OBJECTIVE: To describe a case of sequential bilateral adrenal infarction and hemorrhage resulting in an unusual pattern of adrenal function over time. METHODS: A 50-year-old male with autoimmune antiphospholipid syndrome (APS) presented to the emergency room with severe abdominal pain. Diagnostic studies performed included contrast-enhanced computerized tomographic (IV-CT) imaging of abdomen and pelvis, and laboratory assessment of the hypothalamic-pituitary-adrenal axis. RESULTS: IV-CT of abdomen and pelvis on day 1 showed acute left adrenal gland infarction; cortisol level was 19.9 μg/dL and serum sodium was 133 mEq/L. The patient subsequently developed hyponatremia and hypotension. Repeat IV-CT of abdomen and pelvis on day 3 showed hemorrhagic conversion of the left infarcted adrenal gland and a new right adrenal gland infarction. Cosyntropin stimulation test (CST) confirmed primary glucocorticoid insufficiency. Plasma renin activity and the serum aldosterone level were within normal limits with normokalemia. At 7-month follow-up, CST demonstrated cortisol and aldosterone deficiency. CONCLUSION: Adrenal infarction is a rare complication of APS but is the most common endocrine complication. Evidence of bilateral adrenal infarction on imaging does not predict the type of adrenal dysfunction that might ensue, as demonstrated in this case. Thorough evaluation of glucocorticoid, mineralocorticoid, and androgen deficiency should be conducted both at the time of the event and in follow-up.
OBJECTIVE: To describe a case of sequential bilateral adrenal infarction and hemorrhage resulting in an unusual pattern of adrenal function over time. METHODS: A 50-year-old male with autoimmune antiphospholipid syndrome (APS) presented to the emergency room with severe abdominal pain. Diagnostic studies performed included contrast-enhanced computerized tomographic (IV-CT) imaging of abdomen and pelvis, and laboratory assessment of the hypothalamic-pituitary-adrenal axis. RESULTS: IV-CT of abdomen and pelvis on day 1 showed acute left adrenal gland infarction; cortisol level was 19.9 μg/dL and serum sodium was 133 mEq/L. The patient subsequently developed hyponatremia and hypotension. Repeat IV-CT of abdomen and pelvis on day 3 showed hemorrhagic conversion of the left infarcted adrenal gland and a new right adrenal gland infarction. Cosyntropin stimulation test (CST) confirmed primary glucocorticoid insufficiency. Plasma renin activity and the serum aldosterone level were within normal limits with normokalemia. At 7-month follow-up, CST demonstrated cortisol and aldosterone deficiency. CONCLUSION: Adrenal infarction is a rare complication of APS but is the most common endocrine complication. Evidence of bilateral adrenal infarction on imaging does not predict the type of adrenal dysfunction that might ensue, as demonstrated in this case. Thorough evaluation of glucocorticoid, mineralocorticoid, and androgen deficiency should be conducted both at the time of the event and in follow-up.