DNA-guided hepatitis B treatment, viral load is essential, but not sufficient

Abstract

Hepatitis B virus (HBV) infection is a global public health problem that concerns 350 million people worldwide. Individuals with chronic hepatitis B (CHB) are at increased risk of developing liver cirrhosis, hepatic de-compensation and hepatocellular carcinoma. To maintain undetectable viral load reduces chronic infection complications. There is no treatment that eradicates HBV infection. Current drugs are expensive, are associated with adverse events, and are of limited efficacy. Current guidelines try to standardize the clinical practice. Nevertheless, controversy remains about management of asymptomatic patients with CHB who are hepatitis B e antigen (HBeAg)-positive with normal alanine aminotransferase, and what is the cut-off value of viral load to distinguish HBeAg-negative CHB patients and inactive carriers. We discuss in detail why DNA level alone is not sufficient to begin treatment of CHB.

Keywords: Hepatitis B virus, Viral DNA, Alanine transaminase, Antiviral drug, Hepatitis B e antigen, Antiviral drug resistance

INTRODUCTION

Hepatitis B virus (HBV) infection is a global public health problem. An estimated 350 million people worldwide are chronically infected with HBV. Approximately 500 000 die annually from HBV-related liver disease[1]. The prevalence and concerns to public health institutions about HBV infection vary according to geographical origin.

Individuals with chronic hepatitis B (CHB) are at increased risk of developing serious problems including liver cirrhosis, hepatic de-compensation and hepatocellular carcinoma (HCC). Fifteen to forty percent of these individuals will develop serious sequelae during their lifetime and have greater evolution to cirrhosis or HCC[2,3]. The 5-year rate of progression from CHB to cirrhosis is estimated to be 12%-20%[4–7]. In patients with cirrhosis, the 5-year cumulative risk of developing HCC is 17% in East Asia and 10% in Western Europe and the United States, and the 5-year liver-related death rate is 15% in Europe and 14% in East Asia[8,9]. Seropositivity for the hepatitis B surface antigen (HBsAg) is one of the most important risk factors for HCC[10]. Seropositivity for hepatitis B e antigen (HBeAg) is associated with an increased risk for HCC, and it is significant regardless of serum level of alanine aminotransferase (ALT) and status of liver cirrhosis[8,10,11]. The risk of progression appears to be greatest in patients who progress from an immunotolerant to an immune-clearance phase[12], in patients who have delayed HBeAg seroconversion[13], and in patients who have reactivation of HBV replication after HBeAg seroconversion[14–16].

Disease progression is variable and multifactorial. It is influenced by several factors including replicating activity of the virus, and host and environmental factors[17]. Four phases of CHB have been defined: immunotolerant phase, immune active phase, HBeAg seroconversion to anti-HBeAg, and inactive carrier.

MELASMA DIAGNOSIS AND TREATMENT

How do dermatologists diagnose melasma?

Dermatologists can diagnose most patients by looking at their skin. To see how deeply the melasma penetrates the skin, your dermatologist may look at your skin under a device called a Wood’s light.

Sometimes melasma can look like another skin condition. To rule out another skin condition, your dermatologist may need to remove a small bit of skin. This procedure is called a biopsy. A dermatologist can safely and quickly perform a biopsy during an office visit.

How do dermatologists treat melasma?

Melasma can fade on its own. This often happens when a trigger is causing the melasma, such as a pregnancy or birth control pills. When the woman delivers the baby or stops taking the birth control pills, melasma can fade. 

Some people, however, have melasma for years — or even a lifetime. If the melasma does not go away or a woman wants to keep taking birth control pills, melasma treatments are available. These include: