@entity1887 as a side-effect of combined treatment of XXXX and @entity4184 .

@entity1 @entity251 @entity738 @entity1420 @entity5322 @entity1887 @entity699 @entity53 @entity5929 @entity4184 @entity3800 @entity1577 @entity2059 @entity774
A recent case of @entity699 and complete suppression of the @entity774 in a @entity1 with @entity1577 ( @entity1577 ) and @entity5929 treated with @entity2059 as an antifungal agent, and @entity4184 as an anti-inflammatory agent led to a systematic assessment of this axis and gonadal function in all @entity1 treated with @entity2059 in the authors' @entity1577 centre. @entity2059 can inhibit @entity5322 , thus interfering with synthesis of gluco- and mineralocorticoids, @entity3800 and @entity53 as well as the metabolism of @entity4184 . The aim of this study was to evaluate adrenal and gonadal function in @entity1 treated with @entity2059 with or without @entity4184 . An adrenocorticotrophic hormone (ACTH) test (250 microg tetracosactid) was performed in 25 @entity1577 @entity1 treated with both @entity2059 and @entity4184 , and in 12 @entity1 treated with @entity2059 alone (six @entity1 with @entity1577 and six with chronic @entity738 ). Mineralocorticoid and gonadal steroid function were evaluated by measurements of plasma-renin, follicle stimulating hormone, luteinising hormone, @entity1420 , @entity53 , @entity251 , serum-inhibin A and B. ACTH tests performed as part of a pretransplantation programme in an additional 30 @entity1577 @entity1 were used as controls. Eleven of the 25 @entity1 treated with both @entity2059 and @entity4184 had @entity1887 . None of the @entity1 on @entity2059 therapy alone nor the control @entity1577 @entity1 had a pathological ACTH test. Mineralocorticoid and @entity1887 was not observed in any of the @entity1 . Only one @entity1 with an initial pathological ACTH-test subsequently normalised, the other 10 @entity1 improved but had not achieved normalised adrenal function 2-10 months after @entity2059 treatment had been discontinued. Suppression of the adrenal glucocorticoid synthesis was observed in 11 of 25 @entity1577 @entity1 treated with both @entity2059 and @entity4184 . The pathogenesis is most likely an @entity2059 caused increase in systemic @entity4184 concentration through a reduced/inhibited metabolism leading to inhibition of adrenocorticotrophic hormone secretion along with a direct inhibition of steroidogenesis. In @entity1 treated with this combination, screening for @entity1887 at regular intervals is suggested.
