터너증후군에서 성장호르몬과 성호르몬 치료에 따른 인슐린 저항성의 변화

Abstract

PURPOSE: The aim of this study was to investigate the effects of growth hormone (GH) therapy and sex steroid replacement on glucose metabolism in Turner syndrome (TS). METHODS: We analyzed the clinical and laboratory data of 61 children and adults with TS. The results of oral glucose tolerance test or fasting glucose with insulin levels were obtained, and the changes in insulin resistance index determined using the homeostasis model of assessment (HOMA-IR) and insulin sensitivity (quantitative insulin sensitivity check index, QUICKI) were analyzed. Data were presented in median and range. RESULTS: With GH treatment (n = 21; median duration 38 months, range 5 to 96 months), the HOMA-IR increased to levels higher than that before treatment (2.48 vs. 1.18, P = 0.035), and QUICKI was decreased (0.33 vs. 0.37, P = 0.035). After estrogen was added (n = 13, median duration 11 months, range 2 to 55 months) to the therapy, the decrease in HOMA-IR tended to be greater and QUICKI tended to be higher (0.34 vs. 0.37, P = 0.046) than that during GH treatment alone (2.16 vs. 1.36, P = 0.055). However, there were no significant differences between GH with estrogen treatment and sex hormone cyclic replacement therapy (n = 7) in terms of changes in the HOMA-IR and QUICKI. With GH treatment, insulin resistance tended to increase and the insulin sensitivity was tended to decrease to a level lower than that before treatment, but recovered when estrogen was added to the treatment regimenon and maintained after GH therapy was discontinued and during cyclic treatment with sex steroids. CONCLUSION: The incidence of glucose intolerance or the levels of type 2 diabetes mellitus did not increased during or after GH treatment in patients with TS, but insulin resistance increased transiently; therefore, close monitoring of changes in glucose metabolism is essential during GH treatment. Early replacement of estrogen in addition to GH therapy when growth is nearly accomplished might prevent the aggravation of insulin resistance in TS patients.