INCREASED LEVELS OF PLASMA ANAPHYLATOXINS IN SYSTEMIC LUPUS-ERYTHEMATOSUS PREDICT FLARES OF THE DISEASE AND MAY ELICIT VASCULAR INJURY IN LUPUS CEREBRITIS
INCREASED LEVELS OF PLASMA ANAPHYLATOXINS IN SYSTEMIC LUPUS-ERYTHEMATOSUS PREDICT FLARES OF THE DISEASE AND MAY ELICIT VASCULAR INJURY IN LUPUS CEREBRITIS
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DOI：
10.1002/art.1780310508
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发表时间：
1988-05-01
影响因子：
--
通讯作者：
ABRAMSON, SB
中科院分区：
文献类型：
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作者：
HOPKINS, P;BELMONT, HM;ABRAMSON, SB
我们测量了系统性红斑狼疮（SLE）患者循环中补体过敏毒素裂解产物C3 a和C5 a的水平。在23例连续随访的SLE患者中，疾病稳定期的平均C3 a值为179 ng/ml，疾病发作期为550 ng/ml。在10例患者中，C3 a水平预测疾病活动性，C3 a值从疾病稳定时的平均183 ng/ml上升至疾病临床加重前1-2个月的平均242 ng/ml。5例急性中枢神经系统（CNS）功能障碍患者的C3 a水平为1, 297 ng/ml，明显高于无CNS损害的活动性疾病患者（P < 0.01）。4例急性CNS疾病患者的C5 a水平也显著升高。2例死于急性狼疮发作的患者的病理标本显示中性粒细胞阻塞脑血管和肠血管。中枢神经系统狼疮患者的血管造影显示血管闭塞性视网膜病变。在7例妊娠SLE患者中，5例C3 a水平升高，组平均值为310 ng/ml。SLE妊娠患者C3 a和C3水平呈负相关（r = -0.59），这一发现与补体激活导致C3水平下降一致。我们认为，连续测量C3 a可以预测狼疮患者的疾病发作，并可以证明SLE妇女妊娠期间的补体激活。此外，C3 a和C5 a（炎症介质）释放到循环中可能引起血管损伤，特别是在狼疮性脑炎患者中。
We measured levels of complement anaphylatoxin split products, C3a and C5a, in the circulation of patients with systemic lupus erythematosus (SLE). In 23 SLE patients who were followed serially, the mean C3a values was 179 ng/ml during stable disease and 550 ng/ml during a disease flare. In 10 patients, C3a levels predicted disease activity, with the C3a value rising from a mean of 183 ng/ml at a time of stable disease to a mean of 242 ng/ml 1-2 months prior to a clinical exacerbation of disease. The mean C3a level in 5 patients with acute dysfunction of the central nervous system (CNS) was 1,297 ng/ml, which is significantly higher than that observed in patients with active disease but without CNS involvement (P < 0.01). C5a levels were also significantly elevated in 4 patients with acute CNS disease. Pathologic specimens from 2 patients who died during an acute lupus flare revealed neutrophils occluding the cerebral and intestinal vessels. Fluorescein angiography in a patient with CNS lupus revealed vasoocclusive retinopathy. In 5 of 7 SLE patients who were pregnant, C3a levels were elevated, with a group mean value of 310 ng/ml. There was a negative correlation (r = -0.59) between C3a and C3 levels in pregnant patients with SLE, and this finding is consistent with complement activation as the cause of decreasing C3 levels. We suggest that serial measurements of C3a can predict flares of disease in lupus patients and can demonstrate complement activation during pregnancy in women with SLE. In addition, release of C3a and C5a (mediators of inflammation) into the circulation may elicit vascular injury, particularly in patients with lupus cerebritis.