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牛奶蛋白不耐受婴儿的双糖酶缺乏症。治疗反应。

Disaccharidase deficiency in infants with cow's milk protein intolerance. Response to treatment.

作者信息

Poley J R, Bhatia M, Welsh J D

出版信息

Digestion. 1978;17(2):97-107. doi: 10.1159/000198100.

Abstract

7 infants, aged 5 weeks to 11 months, with clinically documented intolerance to cow's milk protein, chronic diarrhea, and failure to thrive, underwent small intestinal (peroal, suction) biopsy before and after withdrawal of milk proteins. Mucosal specimens were examined by light microscopy and assayed for disaccharidase activities. In all patients, moderate to severe mucosal changes were presented, associated with marked inflammation of lamina propria and damages to the brushborder. Disaccharidase activities (lactase, sucrase, maltase and palatinase) were markedly depressed in all. Follow-up biopsies were obtained in 6 infants, after 3-5 months on a milk-protein-free diet. At the time of the second biopsy, the disaccharidase activities had risen significantly and histologic improvement had occurred in each instance. In infancy, intestinal mucosal lesions due to intolerance to cow's milk protein are histologically indistinguishable from those seen in gluten-sensitive enteropathy and are associated with marked secondary disaccharidase deficiencies. Following therapy, the activity of the disaccharidases become normal or near normal prior to the complete morphologic recovery of the small intestinal mucosa.

摘要

7名年龄在5周至11个月之间的婴儿,临床上有对牛奶蛋白不耐受、慢性腹泻和发育不良的记录,在停用牛奶蛋白前后接受了小肠(经口、抽吸)活检。对黏膜标本进行了光学显微镜检查并测定了双糖酶活性。所有患者均出现中度至重度黏膜改变,伴有固有层明显炎症和刷状缘损伤。所有患者的双糖酶活性(乳糖酶、蔗糖酶、麦芽糖酶和帕拉金酶)均显著降低。6名婴儿在无牛奶蛋白饮食3至5个月后进行了随访活检。在第二次活检时,双糖酶活性显著升高,且每次组织学均有改善。在婴儿期,因牛奶蛋白不耐受导致的肠道黏膜病变在组织学上与麸质敏感性肠病所见病变无法区分,且与明显的继发性双糖酶缺乏有关。治疗后,在小肠黏膜完全形态恢复之前,双糖酶活性恢复正常或接近正常。

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