BACKGROUND/AIMS: Questions remain regarding the etiology of steatosis in hepatitis C, and its impact on disease progression and treatment outcomes. METHODS: We evaluated liver biopsies from 574 patients with chronic hepatitis C from a single center. RESULTS: Severity of steatosis was associated with body mass index, HCV genotype 3 infection, age, and duration of infection (P</=0.01). Serum HCV RNA levels were associated with severity of steatosis in HCV genotype 3 infection (P</=0.03). In HCV genotype 1 infection, fibrosis was associated with severity of steatosis (P<0.01), and patients who achieved SVR had lesser degrees of pre-treatment steatosis compared to nonresponders (4.6+/-1.6 vs. 10.1+/-1.1%, P=0.02). Genotype 1 infected patients with an early virologic response were more likely to have grade 0 steatosis compared to those without an early response (71 vs. 42%; P=0.003). Evaluation of paired biopsies demonstrated a marked decline in steatosis in genotype 3 patients who achieved SVR (P<0.01). CONCLUSIONS: In conclusion, steatosis is an important cofactor in hepatitis C as it is associated with fibrosis and reduces the likelihood of achieving early and sustained virologic response in genotype 1 infected patients.
BACKGROUND/AIMS: Questions remain regarding the etiology of steatosis in hepatitis C, and its impact on disease progression and treatment outcomes. METHODS: We evaluated liver biopsies from 574 patients with chronic hepatitis C from a single center. RESULTS: Severity of steatosis was associated with body mass index, HCV genotype 3 infection, age, and duration of infection (P</=0.01). Serum HCV RNA levels were associated with severity of steatosis in HCV genotype 3 infection (P</=0.03). In HCV genotype 1 infection, fibrosis was associated with severity of steatosis (P<0.01), and patients who achieved SVR had lesser degrees of pre-treatment steatosis compared to nonresponders (4.6+/-1.6 vs. 10.1+/-1.1%, P=0.02). Genotype 1 infectedpatients with an early virologic response were more likely to have grade 0 steatosis compared to those without an early response (71 vs. 42%; P=0.003). Evaluation of paired biopsies demonstrated a marked decline in steatosis in genotype 3 patients who achieved SVR (P<0.01). CONCLUSIONS: In conclusion, steatosis is an important cofactor in hepatitis C as it is associated with fibrosis and reduces the likelihood of achieving early and sustained virologic response in genotype 1 infectedpatients.
Authors: Sekou R Rawlins; Ola El-Zammar; J Michael Zinkievich; Nancy Newman; Robert A Levine Journal: Dig Dis Sci Date: 2010-05-12 Impact factor: 3.199
Authors: Aymin Delgado-Borrego; David Healey; Betania Negre; Marielle Christofi; Sabina Sabharwal; David A Ludwig; Raymond T Chung; Maureen M Jonas Journal: J Pediatr Gastroenterol Nutr Date: 2010-08 Impact factor: 2.839
Authors: David R Blais; Rodney K Lyn; Michael A Joyce; Yanouchka Rouleau; Rineke Steenbergen; Nicola Barsby; Lin-Fu Zhu; Adrian F Pegoraro; Albert Stolow; David L Tyrrell; John Paul Pezacki Journal: J Biol Chem Date: 2010-06-08 Impact factor: 5.157
Authors: Ke-Qin Hu; Sue L Currie; Hui Shen; Ramsey C Cheung; Samuel B Ho; Edmund J Bini; John D McCracken; Tim Morgan; Norbert Bräu; Warren N Schmidt; Lennox Jeffers; Teresa L Wright Journal: Dig Dis Sci Date: 2007-01-17 Impact factor: 3.199