See the letter "Hepatocellular Carcinoma Risk of Compensated Cirrhosis Patients with Elevated HBV DNA Levels according to Serum Aminotransferase Levels" on page 1618.
See the reply "The Author's Response: Anti-Viral Therapy for Compensated Liver Cirrhosis Patients with Normal Alanine Aminotransferase" in Volume 31 on page 825.
Dear Editor-in-Chief
We read with a great interest the article written by Lee and colleagues entitled "Hepatocellular Carcinoma Risk of Compensated Cirrhosis Patients with Elevated HBV DNA Levels according to Serum Aminotransferase Levels" which was recently published in your Journal of Korean Medical Science (1). The authors concluded the beneficial effects of prescribing appropriate anti-viral therapy (AVT) for reducing HCC risk in cirrhotic patients with elevated HBV DNA and normal aminotransferase levels. They have done a valuable work with an appropriate sample size which has considered a really challenging and important subject in chronic hepatitis B (CHB) patients. Despite our interest to the results of the Lee et al. study there are some challenging points about their work; so some comments may be of benefit. The first, the authors have claimed that high levels of ALT were associated with higher risk of HCC in patients with high HBV DNA level. Regarding available data, there is an overlap between high ALT and high HBV DNA levels in their study where they both increase the chance of HCC independently (2). Also high ALT level may be related to high HBV DNA level or possible non-alcoholic fatty liver (NAFLD) in the study individuals that will enhance the risk of HCC (3). Due to limitations of retrospective studies, no information was provided regarding patients??BMI by Lee et al. for considering this subject in their study. Another important issue is that the authors have concluded that AVT duration is associated with lower HCC risk in patients with normal aminotransferase levels and suggested prompt AVT to be considered in these patients. This conclusion involves providing more evidence since there are efficient data on higher risk of HCC in chronic hepatitis B patients with high ALT and HBV DNA levels. However, it is difficult to conclude that AVT can have protective effect on HCC in patients with normal ALT level, high HBV DNA level and without liver damage; as it has been shown that these patients could be considered as HBV inactive carriers (IC) regarding treatment (4). On the other hand, it was concluded that treatment naïve patients who underwent AVT may have even higher risk of HCC development than patients with inactive stage CHB (5). Previous data have clarified the role of HBs Ag in differentiation of CHB from IC patients; however it was mentioned not to be cost-effective (6). It was concluded that CHB patients had higher levels of HBV DNA, HBs Ag and ALT levels in comparison with IC patients (6). In conclusion we appreciate the valuable effort of the authors, however we are wondering if we could kindly ask them to interpret better our concerns.
References
1. Lee J, Sinn DH, Kim JH, Gwak GY, Kim HS, Jung SH, Paik YH, Choi MS, Lee JH, Koh KC, et al. Hepatocellular carcinoma risk of compensated cirrhosis patients with elevated HBV DNA levels according to serum aminotransferase levels. J Korean Med Sci. 2015; 30:1618–1624.
2. Hung IF, Poon RT, Lai CL, Fung J, Fan ST, Yuen MF. Recurrence of hepatitis B-related hepatocellular carcinoma is associated with high viral load at the time of resection. Am J Gastroenterol. 2008; 103:1663–1673.
3. Vanni E, Bugianesi E. Obesity and liver cancer. Clin Liver Dis. 2014; 18:191–203.
4. Keshvari M, Alavian SM, Sharafi H. How can we make decision for patients with chronic hepatitis B according to hepatitis B virus (HBV) DNA level? Hepat Mon. 2014; 14:e15285.
5. Cho JY, Paik YH, Sohn W, Cho HC, Gwak GY, Choi MS, Lee JH, Koh KC, Paik SW, Yoo BC. Patients with chronic hepatitis B treated with oral antiviral therapy retain a higher risk for HCC compared with patients with inactive stage disease. Gut. 2014; 63:1943–1950.
6. Sali S, Sharafi H, Alavian SH, Alavian SM, Etesam F, Salimi S, Merza MA, Keshvari M. Can serum level of HBsAg differentiate HBeAg-negative chronic hepatitis B from inactive carrier state. Diagn Microbiol Infect Dis. 2015; 82:114–119.