Pasteurella multocida endocarditis.
نویسندگان
چکیده
Rifampicin is a potent inducer of hepatic microsomal enzymes and increases the oxidation of cortisol to 63-hydroxycortisol.2 As the major pathway of cortisol metabolism involving tetrahydroreduction of the A ring is not thought to be altered this increased utilisation usually represents only a small percentage of the cortisol produced in patients with normal adrenal function. In patients with pre-existing adrenal insufficiency, however, a higher and probably critical percentage may be involved.' In both of our patients, who had adrenal insufficiency associated with tuberculosis, it is highly probable that rifampicin precipitated the acute adrenal crisis. In case 1 this occurred two weeks after beginning treatment (the time interval at which maximal enzyme induction is occurring)3 and unusually high doses of replacement therapy were required, while in case 2 the biochemical features of adrenal insufficiency improved when rifampicin was discontinued only to recur two weeks after it was reintroduced. Moreover 6 -hydroxycortisol excretion in case 1 was three to four times greater than that usually produced by therapeutic doses of rifampicin.2 To our knowledge the patient described by Edwards et all is the only other case in which rifampicin was thought to have induced an acute adrenal crisis. We emphasise the importance of considering adrenal insufficiency in all patients treated with rifampicin as adrenal crisis may occur within two weeks after beginning the drug even in those whose cortisol production is only mildly impaired (case 2). In addition, replacement therapy should be carefully monitored, as the standard doses of cortisone acetate and fludrocortisone may be inadequate (case 1).1 Other workers have also emphasised that patients receiving therapeutic doses of corticosteroids may need an increased dose when starting rifampicin.
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عنوان ژورنال:
- British medical journal
دوره 286 6381 شماره
صفحات -
تاریخ انتشار 1983