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目的探讨肺炎支原体肺炎并肾脏损害(MPPKI)患儿的免疫发病机制。方法收集本市6家医院3a间收治的128例MPPKI患儿,采用金标渗滤法检测其MPAb-IgM,单克隆抗体碱性磷酸酶抗碱性磷酸酶法检测患儿T淋巴细胞亚群,散射比浊法测定其血清IgA、IgG、IgM,免疫比浊法测定C3补体,并与健康对照组比较。结果1.MPPKI患儿(128例)表现为典型急性肾炎者82例(64.06%),肾外症状性肾炎10例(7.81%),仅血尿和补体降低者24例(18.57%),肾病综合征12例(9.38%)。2.MPPKI患儿CD3+细胞[(66.65±6.46)%]与健康对照组[(65.78±12.34)%]比较无显著性差异(P>0.05);CD4+细胞[(36.46±6.68)%]与健康对照组[(39.25±5.64)%]比较有显著性差异(P<0.01);CD8+[(29.12±3.42)%]较健康对照组[(25.78±4.35)%]显著增高(P<0.01);CD4+/CD8+比值降低(1.06±0.38),与健康对照组比较(1.86±0.46),有显著性差异(P<0.01)。3.MPPKI患儿血清IgG[(16.66±3.42)g/L]、IgM[(3.96±0.66)g/L]水平明显高于健康对照组[(14.48±2.54)g/L,(2.24±0.56)g/L],差异均有显著性(Pa<0.01);IgA水平[(3.06±0.46)g/L]与健康对照组[(2.95±0.55)g/L]比较无显著性差异(P>0.05);C3补体[(506±166)mg/L]明显低于健康对照组[(529±182)mg/L],有显著性差异(P<0.01)。结论MPPKI同时存在细胞免疫和体液免疫功能失调。
Objective To investigate the pathogenesis of mycoplasma pneumonia and renal damage (MPPKI) in children. Methods A total of 128 children with MPPKI were collected from 6 hospitals in our city. MPAb-IgM was detected by gold standard perfusion method. T lymphocyte subsets in children were detected by alkaline phosphatase and alkaline phosphatase , The serum IgA, IgG and IgM were measured by nephelometry and C3 complement by immunoturbidimetry, and compared with the healthy control group. 82 cases (64.06%) of typical acute nephritis, 10 cases of extrarenal nephritis (7.81%), 24 cases (18.57%) of only hematuria and complement reduction, nephrotic syndrome Sign in 12 cases (9.38%). There was no significant difference in the number of CD3 + cells between MPPKI and healthy controls [(66.65 ± 6.46)%] vs (65.78 ± 12.34)%; (36.46 ± 6.68% There was significant difference between the control group [(39.25 ± 5.64)%] and that of the healthy control group (25.78 ± 4.35%) (P <0.01) The ratio of CD4 + / CD8 + decreased (1.06 ± 0.38), compared with the healthy control group (1.86 ± 0.46), there was a significant difference (P <0.01). The levels of serum IgG (16.66 ± 3.42g / L) and IgM (3.96 ± 0.66g / L) in MPPKI group were significantly higher than those in healthy control group (14.48 ± 2.54g / L, 2.24 ± 0.56 (P <0.01). There was no significant difference in the level of IgA between the two groups (P <0.05), while the level of IgA was (3.06 ± 0.46) g / L > 0.05). There was a significant difference (P <0.01) between C3 complement [(506 ± 166) mg / L] and healthy controls [(529 ± 182) mg / L] Conclusion MPPKI has both cellular immunity and humoral immune dysfunction.