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伴有上皮下胶原层增厚的慢性结肠炎(胶原性结肠炎):15例患者的组织病理学 findings

Chronic colitis with thickening of the subepithelial collagen layer (collagenous colitis): histopathologic findings in 15 patients.

作者信息

Jessurun J, Yardley J H, Giardiello F M, Hamilton S R, Bayless T M

出版信息

Hum Pathol. 1987 Aug;18(8):839-48. doi: 10.1016/s0046-8177(87)80059-x.

Abstract

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. Watery 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.

摘要

对14名女性和1名男性的胶原性结肠炎组织病理学特征进行了研究。除1例患者外,所有患者均有慢性水样腹泻:10例有甲状腺疾病或未明确的关节炎病史。所有15例患者在结直肠活检标本中均显示上皮下胶原层(SCL)增厚,但在结直肠远端,增厚有时不明显或仅为临界状态。所有病例均可见表面上皮的斑片状或弥漫性损伤,且与SCL增厚无关。受损的表面上皮有淋巴细胞浸润,有时还有嗜酸性粒细胞和中性粒细胞浸润,使其类似于乳糜泻时小肠所见的表面上皮损伤。隐窝通常有淋巴细胞浸润,但无相关上皮损伤。所有患者的固有层均有淋巴细胞、浆细胞和嗜酸性粒细胞浸润。7例患者可见中性粒细胞性隐窝炎,但通常较稀疏。8例接受皮质类固醇或柳氮磺胺吡啶治疗的患者水样腹泻减轻,且常伴有表面上皮恢复、表面上皮淋巴细胞减少、SCL增厚减轻和固有层嗜酸性粒细胞减少。治疗并未持续改变其他炎症变化。鉴于以下间接证据,应研究自身免疫在胶原性结肠炎中的可能作用:女性占绝大多数;常存在可能由免疫介导的疾病,如甲状腺和关节疾病;表面上皮变化与乳糜泻相似;以及对皮质类固醇的反应。

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