L-精氨酸对宫内发育迟缓胎鼠胰岛素样生长因子及其结合蛋白表达的影响

目的：宫内发育迟缓(IUGR)儿常有脑发育的异常,L精氨酸具有舒张血管、增加胎盘血流的作用,可用于改善胎盘缺氧状态,促进胎儿生长发育。用被动吸烟法制作孕鼠IUGR模型,孕8～20d给予不同剂量L精氨酸,了解其对宫内发育迟缓胎鼠脑内胰岛素样生长因子及其结合蛋白表达的影响,并探讨L精氨酸的作用机制。方法：孕鼠随机分为4组:对照组、模型组、L精氨酸小剂量和大剂量防治组,每组9只。孕21d剖宫取胎,应用酶联免疫吸附法检测各组胎鼠脑组织胰岛素样生长因子Ⅰ(IGFⅠ)、胰岛素样生长因子Ⅱ(IGFⅡ)、胰岛素样生长因子结合蛋白(IGFBP3)含量,应用荧光定量RTPCR法检测各组胎鼠脑组织IGFⅠmRNA表达。结果：与对照组相比较,模型组胎鼠脑组织中IGFⅠ(0.789±0.062ng/mgvs0.947±0.042ng/mg)、IGFⅡ(0.270±0.020ng/mgvs0.374±0.015ng/mg)含量均比对照组明显降低,IGFBP3(0.253±0.011ng/mgvs0.089±0.015ng/mg)含量比对照组明显升高,IGFⅠmRNA表达量(13.12±1.39)×104cps/μgRNAvs(21.28±3.54)×104cps/μgRNA比对照组明显降低,差异均有显著性(P<0.01)。与模型组相比较,小剂量和大剂量L精氨酸防治组IGFⅠ含量明显增高,分别为0.937±0.067ng/mg和0.858±0.077ng/mg,IGFⅡ含量明显增高,分别为0.318±0.018ng/mg和0.354±0.021ng/mg,IGFBP3含量明显降低,分别为0.132±0.006ng/mg和0.146±0.009ng/mg差异有显著性(P<0.01或<0.05)。同时小剂量和大剂量L精氨酸防治组IGFⅠmRNA表达量也明显增高,分别为(19.24±2.48)×104cps/μgRNA和(17.35±2.30)×104cps/μgRNAvs(13.12±1.39)×104cps/μgRNA,差异均有显著性(P<0.01)。结论：L精氨酸可增加被动吸烟致宫内发育迟缓胎鼠脑内IGFⅠ、IGFⅡ含量和IGFⅠmRNA的表达,降低IGFBP3含量。L精氨酸防治IUGR的机制与其对胰岛素样生长因子及其结合蛋白表达的影响有关。     

儿童I型糖尿病青春发育前及青春期血清IGF-I和IGFBP-3水平监测

目的：研究儿童Ⅰ型糖尿病青春发育前及青春期血清胰岛素样生长因子I(IGF-I),胰岛素样生长因子结合蛋白3(IGFBP-3)水平变化,探讨生长激素 胰岛素样生长因子I(GH-IGF-I)轴与血糖控制的关系。方法：分别采用ELISA和免疫放射法测定63例Ⅰ型糖尿病患儿和47例正常对照血清IGF-I,IGFBP-3水平,用胶乳凝集法测定Ⅰ型糖尿病患儿的糖化血红蛋白(HbAIC)。结果：①青春发育前糖尿病患儿血IGF-I为(75.4±26.6) ng/ml,IGFBP-3为(2 756.1±763.8) ng/ml,与对照组［(103.9±46.5) ng/ml,(2 717.1±480.2 ng/ml)相比无统计学差异(P>0.05);但青春期糖尿病患儿血IGF-I和IGFBP-3［(178.2±65.9) ng/ml,(2 956.0±847.6) ng/ml］均低于对照组［(229.6±54.5) ng/ml,(3 393.2±748.9) ng/ml］］P<0.05。②新发病的I型糖尿病患儿胰岛素治疗后血IGF-I为(143.0±67.5) ng/ml,IGFBP-3为(2 740.0±449.8) ng/ml,较治疗前［(54.8±44.3) ng/ml, (2 233.8±336.2) ng/ml］明显升高(P<0.05)。③糖尿病组HbA IC与血IGF-I,IGFBP-3之间存在负相关关系(r=-0.32,-0.29,P<0.01或0.05)。④糖尿病组青春期HbAIC为(9.0±1.8)%,每日胰岛素用量为(0.86±0.30)U/kg,均高于青春期前［(7.8±1.8) %,(0.64±0.38) U/kg］(P<0.05)。结论：儿童Ⅰ型糖尿病血IGF-I,IGFBP-3水平较正常儿降低,尤其青春期患儿比正常同龄儿降低的程度更为显著,提示此类患者青春期存在GH IGF-I轴的严重紊乱,可能是导致这一时期血糖控制不良的重要原因。     

IGFBP-1在胎鼠生长发育中作用的研究

目的　探讨胰岛素样生长因子结合蛋白 - 1(IGFBP - 1)在正常胎鼠发育和胎鼠宫内发育迟滞(IUGR)发生中的作用。方法　钳夹孕鼠双侧子宫动、静脉 2 0min ,建立胎鼠IUGR模型 ,观察实验组 (IUGR组 )和正常对照组胎鼠血清IGFBP - 1水平与胎鼠血糖水平、生长参数 (身长、体重 )和器官重量 (胎盘、肺、脑、肝重 )的关系。结果　实验组胎鼠的体重、肺、脑、肝依次为 (1.93± 0 .2 3) g ,(0 .39± 0 .0 1) g ,(0 .10± 0 .0 1) g ,和 (0 .18±0 .0 2 )g ;身长为 (2 .70± 0 .16 )cm ,血糖水平为 (42 .49± 9.2 5 )mg/ml均明显低于对照组的 (3.87± 0 .85 )g ,(0 .47± 0 .0 4) g ,(0 .15± 0 .0 2 ) g ,和 (0 .2 2± 0 .0 6 ) g ,(3.6 1± 0 .44 )cm ,血糖 (6 7.31± 7.12 )mg/ml。血清IGFBP - 1(94.99± 16 .0 7)ng/ml较对照组 (33.2± 6 .96 )ng/ml明显升高 (均P <0 .0 1) ,血清IGFBP - 1与胎鼠血糖水平、生长参数、器官重量呈显著负相关 (均P <0 .0 1)。结论　血清IGFBP - 1作为生长抑制因子参与正常胎鼠发育及IUGR的发生。     

新生儿缺氧缺血性脑病血清脑脊液中胰岛素样生长因子-Ⅱ水平的变化

目的：很多研究都证实低水平的胰岛素样生长因子-Ⅰ(IGF-Ⅰ)与缺氧缺血性脑损伤的发生有关,认为IGF-Ⅰ具有重要的神经保护作用。胰岛素样生长因子-Ⅱ(IGF-Ⅱ)在结构及功能上与IGF-Ⅰ具有同源性,但对其在脑损伤中的作用尚不明了。该研究通过观察新生儿缺氧缺血性脑病(HIE)血清、脑脊液中IGF-Ⅱ水平的变化,探讨IGF-Ⅱ在新生儿HIE发病机制及预后中的作用。方法：用放射免疫法(RIA)检测41例HIE新生儿在急性期和恢复期血清、脑脊液及10例正常足月新生儿(对照组)血清中IGF-Ⅱ的水平变化。结果：在急性期,轻、中度HIE组血清IGF-Ⅱ分别为203.28±40.09ng/mL,192.33±39.66ng/mL,较对照组的229.38±43.39ng/mL无显著性降低(P>0.05);重度HIE组血清IGF-Ⅱ水平为116.72±39.50ng/mL较轻、中度HIE组及对照组明显降低(P<0.01)。在恢复期,轻、中度HIE组及重度HIE症状恢复组血清中IGF-Ⅱ分别为285.53±49.44ng/mL;278.69±51.34ng/mL;254.08±48.50ng/mL,脑脊液中分别为81.58±9.77ng/mL;78.48±10.44ng/mL;69.42±10.20ng/mL,较急性期时的27.23±7.82ng/mL,23.43±7.79ng/mL,15.05±7.03ng/mL水平明显增高(P<0.01);重度HIE症状未恢复组血清、脑脊液IGF-Ⅱ分别为144.64±46.30ng/mL;25.05±784ng/mL,虽较急性期增高,但差异无显著性意义(P>0.05),且明显低于其他各组的水平(P<0.01)。HIE组血清与脑脊液间的IGF-Ⅱ水平存在明显的正相关关系(r=0.69,P<0.01)。结论：血和脑脊液中IGF-Ⅱ水平的改变与新生儿HIE的发生及转归有关。     

IGF-I及IGFBP-3对生长激素缺乏症患儿诊断及疗效判断的价值

为了探求一次性抽血确诊生长激素缺乏症 (GHD)的方法和寻找一个检测GH治疗效果的可靠而敏感的生化指标 ,分别用RIA法和IRMA法检测25例GHD患儿血清胰岛素样生长因子 -I(IGF -I)、胰岛素样生长因子结合蛋白 -3(IGFBP -3) ,同时进行生长激素 (GH)刺激试验 ;将GHD患儿分为2组 ,完全性缺乏组 (cGHD)及部分缺乏组 (pGHD) ,将2组血清IGF -I、IGFBP -3与年龄、性别配对的正常儿童 (C组 )均值对照 ,并对照不同年龄及不同发育期的50例正常儿童参考范围 ,计算GHD患儿血清IGF -I、IGFBP -3的降低率 ;将IGF -I与GH峰值做相关性分析。用rhGH治疗GHD3个月后将IGF -I增高值 (△IGF -I)与治疗后每年生长速度 (GV)做相关性分析。结果显示 ,GHD组血清IGF -I、IGFBP -3均显著低于正常对照组 ,两组无重叠 ,cGHD组与pGHD组比较 ,两者差异显著 ;IGF -I及IGFBP -3在GHD组及C组均呈显著正相关 ;GHD组血清IGF -I与GH峰值呈显著正相关 (r=0.85,P<0.001) ,回归方程 :y=0.1613 +0.0235x ,由此可根据血清IGF -I测定值求出GH峰值 ;治疗3个月后△IGF -I与治疗后GV呈显著正相关。提示IGF -I、IGFBP -3对GHD患儿的诊断有重要价值 ;GH峰值可根据所测IGF -I由回归方程求出 ,以代替传统的生长激素刺激试验 ;IGF—I是判断rhGH治疗效果的可靠而     

血清生长激素和胰岛素样生长因子-Ⅰ在危重症中的变化及临床意义

目的 探讨血清生长激素（growth hormone,GH）和胰岛素样生长因子-Ⅰ （insulin like growth factor-Ⅰ,IGF-Ⅰ）在危重症患儿中的变化及其临床意义.方法 选择2009年1月至2012年1月同期入住PICU的脓毒症患儿42例为脓毒症组,先天性心脏病择期在体外循环下行开胸手术治疗后的患儿20例为术后组,检测入院次日及手术后次日晨血清GH和IGF-Ⅰ水平,选择健康体检儿童60例为对照组,比较组间GH、IGF-Ⅰ水平的变化.结果 脓毒症组GH水平为（6.71±6.62） ng/ml,术后组GH水平为（8.86±8.06） ng/ml,,两者均显著高于对照组（3.87±3.31） ng/ml,差异有统计学意义（P＜0.05）,而脓毒症组与术后组之间差异无统计学意义;脓毒症组IGF-Ⅰ水平为（63.72±54.17） ng/ml,与术后组（119.06±102.12） ng/ml和健康对照组（154.22±107.10） ng/ml比较,显著降低,差异有统计学意义（P＜0.05）,术后组与对照组比较差异无统计学意义;脓毒症组内存活者与死亡者比较GH无统计学意义差异,IGF-Ⅰ水平显著降低（P＜0.05）.结论 危重症时GH水平升高对机体应激具有积极作用;脓毒症时IGF-Ⅰ水平显著降低,可作为反映重症感染存在的较灵敏指标,并有助于判断预后.     

锌佐治婴幼儿迁延性腹泻的临床研究

目的：探讨迁延性腹泻患儿血、尿锌水平的变化及补锌对迁延性腹泻患儿的临床疗效。方法：测定迁延性腹泻患儿血、尿锌浓度及尿锌与肌酐比值(Zn/Cr)判断其体内锌状态。将124例患儿分为两组,即补锌组60例与非补锌组64例,观察治疗前后两组尿Zn/Cr值的变化及疗效的差异。结果：①迁延性腹泻患儿与正常健康儿对比,血锌浓度分别为(1.02±0.18) μg/ml与(1.20±0.17) μg/ml(P<0.01);尿锌浓度分别为(0.412±0.253) μg/ml与(0.612±0.215) μg/ml(P<0.01);尿Zn/Cr值分别为(0.51±0.19)×10-3与(0.72±0.21)×10-3(P<0.01)。②治疗后尿Zn/Cr值补锌组与非补锌组分别为(0.71±0.22)×10-3与(0.48±0.17)×10-3(P<0.01)。③两组治愈率：补锌组为80%(48/60),非补锌组为 59.4%(38/64),(P<0.01)。两组疗程分别为补锌组(8.1±3.2) d,非补锌组(9.8±3.8) d,(P<0.01)。④对伴营养不良的患儿补锌后可增加其体重。结论：迁延性腹泻患儿体内锌水平降低,补锌可提高其临床治愈率及缩短疗程。     

重组人生长激素治疗不同垂体发育状况生长激素缺乏症患儿疗效的前瞻性研究北大核心CSCD

目的探讨重组人生长激素(recombinant human growth hormone,rhGH)对不同垂体发育状况生长激素缺乏症(growth hormone deficiency,GHD)患儿的治疗效果。方法前瞻性选取2020年6月—2021年12月许昌市妇幼保健院收治的90例GHD患儿为研究对象,根据垂体正中矢状高径将患儿分为垂体发育不良组(45例)、垂体正常组(31例)、垂体发育增大组(14例)。分析比较各组身高、生长速率、身高标准差分值、血清胰岛素样生长因子结合蛋白-3、胰岛素样生长因子-1,以及治疗前后上述指标变化的差值(差值用△表示)。结果治疗后3组身高、生长速率、身高标准差分值及血清胰岛素样生长因子结合蛋白-3、胰岛素样生长因子-1水平均高于治疗前(P<0.05);垂体发育不良组、垂体发育增大组△身高、△生长速率、△身高标准差分值、△胰岛素样生长因子-1、△胰岛素样生长因子结合蛋白-3均大于垂体正常组(P<0.05);3组不良反应发生率比较差异无统计学意义(P>0.05)。结论rhGH治疗不同垂体发育的GHD患儿均有促进骨生长、增加身高的作用,对垂体发育不良及增生患儿效果更明显,且安全性可靠。     

小儿哮喘与肺炎支原体肺炎血中一氧化氮和氧自由基的不同变化及意义

目的：　探讨一氧化氮(NO)、脂质过氧化物(LPO)、血栓素B2 (TXB2 )、循环内皮细胞(CEC)在小儿哮喘及肺炎支原体(MP)肺炎中的作用。方法：　分别检测36例小儿哮喘、40例MP肺炎患儿及15例健康体检儿血NO,LPO,TXB2及CEC水平。结果：　小儿哮喘及MP肺炎急性期血NO,LPO,TXB2,CEC4项指标分别为:哮喘组(162 .27±36.12) μmol/L ,(8.62± 0.87)nmol/ml,(22 9.11± 64.75) pg/ml,(6.13± 1.15)n/0.9μl;MP肺炎组(95.52±33.84)μmol/L ,(5.76± 0 .53)nmol/ml,(388.72±80 .09) pg/ml,(6.36±1.02)n/0 .9μl,分别与对照组 [(68.57±13.80 ) μmol/L ,(4.62± 1.80 )nmol/ml,(105.76±20.10)pg/ml,(4.40±1.04)n/0 .9μl]相比,均增高显著,差异有显著性意义(P<0.01)。其中哮喘组血中NO ,LPO较MP肺炎组增高显著(P<0.01);MP肺炎组TXB2 较哮喘组增高明显 (P<0.01)。恢复期两种疾病所有指标均降低,TXB2,LPO已降至正常范围,而NO ,CEC在两周后[哮喘组(82.64±20.56)μmol/L,(5.41±1.29)n/0.9μl,MP肺炎组 (86.12±21.34)μmol/L,(5.57±1.12 )n/0 .9μl]仍高于正常对照组(P<0.05或0.01)。结论：　本研究提示     

宫内生长迟缓儿脐血瘦素胰岛素生长激素的水平及临床意义

目的：　探讨脐血瘦素、胰岛素、生长激素在胎儿宫内生长迟缓(IUGR)发病中的作用。方法：　采用放射免疫法测定 31例足月IUGR儿(轻度11例,重度20例)和47例足月适于胎龄儿(正常组)脐血瘦素、胰岛素、生长激素水平。结果：　IUGR儿脐血瘦素、胰岛素、生长激素明显低于正常儿,瘦素(5.55±3.79)ng/ml vs (9.47±5.97)ng/ml,胰岛素(9.75± 4.80)mU/L vs (15.59±9.11)mU/L,生长激素(8.71±4.5 4)ng/ml vs (12.77±4.30)ng/ml,(P<0.01),且IUGR儿的不良生长程度越重,三者水平越低。结论：　瘦素、胰岛素、生长激素分泌不足导致内分泌紊乱,形成一个不利于胎儿生长发育的内环境而至胎儿宫内生长迟缓。     

Effect of zinc supplementation on growth hormone secretion, IGF-I, IGFBP-3, somatomedin generation, alkaline phosphatase, osteocalcin and growth in prepubertal children with idiopathic short stature

Controversy exists about the effect of zinc on growth and the GH-IGF system. Zinc supplementation has been shown to stimulate linear growth in zinc-deficient children. However the mechanism of this effect has not been well characterized. Furthermore, the effect of zinc supplementation on non-zinc-deficient short children is unknown. We investigated the effect of zinc supplementation on endogenous GH secretion, serum IGF-I and IGFBP-3 concentrations, IGF-I and IGFBP-3 generation in response to exogenous GH, bone formation markers, and linear growth of non-zinc-deficient children with idiopathic short stature. We analyzed prospectively serum zinc, IGF-I, IGFBP-3, alkaline phosphatase, osteocalcin, and GH response to clonidine test, and performed a somatomedin generation test before and 6 weeks after zinc supplementation in 22 (16 M, 6 F) prepubertal children with idiopathic short stature. Serum IGF-I increased from 67.4+/-70.6 to 98.2+/-77.3 ng/ml (p <0.001), IGFBP-3 from 2326+/-770 to 2758+/-826 ng/ml (p <0.001), alkaline phosphatase from 525+/-136 to 666+/-197 U/l (p <0.0001), and osteocalcin from 16.8+/-10.6 to 25.8+/-12.8 ng/ml (p <0.05) after zinc supplementation despite there being no difference in GH response to clonidine after zinc supplementation (peak GH 11.6+/-6.9 vs 13.4+/-7.8 ng/ml, GH area under the curve during clonidine test 689+/-395 vs 761+/-468, NS). Percent change in IGF-I and IGFBP-3 during the somatomedin generation test was not significantly affected by zinc supplementation (118% vs 136% and 57% vs 44%, respectively). There was no significant correlation between percentage increase in zinc levels and percentage increase in parameters tested. Height SDS or weight SDS did not improve significantly in 17 patients who continued on zinc supplementation for at least 6 months (6-12 months) (-2.59 vs -2.53 SDS and -1.80 vs -1.67 SDS, respectively). Zinc supplementation increased basal IGF-I, IGFBP-3, alkaline phosphatase and osteocalcin without changing GH response to clonidine. Zinc supplementation did not affect sensitivity to exogenous GH as tested by IGF-I and IGFBP-3 generation test. These results suggest a direct stimulatory effect of zinc on serum IGF-IGFBP-3, alkaline phosphatase and osteocalcin. Despite improvements in the above parameters, zinc supplementation to children with idiopathic short stature with normal serum zinc levels did not significantly change height or weight SDS during 6-12 months follow-up.     

Reduced pericellular sensitivity to IGF-I in fibroblasts from girls with Turner syndrome: a mechanism to impair clinical responses to GH

Girls with Turner syndrome (TS) are treated with supraphysiological doses of growth hormone (GH) to improve final height; however in some girls, the growth response can be poor. This may reflect aberrations in GH and/or IGF-I actions at the cellular level, and thus this study compared the response of skin fibroblasts from normal children (n = 5) and girls with TS (n = 8) to GH, IGF-I, or a combination, by assessing the IGF binding protein (IGFBP) profile of conditioned medium harvested over 7 d. The two cell types had a comparable IGFBP profile; IGFBP-3 and IGFBP-4 were the most abundant species. TS fibroblasts produced more IGFBP-3 (d 7, 51.4 ± 45 ng/mL versus 20 ± 22 ng/mL; p < 0.05) than control cells; levels of IGFBP-4 were similar (21 ± 12 ng/mL versus 30 ± 21 ng/mL). GH did not influence IGFBP production. IGF-I treatment did not affect IGFBP-4 levels but enhanced the production of IGFBP-3 by both cell types (p < 0.05). However, the response of TS fibroblasts to IGF-I was approximately half that observed in normal cells (p < 0.05). Altered IGF-I activity, because of reduced bioavailability and/or reduced sensitivity, could contribute to the need for high GH doses in TS and for the poor response to GH in some girls with TS.     

Basal and stimulated levels of growth hormone, insulin-like growth factor-I (IGF-I), IGF-I binding and IGF-binding proteins in beta-thalassemia major

A significant percentage of children with beta-thalassemia major shows retardation in longitudinal growth as they progress towards puberty due to skeletal dysplasia, endocrine gland hypofunction or trace element deficiencies. The aim of this study was to evaluate GH/IGF-I secretion and action in prepubertal patients with beta-thalas-semia major. Eight prepubertal patients with short stature (group A) and seven prepubertal patients with normal stature (group B) were studied. Basal and stimulated (after administration of the hexapeptide Hexarelin) GH levels were measured with IRMA (Nichols); IGF-I and IGFBP-3 levels were measured with RIA (Nichols). IGF-I binding proteins (IGFBPs) were analyzed qualitatively with Western ligand blot. IGF-I binding to B-lymphocytes of the patients was also measured with competitive binding studies using human recombinant IGF-I and 125I-IGF-I (Amersham). Basal GH levels did not differ statistically between the groups. Peak GH levels after Hexarelin stimulation test were higher in group A (A: 27.9 +/- 15.6 ng/ml vs B: 9.1 +/- 4.7 ng/ml) (Wilcoxon test, p < 0.05). IGF-I levels in the two groups were low-normal and comparable (A: 168.0 +/- 81.6 ng/ml vs B: 126.6 +/- 25.5 ng/ml). IGFBP-3 levels were low in both groups (A: 1.21 +/- 0.27 microg/ml vs B: 1.08 +/- 0.20 microg/ml). Western ligand blot did not reveal any discernible difference in IGFBPs. However, IGF-I binding on B-lymphocytes was at least 20% lower in group A compared to group B (t-test, p < 0.01). IGF-I binding inversely correlated with peak GH levels (r = -0.54, p < 0.05). Patients in group A were older and chronological age correlated with IGF-I levels (r = 0.53, p < 0.05) whereas it inversely correlated with IGF-I binding (r = -0.63, p < 0.05). Moreover, patients in group A had higher ferritin levels. No correlation was found between ferritin levels, desferrioxamine dose/compliance or liver enzyme levels and the parameters of the GH axis studied. However, desferrioxamine dose x years correlated with IGFBP-3 (r = 0.56, p < 0.05) and correlated inversely with IGF-I binding (r = -0.74, p < 0.01). In conclusion, we have shown adequate GH secretion, higher secretive capacity after the administration of Hexarelin and lower IGF-I binding in prepubertal beta-thalassemic patients with short stature. Whatever the cause, reduced IGF-I action has to be considered when treating beta-thalassemic patients with short stature.     

Relationship of insulin-like growth factor-I, insulin-like growth factor binding protein-3, insulin, growth hormone in cord blood and maternal factors with birth height and birthweight

BACKGROUND: To determine whether the following factors are related to birthweight or birth height, we measured insulin-like growth factor (IGF)-I, insulin-like growth factor binding protein (IGFBP)-3, insulin and growth hormone (GH) levels in cord blood and also observed the relationship between birthweight, birth height and maternal factors. METHODS: One hundred and ninety-four cord bloods were collected, 106 from males and 88 from females. Three newborns were small for gestational age (SGA), 168 were appropriate (AGA) and 23 were large (LGA); 21 newborns were preterm and 172 were term. RESULTS: Levels of IGF-I and IGFBP-3, measured by enzyme-linked immunosorbent assay, were significantly lower in preterm babies (35.3 +/- 15.1 and 1025.6 +/- 562.8 ng/mL, respectively) than in term babies (61.6 +/- 39.5 and 1252.6 +/- 403.2 ng/mL, respectively; P < 0.01), but neither insulin nor GH levels, measured by radioimmunoassay, showed any significant difference between the two groups (P > 0.05). Among term babies, IGF-I and IGFBP-3 levels were significantly higher in the LGA group (96.1 +/- 34.1 and 1544.7 +/- 418.1 ng/mL, respectively) than in the AGA group (56.4 +/- 37.6 and 1212.8 +/- 383.4 ng/mL, respectively; P < 0.01). Levels of IGF-I and IGFBP-3 showed significant correlation with birthweight and length, respectively (P < 0.01), although GH and insulin levels did not (P > 0.05). There was a significant correlation between IGF-I and IGFBP-3 levels (P < 0.01, r = 0.64), but IGF-I and IGFBP-3 levels showed no relationship with GH or insulin levels. Birthweight correlated significantly with prepartum maternal weight, maternal weight gain and maternal height (P < 0.05), but birth length correlated significantly only with maternal height (P < 0.05). CONCLUSIONS: Our results suggest that fetal growth depends on fetal levels of IGF-I and IGFBP-3 and maternal factors, not on insulin or GH. Levels of IGF-I and IGFBP-3 may not be regulated by insulin alone, but by the complex interactions between several factors, such as insulin, GH and maternal factors.     

Clinical Usefulness of Urinary Growth Hormone Measurement in Short Children

Growth hormone GH) levels in nocturnal urine were measured in 96 short children and 73 children of normal height in order to investigate whether urinary CH levels reflect spontaneous GH secretion and whether they might be used to screen short children for GH treatment. GH levels in 24-hour urine samples were significantly correlated with urinary albumin and β₂-microglobulin levels in normal children, demonstrating an influence of renal function on urinary GH measurements. Nocturnal urinary GH levels showed significant positive correlations with mean serum GH levels during 3 hours of sleep ( r = 0.26. p < 0.05) and plasma insulin-like growth factor 1 (IGF-I) levels, reflecting physiological GH secretion. Urinary GH levels were significantly lower in the eight children with complete GH deficiency (3.1 ± 2.3 ng/g creatinine) than in the normal children (13.8 ± 11.2 ng/g creatinine). Urinary GH levels in three other groups of short children, partial CH deficiency (11.1 ± 16.9 ng/g creatinine), impaired GH secretion during sleep (10.4 ± 12.6 ng/g creatinine) and non-endocrine short stature (18.8 ± 19.5 ng/g creatinine), were not significantly different from those in the normal children. However, when the cut-off point for defining GH insufficiency was set at 5 ng/g creatinine, 87.5% (21 out of 24) of the short children with low urinary GH levels were suitable subjects for GH treatment (i.e. had complete GH deficiency, partial GH deficiency or impaired GH secretion during sleep). It is concluded that urinary GH measurement, though influenced by renal function, is potentially a simple, non-invasive and clinically useful method for screening short children for GH insufficiency. Further refinements of the technique are required before it can be widely applied.     

用尿脱氧吡啶啉及羟脯氨酸排泄率评价肾病综合征患儿骨吸收功能状况

目的　观察糖皮质激素（激素）对肾病综合征(肾病)患儿骨吸收功能的影响。方法　采用酶联免疫竞争法和分光光度比色法,对68例泼尼松治疗不同阶段的肾病患儿及同龄健康儿童16例尿脱氧吡啶啉（DPD）及羟脯氨酸（HOP）进行检测。结果　（1）激素足量治疗组DPD/肌酐(Cr)为（30±17）nmol/mmol,较正常对照组［（21±5）nmol/mmol］、初发激素治疗前组［(20±8)nmol/mmol］及激素减量治疗组［(20±11)nmol/mmol］均有升高（P均<0.05);（2）与DPD/Cr值变化趋势一致,激素足量治疗组HOP/Cr为［(5.3±2.7)mg/mmol］,与正常对照组［(3.2±1.2)mg/mmol］、初发激素治疗前组［(3.5±0.9)mg/mmol］及激素减量治疗组［(3.7±1.7)mg/mmol］比较差异均有显著意义(P＜0.05,<0.01,<0.05);（3）DPD/Cr与HOP/Cr两指标在正常对照组及肾病各组均呈明显正相关(r=0.64、0.65、0.76、0.78,P均<0.01)。结论　超生理剂量的泼尼松治疗能使肾病患儿骨吸收功能增强,易导致骨质疏松。     

多烯康治疗儿童激素敏感型肾病综合征高脂血症疗效观察

目的：观察糖皮质激素治疗后(10周内)多烯康治疗儿童激素敏感型肾病综合征(SSNS)高脂血症的疗效。方法：SSNS患儿随机分为降脂治疗组(治疗组)和对照治疗组(对照组),均给予糖皮质激素标准疗程,治疗组加用多烯康。分别在治疗前,治疗后2～3周,5～6周,8～10周采空腹血观察4种血脂成分：总胆固醇(TC),三酰甘油(TG),高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C)。结果：疗程2～3周治疗组LDL-C(3.19±2.08) mmol,TC(6.42±2.04) mmol均显著低于对照组(5.82±2.73) mmol/L,(10.0±4.75) mmol/L,(P均<0.05)。第5～6周治疗组LDL-C(2.83±1.50) mmol较对照组(4.94±2.04) mmol/L,提前下降至低水平(P<0.01),第8～10周治疗组LDL-C(2.30±0.46) mmol/L仍明显低于对照组（4.20±2.22）mmol/L,(P<0.01)。结论：多烯康能显著缩短SSNS严重高脂血症的时间,尤其是对降(LDL-C)有显著疗效,减轻了高脂血症对肾脏继发性损害的饿威胁。     

Serum levels of insulin-like growth factor (IGF)-I, free IGF-I, IGF binding protein (IGFBP)-1, IGFBP-3 and insulin in obese children.

In simple obesity, spontaneous and stimulated growth hormone (GH) secretions are diminished. However, this diminished GH secretion does not result in decreased somatic growth in obese children. Although the increased insulin level, low insulin-like growth factor binding protein (IGFBP)-1 and the resulting increase of bioavailability of insulin-like growth factor I (IGF-I) have been suggested as being involved, the exact mechanism has not yet been established. We investigated serum IGF-I, free IGF-I, IGFBP-1, IGFBP-3 and insulin levels in 36 obese and 39 non-obese healthy children. Insulin and IGFBP-3 were significantly higher in the obese group than in the control group (p < 0.05, p = 0.001, respectively). IGF-I, free IGF-I, free IGF-I/IGF-I and IGFBP-1 levels in the obese children were not significantly different from those in the control group. A positive correlation was found between body mass index (BMI) and IGF-I in the obese children (r = 0.30, p = 0.05). IGFBP-3 levels correlated positively with IGF-I (r = 0.44, p < 0.005), and free IGF-I levels (r = 0.37, p = 0.05) in the obese children. A negative correlation was found between IGFBP-1 and insulin levels (r = -0.30, p = 0.05) in the obese children. We concluded that normal growth in obese children might be maintained through normal IGF-I and increased IGFBP-3 levels, which are stimulated by increased insulin levels or nutritional factors or by increased responsiveness to GH.