Urinary gonadotrophin excretion in patients with ulcerative colitis and Crohn's disease treated with A.C.T.H. and corticosteroids.

It is generally believed that exogenously administered A.C.T.H. and corticosteroids suppress the secretion of endogenous A.C.T.H. and possibly also of thyroid-stimulating hormone and growth hormone (Ackerman, Smith, and Miller, 1961; Hartog, Gaafar, and Fraser, 1964; Graber, Ney, Nicholson, Island, and Liddle, 1965). However, information regarding the effect of these forms of treatment on pituitary gonadotrophic function is conflicting. In the reports of Maddock, Chase, and Nelson (1953), Lemon (1957), and Brown, Thorburn, and Crooks (1963) patients with a variety of diseases were studied; in the majority of subjects treatment with A.C.T.H. or corticosteroids caused a rise in the output of human pituitary gonadotrophins. On the other hand, Segaloff, Carabasi, Horwitt, Schlosser, and Murison (1954) observed a decrease in levels of pituitary gonadotrophins in a proportion of women with metastatic mammary carcinoma during treatment with corticosteroids. Sohval and Soffer (1951), who conducted their assays in patients suffering from disseminated lupus erythematosus and allied conditions, obtained inconsistent results bearing no obvious relationship to the clinical response to treatment. This problem has been reinvestigated by conducting serial assays of pituitary gonadotrophins in patients with major intestinal conditions, especially ulcerative colitis and Crohn's disease, before, during, and following treatment with A.C.T.H. and synthetic corticosteroid analogues. In all subjects the effects of these forms of treatment on excretion of pituitary gonadotrophins have been correlated with the clinical response. The present communication, a preliminary account of which has been given else597 where (Crean, Bell, Card, Loraine, and Sircus, 1963), reports the results obtained.