Levy R A, Qamar T, Lockshin M D
Hospital for Special Surgery, Cornell University Medical Center, New York, New York.
Clin Exp Rheumatol. 1990 Jan-Feb;8(1):11-5.
To test whether alternative complement pathway activation explains normal C1s-C1 inhibitor complex in hypocomplementemic (low CH50cl) patients with systemic lupus erythematosus, we examined alternative pathway hemolytic complement (CH50alt) factor B, and Ba fragment in hypocomplementemic sera with normal and with elevated C1s-C1 inhibitor complex. Sera with and without high C1s-C1 inhibitor complex were similar in CH50cl, C3, and C4. There was little evidence for important alternative complement pathway activation in either group, but patients with classical pathway activation (elevated C1s-C1 inhibitor complex) had slightly lower CH50alt and slightly higher factor B and Ba compared to patients with normal C1s-C1 inhibitor complex. Pregnant patients did not differ from non-pregnant patients. Alternative complement pathway activation does not account for hypocomplementemia in this group of patients.
为了检验替代补体途径激活是否能解释系统性红斑狼疮低补体血症（低CH50cl）患者中正常的C1s-C1抑制剂复合物，我们检测了具有正常及升高的C1s-C1抑制剂复合物的低补体血症血清中的替代途径溶血补体（CH50alt）、因子B和Ba片段。具有和不具有高C1s-C1抑制剂复合物的血清在CH50cl、C3和C4方面相似。两组中均几乎没有证据表明存在重要的替代补体途径激活，但与C1s-C1抑制剂复合物正常的患者相比，经典途径激活（C1s-C1抑制剂复合物升高）的患者CH50alt略低，因子B和Ba略高。孕妇与非孕妇没有差异。替代补体途径激活并不能解释这组患者的低补体血症。
