ODP015 "Malignant" Hypertension in an Older Male

Abstract

Abstract Background Malignant hypertension connotates extreme elevation of blood pressure with associated acute target organ injury. Secondary causes of hypertension should always be considered in patients presenting with acute organ dysfunction especially when the hypertension is also resistant. Clinical case: A 66-year-old male was transferred to our hospital after two successive admissions to a local hospital with acute confusion. Importantly, he was noted to have acute kidney injury and hypokalemia in the course of those admissions. On review of his records, it was noted that he had been evaluated recently for chest pain with a contrast enhanced chest CT which incidentally detected a left adrenal mass. Biopsy of the mass had been performed and returned positive for adrenocortical carcinoma. Past history was also notable for chronic hypertension, type 2 diabetes and hypothyroidism for which he was on appropriate therapy. On physical examination, the patient was noted to be hypertensive. Other pertinent findings included facial plethora, extensive bruising and supraclavicular fat pad fullness. Abdominal striae were not seen. Laboratory investigations showed hyperglycemia (glucose: 201 mg/dL), hypokalemia (potassium: 3. 0 mmol/L) and metabolic alkalosis (bicarbonate: 30 mmol/L). Endocrine work up showed suppressed aldosterone (<4. 0 ng/dL, n: <21 ng/dL), total testosterone (31 ng/dL, n: 240-950 ng/dL) and ACTH (<5. 0 pg/mL, n: 7.2-63 pg/mL). Dehydroepiandrosterone (474 mcg/dL, n: 12-227 mcg/dL) and androstenedione (219 ng/dL, n: 40-150 ng/dL) levels were elevated. Cortisol levels did not suppress with overnight dexamethasone suppression test (29.8 mcg/dL). A diagnosis of Cushing's syndrome secondary to adrenocortical carcinoma was made. The patient was initiated on chemotherapy with carboplatin and etoposide. He was planned for mitotane therapy but passed away unexpectedly before the drug could be arranged. Conclusion Adrenocortical carcinoma can present with rapid onset of Cushingoid symptoms as well as sudden decompensation of previously controlled chronic hypertension, both of which were seen in this case. Although relatively uncommon, it remains a treatable and yet deadly cause for secondary hypertension, and should be considered in the appropriate clinical and biochemical settings. Presentation: No date and time listed