先天性心脏病手术后生长激素-胰岛素样生长因子轴的变化

目的 探讨先天性心脏病患儿手术后生长激素(growth hormone)和胰岛素样生长因子(insulin-like growth factor,IGF)轴的变化及意义.方法 先天性心脏病25例,采用放射免疫测定法测定治疗前、手术治疗后3个月、6个月和1年空腹血IGF-1及胰岛素样生长因子结合蛋白-3(insulinlike growth factor binding protein-3,IGFBP-3);对照组为正常儿童20名.结果 先天性心脏病患儿手术前血IGF-1和IGFBP-3浓度较正常儿童减低(P＜0.01);先天性心脏病手术治疗后患儿的IGF-1和IGFBP-3浓度随着术后时间增加而逐渐提高,至1年时与同龄儿童持平,差异无统计学意义(P＞0.05).结论 先天性心脏病患儿存在生长发育迟缓及生长激素-胰岛素样生长因子轴功能的紊乱能通过手术治疗纠正,从而改善先天性心脏病患儿生长发育.     

慢性心力衰竭患者血清胰岛素样生长因子-1及其结合蛋白的变化及意义

目的 通过对慢性心力衰竭患者血清中胰岛素样生长因子（insulin-like growth factor,IGF）-1及其相关结合蛋白的浓度测定,研究IGF-1及其相关结合蛋白对慢性心力衰竭的影响.方法 选取2012年6月至2013年12月江西省人民医院心内科慢性心力衰竭患者184例,按纽约心脏病协会心功能分级分为3组（心功能Ⅱ级组、Ⅲ级组和Ⅳ级组）,并选取正常人群63例作为对照组,测定其血清总IGF-1,游离IGF-1（Free IGF-1）、IGF结合蛋白（insulin-like growth factor-binding protein,IGFBP）-1,IGFBP-3浓度.对各组数据进行统计学分析,比较各组之间的血清总IGF-1,Free IGF-1、IGFBP-1,IGFBP-3浓度差异.结果 心功能Ⅳ级组血清总IGF-1,FreeIGF-1,IGFBP-3浓度明显高于心功能Ⅲ级组,心功能Ⅲ级组血清总IGF-1,Free IGF-1,IGFBP-3浓度明显高于心功能Ⅱ级组,差异有统计学意义（P＜0.01）.结论 血清IGF-1浓度随着慢性心力衰竭患者心功能变差而升高,说明IGF-1对患者心功能的恢复可能有明显的促进作用.     

新发病1型糖尿病儿童血生长激素、胰岛素样生长因子(IGF)Ⅰ和IGF结合蛋白3水平的变化

在新发病的1型糖尿病患儿和正常对照儿童测定血GH，胰岛素样生长因子（IGF），IGF结合蛋白（IGFBP）3的水平。结果显示新发病的1型糖尿病患儿可乐定刺激的生长激素分泌，血IGF，IGFBP-3水平低于正常对照儿童。     

肢端肥大症患者胰岛素样生长因子1与生长激素矛盾现象相关因素探讨

<正>人体内的生长激素（growth hormone,GH）、胰岛素样生长因子1(insulin-like growth factor 1,IGF-1)可通过内分泌、旁分泌、自分泌方式，调节体细胞生长、身体组分及代谢等。血清GH和IGF-1测定是GH相关疾病（过量、缺乏及GH不敏感）诊断和随访的重要指标，例如肢端肥大症（以下简称肢大）的诊断及疗效判断依赖于75 g口服葡萄糖耐量试验（oral glucose tolerance test,OGTT）中GH谷值（OGTT-GH谷值）和血清IGF-1水平；     

新生儿脐带血中生化指标的改变与巨大儿形成的关系

目的 探讨新生儿脐带血中生化指标的改变与巨大儿形成的关系。方法84例新生儿根据出生体质量分为巨大儿51例（观察组）和正常儿33例（对照组）,检测两组胰岛素样生长因子-1（IGF-1）、胰岛素样生长因子结合蛋白-3（IGFBP-3）、瘦素（LEP）、胰岛素（INS）、生长激素（GH）、促甲状腺激素（TSH）、血糖（GLU）水平,采用多元线性逐步回归分析巨大儿形成的主要影响因素。结果观察组IGF-1、LEP、IGFBP-3水平高于对照组,GLU低于对照组,P均〈0．05。多元线性逐步回归分析显示IGF-1、LEP、GH与新生儿体质量有明显相关性。结论IGF-1和LEP在调节胎儿生长发育方面起重要作用,可能是胎盘中影响胎儿生长的主要因子,与巨大儿形成有密切关系。     

肢端肥大症药物治疗进展

<正>肢端肥大症（acromegaly）是一类起病缓慢的内分泌代谢性疾病,通常是由于过多的生长激素（growth hormone, GH）促使肝脏产生超量的胰岛素样生长因子1 (insulin-like growth factor 1, IGF-1)为主要临床特征。超过95%的GH异常分泌是由分泌GH的垂体腺瘤所致,剩下少数的是由于异位GH、促GH释放激素（GH releasing hormone,GHRH）瘤所致。     

IGF-1、IGFBP-3在儿童生长激素缺乏症诊断和疗效判断中的应用

目的探讨胰岛素样生长因子1(IGF-1)及其结合蛋白3(IGFBP-3)在儿童生长激素缺乏症(GHD)诊断及疗效判断中的价值。方法68例GHD患儿予以国产0.1 IU/(kg.d)r-hGH治疗12个月,于治疗前及治疗后3、6、12个月分别测定身高、体重、骨龄及血清IGF-1、IGFBP-3,并与60例正常儿童进行对照。结果GHD患儿血清IGF-1和IGFBP-3水平明显低于正常对照组(P均<0.01);r-hGH治疗后身高增长速度明显加快,血清IGF-1、IGFBP-3水平显著升高;治疗前血清IGF-1与治疗6、12个月时的生长速度(GV6,GV12)呈负相关(r=-0.72-、0.78,P均<0.01);治疗3个月时IGFBP-3水平变化与GV6、GV12呈正相关(r=0.82、0.80,P均<0.01)。结论IGF-1、IGFBP-3可用于儿童GHD的诊断及疗效预测。     

生长激素缺乏症治疗前后胰岛素样生长因子及其结合蛋白的变化

20 0 1年 6月至 2 0 0 2年 1 0月 ,我们对 46例生长激素缺乏症 ( GHD)儿童进行生长激素类激素 ( r-h GH)替代治疗 ,观察其血清胰岛素样生长因子( IGF- 1 )、胰岛素样生长因子结合蛋白 ( IGFBP- 3)变化 ,从而为 GHD疗效观察提供依据。1　资料与方法1 .1　临床资料　本文 GHD患儿 46例 ,男 30例 ,女1 2例 ,年龄 4～ 1 2岁。患儿均有典型 GHD症状与生长发育特征 ,身高低于同性别同年龄儿童第三百分位数 ,年身高生长速度 <2 .5 cm,骨龄落后于同类正常儿童至少两年 ;两项生长激素 ( GH)药物激发试验(可乐宁、精氨酸 ) GH峰值 <1 0 μg…     

62例2型糖尿病患者血IGF-1、IGFBP-3水平测定及与糖尿病视网膜病变的相关性

用ELASA法对62例2型糖尿病患者（糖尿病组）及30例健康人（对照组）进行血胰岛素样生长因子-1（IGF-1）、胰岛素样生长因子结合蛋白-3（IGFBP-3）及空腹血糖（FPG）、糖化血红蛋白（HbA1c）水平测定,分析IGF-1、IGFBP-3与糖尿病视网膜病变（DR）的相关性。结果 糖尿病组血IGF-1、IGFBP-3水平显著低于对照组（P〈0.01、0.05）,其中合并增殖性DR者显著高于非增殖性DR者（P〈0.05）;血IGF-1与IGFBP-3水平呈正相关（r^2=0.71,P〈0.01）,糖尿病组IGF-1与HbA1c呈正相关（r^2=0.31,P〈0.01）。认为IGF-1及IGFBP-3可能参与了糖尿病DR的发生和发展。     

结直肠腺瘤患者血清IGF-1和IGFBP-3的变化及其临床意义

目的:研究血清胰岛素样生长因子1(insulin-like growth factor1,IGF-1)和胰岛素样生长因子结合蛋白3(insulin-like growth factor binding protein3,IGFBP-3)在结直肠腺瘤患者中的变化及临床意义.方法:采用放射免疫法和免疫放射法分别检测120例结直肠腺瘤患者、48例结直肠癌患者及34例健康人外周血清IGF-1和IGFBP-3表达水平.结果:血清IGF-1和IGF-1/IGFBP-3比值在结直肠癌组(247.35±60.77;0.063±0.010)、腺瘤性息肉组(224.75±69.45;0.055±0.010)及健康对照组(195.39±63.37;0.047±0.013)依次降低,前两组明显高于后组,差异有统计学意义(P<0.05).腺瘤性息肉患者血清IGF-1、IGFBP-3水平及IGF-1/IGFBP-3比值与患者的性别、年龄、吸烟饮酒情况及肿瘤家族史临床指标间均无统计学意义;与息肉大小、数量、部位、组织学分类也无统计学意义.血清IGF-1和IGF1/IGFBP-3比值在结直肠癌组(247.35±60.77;0.063±0.010)、进展期腺瘤组(235.81±73.72;0.056±0.011)及早期腺瘤组(208.15±59.44;0.052±0.008)依次降低,且前两组较后组比,差异有显著性(P<0.05).结直肠腺瘤性息肉患者血清IGF-1和IGFBP-3呈正相关(r=0.796,P<0.001).结论:血清IGF-1和IGF-1/IGFBP-3比值增高可能在结直肠腺瘤癌变中起一定作用,对适龄人群行血清GF-1和IGF-1/IGFBP-3检测可以简单筛选有息肉恶变倾向者.     

Hemoglobin level is linked to growth hormone-dependent proteins in short children

Erythropoiesis was investigated in 32 children wih short stature and in eight children with skeletal dysplasia by studying blood hemoglobin in relation to growth and to serum concentrations of insulin-like growth factor I (IGF-I), IGF binding protein-3 (IGFBP-3), and erythropoietin (EPO) before, during, and after 12 months of recombinant human growth hormone (GH) treatment. Blood hemoglobin concentration was positively correlated with relative body height and with serum IGF-I and IGFBP-3 levels (P = .001 to .02), but not with the concentrations of EPO. The normal age-dependency of hemoglobin was lacking. Hemoglobin levels and their responses to GH treatment were similar in the patients with GH deficiency and those with normal GH secretion. Treatment with GH accelerated growth and elevated the concentrations of hemoglobin, IGF- I, and IGFBP-3. In the eight patients with skeletal dysplasia, body mass increased similarly, but gain in height was less than in the other patients, and the increase in hemoglobin was markedly pronounced. In this group, the correlations between hemoglobin, IGF-I, and IGFBP-3 were extremely close (r = 0.80 to 0.85, P = .031 to .008). These findings are in accord with earlier observations from in vitro and animal studies, and suggest that the GH-IGF axis is involved in the physiologic elevation of hemoglobin levels during childhood.     

Juvenile rheumatoid arthritis. Effects of disease activity and recombinant human growth hormone on insulin-like growth factor 1, insulin-like growth factor binding proteins 1 and 3, and osteocalcin

Objective. To investigate possible mechanisms of growth impairment in children with juvenile rheumatoid arthritis (JRA). Methods. Eighteen prepubertal children with JRA and growth retardation received recombinant human growth hormone (rHuGH) for 1 year. Growth hormone profiles over 24 hours were obtained before treatment in 12 patients; the levels did not differ from those in “short normal” children. Levels of insulin-like growth factor 1 (IGF-1), IGF binding proteins (IGFBPs) 1 and 3, insulin, osteocalcin, and C-reactive protein (CRP), as well as the erythrocyte sedimentation rate were measured serially. Pretreatment levels were compared with control levels. Results. In JRA patients, IGF-1, IGFBP-3, and osteocalcin levels were significantly lower and insulin levels significantly higher than those in controls, but there was no significant difference in the level of IGFBP-1. With rHuGH treatment, height velocity and mean levels of IGF-1, osteocalcin, and insulin increased significantly, while mean levels of IGFBP-1 fell significantly. Levels of IGFBP-3 correlated with those of IGF-1. The height velocity correlated positively with IGF-1 and osteocalcin, and negatively with IGFBP-1. Levels of IGFBP-1 were inversely related to those of insulin and IGF-1. There was a significant negative correlation between the CRP and height velocity, IGF-1 level, and osteocalcin level. Conclusion. IGF-1 production is impaired in children with active JRA. Treatment with a therapeutic dose of rHuGH can rectify the IGF-1 deficiency within 4 days, but its effect is adversely influenced by the acute-phase response, as reflected by an elevated CRP level.     

Serum insulin-like growth factor type 1, insulin-like growth factor-binding protein-1, and insulin-like growth factor-binding protein-3 concentrations in patients with thyroid dysfunction.

Thyroid hormones play a role in the regulation of insulin-like growth factor type 1 (IGF-1) and insulin-like growth factor-binding protein-3 (IGFBP-3) expression, and both IGF-1 and IGFBPs have been shown to be related to the function and growth of the thyroid. Our aim was to evaluate serum concentrations of IGF-1, IGFBP-1, and IGFBP-3 in patients with thyroid dysfunction before and after normalization of thyroid function. The study was performed in 86 patients with thyroid dysfunction (43 hyperthyroid and 43 hypothyroid patients) and 17 euthyroid subjects. Serum growth hormone (GH), insulin, IGF-1, IGFBP-1, and IGFBP-3 were measured in all patients before and after normalizing serum thyroid hormone concentrations. Hyperthyroid patients showed IGF-1 (198.8 +/- 17.0 microg/L) and IGFBP-3 levels (4.2 +/- 0.2 mg/L) similar to those found in the control group (217.9 +/- 20.3 microg/L and 4.2 +/- 0.3 mg/L, respectively). After therapy these levels significantly decreased to 156.6 + 11.1 microg/L (p < 0.01) and 3.3 +/- 0.1 mg/L (p < 0.001), respectively. IGFBP-1 concentrations were clearly higher than those found in controls (22.7+/- 2.6 vs. 5.7 +/- 1.5 microg/L, p < 0.001) and exhibited a significant reduction after therapy for thyroid hyperfunction (11.0 +/- 1.7 microg/L, p < 0.001). Patients with hypothyroidism showed serum concentrations of IGF-1 (161.5 +/- 13.1 microg/L, p < 0.05) and IGFBP-3 (3.2 +/- 0.3 microg/L, p < 0.05) significantly lower than those found in healthy volunteers. However, replacement therapy with levothyroxine did not induce any significant modification of these concentrations (152.6 +/- 10.6 microg/L and 3.2 +/- 0.2 mg/L, respectively). Similarly, patients with thyroid hypofunction exhibited raised levels of IGFBP-1 (15.5 +/- 0.9 microg/L, p < 0.05 vs. control group) that were significantly decreased after therapy (8.8 +/- 1.4 microg/L, p < 0.01). The results of the present study show that thyroid status affects GH/IGF axis. Hypothyroidism is associated with significant reductions of IGF-1 and IGFBP-3, and IGFBP-1 is elevated in both hypothyroidism and hyperthyroidism.     

The effect of anorexia nervosa and refeeding on growth hormone-binding protein, the insulin-like growth factors (IGFs), and the IGF-binding proteins.

We studied the relationship of serum insulin-like growth factor-I (IGF-I), IGF-II, the IGF-binding proteins IGFBP-1, IGFBP-2, and IGFBP-3, and GH-binding protein (GHBP; which is postulated to be derived from the extracellular portion of the GH receptor) in normal volunteers and patients with anorexia nervosa before and after a refeeding program. Serum GHBP, IGF-I, and IGFBP-3 were all significantly decreased in low weight patients with anorexia nervosa and returned to nearly normal levels with refeeding. Fasting serum GH and serum IGFBP-1 and IGFBP-2 were significantly increased in low weight patients with anorexia nervosa and also returned to nearly normal levels with refeeding. Serum IGF-II was 27% lower in the low weight group than in normal subjects, but this difference was not statistically significant. Both serum IGF-I and IGF-II were positively correlated with serum IGFBP-3 and negatively correlated with serum IGFBP-1 and IGFBP-2. These data are consistent with the hypothesis that nutritional deprivation alters the GH-IGF axis by down-regulation of the GH receptor or its postreceptor mechanisms, and that this effect is reversible with refeeding.     

hrGH treatment of glucocorticoid-induced short stature in children

The treatment of systemic diseases with glucocorticoids is often associated with decreased height velocity (HV), and can result in shorter final height. Interactions between adrenal and GH-IGF axis have been described and can occur at hypothalamic-pituitary level or at the regulation of IGF system, including the IGF1R signaling. The clinical state of these patients may be considered as an absolute and/or functional IGF-1 deficiency. Interventions aiming to restore the normal function of GH-IGF axis might reduce the glucocorticoids-induced growth suppression in these children. It has been shown that recombinant human GH (hrGH) induces an increase in HV and a decrease in protein loss in patients with juvenile idiopathic arthritis treated with glucocorticoids. Significant increment in HV was also described after hrGH treatment in children under glucocorticoid therapy due to inflammatory bowel disease or renal transplantation. There is a positive correlation between HV and the dose of hrGH. The results support that the IGF-1 deficiency in these children may be counteract by hrGH therapy. The effect of hrGH is observed only during the treatment period and depends on the replacement strategy, nutritional status and disease control.     

Modifications of growth velocity and the insulin-like growth factor system in children with acute lymphoblastic leukemia: a longitudinal study

The basis of impaired growth in children with acute lymphoblastic leukemia (ALL) is multifactorial, including the disease itself, infections, undernutrition, and adverse effects of therapy. Because growth is regulated by the GH-insulin-like growth factor (IGF) system, which may be altered in catabolic states, we studied serum IGF-I, free IGF-I, IGF-II, the IGF-binding proteins (IGFBP-1 to -3), and total and free acid-labile subunit (ALS) levels in 26 prepubertal children with ALL at diagnosis (n = 26) and 6 (n = 21), 12 (n = 21), 18 (n = 21), 24 (n = 20), 30 (n = 16), and 36 months (n = 16) after beginning treatment to investigate the effects of disease and therapy on this system and its relationship with growth in these patients. Intensive chemotherapy compromised growth, with a catch-up period beginning when maintenance therapy began and increased growth after stopping therapy. Weight increased 6 months after chemotherapy withdrawal, whereas the body mass index was increased both at 6 months after diagnosis and 6 months after therapy suppression. Serum IGF-I, IGF-II, IGFBP-3, and total and free ALS levels were significantly decreased at diagnosis. Normalization of IGF-II and IGFBP-3 occurred 6 months after diagnosis, and normalization of IGF-I and total and free ALS occurred 1 yr after terminating therapy. IGFBP-1 and IGFBP-2 levels were significantly increased at diagnosis and decreased after stopping therapy. Free IGF-I was elevated throughout the study. IGF and IGFBP-3 levels showed a close relationship to growth velocity at the end of chemotherapy, with this correlation remaining until at least 1 yr after therapy withdrawal. In conclusion, intensive chemotherapy compromises linear growth in prepubertal ALL patients, and this phenomenon is associated with alterations in the IGF system. However, when therapy is reduced or stopped, catch-up growth occurs, but various parameters of the GH-IGF axis remain impaired. This suggests the need for a longer period of follow-up to assess the long-term risks of therapy and disease on this system.     

Effect of short-term medroxyprogesterone acetate on left ventricular mass: role of insulin-like growth factor-1.

Previous studies using 17beta-estradiol and medroxyprogesterone acetate (MPA) have shown that hormone replacement therapy (HRT) increases left ventricular mass (LVM). To determine if insulin-like growth factor-1 (IGF-1) is associated with the increase in LVM, we measured IGF-1 and IGF-binding protein-3 (IGFBP-3) levels in 19 postmenopausal women before and after 8 weeks of oral treatment with MPA 5 mg/d. LVM was measured by two-dimensional echocardiography. Changes in IGF-1, IGFBP-3, and LVM from baseline were analyzed by paired ttest. Regression analysis was used to determine if changes in the IGF-1 axis with MPA treatment affect the increase in LVM. LVM increased 4.4% during the study (P = .006 vbaseline). IGF-1 increased 17% with MPA (P = .008), whereas IGFBP-3 did not change. The IGF-1/IGFBP-3 ratio increased 16.8% (P = .0003). Regression analysis of LVM with IGF-1, IGFBP-3, and the IGF-1/IGFBP-3 ratio suggested that IGF-1 during MPA therapy explains 2.4% and the IGF-1/IGFBP-3 ratio explains 3.2% of the variation in LVM. There was no effect of IGFBP-3 on LVM. Most of the variation in LVM with MPA (90.5%) was explained by baseline LVM. The IGF-1/IGFBP-3 ratio on MPA treatment was inversely related to the change in LVM: women with a lower LVM at baseline had the greatest increase in LVM with MPA. These findings suggest that MPA increases IGF-1 and LVM. Because the increase in IGF-1 with MPA treatment explains a fraction of the increase in LVM, other mechanisms must also be operative.     

Synthesis of insulin-like growth factor binding protein 3 in vitro in human articular cartilage cultures

OBJECTIVE: To quantify the rate of synthesis of insulin-like growth factor binding protein 3 (IGFBP-3) and insulin-like growth factor 1 (IGF-1) by in vitro cultures of normal and osteoarthritic (OA) human articular cartilage. METHODS: Levels of IGF-1 and IGFBP-3 in media from in vitro cultures of human cartilage were determined by radioimmunoassay (RIA). IGFBPs were characterized by immunoblots and ligand blots. Ultrafiltration and RIA analysis of synovial fluid (SF) samples and washings of cartilage samples ex vivo were used to calculate partition coefficients and to estimate the amount of IGF-1 and IGFBP-3 in cartilage in vivo. RESULTS: OA cartilage synthesized 150 ng of IGFBP-3 per gm of cartilage per day, compared with 50 ng synthesized by normal cartilage. The surface zone of normal cartilage produced more IGFBP-3 than did the deep zone. Immunoblots and ligand blots confirmed the presence of IGFBP-3. IGFBP-3 synthesis was stimulated by exogenous IGF-1. No freshly synthesized IGF-1 was detected. The quantities of IGF-1 and IGFBP-3 present ex vivo were 11.3 and 78.7 ng/gm of cartilage in normal cartilage and 21.6 and 225.4 ng/gm in OA cartilage. CONCLUSION: The results show that while IGFBP-3 is synthesized in explant cultures, IGF-1 is not. The rate of IGFBP-3 synthesis is 3 times higher in OA than in normal cartilage. Both IGFBP-3 and IGF-1 penetrate into cartilage from SF in vivo. We estimate that the quantities of IGFBP-3 produced in culture by human cartilage are small compared with the amount supplied in the form of "small complexes" from the circulation. The high value of the partition coefficient of IGFBP-3 implies binding to the matrix.     

Effects of recombinant human insulin-like growth factor I (IGF-I) therapy on the growth hormone-IGF system of a patient with a partial IGF-I gene deletion.

We have previously reported a 17.2-yr-old boy with severe growth retardation and undetectable serum levels of insulin-like growth factor I (IGF-I) due to a partial deletion of the IGF-I gene. The aim of this study was to investigate the effects of recombinant human IGF-I (rhIGF-I) therapy on the GH-IGF system of this patient to gain further insights into its growth-promoting and metabolic actions. To assess the changes in GH, IGFs, IGF-binding proteins (IGFBPs), acid-labile subunit (ALS), and insulin levels, blood samples were obtained before therapy and during the first year of treatment. Hormones were analyzed by specific RIAs. Overnight GH profiles were performed before and at 1, 6, and 12 months of therapy. Fasting ALS, IGF-II, IGFBP-3, IGFBP-2, IGFBP-1, and insulin levels before rhIGF-I treatment were 46.3 mg/L, 1044 microg/L, 5.8 mg/L, 73 ng/mL, 4.7 ng/mL, and 27.3 mU/L, respectively. IGF-II, ALS, and insulin levels were elevated, whereas IGFBP-1 and IGFBP-2 levels were decreased compared to reference values. Twenty-four hours after a single s.c. injection of rhIGF-I (40 microg/kg), the concentrations were 46 mg/L, 888 microg/L, 6.9 mg/L, 112 ng/mL, 5.0 ng/mL, and 21.0 mU/L, respectively. After a single s.c. injection of rhIGF-I of 40 or 80 microg/kg x day and modelling the data using a two-compartment model, the half-lives of elimination were 15.7 and 14.3 h, with a maximum increase in IGF-I levels to 341 and 794 microg/L around 7 h, respectively. An increase in IGFBP-3 levels was observed with both doses of rhIGF-I, with a peak values of 9 mg/L. GH profiles showed a decrease in peak amplitude from 342 to 84 mU/L at 1 month, to 67 mU/L at 6 months, and to 40 mU/L at 1 yr of therapy, with no significant changes in peak number. A significant increase in IGFBP-1 levels was observed during treatment with 80 microg/kg x day IGF-I, reflecting the inhibitory effect of rhIGF-I on insulin secretion. The clinical response to rhIGF-I therapy was an increased height velocity from 3.8 cm/yr before treatment to 6.6 cm/yr. Increased lean body mass correlated with changes in the doses of rhIGF-I and, in turn, with the biochemical changes in the GH-IGF axis. Similar to healthy individuals, this patient had normal IGFBP-3 and ALS levels, which are the major regulators of the pharmacokinetics of rhIGF-I. In summary, rhIGF-I treatment has improved linear growth and insulin sensitivity in this patient by restoring IGF-I levels and by normalizing circulating GH, IGFBP, and insulin levels.     

非霍奇金淋巴瘤患者血清胰岛素样生长因子-1及其结合蛋白-3表达水平的初步观察

目的:探讨非霍奇金淋巴瘤(NHL)患者血清胰岛素样生长因子-1(IGF-1)及其结合蛋白-3(IGFBP-3)表达水平及其临床意义.方法:选择28例诊断初发NHL患者(淋巴瘤组)及28例健康志愿者(对照组),化学发光法测定血清IGF-1及IGFBP-3水平并计算IGF- 1/IGFBP-3值,分析组间的差异.结果:血清IGF-1及IGFBP-3水平淋巴瘤组显著低于正常对照组(均P＜0.01);IGF-1/IGFBP-3淋巴瘤组与正常对照组差异无统计学意义(P＞0.05);不同亚型的淋巴瘤组的血清IGF-1、IGFBP-3水平及IGF-1/IGFBP-3比值的差异均未达到统计学意义(P＞0.05).结论:N HL患者血清IGF-I及IGFBP-3水平明显降低,可能与NHL相关.IGF-1/IGFBP-3比值与NHL无明显相关性,IGF-1及IGFBP-3水平与NHL的分型无明显相关.