Poller D N, Armitage N C
Department of Histopathology, Queen's Medical Centre, Nottingham, England.
Arch Pathol Lab Med. 1993 May;117(5):550-2.
A case of Crohn's colitis with mural bridging lesions is described. The bridging lesions comprised colonic-type mucosa, smooth muscle, nerve fibers, with foci of adipose tissue and fibrous connective tissue. The lesions arose from the muscularis propria proximal to colonic strictures and possibly due to diverticular outpouching of the colonic wall associated with increased intraluminal pressure, although the exact mechanism of their formation appears unclear. This entity has not been previously described in inflammatory bowel disease, to our knowledge. Bridging pseudopolyps are seen in ulcerative colitis and rarely in Crohn's disease but do not contain substantial amounts of smooth muscle and/or nerve fibers. We believe that the mural bridges described in this article represent residual muscularis propria at the site of diverticular formation due to long-standing Crohn's colitis. We speculate that the stricture formation seen distal to the site of the mural bridging lesions may have been an important factor in formation of the colonic diverticula and, hence, these lesions that we interpret as representing residual muscularis propria adjacent to sites of diverticular formation in long-standing Crohn's colitis.
本文描述了一例患有肠壁桥接病变的克罗恩结肠炎病例。桥接病变由结肠型黏膜、平滑肌、神经纤维组成，并伴有脂肪组织和纤维结缔组织灶。这些病变起源于结肠狭窄近端的固有肌层，可能是由于肠腔内压力增加导致结肠壁憩室样膨出，尽管其确切形成机制尚不清楚。据我们所知，这种情况在炎症性肠病中此前尚未有过描述。桥接假息肉可见于溃疡性结肠炎，在克罗恩病中少见，且不包含大量平滑肌和/或神经纤维。我们认为本文所述的肠壁桥是由于长期克罗恩结肠炎导致憩室形成部位的固有肌层残留。我们推测，在肠壁桥接病变部位远端出现的狭窄形成可能是结肠憩室形成的一个重要因素，因此，我们将这些病变解释为长期克罗恩结肠炎中与憩室形成部位相邻的固有肌层残留。
