PATHWAYS OF COAGULATION ACTIVATION INSITU IN RHEUMATOID SYNOVIAL TISSUE

被引：67

作者：

ZACHARSKI, LR

BROWN, FE

MEMOLI, VA

KISIEL, W

KUDRYK, BJ

ROUSSEAU, SM

HUNT, JA

DUNWIDDIE, C

NUTT, EM

机构：

[1] DARTMOUTH MED SCH, DEPT SURG, WHITE RIVER JCT, VT 05009 USA

[2] DARTMOUTH MED SCH, DEPT PATHOL, WHITE RIVER JCT, VT 05009 USA

[3] VET ADM MED CTR, WHITE RIVER JCT, VT 05009 USA

[4] UNIV NEW MEXICO, SCH MED, DEPT PATHOL, ALBUQUERQUE, NM 87131 USA

[5] NEW YORK BLOOD CTR, PLASMA PROT COAGULAT LAB, NEW YORK, NY 10021 USA

[6] MERCK SHARP & DOHME LTD, DEPT PHARMACOL, W POINT, PA 19486 USA

来源：

CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1992年 / 63卷 / 02期

关键词：

D O I：

10.1016/0090-1229(92)90008-C

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Immunohistochemical techniques were applied to rheumatoid synovium in order to detect components of coagulation and fibrinolysis pathways within these tissues. These techniques revealed an intact coagulation pathway and plasminogen activator inhibitor-2 associated with macrophagelike cells that were present throughout these tissues, especially in subsurface areas. Cell-associated thrombin generation appeared to account for conversion of abundant fibrinogen to fibrin. Occasional macrophage-like cells also stained for urokinase but tissue-type plasminogen activator and plasminogen activator inhibitor-1 were restricted to vascular endothelium. Intense synovial fibrin deposition (with the limited evidence for associated fibrinolysis) may contribute to local inflammation and explain certain clinical features of rheumatoid arthritis. These findings suggest novel treatment hypotheses for this disease. © 1992.

引用

页码：155 / 162

页数：8

共 63 条

[1]

ADANY R, 1989, THROMB HAEMOSTASIS, V62, P850

[2] IMMUNOHISTOCHEMICAL FINDINGS IN RHEUMATOID NODULES [J].