Hepatic steatosis in hepatitis B virus infected patients: Meta-analysis of risk factors and comparison with hepatitis C infected patients

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1746.2011.06801.x/abstract

Hepatic steatosis in hepatitis B virus infected patients: Meta-analysis of risk

factors and comparison with hepatitis C infected patients

na V Machado1, António G Oliveira2, Helena Cortez-Pinto1Article first

published online: 25 AUG 2011

DOI: 10.1111/j.1440-1746.2011.06801.x

© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell

Publishing Asia Pty Ltd

Issue

Journal of Gastroenterology and Hepatology

Volume 26, Issue 9, pages 1361–1367, September 2011

Abstract

Background and Aims:  Although hepatic steatosis (HS) has an association with

hepatitis C virus (HCV) infection, an association with hepatitis B virus (HBV)

is controversial. We performed a meta-analysis to evaluate HS prevalence and

risk factors, in HBV infection.

Methods:  Standard guidelines for performance of meta-analyses were followed.

Studies with HS assessed by histology were included. Pooled odd ratios (OR) and

standardized mean differences (SMD) were obtained with the random-effects model

and DerSimonian-Laid method.

Results:  Seventeen out of 21 studies were included, comprising 4100 HBV

infected patients. Overall HS prevalence was 29.6%. Eight studies also included

945 HCV infected patients, showing decreased risk of HS in HBV versus HCV

patients (OR 0.55, 95%CI [0.45–0.67], P < 0.001). In HBV, HS positively

associated with male gender (OR 1.74, 95%CI [1.28–2.38], P < 0.001), body mass

index (SMD 2.17, 95%CI [1.23, 3.11], P < 0.001), obesity (OR 6.59, 95%CI

[3.51–12.257], P = 0.003), diabetes (OR 2.62, 95%CI [1.37–4.00], P = 0.004),

glycemia (SMD 0.84, 95%CI [0.00, 1.67], P = 0.049), triglycerides (SMD 1.18,

95%CI [0.48, 1.89], P = 0.001), cholesterol (SMD 0.88, 95%CI [0.31, 1.45], P =

0.003), moderate alcohol consumption (OR 1.54, 95%CI [1.10–2.15], P = 0.011)

and negatively with HBV DNA (SMD −74.12, 95%CI [−82.93, −65.31], P <

0.001). HS had no association with aminotransferases, HBeAg, genotype or hepatic

histology, necroinflammation or fibrosis.

Conclusion:  HS in HBV seems to be as frequent as in the general population,

and lower than in HCV infected patients, relating to metabolic factors but not

with hepatic histology severity. A puzzling strong negative association between

viral load and HS, may even suggest a protective effect of the virus on HS.

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1746.2011.06801.x/abstract

Hepatic steatosis in hepatitis B virus infected patients: Meta-analysis of risk

factors and comparison with hepatitis C infected patients

na V Machado1, António G Oliveira2, Helena Cortez-Pinto1Article first

published online: 25 AUG 2011

DOI: 10.1111/j.1440-1746.2011.06801.x

© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell

Publishing Asia Pty Ltd

Issue

Journal of Gastroenterology and Hepatology

Volume 26, Issue 9, pages 1361–1367, September 2011

Abstract

Background and Aims:  Although hepatic steatosis (HS) has an association with

hepatitis C virus (HCV) infection, an association with hepatitis B virus (HBV)

is controversial. We performed a meta-analysis to evaluate HS prevalence and

risk factors, in HBV infection.

Methods:  Standard guidelines for performance of meta-analyses were followed.

Studies with HS assessed by histology were included. Pooled odd ratios (OR) and

standardized mean differences (SMD) were obtained with the random-effects model

and DerSimonian-Laid method.

Results:  Seventeen out of 21 studies were included, comprising 4100 HBV

infected patients. Overall HS prevalence was 29.6%. Eight studies also included

945 HCV infected patients, showing decreased risk of HS in HBV versus HCV

patients (OR 0.55, 95%CI [0.45–0.67], P < 0.001). In HBV, HS positively

associated with male gender (OR 1.74, 95%CI [1.28–2.38], P < 0.001), body mass

index (SMD 2.17, 95%CI [1.23, 3.11], P < 0.001), obesity (OR 6.59, 95%CI

[3.51–12.257], P = 0.003), diabetes (OR 2.62, 95%CI [1.37–4.00], P = 0.004),

glycemia (SMD 0.84, 95%CI [0.00, 1.67], P = 0.049), triglycerides (SMD 1.18,

95%CI [0.48, 1.89], P = 0.001), cholesterol (SMD 0.88, 95%CI [0.31, 1.45], P =

0.003), moderate alcohol consumption (OR 1.54, 95%CI [1.10–2.15], P = 0.011)

and negatively with HBV DNA (SMD −74.12, 95%CI [−82.93, −65.31], P <

0.001). HS had no association with aminotransferases, HBeAg, genotype or hepatic

histology, necroinflammation or fibrosis.

Conclusion:  HS in HBV seems to be as frequent as in the general population,

and lower than in HCV infected patients, relating to metabolic factors but not

with hepatic histology severity. A puzzling strong negative association between

viral load and HS, may even suggest a protective effect of the virus on HS.