Adrenal function in hospitalised patients with pulmonary tuberculosis treated with rifampicin
Date
2009-02-13T08:49:51Z
Authors
Venter, Willem Daniel Francois
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Abstract
Abstract
Introduction: Tuberculosis carries a high mortality in the days immediately after
treatment. It is also the commonest cause of adrenal insufficiency in the developing
world. Rifampicin is a potent hepatic enzyme inducer, and may contribute to adrenal
insufficiency by accelerating cortisol breakdown. The aim of the study was to determine
whether rifampicin induced accelerated catabolism of corticosteroids.
Methods: A prospective, randomised study comparing adrenal function in 20 patients
with pulmonary tuberculosis in the first five days treated with two different
antituberculosis regimens, one containing rifampicin, and the other ciprofloxacin.
Results: Demographic, clinical and laboratory results were similar in both groups. Both
groups showed a statistically significant and similar decrease in morning cortisol, with
similar responses to ACTH stimulation at both 30 and 60 minutes before and after four
days of treatment. In the entire cohort, 40% demonstrated an incremental cortisol rise of
<250nmol/l after ACTH stimulation on day 1. Mean basal cortisol concentrations were
substantially elevated and DHEA-S levels were consistently subnormal, resulting in a
high cortisol:DHEA-S ratio. No patient demonstrated overt adrenal insufficiency. There
were no significant differences between the two groups before or during therapy for any
electrolytes, hormones or calculated serum osmolality.
Conclusions: Rifampicin did not additionally impair adrenocortical function during the
initial period of therapy.
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Keywords
tuberculosis, TB, rifampicin, adrenal function, hospital patients