Search PubMedSearch

PubMed · 3004550

Adrenal function in tuberculosis.

Abstract

In a study of 41 African Zulus with acute pulmonary tuberculosis, 55% were found to have a suboptimal cortisol response to Synacthen and all had very low plasma dehydroepiandrosterone levels. Following a 2-week course of antituberculous chemotherapy there was an improvement in adrenal corticosteroid function with a reduction to 30% of those showing an impaired cortisol response to Synacthen, but adrenal androgen function did not improve in any. Patients who received rifampicin as part of their treatment appeared to show less improvement in adrenal corticosteroid function when compared to a group who received antituberculous treatment which did not include rifampicin.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M E Ellis, F Tayoub. 1986. Adrenal function in tuberculosis.. https://doi.org/10.1016/0007-0971(86)90003-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

A major role for the Fas pathway in acute graft-versus-host disease.

Recent studies have suggested a role for the Fas pathway in the wasting syndrome associated with lpr-->wild-type bone marrow transplants. To directly examine whether Fas ligand has a major role in the development of acute graft-vs-host disease (GVHD), Fas ligand-deficient (gld) mice were used as donors and C3H/HeJ x C57BL/6F1 as recipients in the parent-into-F1 model of acute GVHD. Transplantation of C3H/gld spleen cells induced significantly less host lymphoid depletion and was associated with less antihost cytotoxic activity in vitro when compared with wild-type C3H donor cells. The reduced depletion of host lymphocytes was explained by both impaired antihost T cell cytolytic activity and by reduced expansion of gld donor T cells in F1 recipients. These findings not only indicate that the Fas ligand is an important effector molecule in acute GVHD, but also provide in vivo evidence supporting a role for Fas/Fas ligand interactions in T cell expansion and maturation.

Acute Disease