The cellular infiltrate of the jejunum in adult coeliac disease and dermatitis herpetiformis following the reintroduction of dietary gluten.
The cellular infiltrate of the jejunum in adult coeliac disease and dermatitis herpetiformis following the reintroduction of dietary gluten.
复制标题
成人乳糜泻和疱疹样皮炎重新引入膳食麸质后空肠的细胞浸润。
作者：
M. Lancaster;P. Kumar;A. Dawson
对治疗和未治疗的成人乳糜泻和疱疹样皮炎患者的空肠粘膜细胞浸润进行了研究，并连续研究了在饮食中重新添加面筋之前和之后的治疗患者的空肠粘膜细胞浸润。在成人乳糜泻和疱疹样皮炎中，空肠粘膜表现出类似的细胞浸润性异常，其特征是上皮内淋巴细胞、固有层浆细胞和嗜酸性粒细胞增多，以未经治疗的患者最多。在单一的25g面筋蛋白攻击后24-48小时，固有层浆细胞、淋巴细胞、嗜酸性粒细胞和上皮内淋巴细胞增加。除了固有层淋巴细胞外，所有这些细胞组在服用含面筋的饮食七天后都保持了这种上升。这些反应在成人乳糜泻和治疗前有空肠病变的疱疹样皮炎患者中基本上是相似的。在正常饮食下空肠形态正常的疱疹样皮炎患者中，服用额外的谷蛋白后一到三周内，固有层浆细胞和上皮内淋巴细胞有上升的趋势。这些结果与以下观点是一致的，即乳糜泻和疱疹样皮炎的空肠病变的发病机制可能不止一种。
The cellular infiltrate of the jejunal mucosa has been studied in patients with both treated and untreated adult coeliac disease and dermatitis herpetiformis and serially in treated patients before and after the reintroduction of gluten to the diet. In adult coeliac disease and dermatitis herpetiformis the jejunal mucosa showed similar abnormalities of the cellular infiltrate which was characterized by an increase in intraepithelial lymphocytes and lamina propria plasma cells and eosinophils, with the greatest numbers of cells occurring in untreated patients. At 24-48 hours following a single 25-g gluten challenge there was an increase in lamina propria plasma cells, lymphocytes and eosinophils and intraepithelial lymphocytes. This rise was sustained after seven days on a gluten-containing diet for all of these cell groups except lamina propria lymphocytes. These responses were essentially similar in both adult coeliac disease and in those dermatitis herpetiformis patients who had jejunal lesions before treatment. In dermatitis herpetiformis patients with normal jejunal morphology on a normal diet there was an upward trend in lamina propria plasma cells and intraepithelial lymphocytes within one to three weeks of taking extra dietary gluten. These results are compatible with the view that more than one immunological mechanism may be responsible for the pathogenesis of the jejunal lesion of coeliac disease and dermatitis herpetiformis.