Cummins A, Chu G, Faust L, Chandy G, Argyrides J, Robb T, Wilson P
Gastroenterology Unit, Queen Elizabeth Hospital, Woodville South, South Australia.
JPEN J Parenter Enteral Nutr. 1995 May-Jun;19(3):193-8. doi: 10.1177/0148607195019003193.
The purpose of this study was to assess the structure and function of the small intestine before and after enteral feeding given via a percutaneous feeding gastrostomy (PEG). It is not known whether this method of feeding provides a good luminal drive to the small intestine.
Studies were performed of patients at the time of PEG placement, in a cross-sectional group after a period of feeding and in a smaller longitudinal subgroup. Enteral feeds were adjusted in volume and caloric content for each patient. Duodenal biopsies were taken during endoscopy for quantitative morphometry, and lactulose-rhamnose permeability tests were performed during the next day. Duodenal fluid was cultured quantitatively in the first study, and disaccharidases determined in the second study.
The first study of 15 patients, who had enteral feeding for a median (range) period of 13 (8 to 104) weeks, showed partial villous atrophy with normal crypt length, no increase in duodenal bacteriology, and abnormal lactulose-rhamnose sugar permeability due to rhamnose malabsorption. These changes were also present in 38 similar patients before enteral feeding. A second study before enteral feeding showed lowered maltase activity (24 patients), and similar intestinal permeability findings (22 patients). Twelve of these patients were followed longitudinally for 3 months of enteral feeding that maintained but did not improve nutrition, as assessed by body mass index and mid-arm muscle circumference, and there was no change in duodenal morphometry (11 patients), rhamnose malabsorption (4 patients), or disaccharidases (11 patients).
These studies suggest villous atrophy was not due to an inflammatory enteropathy but resulted from a poor luminal "drive" associated with the enteral feeding. Enteral feeding maintained but did not improve nutrition status.
本研究的目的是评估经皮胃造瘘术（PEG）进行肠内喂养前后小肠的结构和功能。目前尚不清楚这种喂养方法是否能为小肠提供良好的腔内驱动力。
对患者在放置PEG时、经过一段时间喂养后的横断面组以及较小的纵向亚组进行研究。根据每位患者的情况调整肠内喂养的体积和热量含量。在内镜检查时取十二指肠活检组织进行定量形态测定，并在次日进行乳果糖-鼠李糖渗透性测试。在第一项研究中对十二指肠液进行定量培养，在第二项研究中测定双糖酶。
第一项研究纳入了15例患者，他们接受肠内喂养的中位（范围）时间为13（8至104）周，结果显示存在部分绒毛萎缩但隐窝长度正常，十二指肠细菌学无增加，且由于鼠李糖吸收不良导致乳果糖-鼠李糖糖渗透性异常。这些变化在38例肠内喂养前的类似患者中也存在。第二项肠内喂养前的研究显示麦芽糖酶活性降低（24例患者），以及类似的肠道渗透性结果（22例患者）。其中12例患者接受了3个月的肠内喂养并进行纵向随访，根据体重指数和上臂中部肌肉周长评估，营养状况得以维持但未改善，十二指肠形态测定（11例患者）、鼠李糖吸收不良（4例患者）或双糖酶（11例患者）均无变化。
这些研究表明绒毛萎缩并非由于炎症性肠病，而是与肠内喂养相关的腔内“驱动力”不足所致。肠内喂养维持了营养状况，但未改善营养状态。
