The effects of corticotropin (ACTH) and cortisone in fifteen cases of pulmonary tuberculosis.

Despite numerous studies reported during the past six years, the controversy concerning the effects of ACTH and cortisone on tuberculous infections continues. When one considers the many known and unknown factors that influence host-parasite relationships, the different reactions of different species to tuberculous infections, and the varied effects of different drugs and hormones on the infecting organism, the persisting controversy is not surprising. Administration or exogenous ACTH stimulates increased production of not only catabolic glucocorticoids, such as hydrocortisone and cortisone, but also anabolic androgenic and estrogenic “N” hormones and mineral corticoids. In contrast to ACTH, the administration of exogenous cortisone or hydrocortisone may increase the blood level of the hormone given but otherwise reduces the endogenous production of the anabolic “N” hormones and mineral corticoids as well as adrenal glucocorticoids. Hydrocortisone or cortisone therapy will also suppress the pituitary gland and its production of ACTH, TSH, gonadotropin, etc. and thereby secondarily reduce the production of adrenocortical, thyroid, sex, and other hormones. ACTH therapy stimulates hypertrophy of the adrenal cortex and increased endogenous production of many adrenocortical hormones, whereas cortisone or hydrocortisone therapy results in atrophy of the adrenal cortex (diminished ACTH stimulation) and reduced endogenous production of adrenocortical hormones. Thus cortisone therapy more grossly alters the over-all normal hormonal balance and interferes with more factors affecting host-resistance to stress or infection, than does ACTH therapy, because of deficencies of endogenous production of many more hormones. Theoretically, at least, these differences would suggest that ACTH might be less harmful than cortisone in infections. Fifteen cases of active pulmonary tuberculosis were selected for complete metabolic studies of ACTH and cortisone, and the influence of these hormones upon toxic manifestations. However, because of the continuing uncertainty, confusion, and disagreement among equally reliable investigators who have used hormonal therapy in tuberculosis, a report of