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Liver disease occurs frequently in short bowel syndrome. Whether small bowel dilation in short bowel syndrome could influence the risk of liver injury through increased bacterial translocation remains unknown. Our aim was to analyze associations between small bowel dilation, mucosal damage, bloodstream infections, and liver injury in short bowel syndrome patients.Among short bowel syndrome children (n = 50), maximal small bowel diameter was measured in contrast series and expressed as the ratio to the height of the fifth lumbar vertebra (small bowel diameter ratio), and correlated retrospectively to fecal calprotectin and plasma citrulline—respective markers of mucosal inflammation and mass—bloodstream infections, liver biochemistry, and liver histology.Patients with pathologic small bowel diameter ratio >2.17 had increased fecal calprotectin and decreased citrulline (P < .04 each). Of 33 bloodstream infections observed during treatment with parenteral nutrition, 16 were caused by intestinal bacteria, cultured 15 times more frequently when small bowel diameter ratio was >2.17 (P < .001). Intestinal bloodstream infections were predicted by small bowel diameter ratio (odds ratio 1.88, P = .017), and their frequency decreased after operative tapering procedures (P = .041). Plasma bilirubin concentration, gamma-glutamyl transferase activity, and histologic grade of cholestasis correlated with small bowel diameter ratio (0.356–0.534, P < .014 each), and were greater in the presence of intestinal bloodstream infections (P < .001 for all). Bloodstream infections associated with portal inflammation, cholestasis, and fibrosis grades (P < .031 for each). In linear regression, histologic cholestasis was predicted by intestinal bloodstream infections, small bowel diameter ratio, and parenteral nutrition (β = 0.36–1.29; P < .014 each), while portal inflammation by intestinal bloodstream infections only (β = 0.62; P = .033).In children with short bowel syndrome, small bowel dilation correlates with mucosal damage, bloodstream infections of intestinal origin, and cholestatic liver injury. In addition to parenteral nutrition, small bowel dilation and intestinal bloodstream infections contribute to development of short bowel syndrome-associated liver disease.