Cushing's syndrome and hypertension.

Abstract

A 69-year-old man was admitted to the Massachusetts General Hospital in December 1983, following referral from another hospital, for evaluation of hypoproteinemia, peripheral edema, and weakness. He was known to have type II diabetes when he underwent a gastroenterostomy and, later, a vagotomy, two-thirds gastrectomy, and gastroenterostomy in 1972 for peptic ulcer disease. His blood glucose levels had been well controlled with an oral hypoglycemic agent until September 1983, when he was admitted to another hospital for investigation and treatment of uncontrolled hyperglycemia (blood glucose level, 543 mg/dl) and lower extremity edema. He was commenced on a regimen of NPH insulin, and an evaluation of his edema led to discovery of diffuse hypoproteinemia (total protein, 5.6 g/dl; albumin, 2.7-3.3 g/dl). Initially, the hypoproteinemia was thought to be due to a protein-losing enteropathy, but this suspicion could not be substantiated.

Pathophysiology of Hypertension

“…Increased peripheral vascular sensitivity to adrenergic agonists may play a role in the HTN [418]. Hepatic synthesis of angiotensinogen, which stimulates the RAAS, is activated, and phospholipase A2, which releases arachidonic acid from phospholipids and plays an important role in the synthesis of vasodilatory prostaglandins, is inhibited [419]. Glucocorticoids also reduce the activity of the depressor kallikrein-kinin system, enhance pressor sensitivity to endogenous vasoconstrictors (epinephrine and angiotensin II) [420,421], and promote sodium influx into vascular smooth muscle cells [422].…”