HBF is pleased to connect our blog readers to Christine Kukka’s monthly HBV Journal Review that she writes for the HBV Advocate. The journal presents the latest in hepatitis B research, treatment, and prevention from recent academic and medical journals. This month, the following topics are explored:
- Tests for Antigens and Drug-Resistant Virus Emerge as Valuable Diagnostic Tools
- Experts Issue a Report Card on Side Effects from Antivirals
- Experts Weigh in on Why They Prefer Either Antivirals or Interferon
- Doctors Explain Which Medical Guidelines They Follow, Or Ignore
- Truvada Effective in Lowering Viral Load in Young Adults with High Viral Load
- Hepatitis B Causes Most Liver Cancer Deaths in China
- Smoking Shortens Survival after Liver Cancer Surgery
HBV Journal Review
February 1, 2014
Vol 11, no 2
by Christine M. Kukka
Tests for Antigens and Drug-Resistant Virus Emerge as Valuable Diagnostic Tools
Measuring the amount of hepatitis B surface antigen (HBsAg) in your bloodstream or conducting quick tests for drug-resistant hepatitis B virus (HBV) may soon be part of your office visit in the brave new molecular world of hepatitis B treatment.
Doctors increasingly are measuring HBsAg levels to determine if treatment is needed or if current medications are working. HBsAg tests—along with measuring alanine aminotransferase (ALT) for signs of liver damage and HBV DNA for viral load—may become essential tools to assess hepatitis B progression or remission.
HBsAg is the protein that makes up the outer covering of HBV. When a patient has a high viral load (and is positive for the hepatitis B “e” antigen—HBeAg), there are often large quantities of HBsAg circulating in the blood stream. When viral replication slows and HBeAg disappears, there can be lower quantities of HBsAg.
But experts are learning that high HBsAg levels can increase cancer risk, even in HBeAg-negative patients, according to a study published in the journal Annales de Biologie Clinique. (1) As a result, there is heightened attention on HBsAg as a key indicator of a patient’s health. For example:
- In HBeAg-negative patients, HBsAg levels less than 1,000 international units per milliliter (IU/mL) along with low viral load (HBV DNA) under 2,000 IU/mL indicate the patient is an “inactive” patient.
- When patients are treated with pegylated interferon, doctors can tell if the treatment is working if there is a decline in HBsAg levels within 12 weeks. This early indicator can save money if the drug isn’t working and help to avoid uncomfortable side effects. Doctors recommend patients with genotypes B and C should stop interferon at week 12 if their HBsAg levels remain at 20,000 UI/mL or higher.
Another team of French researchers, also exploring the implications of HBsAg in an article published in the February 2014 issue of the journal Liver International, suggest that as HBsAg levels decline, so does the risk of liver cancer.
They also suggest that during antiviral treatment, a rapid decline in HBsAg may indicate which patients will eventually clear HBsAg. A 100-fold decline or more of HBsAg over six months of treatment, “… could be a marker of a sustained response after treatment cessation,” they wrote.(2)
In another diagnostic breakthrough, researchers writing in the December journal of Clinical Molecular Hepatology promoted the value of a HepB Typer-Entecavir kit that can precisely detect HBV that have viral mutations that can “resist” the antiviral drug entecavir (Baraclude). This diagnostic tool allows doctors to select the most effective antiviral for each individual patient based on the molecular makeup of their HBV.(3)
Experts Issue a Report Card on Side Effects from Antivirals
Hong Kong researchers evaluated the side effects of commonly-used antivirals in the December 2013 issue of the Journal of Gastroenterology and Hepatology. Antivirals disrupt the genetic make-up of HBV, making it difficult for the virus to replicate. While generally safe, patients must take antiviral pills daily over several years and side effects include damage to the mitochondria of the body’s cells (called mitochondria toxicity.)