摘要
目的探讨急性脑梗死(ACI)患者血清中抗心磷脂抗体(ACA)和血浆血栓烷B2(TXB2)、6酮前列腺素1α(6KPGF1α)含量变化及其在ACI致病作用中的相互关系。方法应用酶联免疫吸附法测定143例ACI患者血清ACA及血浆TXB2、6KPGF1α的水平,与59名健康人比较;在ACA阳性的ACI患者中,对有、无卒中危险因素两组之间比较血浆TXB2、6KPGF1α水平。结果(1)ACI组ACA阳性率(46.85%)明显高于对照组(11.63%)(P<0.01);ACA分型中,ACI组IgA、IgG阳性率分别为34.03%、20.78%,也明显高于对照组(6.98%、6.98%)(P<0.01,P<0.05)。(2)ACI组TXB2[(106.54±59.82)pg/ml]较对照组[(77.09±30.39)pg/ml]明显增高(P<0.01),6KPGF1α[(21.30±11.63)pg/ml]较对照组[(28.12±13.63)pg/ml]明显降低(P<0.01),TXB2/6KPGF1α(6.92±7.69)较对照组(4.12±2.67)明显增高(P<0.01);在ACA阳性ACI患者中,有、无卒中危险因素两组之间比较,以上指标差异均无显著性(P>0.05)。结论ACA中IgA可能为主要的ACI致病性抗体;ACA可能通过作用于血管内皮细胞及血小板膜磷脂,影响前列环素与血栓烷A2的代谢及两者间的平衡,诱导血栓形成。
Objective To study the changes and roles of serum anticardiolipin antibodies （ACA） and plasma TXB2,6-K-PGF1α in acute cerebral infarction （ACI）, Methods Serum ACA and plasma TXB2, 6-K-PGF1α levels were measured by enzyme linked immunosorbent assay （ELISA） in 143 patients with ACI and were compared with 59 healthy controls. The patients with ACA positive in ACI group were further divided into subgroup I with stroke risk factors and subgroup Ⅱ without stroke risk factors. The levels of TXB2 and 6-K-PGF1α in the two groups were compared. Results The positive rate of ACA in ACI group （46.85%） was significantly higher than that in control group （ 11.63% ） （P 〈0. 01 ）. The positive rates of ACA-IgA and ACA-IgG in ACI group （ 34.03%, 20.78% ） were also significantly higher than those in control group （ 6.98%, 6.98% ） （ P 〈0.01, P 〈 0. 05 ）. Plasma TXB2 level （ 106.54±9.82pg/ml） in ACI group was significantly higher than that in control group （77.09±30.39 pg/ ml） （P 〈0. 01 ）. Plasma 6-K-PGF1αlevel （21.30±11.63 pg/ml） was significantly lower than that in control group （28.12± 13.63 pg/ml） （P 〈0. 01 ）. The ratio of TXB2/6-K-PGF1α in ACI group （6.92±7.69） was higher than in control group （ 4. 12±2.67 ） （ P 〈0.01 ）. But there wele no remarkable differences of these indexes between subgroup I and subgroup Ⅱ. Conclusions ACA-IgA may play a central role in its etiopathogenesis. ACA induces thrombokinesis by destructing the balance between PGI2 and TXA2, which affects membrane phospholipid of vascular endothelial phagocyte and blood platelet.
出处
《临床神经病学杂志》
CAS
北大核心
2006年第4期281-283,共3页
Journal of Clinical Neurology
