Glucocorticoid-phenylethanolamine-N-methyltransferase interactions in humans.
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HISTORY: A 56-year-old man was admitted for investigation of abdominal pain radiating to the back. The patient was known to suffer from APS and autoimmune thrombocytopenia, and was therefore treated with oral anticoagulants. The clinical examination was normal. INVESTIGATIONS: Ultrasound detected an area with low echogenicity in the region of the right adrenal gland. A CAT scan identified this mass as an adrenal hemorrhage. DIAGNOSIS AND TREATMENT: Anticoagulation treatment was discontinued because the bleeding and thrombocytopenia and the patient's pain subsided. A few days later, he experienced similar pain, this time radiating to the left side. A second hematoma was discovered in the left adrenal gland. The patient developed symptoms of acute adrenal insufficiency, which subsided after therapy. The bilateral adrenal hemorrhage was considered to be secondary bleeding following thromboses in the venous system of the adrenal gland. The thromboses were due to the underlying APS. Anticoagulation therapy was resumed, and the patient's condition stabilised without further complications. CONCLUSION: The cessation of anticoagulation therapy in this patient paradoxically led to hemorrhage, this time of the contralateral adrenal gland. Unilateral and, especially, bilateral adrenal bleeding should give rise to the suspicion of thrombophilic disorders such as APS or heparin-induced thrombocytopenia (HIT); for which careful anticoagulation is the treatment of choice.
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Bilateral adrenal gland hemorrhage was found in 22 of 2,000 (1.1%) consecutive general hospital autopsies. Clinical features of these 22 patients with diffuse or focal bilateral adrenal hemorrhage have been analyzed and compared with previous series. In our experience, patients with this postmortem finding rarely manifest features of adrenocortical insufficiency and appear instead to die as a consequence of concomitant overwhelming illness, such as septicemia, body surface burns or cardiovascular catastrophe. Two-thirds of the current series had impaired renal function at the time of adrenal hemorrhage and three patients had pituitary gland necrosis. Experimental and clinical observations indicate that the "stressed" adrenal gland--under substantive endogenous or exogenous ACTH stimulation--is unusually susceptible to hemorrhage. While our own experience indicates that bilateral adrenal hemorrhage can infrequently be implicated as a factor contributing to patients' death, the possibility of adrenocortical insufficiency must be considered in patients at risk for adrenal hemorrhage. Such patients are those who are azotemic and have bacteremia, burns, or recent cardiovascular catastrophe, particularly when the latter is managed with anticoagulant administration. In these patients, unexplained clinical deterioration or the appearance of findings consistent with adrenocortical insufficiency mandate measurement of serum cortisol concentration and institution of stress-level corticosteroid replacement therapy until a diagnosis of acute adrenocortical insufficiency can be established or refuted.
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