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放血疗法对遗传性血色素沉着症下丘脑 - 垂体功能异常的影响。

Influence of phlebotomy treatment on abnormal hypothalamic-pituitary function in genetic hemochromatosis.

作者信息

Lufkin E G, Baldus W P, Bergstralh E J, Kao P C

出版信息

Mayo Clin Proc. 1987 Jun;62(6):473-9. doi: 10.1016/s0025-6196(12)65472-x.

Abstract

To test the hypothesis that deficiencies in hypothalamic-pituitary function in genetic hemochromatosis result from cellular injury by iron deposits, we conducted provocative tests in 11 men with genetic hemochromatosis before and after iron depletion by serial phlebotomy and in 10 control subjects. We gave combination intravenous injections of insulin (0.15 U/kg), luteinizing hormone releasing hormone (LHRH, 100 micrograms), and thyrotropin releasing hormone (400 micrograms) and then measured plasma glucose, growth hormone, corticosteroids, follicle-stimulating hormone, luteinizing hormone, prolactin, and thyroid-stimulating hormone at 30-minute intervals for 90 minutes. Phlebotomy caused a substantial decrease in median values for serum ferritin, deferoxamine-chelatable iron, and hepatic iron concentration. Before phlebotomy, stimulation by hypoglycemia and thyrotropin releasing hormone caused significantly less secretion of growth hormone (P = 0.004) and prolactin (P = 0.03) in patients than in control subjects. No significant improvement was noted, however, in growth hormone or prolactin secretion after phlebotomy. Of the 11 patients, 7 had secondary hypogonadism, and phlebotomy did not improve the serum testosterone, follicle-stimulating hormone, luteinizing hormone, or responses to LHRH in any case. Chlorpromazine injections failed to elevate serum prolactin in all patients, and administration of levodopa caused a partial reduction in serum prolactin; thus, the hypothalamus may be an important locus of endocrine malfunction in these patients. We conclude that abnormal hypothalamic-pituitary function in genetic hemochromatosis is not substantially improved by iron-depletion therapy.

摘要

为了验证遗传性血色素沉着症患者下丘脑 - 垂体功能缺陷是由铁沉积导致的细胞损伤引起这一假说,我们对11名遗传性血色素沉着症男性患者在进行系列放血排铁前后,以及10名对照受试者进行了激发试验。我们静脉联合注射胰岛素(0.15 U/kg)、促黄体生成素释放激素(LHRH,100微克)和促甲状腺激素释放激素(400微克),然后在90分钟内每隔30分钟测量血浆葡萄糖、生长激素、皮质类固醇、促卵泡激素、促黄体生成素、催乳素和促甲状腺激素。放血导致血清铁蛋白、去铁胺可螯合铁和肝脏铁浓度的中位数大幅下降。放血前,低血糖和促甲状腺激素释放激素刺激引起的患者生长激素(P = 0.004)和催乳素(P = 0.03)分泌明显少于对照受试者。然而,放血后生长激素或催乳素分泌未见明显改善。11名患者中有7名患有继发性性腺功能减退,放血在任何情况下均未改善血清睾酮、促卵泡激素、促黄体生成素或对LHRH的反应。氯丙嗪注射未能使所有患者的血清催乳素升高,左旋多巴给药导致血清催乳素部分降低;因此,下丘脑可能是这些患者内分泌功能障碍的重要部位。我们得出结论,铁耗竭疗法并不能显著改善遗传性血色素沉着症患者异常的下丘脑 - 垂体功能。

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