed pulmonary oedema and left adrenal haemorrhage. Urinary catecholamines were marginally elevated (24 h Urinary Metadrenalines 7.58 μmol/24 h) raising the possibility of an underlying phaeochromocytoma. Short synacthen test showed a sub-optimal response (0 min cortisol 199 nmol/l, 30 min 433 nmol/l).

Routine coagulation screen showed a prolonged APTT (APTT 81.5, PT1 4.0), prompting antiphospholipid syndrome (APS) screen. Anticardioplipin antibodies and lupus anticoagulant were present (IgG Cardiolipin Abs 21 GPLU/ml, IgM Cardiolipin Abs 45 MPLU/ml) consistent with an underlying diagnosis of APS. Autoimmune screen was negative consistent with primary APS. Diagnosis was confirmed on repeat testing 12 weeks later.

Blood pressure was well controlled with appropriate combination therapy. Significant acute kidney injury developed with peak creatinine 517 μmol/l. Urinalysis showed blood and protein. A further vasculitic screen was negative and renal biopsy performed. This showed features of microvascular ischaemia alone.

Adrenal haemorrhage has reduced in size on serial imaging. Twenty-four hours catecholamine levels have fallen back into the normal range. Antihypertensive treatment has been withdrawn and renal function has improved significantly (creat 165 μmol/l). Therapeutic anticoagulation had been deferred due adrenal haemorrhage, but has now been instituted following serological confirmation of APS.

Conclusions: 1. Adrenal haemorrhage more commonly presents with hypotension and hypoadrenalism rather than hypertensive crisis.

2. Adrenal haemorrhage should always raise the possibility of underlying APS in absence of sepsis, trauma and coagulopathy.

3. Rise in urinary catecholamines may be associated adrenal haemorrhage. Elevation is typically marginal and transient.

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