Tuberculous Addison's disease: lack of normalization of adrenocortical function after anti-tuberculous chemotherapy

Tuberculosis of the adrenal glands is a common cause of Addison's disease in developing countries. We conducted a study to determine if treatment of such patients with modern anti-tuberculous chemotherapy would lead to an improvement in plasma cortisol and aldosterone levels.

Prospective study.

5 patients with Addison's disease secondary to tuberculosis.

Basal and ACTH stimulated plasma cortisol and aldosterone levels were measured prior to instituting anti-tuberculous chemotherapy, as well as one month after its conclusion. Four patients were again studied over the next 2-5 years.

Peak plasma cortisol levels prior to treatment were markedly reduced (range, < 14-110 mumol/l). There was no improvement one month (< 14-143 mumol/l) or 2-5 years (< 14-69 mumol/l) after completing anti-tuberculous chemotherapy. Peak plasma aldosterone at diagnosis was < 56-210 pmol/l; it was undetectable in 4 patients. No improvement was observed one month (< 56-210 pmol/l), or 2-5 years (< 56-389 pmol/l) after stopping anti-tuberculous chemotherapy. Plasma aldosterone levels at both these time points were far lower than those in control subjects (median 736 pmol/l, 560-1512 pmol/l; p < 0.01). One patient had an increase in peak aldosterone from < 56 pmol/l to 389 pmol/l, though peak cortisol actually declined in this subject (from 110 mumol/l to 69 mumol/l).

Treatment of tuberculous Addison's disease with anti-tuberculous chemotherapy does not lead to normalization of ACTH stimulated plasma cortisol or aldosterone levels during the 2-5 year period of study. However, prolonged follow up with regular adrenal function tests is warranted in all such patients.