SUMMARY Total and free serum thyroxine (T4) and triiodothyronine (T3), basal serum thyrotrophin (TSH) and the serum TSH response to a standard intravenous dose of thyrotrophin releasing hormone (TRH) have been measured in fifteen men with liver cirrhosis and in eight alcoholic men with fatty liver change. All the patients studied were clinically euthyroid. In cirrhotics, total T4 and free T4 (FT4) concentrations were normal as were free T3 (FT3) concentrations but total T3 concentrations were significantly reduced and basal TSH concentrations were significantly higher than normal. Alcoholics with fatty liver change had normal basal TSH concentrations and normal total and free thyroid hormone concentrations apart from reduced FT4. Correlation of thyroid function tests with liver function (serum albumin concentration) showed significant positive correlations for serum albumin with both total T3 and FT3 and significant negative correlations with both FT4 and basal TSH. Nine of fifteen cirrhotics had an abnormal serum TSH response to TRH, the commonest abnormal pattern being a delayed response (seven patients). Three of eight alcoholics with fatty liver change also had an abnormal TSH response to TRH. These findings not only show complex disturbances in hypothalamic‐pituitary‐thyroid relationships in chronic liver disease but also provide indirect evidence of reduced extra‐thyroidal conversion of T4 to T3.

There is conflicting evidence regarding the adequacy of hypothalamic-pituitary function in children and adolescents with chronic inflammatory bowel disease complicated by growth retardation and delayed sexual maturation. A child with Crohn's disease, who has never received corticosteroid therapy, had delay of both growth and sexual maturation and has been investigated over the course of his disease. In addition to a skull X-ray (normal) and thyroid function tests (normal), a standard insulin tolerance test (insulin 0.15 u/kg) and a standard gonadotropin-releasing hormone (Gn-RH) test (100 microgram Gn-RH i/v) were performed when the bowel disease was in relapse and again during a remission of the bowel disease, achieved by surgery. When the bowel disease was in relapse (coincident with growth arrest) results showed an inadequate release of gonadotrophins and of growth hormone (even after pre-treatment with stilboestrol) but normal release of cortisol and prolactin. During a remission of the bowel disease coinciding with a period of rapid "catch-up" growth, release of growth hormone was normal and that of gonadotrophins supranormal. The demonstration of a reversible apparent partial hypopituitarism in this boy not only re-questions the adequacy of hypothalamic-pituitary function in inflammatory bowel disease but also indicates a potential diagnostic pitfall in the routine investigation of growth retardation if gastrointestinal symptoms are not prominent at presentation.

No abstract