Raluca Pais1, Elena Rusu2, Diana Zilisteanu3, Alexandra Circiumaru4, Laurentiu Micu5, Mihai Voiculescu6, Thierry Poynard7, Vlad Ratziu8. 1. Université Pierre et Marie Curie, Hôpital Pitié Salpêtrière, Paris, France; INSERM, UMRS 938, Paris, France. Electronic address: ralu_pais@yahoo.com. 2. "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania; Clinic of Internal Medicine and Nephrology, Fundeni Clinical Institute, Bucharest, Romania. Electronic address: ela.rusu@gmail.com. 3. "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania; Clinic of Internal Medicine and Nephrology, Fundeni Clinical Institute, Bucharest, Romania. Electronic address: diamicu@gmail.com. 4. Clinic of Internal Medicine and Nephrology, Fundeni Clinical Institute, Bucharest, Romania. Electronic address: alexandra.circiumaru@gmail.com. 5. Clinic of Internal Medicine and Nephrology, Fundeni Clinical Institute, Bucharest, Romania. Electronic address: laurentiumicu2000@yahoo.com. 6. "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania; Clinic of Internal Medicine and Nephrology, Fundeni Clinical Institute, Bucharest, Romania. Electronic address: mihaiv45@gmail.com. 7. Université Pierre et Marie Curie, Hôpital Pitié Salpêtrière, Paris, France; INSERM, UMRS 938, Paris, France. Electronic address: tpoynard@teaser.fr. 8. Université Pierre et Marie Curie, Hôpital Pitié Salpêtrière, Paris, France; INSERM, UMRS 938, Paris, France. Electronic address: vlad.ratziu@upmc.fr.
Abstract
UNLABELLED: The association of NAFLD with chronic hepatitis C (CHC) has been extensively studied but little is known about its coexistence with chronic hepatitis B (CHB). AIMS: To investigate the prevalence and determinants of steatosis and insulin resistance (IR) in CHB and its consequences on liver injury compared with CHC and NAFLD. METHODS: Patients with CHB (N=110), CHC (N=111) and NAFLD (N=136) were evaluated by biomarkers of steatosis (SteatoTest>0.38 as a surrogate for steatosis >5%), IR (HOMA-IR>2.7 as a surrogate for IR) and fibrosis (FibroTest>0.48 as a surrogate for significant fibrosis, ≥F2). RESULTS: HOMA-IR gradually increased in CHB, CHC and NAFLD: 2.3±1.8; 3±2.6 and 3.8±2.7 (p<0.001). The prevalence of steatosis >5% was 21% (CHB), 43% (CHC) and 82% (NAFLD), (p<0.001). The prevalence of fibrosis≥F2 was 10% (CHB), 42% (CHC) and 21% (NAFLD), p<0.001. In CHB, IR was related to host and not viral factors. CHB patients with steatosis had higher BMI (29±5.7kg/m(2) vs. 24±4kg/m(2), p<0.001), waist circumference (96±14cm vs. 84±11cm, p=0.001) and HOMA-IR (3.9±2.6 vs. 1.8±1.2, p<0.001) than those without steatosis. HOMA-IR independently predicted steatosis in CHB (OR=1.9, 95% CI, 1.09-3.27, p<0.05) and CHC (OR=1.38; 95% CI, 1.07-1.78, p<0.02). In CHB, metabolic risk factors and HOMA-IR were not associated with significant fibrosis. HOMA-IR was an independent predictor of fibrosis in CHC. CONCLUSIONS: Steatosis may co-exist in CHB patients but with a lower prevalence than in CHC and NAFLD. In CHB steatosis is related to host and not viral factors, and is not associated with the severity of fibrosis.
UNLABELLED: The association of NAFLD with chronic hepatitis C (CHC) has been extensively studied but little is known about its coexistence with chronic hepatitis B (CHB). AIMS: To investigate the prevalence and determinants of steatosis and insulin resistance (IR) in CHB and its consequences on liver injury compared with CHC and NAFLD. METHODS:Patients with CHB (N=110), CHC (N=111) and NAFLD (N=136) were evaluated by biomarkers of steatosis (SteatoTest>0.38 as a surrogate for steatosis >5%), IR (HOMA-IR>2.7 as a surrogate for IR) and fibrosis (FibroTest>0.48 as a surrogate for significant fibrosis, ≥F2). RESULTS: HOMA-IR gradually increased in CHB, CHC and NAFLD: 2.3±1.8; 3±2.6 and 3.8±2.7 (p<0.001). The prevalence of steatosis >5% was 21% (CHB), 43% (CHC) and 82% (NAFLD), (p<0.001). The prevalence of fibrosis≥F2 was 10% (CHB), 42% (CHC) and 21% (NAFLD), p<0.001. In CHB, IR was related to host and not viral factors. CHB patients with steatosis had higher BMI (29±5.7kg/m(2) vs. 24±4kg/m(2), p<0.001), waist circumference (96±14cm vs. 84±11cm, p=0.001) and HOMA-IR (3.9±2.6 vs. 1.8±1.2, p<0.001) than those without steatosis. HOMA-IR independently predicted steatosis in CHB (OR=1.9, 95% CI, 1.09-3.27, p<0.05) and CHC (OR=1.38; 95% CI, 1.07-1.78, p<0.02). In CHB, metabolic risk factors and HOMA-IR were not associated with significant fibrosis. HOMA-IR was an independent predictor of fibrosis in CHC. CONCLUSIONS:Steatosis may co-exist in CHB patients but with a lower prevalence than in CHC and NAFLD. In CHB steatosis is related to host and not viral factors, and is not associated with the severity of fibrosis.
Authors: Michael O Baclig; Karen G Reyes; Veni R Liles; Cynthia A Mapua; Mark Pierre S Dimamay; Juliet Gopez-Cervantes Journal: Int J Mol Epidemiol Genet Date: 2018-04-05
Authors: Joachim Lupberger; Tom Croonenborghs; Armando Andres Roca Suarez; Nicolaas Van Renne; Frank Jühling; Marine A Oudot; Alessia Virzì; Simonetta Bandiera; Carole Jamey; Gergö Meszaros; Daniel Brumaru; Atish Mukherji; Sarah C Durand; Laura Heydmann; Eloi R Verrier; Hussein El Saghire; Nourdine Hamdane; Ralf Bartenschlager; Shaunt Fereshetian; Evelyn Ramberger; Rileen Sinha; Mohsen Nabian; Celine Everaert; Marko Jovanovic; Philipp Mertins; Steven A Carr; Kazuaki Chayama; Nassim Dali-Youcef; Romeo Ricci; Nabeel M Bardeesy; Naoto Fujiwara; Olivier Gevaert; Mirjam B Zeisel; Yujin Hoshida; Nathalie Pochet; Thomas F Baumert Journal: Gastroenterology Date: 2019-04-09 Impact factor: 33.883