补体活化对SLE孕妇胎儿不良结局影响的研究
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摘要
目的:探讨自身抗体介导的补体活化与胎儿不良结局的关系,以改善SLE孕妇妊娠结局。方法:选取2011年1月至2013年1月福建省立医院产科收治的16例妊娠合并SLE患者和20例正常妊娠活产孕妇(对照组)产后的胎盘,对胎盘进行常规病理检查,免疫组化法检测C1q及C4d表达。结果:SLE孕妇胎盘镜下观察均可见绒毛组织不同程度退变、局部梗死、灶性钙化及不同程度急慢性炎症细胞浸润。胎盘免疫组化C4d染色结果显示,16例SLE孕妇中9例胎盘母儿交界处弥漫性染色、7例局灶性染色,与对照组比较差异有统计学意义(P<0.05);胎盘免疫组化C1q染色结果显示,SLE组与对照组比较差异无统计学意义(P>0.05)。胎盘C4d弥漫性染色的9例SLE孕妇中FGR发生率(55.6%)及早产发生率(66.7%)均高于C4d局灶性染色者,C4d染色阴性的对照组未发现FGR及早产病例。结论:SLE孕妇胎盘母儿交界处C4d大量沉积与围产儿不良结局密切相关,C4d可作为自身抗体介导的妊娠合并SLE围产儿不良结局的生物标记,为有不良妊娠结局的SLE患者再次妊娠的治疗提供依据。
Objective: To investigate the relationship between autoantibodies mediated complement activation and adverse pregnancy outcomes,to improve the outcome of pregnancy.Methods: Placenta pathology and immunohistochemistry of C1 q and C4 d were compared between 16 placentas of pregnant women with SLE and 20 placentas of normal pregnant women accepted in Fujian Provincal Hospital from 2011 Jan. to 2013 Jan. Results: 16 placentas of pregnant women with SLE were found degeneration of villus,partly infartion,thrombopoiesis,partly calcification and acute or chronic inflammatory cell infiltration. C4 d diffuse staining was found in maternal-fetal junction of 9 SLE pregnancies with 7 non-guidance-pregnancy( 77. 8%),2 guidance-pregnancy( 22. 2%),5 FGR( 55. 6%) and 6 preterm delivery( 66. 7%). C4 d focal dyeing was found in 7 pregnancies,which were higher than control group.There was no statistical difference about placentas immunohistochemistry of C1 q staining between two groups. Conclusions: The excessive deposition of C4 d in maternal-fetal junction of SLE pregnancies was associated with poor neonatal outcome,for non-guidance-pregnancy specially,C4 d counld be seemed as a biomarker for autoantibodies mediated adverse fetal outcome and as evidence to improve outcome of secondary pregnancy.
Objective: To investigate the relationship between autoantibodies mediated complement activation and adverse pregnancy outcomes,to improve the outcome of pregnancy.Methods: Placenta pathology and immunohistochemistry of C1 q and C4 d were compared between 16 placentas of pregnant women with SLE and 20 placentas of normal pregnant women accepted in Fujian Provincal Hospital from 2011 Jan. to 2013 Jan. Results: 16 placentas of pregnant women with SLE were found degeneration of villus,partly infartion,thrombopoiesis,partly calcification and acute or chronic inflammatory cell infiltration. C4 d diffuse staining was found in maternal-fetal junction of 9 SLE pregnancies with 7 non-guidance-pregnancy( 77. 8%),2 guidance-pregnancy( 22. 2%),5 FGR( 55. 6%) and 6 preterm delivery( 66. 7%). C4 d focal dyeing was found in 7 pregnancies,which were higher than control group.There was no statistical difference about placentas immunohistochemistry of C1 q staining between two groups. Conclusions: The excessive deposition of C4 d in maternal-fetal junction of SLE pregnancies was associated with poor neonatal outcome,for non-guidance-pregnancy specially,C4 d counld be seemed as a biomarker for autoantibodies mediated adverse fetal outcome and as evidence to improve outcome of secondary pregnancy.
引文
[1]龚非力.医学免疫学[M].第3版.北京:科学出版社,2009:31-39
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[3]Cohen D,Buurma A,Goemaere NN,et al.Classical complement activation as a footprint for murine and human antiphospholipid antibody-induced fetal loss[J].J Pathol,2011,225(4):502-511
[4]卜宪敏,郑智勇,余英豪,等.肝移植排斥反应中C4d的表达意义[J].世界华人消化杂志,2005,13(11):1314-1316
[5]Ornoy A.Maternal autoimmune diseases and immunologically induced embryonic and fetoplacental damage[J].Birth Defects Res A Clin Mol Teratol,2004,70(6):371-381
[6]Buurma A,Cohen D,Veraar K,et al.Preeclampsia is characterized by placental complement dysregulation[J].Hypertension,2012,60(5):1332-1337
[7]Sachiko M,Yoshiki M,Naoki N,et al.Complement split product C4d deposition in placenta in systemic lupus erythematosus and pregnancy-induced hypertension[J].Pathol Int,2013,63(3):150-157
[8]Girardi G,Redecha P,Salmon JE.Heparin prevents antiphospholipid antibody-induced fetal loss by inhibiting complement activation[J].Nat Med,2004,10(11):1222-1226
[9]Kishore U,Sim RB.Factor H as a regulator of the classical pathway activation[J].Immunobiol,2012,217(2):162-168
[10]Davis AE,Lu F,Mejia P.C1 inhibitor,a multi-functional serine protease inhibitor[J].Thromb Haemost,2010,104(5):886-893
[2]Tincani A.Complement Activation and Pregnancy Failure[J].Clinic Rev Allerg Immunol,2010,39(3):153-159
[3]Cohen D,Buurma A,Goemaere NN,et al.Classical complement activation as a footprint for murine and human antiphospholipid antibody-induced fetal loss[J].J Pathol,2011,225(4):502-511
[4]卜宪敏,郑智勇,余英豪,等.肝移植排斥反应中C4d的表达意义[J].世界华人消化杂志,2005,13(11):1314-1316
[5]Ornoy A.Maternal autoimmune diseases and immunologically induced embryonic and fetoplacental damage[J].Birth Defects Res A Clin Mol Teratol,2004,70(6):371-381
[6]Buurma A,Cohen D,Veraar K,et al.Preeclampsia is characterized by placental complement dysregulation[J].Hypertension,2012,60(5):1332-1337
[7]Sachiko M,Yoshiki M,Naoki N,et al.Complement split product C4d deposition in placenta in systemic lupus erythematosus and pregnancy-induced hypertension[J].Pathol Int,2013,63(3):150-157
[8]Girardi G,Redecha P,Salmon JE.Heparin prevents antiphospholipid antibody-induced fetal loss by inhibiting complement activation[J].Nat Med,2004,10(11):1222-1226
[9]Kishore U,Sim RB.Factor H as a regulator of the classical pathway activation[J].Immunobiol,2012,217(2):162-168
[10]Davis AE,Lu F,Mejia P.C1 inhibitor,a multi-functional serine protease inhibitor[J].Thromb Haemost,2010,104(5):886-893