Acute adrenocortical crisis: three different presentations.

The adrenal cortex normally produces three principal steroid hormones: the glucocorticoid cortisol, the mineralocorticoid aldosterone, and a small quantity of sex steroids. In primary adrenocortical insufficiency, there is a deficiency of both cortisol and aldosterone with characteristic clinical and laboratory findings. In contrast, with a pituitary disorder there is isolated hypocortisolism, because its production is dependent on pituitary adrenocorticotropic hormone (ACTH), whereas aldosterone production is controlled by extracellular fluid volume, renin and serum potassium. Acute adrenocortical crisis is an absolute medical emergency and its presentation is not always typical. We describe three recent cases of acute adrenocortical crisis in our hospital who presented in three different ways in three different wards.

Long-term amiodarone therapy raises serum cholesterol.

Serum total cholesterol and triglyceride levels were measured in 12 patients before and 3.6 and 9 months after treatment with amiodarone. In addition, we monitored serum T4, T3, reverse T3 and TSH levels. Amiodarone and its desethyl metabolite levels were measured on each occasion. Serum total cholesterol and T4 levels rose from 5.95 mmol/l, and 102.7 mmol/l respectively at baseline to 6.95 and 115.8 at 6 months and reverse T3 increased at 3, 6 and 9 months from baseline. Serum triglycerides did not change. No relationship existed between cholesterol, T4 and T3 and amiodarone (or its metabolite) levels nor between cholesterol and thyroid hormone levels. These data demonstrate that amiodarone therapy is associated with an elevation in serum cholesterol. This may have clinical implications in view of the current widespread use of the drug.

Amiodarone therapy and glucose tolerance--a prospective trial.

It has previously been suggested that amiodarone, used widely to treat refractory cardiac arrhythmias, may induce glucose intolerance. In view of this, we have undertaken a prospective study in a group of 10 patients with normal glucose tolerance profiles requiring amiodarone therapy for control of supraventricular or ventricular dysrhythmias. The patients were followed for a total of 9 months, and glucose tolerance tests and glycosylated haemoglobin were done at 3 monthly intervals in all patients. Both fasting blood glucose levels and glucose tolerance tests were entirely within normal limits in all patients at each stage during the study. Glycosylated haemoglobin did rise significantly at 6 months, but this did not exceed the normal range in the majority of patients and the rise was not sustained at 9 months. In this prospective study therefore, there is no evidence of either glucose intolerance or a diabetogenic effect during prolonged therapy with amiodarone.