淋巴细胞亚群检测在小儿过敏性紫癜诊治中的应用
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摘要
目的探讨淋巴细胞亚群检测在小儿过敏性紫癜(HSP)诊治中的作用及意义。方法选取73例HSP患儿作为HSP组,并根据是否感染溶血性链球菌分为链球菌感染组(31例)和链球菌未感染组(35例),并设同期正常体检的30例儿童为健康对照组。分析两组患儿入院时及采用相同治疗方案2周后的临床症状和淋巴细胞亚群检测结果。结果与健康对照组比较,HSP组存在CD4+[33.572±7.408)%比(37.225±5.789)%]、CD4+/CD8+[1.270±0.218)%比(1.582±0.176)%]及CD16+CD56+[12.301±4.946)%比(15.553±4.249)%]细胞比值下降,CD8+[29.887±5.538)%比(24.500±3.589)%]、CD19+[20.603±4.713)%比(14.100±3.699)%]细胞比值上升,差异有统计学意义(P<0.05)。治疗2周后,链球菌感染组患儿淋巴细胞亚群检测数值及临床症状改善均不明显,而链球菌非感染组患儿的淋巴细胞亚群数值和临床症状明显改善,差异有统计学意义(P<0.05)。结论 HSP患儿急性期存在细胞免疫紊乱,溶血性链球菌感染会进一步加重该类患者细胞免疫功能紊乱,淋巴细胞亚群检测对小儿HSP诊治具有重要的作用与意义。
Objective To investigate the change of lymphocyte subsets in children with Henoch-Schonlein purpura and beneficial for clinical care. Methods Seventy-three cases of Henoch-Schonlein purpura were divide into infected and uninfected groups with hemolytic streptococcus. Compared with 30 normal children,the lymphocyte data and clinical symptoms at admission and after two weeks' treatment were analyzed. Results Compared to the normal control group,the number of CD4+[33. 572 ± 7. 408) % vs.(37. 225 ±5. 789) % ],the ratio of CD4+/CD8+[1. 270 ± 0. 218) % vs.(1. 582 ± 0. 176) %] and CD16+CD56+[12. 301 ± 4. 946) % vs.(15. 553 ± 4. 249) %]were all decreased. The number of CD8+[29. 887 ± 5. 538) % vs.(24. 500 ± 3. 589) %]and CD19+[20. 603± 4. 713) % vs.(14. 100 ± 3. 699) %] were increased(P < 0. 05). At admission,the number of CD19+of infected group was higher than uninfected group,and the number of patients with hematuresis and proteinuria were higer than uninfected group. After two weeks' treatment,there was no obviously improved about the lymphocyte data and clinical symptoms of infected group,while uninfected group improved(P < 0. 05). Conclusion Cellular immune disorders in the acute phase of HSP,hemolytic streptococcal infection can further aggravate the cellular immune disorders. Diagnosis and treatment of lymphocyte subsets are with great significance in children with HSP.
Objective To investigate the change of lymphocyte subsets in children with Henoch-Schonlein purpura and beneficial for clinical care. Methods Seventy-three cases of Henoch-Schonlein purpura were divide into infected and uninfected groups with hemolytic streptococcus. Compared with 30 normal children,the lymphocyte data and clinical symptoms at admission and after two weeks' treatment were analyzed. Results Compared to the normal control group,the number of CD4+[33. 572 ± 7. 408) % vs.(37. 225 ±5. 789) % ],the ratio of CD4+/CD8+[1. 270 ± 0. 218) % vs.(1. 582 ± 0. 176) %] and CD16+CD56+[12. 301 ± 4. 946) % vs.(15. 553 ± 4. 249) %]were all decreased. The number of CD8+[29. 887 ± 5. 538) % vs.(24. 500 ± 3. 589) %]and CD19+[20. 603± 4. 713) % vs.(14. 100 ± 3. 699) %] were increased(P < 0. 05). At admission,the number of CD19+of infected group was higher than uninfected group,and the number of patients with hematuresis and proteinuria were higer than uninfected group. After two weeks' treatment,there was no obviously improved about the lymphocyte data and clinical symptoms of infected group,while uninfected group improved(P < 0. 05). Conclusion Cellular immune disorders in the acute phase of HSP,hemolytic streptococcal infection can further aggravate the cellular immune disorders. Diagnosis and treatment of lymphocyte subsets are with great significance in children with HSP.
引文
[1]YUKIHIKO KAWASAKI.The pathogenesis and treatment of pediatric Henoch-Schonlein purpura nephritis[J].Clin Exp Nephrol,2011,15(5):648-657.
[2]RESTIVO V,COSTANTINO C,TRAMUTO F et al.Hospitalization rates for intussusception in children aged 0-59 months from 2009 to2014 in Italy[J].Hum Vaccin Immunother,2017,13(2):445-449.
[3]潘瑞,杨春芳,潘家华.过敏性紫癜伴肺出血1例报道[J].安徽医药,2015,19(3):526-526.
[4]OZEN S,PISTORIO A,IUSAN SM,et al.EULAR/PRINTO/PRES criteria for Henoch-Schonlein purpura,childhood polyarteritis nodosa,childhood Wegener granulomatosis and childhood Takayasu arteritis:Ankara 2008.Part II:Final classification criteria[J].Ann Rheum Dis,2010,69(5):798-806.
[5]HE L,PENG Y,LIU H,et al.Activation of the interleukin-4/signal transducer and activator of transcription 6 signaling pathway and homeodomain-interacting protein kinase 2 production by tonsillar mononuclear cells in Ig A nephropathy[J].Am J Nephrol,2013,38(4):321-332.
[6]EI HUSSEINI A,AHMED A,SABUCEDO A,et al.Refractroy Henoch-Sch9nlein purpura:anypical aetiology and management[J].J Ren Care,2013,39(2):77-81.
[7]王士杰,鹿玲.过敏性紫癜患儿血IL-21、TGF-β1、TNF-α和免疫球蛋白变化及意义[J].临床儿科杂志,2011,29(2):159-161.
[8]钱毅,封其华.儿童过敏性紫癜急性期免疫状态研究[J].中国实用儿科杂志,2009,24(3):203-205.
[9]YUKIHIKO KAWASAKI.The pathogenesis and treatment of pediatric Henoch-Schonlein purpura nephritis[J].Clin Exp Nephrol,2011,15(5):648-657.
[10]丁艳,尹薇,何学莲,等.儿童过敏性紫癜急性期免疫功能探讨[J].中国免疫学杂志,2013,29(5):518-521,525.
[11]KAWASHIMA N,KAWADA JI,NISHIKADO Y,et al.Abnormal urinalysis on day 7 in patients with Ig A vasculitis(HenochSch9nlein purpura)[J].Nagoya J Med Sci,2016,78(4):359-368.
[12]胡海玉,鹿玲.过敏性紫癜患儿复发与反复的危险因素分析[J].中华实用儿科临床杂志,2012,27(21):1663-1665.
[13]TENG MC,WANG LC,YU HH,et al.Kawasaki disease and Henoch-Sch9nlein purpura-10 years’experience of childhood vasculitis at a university hospital in Taiwan[J].Journal of Microbiology Immunology&Infection,2012,45(1):22-30.
[14]LIU Z,WEI YD,HOU Y,et al.Differences in pathological characteristics and laboratory indicators in adult and pediatric patients with Henoch-Sch9nlein purpura nephritis[J].J Huazhong Univ Sci Technolog Med Sci,2016,36(5):659-666.
[15]DAVIN JC,COPPO R.Henoch-Schonlein purpura nephritis in children[J].Nat Rev Neprol,2014,10(10):563-573.
[2]RESTIVO V,COSTANTINO C,TRAMUTO F et al.Hospitalization rates for intussusception in children aged 0-59 months from 2009 to2014 in Italy[J].Hum Vaccin Immunother,2017,13(2):445-449.
[3]潘瑞,杨春芳,潘家华.过敏性紫癜伴肺出血1例报道[J].安徽医药,2015,19(3):526-526.
[4]OZEN S,PISTORIO A,IUSAN SM,et al.EULAR/PRINTO/PRES criteria for Henoch-Schonlein purpura,childhood polyarteritis nodosa,childhood Wegener granulomatosis and childhood Takayasu arteritis:Ankara 2008.Part II:Final classification criteria[J].Ann Rheum Dis,2010,69(5):798-806.
[5]HE L,PENG Y,LIU H,et al.Activation of the interleukin-4/signal transducer and activator of transcription 6 signaling pathway and homeodomain-interacting protein kinase 2 production by tonsillar mononuclear cells in Ig A nephropathy[J].Am J Nephrol,2013,38(4):321-332.
[6]EI HUSSEINI A,AHMED A,SABUCEDO A,et al.Refractroy Henoch-Sch9nlein purpura:anypical aetiology and management[J].J Ren Care,2013,39(2):77-81.
[7]王士杰,鹿玲.过敏性紫癜患儿血IL-21、TGF-β1、TNF-α和免疫球蛋白变化及意义[J].临床儿科杂志,2011,29(2):159-161.
[8]钱毅,封其华.儿童过敏性紫癜急性期免疫状态研究[J].中国实用儿科杂志,2009,24(3):203-205.
[9]YUKIHIKO KAWASAKI.The pathogenesis and treatment of pediatric Henoch-Schonlein purpura nephritis[J].Clin Exp Nephrol,2011,15(5):648-657.
[10]丁艳,尹薇,何学莲,等.儿童过敏性紫癜急性期免疫功能探讨[J].中国免疫学杂志,2013,29(5):518-521,525.
[11]KAWASHIMA N,KAWADA JI,NISHIKADO Y,et al.Abnormal urinalysis on day 7 in patients with Ig A vasculitis(HenochSch9nlein purpura)[J].Nagoya J Med Sci,2016,78(4):359-368.
[12]胡海玉,鹿玲.过敏性紫癜患儿复发与反复的危险因素分析[J].中华实用儿科临床杂志,2012,27(21):1663-1665.
[13]TENG MC,WANG LC,YU HH,et al.Kawasaki disease and Henoch-Sch9nlein purpura-10 years’experience of childhood vasculitis at a university hospital in Taiwan[J].Journal of Microbiology Immunology&Infection,2012,45(1):22-30.
[14]LIU Z,WEI YD,HOU Y,et al.Differences in pathological characteristics and laboratory indicators in adult and pediatric patients with Henoch-Sch9nlein purpura nephritis[J].J Huazhong Univ Sci Technolog Med Sci,2016,36(5):659-666.
[15]DAVIN JC,COPPO R.Henoch-Schonlein purpura nephritis in children[J].Nat Rev Neprol,2014,10(10):563-573.