重组人生长激素对全身炎症反应综合征患儿细胞免疫及炎症因子的影响

摘要

目的 研究重组人生长激素(rhGH)合并肠内营养支持治疗,对全身炎症反应综合征(SIRS)患儿的临床疗效及对细胞免疫和血清炎症递质的影响,并探讨其可能的抗炎机制.方法 SIRS患儿随机分为rhGH治疗组和常规治疗组,两组均给予肠内营养及综合治疗,rhGH治疗组于入院第2天晚上10:00给予生长激素(0.1 U/kg)腹部皮下注射,连续治疗7 d.检测两组患儿于入院第2天的(治疗前)和入院第9天(治疗后)的细胞免疫功能和血清炎症因子水平.另选同期健康体检婴幼儿20例作为正常对照组.结果 SIRS患儿与正常对照儿童比较,CD3、CD8、NK细胞水平降低,差异有统计学意义(P均＜ 0.01).经治疗后,rhGH治疗组SIRS患儿的CD4、CD4/CD8、NK细胞较常规治疗组明显增高,差异有统计学意义(P均＜ 0.05);而IL-2、IL-4、TNF-α、IFN-γ水平则降低,差异亦有统计学意义(P均＜ 0.05).结论 SIRS患儿体内存在细胞免疫功能的紊乱;rhGH能增强SIRS患儿的细胞免疫功能,并缓解机体炎症反应.%Objective To evaluate the remedial effects of the combination of nutrition support with recombinant human growth hormone (rhCH) and to investigate the changes of cellular irnmunological function ana serum inflammatory cytokme levels in patients with systemic inflammatory response synarorne (SIRS). Methods Fifty SIRS pediatric patienLs were rancomly civided ]nto niGM treatment group (25 cases) anc conventional treatment group ( 25 cases) - ooth groups were given enteral nutrition and comprehensive treatment. The patients in rhGH treatment group were given rhGH (0,1 u/Ckg-d) at 10 pm starting on day 2 of the hospilalization for 7 days. Cellular immunity (CD3, CD4, CDS, CD4/CD8, NK ceil) and inflammatory cytokme (IL-2, IL--4, IFN-γ, TNF-α) were measured on day 2 of the hospitai-ization (before treatment) and on day 9 of the hospitalization (after treatment) - Another 20 healthy children were selected as control group. Results Compared with healthy control, the levels of serum CD3, CDS and NK cell were significantly lower in SIRS pediatric patients (P < 0.01). After treatment, serum CD4, NK cell and CD4/CD8 were significantly increased in rhGH treatment group than in conventional treatment group (P < 0-05) ; and inflammatory cytokme (IL-2, IL 4, TNF α, IFN-β were significant decreased m rhGH treatment group than in conventional treatment group (P < 0.05 ). Conclusions The cellar immune function is inhibited in the SIRS pediatric patients. rhCH treatment can significantly improve the cellular immunity function and alleviate the inflammatory response in SIRS pediatric patients.