ETIOLOGY AND PATHOGENESIS OF CHRONIC INFLAMMATORY BOWEL-DISEASE

被引:56
|
作者
MACDONALD, TT [1 ]
MURCH, SH [1 ]
机构
[1] QUEEN ELIZABETH HOSP CHILDREN, LONDON E2, ENGLAND
来源
基金
英国惠康基金;
关键词
D O I
10.1016/S0950-3528(06)80017-5
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
While Crohn's disease and ulcerative colitis are both conditions characterized by intestinal inflammation, with some overlap in their clinical and histological features, they are essentially different in pathogenesis. Crohn's disease appears to be primarily a condition of chronic T-lymphocyte activation, with tissue damage induced by secondary macrophage activation. What activates the T-cells is unknown. In this chapter we look at the evidence for and against cell-wall deficient mycobacteria species, viral infection of vascular endothelium and luminal contents as potential mechanisms of chronic activation. In ulcerative colitis, by contrast, there is no strong evidence for T-cell activation, and humoral mechanisms predominate. While the finding of atypical anti-neutrophil cytoplasmic antibodies (P-ANCAs) may be useful in screening, the only novel pathogenetic discovery is the co-localization of a 40 kD colonic autoantibody with immunoglobulins and complement on the apical enterocyte surface. Despite the fundamental differences in initiating mechanisms, the twoconditions have many 'downstream' inflammatory processes in common. We discuss the evidence for local production of cytokines, arachidonic acid metabolites and reactive oxygen and nitrogen radicals, highlighting the potential adverse consequences for intestinal vascular integrity. © 1994 Baillière Tindall. All rights reserved.
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页码:1 / 34
页数:34
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