Center for Human Nutrition, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Department of Internal Medicine and Surgery, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA.
Nutr Clin Pract. 2018 Aug;33(4):454-466. doi: 10.1002/ncp.10113. Epub 2018 Jun 21.
Short bowel syndrome (SBS) occurs in patients who have had extensive resection. The primary physiologic consequence is malabsorption, resulting in fluid and electrolyte abnormalities and malnutrition. Nutrient digestion, absorption, and assimilation may also be diminished by disturbances in the production of bile acids and digestive enzymes. Small bowel dilation, dysmotility, loss of ileocecal valve, and anatomical changes combined with acid suppression and antimotility drugs increase the risk of small intestinal bacterial overgrowth, further contributing to malabsorption. Metabolic changes that occur in SBS due to loss of colonic regulation of gastric and small bowel function can also lead to depletion of calcium, magnesium, and vitamin D, resulting in demineralization of bone and the eventual development of bone disease. Persistent inflammation, steroid use, parenteral nutrition, chronic metabolic acidosis, and renal insufficiency may exacerbate the problem and contribute to the development of osteoporosis. Multiple factors increase the risk of nephrolithiasis in SBS. In the setting of fat malabsorption, increased free fatty acids are available to bind to calcium, resulting in an increased concentration of unbound oxalate, which is readily absorbed across the colonic mucosa where it travels to the kidney. In addition, there is an increase in colonic permeability to oxalate stemming from the effects of unabsorbed bile salts. The risk of nephrolithiasis is compounded by volume depletion, metabolic acidosis, and hypomagnesemia, resulting in a decrease in renal perfusion, urine output, pH, and citrate excretion. This review examines the causes and treatments of small intestinal bacterial overgrowth, bone demineralization, and nephrolithiasis in SBS.
短肠综合征（SBS）发生于广泛切除的患者。主要的生理后果是吸收不良，导致液体和电解质异常和营养不良。胆汁酸和消化酶的产生紊乱也可能会影响营养消化、吸收和同化。小肠扩张、运动障碍、回盲瓣丧失以及解剖结构改变，加上酸抑制和抗动力药物的使用，增加了小肠细菌过度生长的风险，进一步导致吸收不良。SBS 中由于结肠对胃和小肠功能的调节丧失而发生的代谢变化也可能导致钙、镁和维生素 D 的消耗，导致骨质脱矿，并最终发展为骨病。持续的炎症、类固醇的使用、肠外营养、慢性代谢性酸中毒和肾功能不全可能会使问题恶化，并导致骨质疏松症的发生。多种因素会增加 SBS 患者肾结石的风险。在脂肪吸收不良的情况下，更多的游离脂肪酸可与钙结合，导致未结合的草酸盐浓度增加，这些草酸盐很容易穿过结肠黏膜被吸收，并在那里进入肾脏。此外，未被吸收的胆盐会导致结肠对草酸盐的通透性增加。肾结石的风险因容量不足、代谢性酸中毒和低镁血症而加剧，导致肾脏灌注、尿量、pH 值和柠檬酸盐排泄减少。本文综述了 SBS 中小肠细菌过度生长、骨质脱矿和肾结石的病因和治疗方法。
