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Tag Archives: HBsAg

You’ve Lost the Hepatitis B Surface Antigen, Go Celebrate, But Keep Monitoring

By Christine Kukka

Image courtesy of stockimages at FreeDigitalPhotos.net
Image courtesy of stockimages at FreeDigitalPhotos.net

After years of living with “inactive’ chronic hepatitis B—with low viral load and no signs of liver damage–some patients may finally lose the hepatitis B surface antigen (HBsAg) and even develop surface antibodies.

This event merits a celebration and a huge sigh of relief, but if you think you will never have to get another blood draw or worry about your liver, think again. We hate to be the bearer of bad news, but hepatitis B really never goes away.

Image courtesy of stockimages at FreeDigitalPhotos.net
Image courtesy of stockimages at FreeDigitalPhotos.net

Think herpes, mono, or chicken pox and shingles. Children infected with chickenpox get rid of the infection and the ugly blisters, but very small amounts of the chickenpox (varicella) virus remains in the spinal nerves. As we grow older and our immune systems weaken with age,  our bodies aren’t able to suppress the varicella virus any more and it reactivates, causing painful shingles.

The hepatitis B virus (HBV) behaves in the same way. When we lose HBsAg and even develop surface antibodies (anti-HBs), there are still HBV lurking in our livers. When we’re healthy, our immune systems suppress the virus and prevent any reactivation, but old age or another disease or medical condition can weaken our bodies and allow the viral infection to reactivate.

So, even after we clear HBsAg, we need to stay vigilant and continue to get our liver health monitored regularly. Here is what you need to know:

First, what are my chances of ever getting rid of HBsAg and developing the surface antibody? It can happen, especially in older adults after a long period of “inactive” hepatitis B infection.

About 1 to 3 percent of people with chronic hepatitis B lose HBsAg each year, and about half of all people with chronic infections who live up to age 75 will lose HBsAg, depending on the amount of HBV DNA in their blood.

Your chances of losing HBsAg and developing the surface antibody increase if you have a healthy lifestyle and avoid alcohol, cigarettes and obesity (fatty liver). Another report found that people with the hepatitis B strain or genotype C have higher rates of clearing HBsAg over time than those with genotype B.

Image courtesy of taoty at FreeDigitalPhotos.net
Image courtesy of taoty at FreeDigitalPhotos.net

Once you clear HBsAg, the chance of developing surface antibodies over the next two, five and 10 years are 24 percent, 58 percent and 78 percent respectively, according to a recent report in the September 2016 journal of Epidemiology and Infection.

After I clear HBsAg, how often do I need to get my liver health monitored? According to Dr. Robert Gish, medical director of the Hepatitis B Foundation and professor consultant of gastroenterology and hepatology at Stanford University, once you have cleared HBsAg, 12 months later you need to:

  • Check all of your liver enzymes and liver function
  • Get your platelet count and hepatitis B blood tests done, and
  • Have an ultrasound of your liver and spleen.

These tests become your new “baseline” that your doctor can refer too in the years ahead while monitoring your liver health.

Your baseline ultrasound should examine your liver and measure its portal vein (it should be under 12 mm) and spleen (it should be under 12 cm) to make sure it’s normal with no signs of cirrhosis or portal hypertension.

If you had cirrhosis before you cleared HBsAg: You need to be surveyed for liver cancer (with an ultrasound, alpha fetoprotein (AFP) blood test and a Des-gamma-carboxy prothrombin (DCP) test) every six months for at least five years, because cirrhosis puts you at high risk of liver cancer. Once an ultrasound finds no evidence of cirrhosis and all other tests are normal, including the cancer tests, then the testing can become less frequent and your doctor can prescribe a new monitoring schedule.

If you’ve had elevated liver enzymes (called ALT or SGPT) in the past, (higher than 19 in women and 30 in men), you need to continue to get tested every six months until you’ve had two consecutive healthy ALT readings. If your ALT remains elevated, make sure you are not drinking alcohol and do not have fatty liver disease. Talk to your doctor about a new monitoring schedule.

Tell all of your current and future doctors you’ve had hepatitis B, and beware of immune-suppressing drugs used to treat various cancers and rheumatoid arthritis. Our immune systems, which are working to keep the residual HBV in our bodies in check, can also take a hit from medications that deliberately suppress our immune systems in order to fight cancer, psoriasis or rheumatoid arthritis.

According to medical guidelines, all oncologists and other specialists who use these powerful drugs are supposed to test all  their patients for hepatitis B and carefully monitor anyone who had hepatitis B in the past, which is indicated by a positive test for the hepatitis B core antibody (anti-HBc).

Even if you’ve cleared HBsAg, doctors may pre-emptively treat you with antivirals during and after your treatment for cancer, immune disorders such as arthritis or psoriasis, and hepatitis C and monitor your HBsAg and viral load regularly to make sure your hepatitis B does not reactivate.

These screening guidelines exist, but no one is perfect and your oncologist may not know you’ve been infected, may forget to screen you for hepatitis B, or may not understand the testing. So, tell everyone if you have an active or resolved hepatitis B infection. The last thing you want is to be battling both cancer and a reactivated hepatitis B infection simultaneously.

While hepatitis B never really goes away, once you clear HBsAg your risk of liver damage and liver cancer diminish tremendously. It’s worth a celebration, but you need to continue to be monitored as you age.

Forget Surface Antibodies, If You Have Both Undetectable Viral Load and HBsAg, You Might Be Functionally “Cured”

Dr. Robert Gish
Dr. Robert Gish

By Christine Kukka

For decades, people living with chronic hepatitis B were told they would be “cured” only when they lost the hepatitis B surface antigen (HBsAg) and developed surface antibodies. It represented the holy grail of recovery that everyone hoped for, but very few achieved.

Today, experts are redefining what constitutes a “functional cure” from chronic hepatitis B and taking the surface antibody out of the equation.

Researchers, including expert Dr. Robert Gish, suggest if people have an undetectable viral load (HBV DNA), undetectable HBsAg, and no signs of liver damage, they may be “functionally cured,” even if they haven’t developed surface antibodies. The cure is called “functional” because the only cure for hepatitis B is when the immune system controls or suppresses the virus. Continue reading "Forget Surface Antibodies, If You Have Both Undetectable Viral Load and HBsAg, You Might Be Functionally “Cured”"

HBsAg Levels Linked with Fibrosis in HBeAg-Positive Patients

Below is a publication from “Healio Hepatology, February 21, 2013 – HbsAg Levels Linked with Fibrosis in HBeAg-Positive Patients” , showing the correlation between HBsAg and HBV DNV virus levels and the risk of moderate to severe fibrosis in HBeAg positive patients.

Patients with hepatitis B who tested positive for hepatitis B e antigen were at increased risk for moderate-to-severe fibrosis with lower levels of hepatitis B surface antigen in a recent study.

Researchers evaluated serum samples and liver biopsy results from 406 treatment-naive patients with chronic hepatitis B. HBV genotype and hepatitis B e antigen (HBeAg) status were recorded along with levels of HBV DNA and hepatitis B surface antigen (HBsAg).

HBeAg-positive patients (n=101) had a higher mean fibrosis stage than HBeAg-negative patients (1.86 ± 1.18 vs. 1.40 ± 0.99; P<.001) and had greater levels of HBV DNA (7.06 ± 1.71 vs. 4.12 ± 1.67)and HBsAg (4.24 ± 0.9 vs. 3.53 ± 0.92) (P<.0001 for both). Investigators observed strong correlations between HBV DNA and HBsAg levels (r=0.44; P<.0001) and between fibrosis severity and HBsAg levels (r=0.43; P<.0001) among HBeAg-positive patients, but not among HBeAg-negative participants.

HBeAg-positive patients with moderate-to-severe fibrosis had lower HBsAg (3.84 ± 1.01 vs. 4.63 ± 0.58; P<.0001)and HBV DNA levels (6.47 ± 1.81 vs. 7.62 ± 1.40; P<.001) than those with mild or no fibrosis. HBeAg-positive patients with genotypes B, D or E had significantly higher HBsAg levels than HBeAg-negative patients, along with higher HBV DNA levels regardless of genotype.

Modeling analysis established an HBsAg cutoff of 3.85 log IU/mL-1 with a theoretical sensitivity of 100%, specificity of 86% and NPV of 100% for predicting moderate-to-severe fibrosis among HBeAg-positive patients with genotypes B or C. Investigators noted that the small cohort size used to establish this cutoff requires further validation to be clinically useful.

“To our knowledge, the current study is only the second to associate an HBsAg cutoff with the prediction of fibrosis severity in CHB patients,” the researchers wrote. “It will be of considerable interest to see whether the serum HBsAg and HBV DNA levels in the patients infected with different genotypes are significantly different from the mean values of the overall HBeAg-positive group, and if they will require the development of genotype-specific cutoffs, or whether a single cutoff is applicable to all HBV genotypes.”

Disclosure: See the study for a full list of relevant disclosures.