Poley J R, Hofmann A F
Gastroenterology. 1976 Jul;71(1):38-44.
To clarify the role of fat maldigestion in the pathogenesis of steatorrhea in patients with ileal resection the total and aqueous phase concentrations of bile acid and fatty acid were characterized in 8 such patients (5 patients with small ileal resection, bile acid diarrhea, and steatorrhea less than 20 g per day; 3 patients with large ileal resection, fatty acid diarrhea, and steatorrhea greater than 20 g per day) as well as 4 healthy control subjects after a morning and an afternoon liquid test meal. The study was then repeated with cholestyramine, 4 g being administered before each meal to induce fat maldigestion. After a conventional test meal, patients with large resections and severe steatorrhea had significantly lower aqueous phase concentrations of bile acids (and fatty acids) than patients with smaller resections or control subjects, explained in part by intraluminal precipitation of about one-half of the bile acids during digestion. When cholestyramine was administered before the meal, aqueous phase bile acid concentrations decreased in all patients, including the normal control subjects; the degree of fat maldigestion induced in the patients with small resections (and the control subjects) became similar to that present after the conventional test meal in the patients with large resections. Because steatorrhea increased little in the patients with small resections when cholestyramine was administered continuously, the data suggest that fat maldigestion per se does not induce severe fat malabsorption in patients with sufficient anatomical reserve, because such patients can absorb fat efficiently by utilizing the distal small intestine. In patients with large ileal resections, severe steatorrhea is explained in part by the combination of fat maldigestion and decreased surface area. It is also speculated that the steatorrhea occurring in patients with small resections and relatively normal fat digestion during two test meals may be explained by impaired fat digestion which occurs during the final meal of the day, which is often the largest meal.
为阐明脂肪消化不良在回肠切除术后患者脂肪泻发病机制中的作用,对8例此类患者(5例小肠切除、胆汁酸腹泻且每日脂肪泻少于20克;3例大肠切除、脂肪酸腹泻且每日脂肪泻大于20克)以及4名健康对照者在早、晚两次液体试验餐后的胆汁酸和脂肪酸的总浓度及水相浓度进行了测定。然后用消胆胺重复该研究,每餐饭前给予4克以诱导脂肪消化不良。在常规试验餐后,大肠切除且脂肪泻严重的患者胆汁酸(和脂肪酸)的水相浓度显著低于小肠切除患者或对照者,部分原因是消化过程中约一半的胆汁酸在肠腔内沉淀。当饭前给予消胆胺时,所有患者包括正常对照者的水相胆汁酸浓度均降低;小肠切除患者(和对照者)诱导的脂肪消化不良程度与大肠切除患者常规试验餐后的程度相似。由于持续给予消胆胺时小肠切除患者的脂肪泻增加不多,数据表明对于有足够解剖学储备的患者,脂肪消化不良本身不会导致严重的脂肪吸收不良,因为这类患者可通过利用远端小肠有效吸收脂肪。在大肠切除的患者中,严重脂肪泻部分是由脂肪消化不良和表面积减少共同导致的。还推测小肠切除且在两次试验餐期间脂肪消化相对正常的患者出现的脂肪泻可能是由一天中最后一餐(通常是最大的一餐)期间发生的脂肪消化受损所解释的。