Tauber M, Moulin P, Pienkowski C, Jouret B, Rochiccioli P
Service de Pédiatrie Endocrinologie, Centre, Hospitalier Universitoine, Purpan, Toulouse, France.
J Clin Endocrinol Metab. 1997 Feb;82(2):352-6. doi: 10.1210/jcem.82.2.3726.
GH state and auxological data after completion of GH therapy are reported in 131 patients (79 males, 52 females). They were treated from 1980-1994 for partial (n = 98) or complete (n = 33) GH deficiency (GHD), either idiopathic (n = 121) or organic (n = 10). A single stimulation test (clonidine+betaxolol) was used, and only 50 patients (38%) maintained a blunted response (GH peak below 10 micrograms/L). Although 9 of the 10 patients with organic GHD had an abnormal low GH peak, 67% of patients with idiopathic GHD normalized their GH secretion. This was particularly true of partial GHD patients (71% vs. 36% of complete GH-deficient patients). Based on a retest GH peak below 5 micrograms/L, only 23% of the patients were considered to be GH deficient and therefore candidates for GH treatment during adulthood. We found no significant difference between hormonal state at completion of treatment and initial GH deficiency, pubertal state, or sex, although we did find a significantly lower GH peak value before and after treatment in patients with elevated body mass index. Of the 14 obese children who were treated, 50% had an abnormally low serum insulin-like growth factor-I level, arguing for true GHD, and only two children remained obese at cessation of treatment. Auxological data showed that with a mean duration of treatment of 3.6 +/- 2.0 yr, patients classified as having complete GHD before treatment had significantly greater catch-up growth as expressed in SDS for height than patients with partial GHD (0.6 +/- 1.1 vs. 1.1 +/- 0.7 SDS, P < 0.05), and that boys grew better than girls (1.4 +/- 0.8 vs. 1.6 +/- 0.6 SDS) for height, P < 0.01). That catch-up growth was not correlated with the result of GH peak after cessation of treatment.
报告了131例患者(79例男性,52例女性)生长激素(GH)治疗结束后的GH状态及生长发育数据。他们在1980年至1994年期间接受治疗,病因是部分性(n = 98)或完全性(n = 33)GH缺乏(GHD),其中特发性(n = 121)或器质性(n = 10)。采用单次刺激试验(可乐定+倍他洛尔),只有50例患者(38%)维持迟钝反应(GH峰值低于10μg/L)。虽然10例器质性GHD患者中有9例GH峰值异常低,但67%的特发性GHD患者GH分泌恢复正常。部分性GHD患者尤其如此(71%对比完全性GH缺乏患者中的36%)。基于复测GH峰值低于5μg/L,只有23%的患者被认为存在GH缺乏,因此在成年期有接受GH治疗的指征。我们发现治疗结束时的激素状态与初始GH缺乏、青春期状态或性别之间无显著差异,尽管我们确实发现体重指数升高的患者治疗前后的GH峰值显著更低。在接受治疗的14例肥胖儿童中,50%的血清胰岛素样生长因子-I水平异常低,提示存在真正的GHD,且治疗结束时只有2例儿童仍肥胖。生长发育数据显示,治疗平均时长为3.6±2.0年,治疗前分类为完全性GHD的患者在身高标准差评分(SDS)方面的追赶生长显著大于部分性GHD患者(0.6±1.1对比1.1±0.7 SDS,P<0.05),而且男孩在身高方面的生长比女孩更好(1.4±0.8对比1.6±0.6 SDS,P<0.01)。追赶生长与治疗停止后的GH峰值结果无关。