Rotonya M Carr1, Arpan Patel2, Hillary Bownik3,4, Amanke Oranu3, Caroline Kerner3,5, Amy Praestgaard6,7, Kimberly A Forde3,8, K Rajender Reddy3,9, Gary R Lichtenstein3,10. 1. Division of Gastroenterology, University of Pennsylvania, 421 Curie Boulevard, 907 Biomedical Research Building II/III, Philadelphia, PA, 19104, USA. rotonya.carr@uphs.upenn.edu. 2. UCLA GI Fellowship Training Program, Division of Digestive Diseases, UCLA, 10945 Le Conte Ave, PVUB 2114, MC 694907, Los Angeles, CA, 90095-6949, USA. 3. Division of Gastroenterology, University of Pennsylvania, 421 Curie Boulevard, 907 Biomedical Research Building II/III, Philadelphia, PA, 19104, USA. 4. , 106 W. 14th Street Unit 3002, Kansas City, MO, 64105, USA. 5. Pennsylvania Hospital Gastroenterology, 230 West Washington Square, 4th Floor, Philadelphia, PA, 19106, USA. 6. Biostatistics Analysis Center, University of Pennsylvania, Philadelphia, PA, USA. 7. Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, 518 Blockley Hall 423 Guardian Drive, Philadelphia, PA, 19104, USA. 8. Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, 423 Guardian Drive 722 Blockley Hall, Philadelphia, PA, 19104, USA. 9. Hospital of the University of Pennsylvania, 2 Dulles, 3400 Spruce Street, Philadelphia, PA, 19104, USA. 10. Hospital of the University of Pennsylvania, 7-South Perelman Center, Room 753, One Convention Avenue, Philadelphia, PA, 19104, USA.
Abstract
BACKGROUND AND AIM: Nonalcoholic fatty liver disease (NAFLD) is a common cause of hepatic steatosis in patients with inflammatory bowel disease (IBD). Both metabolic syndrome (MetS) and intestinal inflammation are implicated in NAFLD pathogenesis. METHODS: We performed a retrospective cohort study of patients with IBD and NAFLD seen in our health system from January 1997 to December 2011 to examine associations between IBD severity and phenotype; MetS; and NAFLD fibrosis as estimated by the NAFLD Fibrosis Score (NFS). RESULTS: A total of 84 patients were included in our analysis (24 UC, 60 CD). 23% of patients had MetS. IBD patients with MetS were significantly older at the time of IBD diagnosis (44 vs. 33, p = 0.005) and NAFLD diagnosis (55 vs. 47, p = 0.018). IBD patients with MetS had higher ALT (54 vs. 38 U/L, p = 0.02) and AST (52 vs. 35 U/L, p = 0.004). Comparing MetS patients to non-MetS IBD patients, there was no significant difference between IBD medication use (i.e., steroids, anti-TNFs, and immunomodulators) or NAFLD medication use, other than statins. Both UC and CD patients with concomitant MetS had significantly higher NFS scores than non-MetS patients: UC (-0.4 vs. -2.5, p = 0.02) and CD (-0.8 vs. -2.3, p = 0.03). IBD disease severity, disease location, or IBD medication use was associated with NAFLD severity. CONCLUSIONS: To our knowledge, this is the first study to demonstrate that NAFLD severity in both UC and CD IBD patients is associated with the presence of MetS but not with the severity of IBD.
BACKGROUND AND AIM: Nonalcoholic fatty liver disease (NAFLD) is a common cause of hepatic steatosis in patients with inflammatory bowel disease (IBD). Both metabolic syndrome (MetS) and intestinal inflammation are implicated in NAFLD pathogenesis. METHODS: We performed a retrospective cohort study of patients with IBD and NAFLD seen in our health system from January 1997 to December 2011 to examine associations between IBD severity and phenotype; MetS; and NAFLD fibrosis as estimated by the NAFLD Fibrosis Score (NFS). RESULTS: A total of 84 patients were included in our analysis (24 UC, 60 CD). 23% of patients had MetS. IBD patients with MetS were significantly older at the time of IBD diagnosis (44 vs. 33, p = 0.005) and NAFLD diagnosis (55 vs. 47, p = 0.018). IBD patients with MetS had higher ALT (54 vs. 38 U/L, p = 0.02) and AST (52 vs. 35 U/L, p = 0.004). Comparing MetS patients to non-MetS IBD patients, there was no significant difference between IBD medication use (i.e., steroids, anti-TNFs, and immunomodulators) or NAFLD medication use, other than statins. Both UC and CD patients with concomitant MetS had significantly higher NFS scores than non-MetS patients: UC (-0.4 vs. -2.5, p = 0.02) and CD (-0.8 vs. -2.3, p = 0.03). IBD disease severity, disease location, or IBD medication use was associated with NAFLD severity. CONCLUSIONS: To our knowledge, this is the first study to demonstrate that NAFLD severity in both UC and CD IBD patients is associated with the presence of MetS but not with the severity of IBD.
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