Aldehyde

I have hepatitis B surface antigen (+) and hepatitis B core antibody (+) but negative for IgM anti core antigen (-), then it means that I am chronically infected with hep B. However, what if I also have the surface antibody against Hepatitis B?

I've searched though countless websites and discussed this with my doctor and the only reasons behind this strange test result are:
1. I am took the vaccine after getting infected and the virus mutated
2. I can fight off the virus.

Reason number 2 seems unlikely because I had the virus for over 4 years now since date of diagnosis (~age 15).

The first reason is more likely because I did get immunized during grade 6 (age 12) BUT I simply do not know how I got infected in the first place because my parents and brothers are negative even though my parents are the most likely cause of my infection.

Any ideas towards this phenomenon and how the virus mutated (i.e. why wouldn't you give the vaccine to a chronic hep B patient?)

Aldehyde

oops, wrong board. I wonder how can I move this topic

Dr Rick

Ask your doctor to fax the lab results to
(970) 928-9402 attn. to me and I'll email my interpretation and recommendations to you.

Rick Bochner, MD;
Diplomate ABIM,
Board Certified in Gastroenterology/Hepatology

Aldehyde

Thank you for replying. I actually have a copy of my lab results right here since I work in a lab and did some tests myself:

HBsAg = reactive
HBcAb = reactive
HBcAb IgM = non reactive
HBsAb = 22 mIU/mL (>10 mIU/mL = protective)
HB DNA = positive

My case was considered as a 'rare case' and a copy of my results was put into a record book never to be looked at again.

The chemistry and hematology panel were normal, and alpha fetoprotein is 3.1 (<15.0 ug/L)

Dr Rick

Chronic hepatitis B virus (HBV) affects over 5% of the world's population and is the primary cause of cirrhosis and hepatocellular carcinoma and the ninth leading cause of death worldwide. In the United States, about 1 million persons are chronically infected with HBV, but only a minority of these are carriers. Your situation is atypical but by no means rare, and overall, based on the information you've provided, your outlook is good.

The clinical presentation of acute HBV ranges from subclinical hepatitis (70%) to icteric hepatitis (30%) with rare cases of fulminant hepatitis (0.1% to 0.5%). Elevation of liver enzyme levels, primarily alanine aminotransferase (ALT) and aspartate aminotransferase (AST). In patients who recover, ALT levels normalize within 1 to 4 months. Persistent elevation of serum ALT levels greater than 6 months usually indicates progression to chronic HBV. Carriers of HBV maintain normal ALT levels with persistence of serologic markers of infection without serologic markers of active viral replication


The outcome of HBV infection depends on age of acquisition, immune status of the host, and rate of replication of the virus. It appears that you aquired the infection at a young age which is often associated with mild or no symptoms but a high risk of chronicity. In adults, infection is usually symptomatic with a low risk of chronicity. With perinatal infection, the initial phase is characterized by high levels of HBV replication, hepatitis B e antigen (HBeAg) in serum, and high levels of HBV DNA, but no evidence of active liver disease. The patient is asymptomatic, has normal ALT levels, and minimal changes on liver biopsy. Minimal liver disease, despite high levels of HBV replication, may be caused by immune tolerance in infants and children. These patients usually experience an immune-clearance phase during the second and third decade when spontaneous HBeAg seroconversion to antibody to HBeAg (anti-HBe) increases to an annual rate of 10% to 20%, so it's quite possible you will fall into this group sometime in the future if you haven't already.

Chronic HBV ranges from the asymptomatic carrier, to chronic active HBV, to cirrhosis and hepatocellular carcinoma. The rate of progression from acute to chronic HBV is about 90% for perinatal infection, 20% to 50% for infection acquired between the ages of 1 to 5 years, and less than 5% for adult-acquired infection. Of these adults, some develop chronic active HBV while others are asymptomatic carriers.

In healthy hepatitis B surface antigen (HBsAg) carriers, the prognosis is very good with a low rate of progression to cirrhosis. However, in HBV patients from endemic areas of the world such as Southeast Asia and sub-Sahara Africa and in patients with chronic, non-carrier HBV, the risk of progression over 5 years from chronic hepatitis to cirrhosis is much higher.


HBsAg is the serologic hallmark of HBV infection and arises from excess surface particles produced by virions multiplying in liver cells. HBsAg appears after acute infection and, in patients who recover, disappears 4 to 6 months later. Persistence of HBsAg beyond 6 months suggests progression to chronic HBV. Antibody to HBsAg (anti-HBs) appears as HBsAg disappears, and in most cases anti-HBs persists and confers lifelong immunity. In 25% of cases, however,k the titers of anti-HBs are not sufficient to neutralize circulating virions, and HBsAg and anti-HBs coexist. Individuals with this combination are considered carriers.


Hepatitis B core antigen (HBcAg) is an intracellular antigen in infected hepatocytes and is not detectable in serum. Antibody to HBcAg (anti-HBc) appears early in the infection and is then detected throughout the course of infection. In the acute phase, it is primarily an immunoglobulin (Ig) M antibody. In patients who recover, the anti-HBc changes to IgG and remains detectable with anti-HBs. It is also detectable in patients with chronic active HBV with HBsAg. IgM anti-HBc may be detectable during HBV exacerbations.


HBeAg is a marker of active HBV replication and infectivity. HBeAg is usually associated with high titers of HBV DNA in the serum, active liver disease, and high rates of infectivity; however, patients with perinatal HBV infection can be HBeAg positive but have minimal liver inflammation and normal ALT levels. Seroconversion from HBeAg to anti-HBe is associated with recovery and the disappearance of serum HBV DNA. Although rare, some patients have a viral mutation in the precore region that prevents expression of HBeAg; these patients have active liver disease and HBV DNA in the serum but are HBeAg negative.


The presence of serum HBV DNA is sensitive and specific for viral replication. Since HBV DNA arises from hepatitis virions replicating in the liver, one would expect it to be positive in patients with positive HBsAg. Having said that, the less sensitive non-PCR-based HBV DNA assays can be negative in such a patient, but the more sensitive PCR-based assay will always be positive. The PCR assays are so sensitive that they can remain positive for years after the virus is cleared from the blood. Recovery from acute HBV and HBeAg seroconversion in chronic HBV is associated with the disappearance of HBV DNA by non-PCR-based assays. PCR-based assays may remain positive for many years, which suggests the persistence of small numbers of virions that are contained by the host immune system. The main use of HBV DNA assays is to assess chronic active HBV patients for treatment and to evaluate their response.

Chronic HBV is characterized by the persistence of HBsAg for over 6 months. During active viral replication, HBeAg and HBV DNA are positive, and ALT levels are usually elevated. These tests are necessary to decide if therapy is warranted. A carrier state is characterized by positive HBsAg and anti-HBs, negative HBeAg, normal ALT levels, and undetectable HBV DNA (by non-PCR-based assays).

Liver biopsy is helpful in assessing the severity of liver damage, predicting prognosis, determining treatment, and monitoring response. Liver biopsy is generally indicated if any of the parameters for chronic active HBV are present -- HBsAg along with either elevated ALT levels, HBeAg, or HBV DNA, or all 3 of them. In most cases all 3 parameters are present but in some the ALT levels may be normal or HBeAg may be negative.


There are no definitive studies to guide the treatment and follow-up of patients who are carriers - that is HBsAg positive and surface antibody positive, HBeAg negative, with no DNA detected by hybridization assay - but a reasonable approach based on our understanding of the HBV carrier state would be for you to have your HBeAG and anti-HBeAG levels checked and to consider liver biopsy if the former is positive. If the biopsy demonstrates significant inflammation and/or fibrosis, therapy with interferon and lamuvidine may be warranted. On the other hand, if your HBV DNA was positive by PCR but not hybridization assay, the HBeAG is negative and your ALT level is normal, continued observation and retesting of these parameters every 6 to 12 months may be all that is necessary.

The above is general advice only and not medical care nor a substitute for it. I hope you find it helpful. Let me know what the results of the studies I recommended are, or if I can offer any other advice.

Rick

Dr Rick

BTW; if you are anti-HAV negative (negative for antibodies to Hepatitis A), begin and complete a Hepatitis A vaccination series now. Hepatitis A is usually a benign, short-lived infection, but can be fulminant and rarely even fatal if it occurs in the presence of a chronic Hepatitis B infection.

The Hepatitis B vaccination series would not be beneficial to you.

Rick

Marduk

How odd, I test positive for the core antibodies but none of the other 3??? All my liver stuff was fine to. Even though I have never had hepatitus B, to my knowledge, I used to give blood every 3 months, they always run that test, one time it came back + for core antibodies, they checked again, same results. Had my Dr. repeat the test, same results. Don't even know where I got it from
(it couldn't have been from my dismal non exisistent sex life and I don't inject drugs???)
<img src="confused.gif" border="0">

Aldehyde

Thank you very much Dr.Rick Bochner. I searched through a lot of stuff but I wasn't able to find a more concise and informative source (or at least not as easily understood reading material). It seemed much clearer hearing from another doctor rather than from a textbook.

Currently, I am having shots for Hep A.

And marduck, Hep B can be transfer through blood, urine and saliva too (the latter 2 are very uncommon). I really feel for you, we're quite similar you see. We both had no sex life and are no druggie. It really sucks to have a STD for unknown reasons. Maybe you should get whoever living with you to test for Hep B too. Sharing razors or even sharing food with saliva in them can transmit Hep B if you're very unlucky.

[ July 28, 2002: Message edited by: Aldehyde ]</p>