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-Pinto1,*

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

Accepted Article (Accepted, unedited articles published online for future

issues)

ABSTRACT

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. 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. 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. Conclusions: 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-Pinto1,*

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

Accepted Article (Accepted, unedited articles published online for future

issues)

ABSTRACT

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. 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. 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. Conclusions: 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.