Individuals infected with the hepatitis C virus who have a higher ratio of alanine aminotransferase to aspartate aminotransferase may be at greater risk of developing nonalcoholic fatty liver disease and hepatosteatosis, new data suggest.
A community-based observational study in 1,354 Taiwanese individuals seropositive for hepatitis C virus – including 433 with nonalcoholic fatty liver disease – found a high alanine aminotransferase to aspartate aminotransferase ratio was significantly and independently associated with nonalcoholic fatty liver disease (OR, 1.90; 95% CI, 1.37 to 2.65; P less than .001) and high-degree nonalcoholic fatty liver disease (OR, 2.44; 95% CI, 1.58 to 3.77; P less than .001).
This effect was observed even after researchers accounted for potential confounders: age, body mass index, metabolic syndrome, cholesterol level, hepatitis B virus infection, and smoking.
The study found the ALT/AST ratio was significantly higher among patients with nonalcoholic fatty liver disease (1.2 ± 0.4 vs. 1.1 ± 0.4; P less than .001) – defined as hepatic steatosis by echogenic imaging – according to a paper published online Sept. 14 in BMJ Open.
Nonalcoholic fatty liver disease is a particular issue because not only can it progress to severe liver disease but it is also associated with a lower likelihood of achieving a sustained virologic response to antiviral therapy. In addition, the majority of cases of nonalcoholic fatty liver disease are silent and are discovered incidentally, the authors wrote.
“This is the first study to reveal a strong relationship between the ALT/AST ratio and NAFLD in patients with HCV, and the ALT/AST ratio was also an independent risk factor apart from the conventional risk factors for hepatosteatosis including the MetS [metabolic syndrome], LDL, TC, waist/hip ratio, and body mass index,” wrote Dr. Ming-Shyan Lin of Chang Gung Memorial Hospital, Taiwan, and coauthors.
While the AST/ALT ratio is a marker of liver cirrhosis and advanced liver disease, the ALT/AST ratio is also a marker for insulin resistance and metabolic syndrome.
Researchers also noted that individuals with hepatitis C infection and nonalcoholic fatty liver disease had a significantly higher incidence of metabolic syndrome, significantly higher fasting glucose, uric acid, and triglycerides, and a lower HDL than did those with low-degree nonalcoholic fatty liver disease.
“The prevalence of hepatosteatosis in chronic hepatitis C infection has been reported in up to 31%-72%, which is significantly higher than that in participants with other chronic liver disease such as hepatitis B or autoimmune hepatitis, suggesting a direct effect of HCV replication in the development of excess fat accumulation in the liver,” the authors wrote.
In this cohort, the prevalence of nonalcoholic fatty liver disease was 31.9%, and 19.6% of participants had moderate to severe hepatosteatosis (BMJ Open 2015, Sep 14. doi:10.1136/bmjopen-2015-008797).
Given the silent nature of nonalcoholic fatty liver disease, the authors suggested that the findings could help clinicians identify individuals with hepatosteatosis and implement interventions such as weight loss to reduce their risk of further progression.
No conflicts of interest were declared.