CHRONIC COLITIS WITH THICKENING OF THE SUBEPITHELIAL COLLAGEN LAYER (COLLAGENOUS COLITIS) - HISTOPATHOLOGIC FINDINGS IN 15 PATIENTS
CHRONIC COLITIS WITH THICKENING OF THE SUBEPITHELIAL COLLAGEN LAYER (COLLAGENOUS COLITIS) - HISTOPATHOLOGIC FINDINGS IN 15 PATIENTS
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DOI：
10.1016/s0046-8177(87)80059-x
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发表时间：
1987-08-01
期刊：
影响因子：
3.3
通讯作者：
BAYLESS, TM
中科院分区：
文献类型：
--
作者：
JESSURUN, J;YARDLEY, JH;BAYLESS, TM
研究了14名女性和1名男性胶原性结肠炎的组织病理学特征，除1名患者外，所有患者均表现为慢性水样腹泻，10名患者有甲状腺疾病或不明关节炎病史。所有15例患者在结直肠活检标本中均表现出上皮下胶原层（SCL）的特征性增厚，但在远端结直肠中，增厚有时不存在或呈边界性。在所有病例中均观察到表面上皮的斑片状或弥漫性损伤，并且与SCL增厚无关。损伤的表面上皮细胞被淋巴细胞浸润，并被嗜酸性粒细胞和中性粒细胞浸润，导致其类似于乳糜泻中小肠中观察到的表面上皮损伤。隐窝通常被淋巴细胞浸润，但没有相关的上皮损伤。所有患者的固有层均被淋巴细胞、浆细胞和嗜酸性粒细胞扩张。嗜中性粒细胞隐窝炎被认为是在7名患者，但通常是稀疏的。 水腹泻减轻8例皮质类固醇或柳氮磺胺吡啶治疗，往往是由恢复表面上皮细胞，减少表面上皮淋巴细胞，减少SCL增厚，减少固有层嗜酸性粒细胞。治疗并没有持续改变其他炎症变化。自身免疫在胶原性结肠炎中的可能作用应进行研究，因为有以下间接证据：女性占压倒性优势;经常存在可能的免疫介导的疾病，如甲状腺和关节疾病;表面上皮变化与乳糜泻相似;对皮质类固醇的反应。
The histopathologic features of collagenous colitis were studied in 14 women and one man. All but one patient presented with chronic watery diarrhea; 10 had a history of thyroid disease or unspecified arthritis. All 15 patients showed characteristic thickening of the subepithelial collagen layer (SCL) in colorectal biopsy specimens, but in the distal colorectum the thickening was sometimes absent or borderline. Patchy or diffuse injury to the surface epithelium was seen in all cases and was independent of SCL thickening. The injured surface epithelium was infiltrated by lymphocytes and variably by eosinophils and neutrophils, causing it to resemble the surface epithelial injury seen in the small intestine in celiac disease. Crypts were commonly infiltrated by lymphocytes but without associated epithelial injury. The lamina propria in all patients was expanded by lymphocytes, plasma cells, and eosinophils. Neutrophilic cryptitis was seen in seven patients but was usually sparse. Water diarrhea abated in eight patients treated with corticosteroids or sulfasalazine and was often paralleled by restoration of surface epithelium, reduction in surface epithelial lymphocytes, diminished SCL thickening, and reduced lamina propria eosinophils. Therapy did not consistently alter other inflammatory changes. The possible role of autoimmunity in collagenous colitis should be investigated because of the following circumstantial evidence: the overwhelming female predominance; the frequent presence of possible immunologically mediated disorders such as thyroid and joint disease; the resemblance of surface epithelial changes to those in celiac disease; and the response to corticosteroids.