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作 者:唐丹[1] 王峻峰[1] 吴从愿[1] 邓洁英[1] 史轶蘩[1]
机构地区:[1]中国医学科学院中国协和医科大学北京协和医院内分泌科
出 处:《中华内科杂志》1997年第11期754-758,共5页Chinese Journal of Internal Medicine
摘 要:为探讨生长激素治疗对甲状腺功能的影响及其机制,给19例特发性生长激素缺乏症患者每日皮下注射重组人生长激素(rhGH)Genotropin0.1IU/kg体重,治疗1年,观察治疗前后甲状腺功能及血促甲状腺激素(TSH)对静脉推注促甲状腺素释放激素(TRH)的反应。经Genotropin治疗后,患者血清T4及FT4水平较治疗前明显下降(P<0.01);治疗半年后,血清FT3水平亦较治疗前下降(P<0.05);而血清T3、3,3′,5′-三碘甲状腺原氨酸及TSH水平无明显变化(0.2<P<0.3)。治疗1年后,8例患者血清FT4水平降至正常范围以下,依此将患者分为治疗后甲状腺功能正常组及降低组,结果证实甲状腺功能降低组在治疗前或治疗后TSH对TRH兴奋的反应均较甲状腺功能正常组高(P<0.05)。血清TSH对TRH的反应增强提示患者治疗前就已有潜在的TRH缺乏,后者可能是rhGH治疗过程中FT4及T4水平下降的潜在基础。因此在rhGH治疗过程中需监测特发性生长激素缺乏症患者的甲状腺功能,以及时给予替代治疗。To evaluate the effect of growth hormone treatment on thyroid function of growth hormone deficient children, 19 (18M/1F) euthyroid children of growth hormone deficiency (GHD) were treated with Genotropin, a recombinant human growth hormone (rhGH) for 12 months. rhGH was injected subcutaneously with a daily dosage of 0.1 IU/kg. All the patients were diagnosed by two GH provocative stimulating tests with the serum GH peak level <7 μg/L. During the treatment, blood was drawn before or 6 and 12 months after the initiation of therapy to measure serum T3, T4, FT3, FT4, rT3 and thyroidstimulating hormone (TSH) levels. In the meantime, thyrotropin releasing hormone (TRH) stimulating test was performed by an i.v. injection of 200 μg synthetic TRH. The results showed that (1) the average serum levels of T4 and FT4 decreased significantly 6 at the 6th and 12th month (P<0.001), while the serum FT3 level decreased only at the 6th month (P<0.05). The serum T3, rT3 and TSH concentrations remained unchanged. (2) 8 euthyroid patients (45%) became subclinical hypothyroidism after 12 months′ treatment with rhGH for their serum FT4 levels fell to below the normal range. The 19 patients were divided into thyroid function normal (n=11) and subnormal group (n=8) according to their posttreatment thyroid functions. (3) The TSH response to TRH was evaluated by the area under the curve (AUC) of serum TSH. The average AUC was greater in the subnormal group than in the normal group whether before or 6 and 12 months after the treatment. The greater TSH response to TRH among patients with decreased posttreatmental FT4 levels suggests that latent TRH deficiency has already existed, which may be the pathogenetic basis of the hypothyroidism developped after rhGH treatment. Thus the thyroid function of GHD patients should be monitored during rhGH treatment in order that the thyroxine replacement therapy can be given in time.
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