肺炎支原体肺炎患儿血清免疫球蛋白水平的变化及结果分析

Serum Immunoglobulin Levels Alteration in Pediatric Mycoplasma Pneumoniae Infected Patients and Analysis

目的探讨肺炎支原体肺炎患儿体液免疫(免疫球蛋白)在肺炎支原体肺炎(MPP)发病机制中的作用。方法采用免疫透射比浊法检测MP-IgM阳性患儿和正常对照组儿童各60例的血清免疫球蛋白(IgGI、gA、IgM)。结果健康男童血清IgGI、gA水平比女童高,两者比较差异有显著性(P<0.01);男童血清IgM水平比女童稍高,两者比较无显著性差异(P>0.05)。MP阳性患儿血清IgG水平明显低于正常对照组(P<0.05);血清IgA水平较对照组稍高,但无明显差异(P>0.05);而血清IgM水平明显高于正常对照组(P<0.01)。结论健康男童血清IgG和IgA水平均明显高于健康女童(P<0.01),而血清IgM的水平无明显差异,可能与男童对感染性疾病的抵抗力强于女童有关;患儿血清IgM水平较对照组显著升高,IgA升高不明显,IgG水平则低于对照组,显示体液免疫(免疫球蛋白)可能在MP感染的发病机制中起到一定的作用。

Objective To explore the influence of humoral immunity in the mycoplasma pneumoniae pneumonia （MPP） pathogenesis. Methods Immunity transmission turbidimetry technique was used to determine the serum immunoglobulin （IgG, IgA, IgM） levels in a MPP patients group and an apparently healthy control children group; each group consisted with age matched 30 boys and 30 girls. Results The IgG, IgA levels in healthy control group showed significant sex difference with boys higher than that of the girls（ P〈 0.01 ）, but not the IgM levels （P〉0.05）. There were significant differences in the serum IgG levels between the mycoplasma pneumoniae pneumonia patients group and the healthy group, the MPP patient group levels were significantly lower （P〈 0.05） ; while the serum IgA levelof MPP patients was a little higher than the healthy group, but showed no significant difference （P〉 0.05）. Comparing the IgM levels between these two groups, we found significant difference： the levels of patients were significantly higher than the healthy group （P〈 0.01）. Serum IgG and IgA levels in health boys were significantly higher than that of the healthy girls, but not in the IgM levels, which might explain why girls were more vulnerable. IgM levels in the patient group were significantly higher than that of the healthy group, while the difference of IgA level was insignificant, and the IgG levels in patient group were lower. Conclusions These results indicate that humoral immunity may play an important role in the pathogenesis of MP infection.