Bacteria, Bones, and Stones: Managing Complications of Short Bowel Syndrome

Abstract

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.

Small intestine resection increases oxalate and citrate transporter expression and calcium oxalate crystal formation in rat hyperoxaluric kidneys

“…Severe hyperoxaluria in our SB rats was induced by feeding the rats with an oxalogenic diet; this was not a spontaneous formation in terms of the disease progression in SB patients. However, our animal model shared some important features similar to SB patients, such as hypocalcemia, hypocalciuria, hypocitraturia, and hyperoxaluria [ 33 ]. This study only focused on changes related to secondary parathyroidism in our experimental models.…”

Updates on bone health in children with gastrointestinal diseases

“…In children with short-bowel syndrome, prognosis factors include the length of the remnant bowel, bowel condition, preservation of the ileocecal valve, and stomy formation. 21) Usually, a total small-bowel length less than 40cm necessitates more than 2 years of adaptation by the remnant bowel.…”

“…Metabolic changes due to loss of colonic regulation of gastric and small-bowel function lead to depletion of calcium, magnesium, and vitamin D, resulting in demineralization of bone and low BMD. 21) Parenteral nutrition, persistent inflammation, steroid use, chronic metabolic acidosis, and renal insufficiency are additional factors that contribute to development of bone disease in patients with short-bowel syndrome. 21) According to a retrospective study of 36 pediatric intestinal failure patients on parenteral nutrition for more than 30 days, BMD z-score less than -1.0 on DXA scanning was noted in 50% (n=18) of the patients, serum 25(OH) vitamin D level less than 30 ng/mL was found in 63.8%, and pathologic fracture was observed in 11.1% (n=4).…”

“…21) Parenteral nutrition, persistent inflammation, steroid use, chronic metabolic acidosis, and renal insufficiency are additional factors that contribute to development of bone disease in patients with short-bowel syndrome. 21) According to a retrospective study of 36 pediatric intestinal failure patients on parenteral nutrition for more than 30 days, BMD z-score less than -1.0 on DXA scanning was noted in 50% (n=18) of the patients, serum 25(OH) vitamin D level less than 30 ng/mL was found in 63.8%, and pathologic fracture was observed in 11.1% (n=4). 22) In this pediatric study, duration of parenteral nutrition was significantly associated with low BMD.…”

Renal involvement in paediatric inflammatory bowel disease

“…Nephrolithiasis treatment should be directed towards reversing the metabolic abnormalities, such as increasing fluid intake in patients with excessive GI losses to guard against stoma losses and diarrhoea, alkalinisation of urine and citrate administration [10]. Low-fat diet and bile salt sequestrants can help in cases of steatorrhea or bile salt malabsorption, respectively [18].…”