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Hepatitis B Diagnosis & Monitoring, Living with Hepatitis B

Diagnosed With Chronic Hepatitis B? What Stage – HBeAg-Positive Chronic Infection / Immune Tolerant?

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Do you know the stage or phase of your chronic hepatitis B infection? Quite often people may refer to themselves as “hepatitis B carriers”. This statement by itself does not say anything about your chronic hepatitis B infection except that you are someone who tests positive for hepatitis B, and that you are HBsAg positive.

The names of the stages or phases of HBV may vary with the liver society or over the years, but they reflect the natural history of the virus. It can be helpful for your doctor to determine if you are in the immune tolerant, immune active or clearance phase, the inactive carrier phase, have developed HBe negative chronic hepatitis B, or if you are in an HBsAg negative phase. It may take a few months or even half a year to accurately determine the phase, and then your doctor can talk to you about possible treatment options and whether or not treatment would benefit you at this time.  Remember, hepatitis B is typically not an emergency, so try to relax with the process knowing you may not have immediate answers.

If you are acutely infected, you also follow the natural course of the virus in a matter of months (clearance of an acute HBV infection within 6 months is considered an acute hepatitis B  infection). However, at the end of 6 months, those acutely infected will have a resolved infection, and will no longer be HBsAg+. If you are chronically infected, you will pass through many of these phases too, but unfortunately you will likely never get to an HBsAg negative or resolved phase.  The journey from phase to phase is different for each person and the time it takes to move through these phases varies along with the amount of liver damage that occurs.

The importance of a good liver specialist or knowledgeable doctor  cannot be over emphasized. These stages and phases may seem simple to understand, but not everything is black and white. There are often “gray areas” between phases  or time between phases where bloodwork and other diagnostic data must be carefully monitored. Results vary with the patient. New evidence indicates there may be more damage occurring during this gray area than originally thought. There may be a missed opportunity for treatment during this time.

The importance of being actively involved in your hepatitis B care can not be overstated. Tracking your lab data over time and putting it into an excel spreadsheet or graphing the data may help you understand what is happening with the virus and may even be helpful for your doctor, so don’t forget to request copies of all lab results. You are more in control than you think. Get involved with your care!

Once you have confirmed that you have chronic hep B, you need further testing to determine your HBeAg status. Those with chronic hepatitis B  are either HBeAg positive or negative. If you are HBeAg positive, you have a higher hepatitis B viral load/HBV DNA and are more infectious to others. People who are HBeAg positive are either in the immune tolerant stage or the immune clearance stage or in a gray zone. Repeated labs over time will help clarify this for your doctor.

If you are in the immune tolerant stage, you are HBeAg positive and have a high viral load. You will have normal or very mildly elevated ALT (SGPT) levels and mild or no inflammation or damage to the liver. This is very common with chronically infected young children who may have viral loads in the millions or even billions. During this time the virus is actively replicating in the liver, but the immune system has not recognized the virus so it is not trying to kill the infected liver cells. It is not the replication of the virus that kills liver cells, causing liver damage, but it is the response of your immune system to these infected liver cells.

During the immune tolerant phase the virus is happily replicating, completely unchecked by the immune system, which accounts for the high viral load and lack of liver damage during this time. People in the immune tolerant phase may remain in this phase for a couple of years, or it may be decades.  Treatment is not typically recommended during this phase.  However, for those that have been in this phase for decades, treatment is something likely  recommended by a  liver specialist. There is also the concern that a person may be in a gray zone where ALT elevations and subsequent liver damage may be occurring but may be missed. This emphasizes the need for very careful monitoring by a knowledgeable doctor and the possible discussion for treatment.

What happens when you move into the HBeAg-positive chronic hepatitis /Immune Reactive / Immune clearance  phase? Read more. 

Hepatitis B Prevention, Living with Hepatitis B

Personal Reflection on Yesterday’s FDA Vaccine Advisory Panel Review of Dynavax’s New HBV Vaccine

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I was fortunate to have the opportunity to represent the Hepatitis B Foundation at yesterday’s FDA vaccine advisory panel review of Dynavax’s new HEPLISAV vaccine for hepatitis B.  I was there for the public comment period on the second day of the meeting with my prepared statement. I was surprised to find I was the only one there for public comment. Since I’ve never been to anything like this, I don’t know if that is typical or not.  I think my personal story with HBV, and the message from the HBF was important for the FDA panel to hear, so they were sure to be reminded that there are real people affected by chronic hepatitis B.

There has been a great deal of good press about the new Dynavax vaccine. In studies it has superior immunogenicity when compared to the currently available vaccines. Immunity is generated in 2 doses given one month apart, versus the currently available vaccines where it is a three shot series over 6 months. This is particularly important to subpopulations such as those undergoing dialysis, and diabetic adults who are encouraged to be vaccinated against hepatitis B – a new recommendation by the CDC this year. It is also important to the general adult population, where it is found that 30-50% of adults may not complete the 3 shot HBV vaccine series making them vulnerable to infection. This  need for HBV prevention via a more effective vaccine, particularly in needy subpopulations was what was stressed in HBF’s public statement.

I do believe the panel was well aware of the importance of HBV prevention and one doctor made mention of the importance based on “the public comment”, so they were listening. Another doctor mentioned the burden of the disease not only globally, but also in the US. That is often understated.

The FDA panel met both Wednesday and Thursday. The public comment period was Thursday, and I remained there for the vote on two vital questions.  The first question was about whether the immunogenicity data was adequate to support the effectiveness of HEPLISAV for the prevention of hepatitis B infection in adults 18 through 70 years of age? The vote cast showed unanimous agreement in the efficacy of the vaccine.

The other question was about whether the data was adequate to support the safety of HEPLISAV when administered to adults 18 through 70 years. Five members said “yes”, 1 abstained and 8 voted “no”.

Prior to both votes there was a great deal of discussion amongst the panelists, and the representative from Dynavax who responded directly to questions.

Ultimately it came down to a few key points.  It was clear that the panel was impressed with efficacy or level of immunity generated by this new, 2 shot series. This vaccine uses a unique adjuvant. An adjuvant is a substance that is added to the vaccine in order to increase the body’s immune response to the vaccine.  In this case it was a nucleic acid versus a lipid – details of which I do not even pretend to understand. Although this new adjuvant was exciting based on the great immunogenicity data presented by Dynavax, it was also a source of concern because the panel was not sure if there was enough study data that represented all demographics. In other words, this vaccine performed really well, but they weren’t sure if it had been proven safe in different ethnic groups such as African Americans, Asian-Americans, and Hispanics. Since the US is a melting pot, this is important.

The other concern was that the vaccine had not been administered along with other vaccines. Because this vaccine is to be given to adults, they felt it was important that it could be given when an adult came in for their annual flu shot, or another immunization. Adults just don’t get to the doctor’s office that often! Although this was clearly of interest, it was not a deal breaker like the lack of safety data among all demographics. There was the suggestion to introduce the vaccine into the current sub-populations that were in particular need, but not much discussion beyond.

The votes were cast and the panel and the audience dispersed. Looks like Dynavax will need to complete further studies before the vaccine is once again reviewed by the FDA panel for approval. Personally, I believe there’s a real  need and a place for this vaccine, but of course safety always comes first.

Liver Cancer, Living with Hepatitis B

More on Metformin and Statins: Drugs Approved by the FDA for Other Purposes That May Prevent Liver Cancer

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From HBF’s expert Guest Blogger, Dr. Thomas London…

In an earlier blog, I pointed out that the available drugs to treat or prevent primary liver cancer (hepatocellular carcinoma, HCC) have been disappointing.  I noted that there may be drugs used for other purposes that may work against HCC.  The most promising of these was an old drug called metformin that has been used to treat type II diabetes for 17 years.  Now a new study on metformin provides the most intriguing results yet.

At the 2012 Digestive Disease Week meeting in San Diego, an enormous study from Taiwan was reported that encompassed almost all of Taiwan’s 23 million people. (I am indebted to Christine Frangou for her excellent report in Gastroenterology and Endoscopy News and have quoted from it extensively.) The investigators used the Taiwan National Insurance Database to identify all cases of HCC diagnosed from 1997 to 2008. There were 97,430 patients with HCC (most of whom would have had chronic hepatitis B). They were compared with 200,000 controls matched to the HCC cases by age, gender, and date of first physician visit.  Using the same database they linked all patients with diabetes and their treatment methods to patients with and without HCC.

From this they were able to show that patients with diabetes had a 2.3-fold increased risk of developing HCC.  In those patients who were taking metformin, however, HCC occurred about 20% less often than in those who were not treated with metformin. Furthermore, the longer patients took metformin, the lower their risk of HCC; about 7% lower for each year that they took the drug.

This study is not the final answer.  We don’t know why some diabetic patients were treated with metformin and some were not.  It is possible that the patients who did not take metformin had some unknown liver abnormality and were deliberately not treated with metformin.  Nevertheless, anti-tumor effects of metformin in experimental animals and in cell culture systems continue to be reported.  I will keep my eye out for more research on metformin and HCC and report it as it hits the medical press.

Statins are another group of drugs that are in common use. They were first approved by the FDA in 1987 to lower serum cholesterol levels and thereby prevent heart disease.  Statins inhibit an enzyme in the liver used to make cholesterol.  Several isolated reports suggested that statins might also help prevent HCC.  This month investigators at the Mayo Clinic in Rochester, Minnesota reported a meta-analysis (a statistical method to combine results from different studies) of all the reports in the medical literature of new cases (incidence) of HCC and exposure to statin therapy.  Ten studies reporting a total of 4,928 HCC cases in 1,459,417 patients were analyzed.  Overall, patients who were treated with statins had a 40% lower risk of developing HCC than those who were untreated.  The results varied from population to population. Asian populations which were more likely to also have chronic hepatitis B, had a 50% lower risk of developing HCC, while western populations had about a 30% lower risk.

At this time we do not know what the mechanism of a preventative effect of statins on HCC might be.  Nor do we know whether statins might have been withheld from patients with high cholesterol levels because they had a liver abnormality. It is likely, however, that more information on these issues will become available in the near future.  When that happens I will report it to you.

 

Hepatitis B Diagnosis & Monitoring, Hepatitis B Prevention, Living with Hepatitis B

Why Give the Hepatitis B Vaccine to Infants?

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The CDC recommends a birth dose of the hepatitis B vaccine for all babies. Pediatrician, Dr. Allison Shuman explains why in this informative video.

If you live in a part of the world where chronic HBV is at a medium (2-7% of population) or high prevalence rate (greater than 8% of population), your child is especially susceptible and at-risk for hepatitis B, with HBV transmission often occurring vertically from mother to child at birth, and horizontally from an HBV infected adult or another child’s infected body fluids to an unvaccinated baby or child. Please be sure that pregnant women are screened for hepatitis B. If mom tests positive for HBV, be sure baby receives a birth dose of the HBV vaccine and a shot of HBIG within 12 hours of birth. If mom tests negative for HBV, be sure that baby receives a birth dose of the HBV vaccine before leaving the hospital. Both babies of HBV infected and uninfected mom’s should receives shots 2 and 3 of the series according to schedule. Babies of infected mom’s should be tested at 18 months to be sure baby is hepatitis B free.

Please make arrangements with your doctor and the hospital to receive the HBV vaccine for your baby, prior to delivery, so you are sure the vaccine and/or HBIG are available at the hospital so prophylaxis can be given within 12 hours of birth. Please feel free to print and distribute  Chronic Hepatitis B in Pregnancy: Screening, Evaluation and Management (Part I and Part II) to your doctor.

 

Hepatitis B Advocacy, Living with Hepatitis B

Consider Viral Hepatitis Issues When you Vote

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Election Day is fast approaching, and while there are many important issues to ponder, don’t forget to consider the candidates’ positions on vial hepatitis and health care issues.  There are 435 seats in the House of Representatives on the ballot, along with 33 senate seats.  The National Viral Hepatitis Roundtable (NVHR) sent surveys to the House and Senate asking them their position on viral hepatitis funding, the Affordable Care Act, the syringe exchange ban, HHS strategic plan, and the Viral Hepatitis Testing Act. Surveys continue to be returned, but were updated October 24th to reflect new additions. To read the returned candidate responses, go to NVHR’s Candidate Survey .  If you don’t see your state’s candidate included in the collection of surveys, contact the candidate, educate them on viral hepatitis issues, and personalize the cause if you are able.  If you need help, contact Ryan Clary, Director or Programs, and ask him about your Congressional candidate’s position on viral hepatitis prevention and treatment efforts, and what you might do to help the cause. Be sure to get out there and vote – Tuesday, November 6th.

 

Hepatitis B Diagnosis & Monitoring, Hepatitis B Treatment, Living with Hepatitis B

Diagnosed with Chronic Hepatitis B? What do the HBe Blood Tests Mean?

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Your liver specialist has informed you that you have a chronic hepatitis B infection, and that he wants to run additional blood work so he can learn more about your HBV. Some of this blood work may need to be repeated over a period of time, but over the next 6 months or so, your doctor will determine whether or not you are a good candidate for treatment.  Regardless, he will definitely want to continue monitoring. Remember, treatment is important, but rarely an emergency, so be patient.

Now you need additional lab work to determine your HBe status, which will tell you whether or not you are HBeAg and HBeAb (anti-HBe) negative or positive. This reveals a great deal about your HBV such as whether or not the virus is replicating, and how infectious you are to others.

At this point, it is helpful to have a little background on antigens and antibodies.  An antigen is a foreign substance in your body that evokes an immune response. This may include viruses, bacteria or other environmental agents such as pollen or a chemical. In this case, it is the HBV e antigen. Your previous hepatitis B panel tested for the surface antigen, or HBsAg.

Antibodies are produced as a result of an immune system response to antigens. These antigen/antibody pairings are unique. An antibody response can be generated as a result of an immune response to an actual infection, or as a result of vaccination.  An uninfected person vaccinated against hepatitis B will generate an immune response, or surface antibody (HBsAb, or anti-HBs) to the HBV vaccine.

The hepatitis e antigen, or HBeAg, is a marker of an actively replicating HBV virus infection. Those with a positive HBeAg have active replication in their liver cells, more of the virus circulating in their blood, and as a result, they are more infectious, with a higher likelihood of transmitting HBV to others.  Most often, when a person is HBeAg positive, they tend to be HBeAb negative and vice-versa. This active, replicating phase may go on for weeks, as in the case of an acute infection, or for years, or even decades in those chronically infected.

Eventually most move into a non-replicative stage. During this time, e antigen (HBeAg) is no longer in the blood, and the anti-HBe antibody (HBeAb) is generated and appears in blood work. This HBeAg serconversion, or loss of HBeAg and the gaining of the antibody, HBeAb, can happen due to treatment, or spontaneously without treatment. Entering this stage is typically a good thing, and is often a goal of treatment.  However, monitoring by your liver specialist bi-annually or at least annually is essential, even if you have had an HBeAg serconversion years ago and are considered in the non-replicative phase.

HBV is complicated, and sometimes you may relapse. In other words, you may seroconvert losing HBeAg and gaining the HBeAb antibody, but it may not be durable, and you may have an HBeAg reversion to an actively replicating stage where you are once again HBeAg positive and HBeAb negative.  Years ago they called it “flip-flopping”.  This possibility is one of many reasons why regular monitoring by your liver specialist is so important.

The other possibility is the development of HBe-negative hepatitis B, which is the result of hepatitis B mutations. These precore or core promoter mutations replicate without generating the HBe antigen. However, they are actively generating the virus, though typically not at the levels of those with HBeAg positive HBV.  Once again, it is critical to continue regular monitoring by your liver specialist, so you are sure you have not begun active generation of HBe negative mutations.

Additional blood work ordered by your liver specialist will further clarify your HBeAg and over-all HBV status, and whether or not treatment may benefit you.

More next time…

Hepatitis B Diagnosis & Monitoring, Hepatitis B Treatment, Living with Hepatitis B

Diagnosed with Hepatitis B? Do You Need Treatment?

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When people learn they are infected with hepatitis B, the first thing they want to know is “what can I take to get rid of this disease?” It can be complicated, and what can be even more difficult to understand is that during different stages of the disease there may be absolutely no benefit from currently available treatments.

Just diagnosed with HBV? Are you acute or chronic? 

First, if you have just been diagnosed with HBV, it is imperative that you determine if you have an acute or chronic infection. If you have an acute, or new infection, then it is important to know that very few people require any sort of treatment. Just be sure you are being monitored by your doctor, and take good care of your health and be sure to prevent transmission to others during this time.

Chronically infected, now what?

If your doctor determines you are chronically infected, then you will need additional information to determine what your next steps should be.

Remember that unless you display urgent symptoms, such as jaundice, or a bloated abdomen, or severe illness, you really can wait a few weeks, or even a few months, to see a liver specialist. Many people panic if they are unable to see a liver specialist immediately.  Relax, find a good doctor, learn what you can about hepatitis B, and take care while you wait.

How will you be evaluated?

Your liver specialist will do a complete work-up on you. He will perform a physical examination, get a complete medical history, and he will run additional blood tests to learn more about your hepatitis B status and your liver health. He may also get a baseline ultrasound or perform other diagnostic imaging procedures to gain more data so he can make a decision whether or not you would benefit from treatment at this time.  Some of the blood work may need to be repeated over a period of time before your doctor decides whether or not to move forward with treatment. Do not beg your doctor for treatment. Waiting and watching is sometimes the smartest thing to do.  Treatment is rarely an emergency. Time is on your side, so please be patient.

What can you do while you wait?

This is a good time to look at some of your personal lifestyle choices and consider some basic changes that might benefit you at this time. Avoid alcohol, and stop smoking. Focus on eating a well-balanced diet filled with fresh vegetables, fruit, whole grains and lean meats. Avoid fast and processed foods when possible. They may contain trans fats, partially hydrogenated fats, high fructose corn syrup and other less desirable “ingredients”. Don’t’ forget to get everyone in the household screened and vaccinated against HBV if you have not already done so.

What’s next? Tune in next time to learn about some of your blood work…

Hepatitis B Diagnosis & Monitoring, Hepatitis B Prevention, Hepatitis Delta (HDV)

Hepatitis D Coinfection with Hepatitis B

Hepatitis D virus (HDV) – the “D” is for delta – is a viral enigma that doesn’t act like a normal virus. It is helpless – that is, it can’t infect a cell – without its viral accomplice, the hepatitis B virus (HBV), and makes infection with HBV worse.

Delta virus can only cause illness in those already infected with HBV, said Timothy Block, Ph.D., President and Co-Founder of the Hepatitis B Foundation, Professor and Director, Drexel University Institute for Biotechnology and Virology Research.

“It can take quiescent HBV and turn it into an acute, lethal viral infection,” Block said. “Liver disease – cirrhosis, liver failure – that might take decades to develop or could only take a year or two. Delta virus converts HBV infection into an emergency situation.”

“It’s one of the most severe forms of human viral hepatitis,” said Jeffrey Glenn, MD, Ph.D., Associate Professor of Medicine at Stanford Cancer Institute.

“Delta virus is a parasite of HBV because it encodes its own genome and coat-like protein but it doesn’t make its own envelope protein,” Glenn explained. “It steals that from HBV. It needs the B envelope protein to make its own, and this provides a means to infect new cells and subsequently make a fully formed viral particle to get out of those cells to infect others.”

Individuals can acquire delta virus two ways: Either after infection with HBV, which is called a “superinfection” and more likely to stay chronic, or a “co-infection”, which entails becoming infected with both viruses at the same time. In the latter, acute infections are more severe and increase the likelihood of developing liver disease much more quickly.

Worldwide, more than 15 million are infected, though fewer than 100,000 in the U.S. have the virus. It is concentrated in particular regions worldwide. Mediterranean areas such as southern Italy and southern Greece, for example, have larger than usual numbers of affected individuals, and in Turkey it is endemic. There are eight reported genotypes of HDV, which vary by geographical distribution and pathogenicity. Some believe that HDV’s incidence is declining. This is likely due to the hepatitis B vaccined and the resulting decrease in HBV carriers.

Because HDV is not a huge problem in the U.S., it flies under the radar screen of public awareness. Screening for HDV is not routinely ordered; however, infection with delta virus should always be considered when a patient with chronic liver disease suddenly gets worse.

Researchers have been frustrated in their attempts to develop effective treatments against HDV. Newer antiviral drugs that keep down levels of HBV DNA don’t do much against delta virus because they don’t affect the HBV envelope protein. The response rate to pegylated interferon alpha is typically poor.

With research there is always hope. Currently, there is a clinical trial of lonafarnib for the treatment of those coinfected with hepatitis B and D in the United States. It was originally developed for the treatment of different types of cancers. Perhaps additional information will come out of this year’s International Meeting on Molecular Biology of Hepatitis B Viruses. We shall soon hear.

Hepatitis D Fast facts:

—   Delta hepatitis is one of the most severe forms of viral hepatitis.

—   It is an incomplete viral particle that was discovered in 1977.

—   Approximately 15 million people are infected with HDV worldwide.

—   In the U.S., an estimated 6,000-13,000 people suffer acute HDV infection 
each year; 30,000 suffer from chronic HDV; and 1,000 Americans die 
from HDV-related diseases annually.

—   It is transmitted by blood from people already infected with hepatitis B.

—   Preventing hepatitis B, especially vaccination, will prevent HDV.

—   There is currently no effective treatment for HDV

Living with Hepatitis B

Which is Worse Chronic Hepatitis B or C? What Do You Think?

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From HBF’s expert Guest Blogger, Dr. Thomas London…

If you ask doctors in the United States, or patients with liver disease, or the average person on the street, the answer that you usually get is that Hepatitis C is worse.  Hepatitis C has a bad reputation in the media and with the public. We, at the Hepatitis B Foundation, tend to think that hepatitis B is the worse disease, but until now we have not had any basis for that answer. Now we do.

Recently a group of investigators from Johns Hopkins University published a paper with the title “Comparative Risk of Liver-Related Mortality from Chronic Hepatitis B Versus Chronic Hepatitis C Virus Infection”.  The answer from this publication is that hepatitis B is more likely to cause liver related death than hepatitis C.  It is worth dwelling on how the authors came to this conclusion: unexpectedly, the AIDS epidemic triggered the studies, which made the conclusion possible.

Acquired immune deficiency disease (AIDS) was first reported in the United States in 1981. The disease appeared to be deadly, and it was thought-to-be confined to homosexual men. In fact, it was initially called Gay Related Immune Deficiency or GRID.  Although it was soon proven that this new immune deficiency disease was not limited to gay men, it is true that men who had sex with men (MSM) accounted for most of the early cases.  In the 1970’s there were several reports that MSM had a high incidence of hepatitis B.  For the initial clinical trial of the then new hepatitis B vaccine, MSM in New York City were selected as the study population because of their high risk for hepatitis B infection. In the trial about 27% of the unvaccinated population became infected with hepatitis B virus (HBV) within 18 months, whereas less than 3% of the men who received the vaccine became infected over the same time interval.  This result proved the efficacy of the vaccine.

Fast forward to 1984 before the virus causing AIDS was clearly identified, several researchers suggested that a variant of hepatitis B was the cause. A group of investigators proposed a prospective study of MSM who had been tested for hepatitis B and a newly reported anti-HIV antibody, but who did not have immune deficiency disease.  By following the men over time, the thought was that it would be possible to observe which infection – HIV or hepatitis B or a combination of both – led to AIDS.

MSM were recruited from 4 cities in the USA (Baltimore, Chicago, Pittsburgh, Los Angeles); thereafter called the Multicenter Cohort Study (MACS).  Over four time intervals from 1984 to 2002, 6972 MSM were enrolled.  The men were followed until 2010, on average for more than 8 years. Serum samples were collected every 6 months, frozen and stored.  Although the hepatitis C virus had not yet been identified in 1984, all the samples were later tested for HIV, HBV and hepatitis C virus (HCV).  All deaths were recorded as were all liver related deaths.

The results were surprising. Comparable numbers of men were infected with HBV and HCV, but MSM with chronic hepatitis B were twice as likely to die a liver related death as the men with chronic hepatitis C.  The statistical analyses were carefully done to account for the treatments of HCV, HBV, and HIV that were used during the course of the study.  Immunodeficiency further increased the risk of liver death in the men with hepatitis B over that in the men with chronic hepatitis C.

The study showed that in the two and a half decades after 1984, hepatitis B infection was more serious than hepatitis C. Now, in 2012, this difference is even greater. Chronic hepatitis C has become a curable disease.  Chronic hepatitis B is manageable, but not yet curable.  This means that hepatitis B, which was already a worse disease than hepatitis C before the new therapies for HCV, is now a much more important unsolved health problem.

– Dr. Tom London

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The Hepatitis B Foundation Mourns the Loss of Dr. R. Palmer Beasley

Dr. Palmer Beasley (center), with his wife Dr. Lu-Yu Hwang at his side, received the HBF's Distinguished Scientific Award from Dr. Timothy Block (left) and Nobel Laureate Dr. Baruch Blumberg, HBF co-founder (far right) in 2010.

The Hepatitis B Foundation mourns the loss of a great hepatitis B champion. Dr. R. Palmer Beasley. The Hepatitis B Foundation was proud to have honored Dr. Beasley with the Distinguished Scientist Award 2010, at HBF’s annual Crystal Ball. Dr. Beasley’s groundbreaking research discoveries in Taiwan included identifying mother-to-infant hepatitis B transmission, and the fatal link between hepatitis B and hepatocellular carcinoma (primary liver cancer). Additionally, Dr. Beasley’s initiation of a national hepatitis B immunization program has protected a generation of people in Taiwan against hepatitis B and liver cancer.

Dr. Timothy Block, President and Co-Founder of the Hepatitis B Foundation wrote: “Our cause has lost another great one with the passing of Palmer Beasley. He was passionate and visionary in working to advance hepatitis B awareness and research. His work with the HBV vaccine, particularly in Taiwan, is considered definitive and as having set the stage for saving millions of people. The HBF recognized him as our honoree in 2010, and for that, I am glad.”

The Washington Post obituary of Dr. Beasley, dated August 5th, presented a wonderful review of some of Dr. Beasley’s many accomplishments and touches on his unique personality. Please see the reprint below –

Adventurous, meticulous and intensely curious about the world and its people, Dr. R. Palmer Beasley, epidemiologist and infectious-disease expert, used those skills to discover the link between the hepatitis B virus and liver cancer — proof that a virus could cause a human cancer, and a finding that ultimately led to vaccinations that saved hundreds of thousands of lives.

Dr. Beasley, a former University of Washington faculty member and dean of the University of Texas School of Public Health, died Aug. 25 at his home in Houston. He was 76. His death, from pancreatic cancer, was confirmed by his wife Lu-Yu Hwang.

Measles, plague, HIV — they all intrigued Dr. Beasley, who had decided as a student at Harvard Medical School that he wanted to be an epidemiologist, studying infectious diseases. In the early 1970s, as a fellow at what later became the University of Washington School of Public Health, he jumped at the chance to go to Taiwan to research rubella (German measles). There, he became determined to delve into the mysteries of hepatitis B, which he considered the least understood unconquered virus of the time.

“He took an approach like Albert Schweitzer,” said Herbert DuPont, director of the Center for Infectious Diseases at the University of Texas. “He lived in the field, he worked with patients, with the people. He didn’t go back to Seattle and sit in an office at the University of Washington and contact people in Taiwan.”

J. Thomas Grayston, then Dr. Beasley’s supervisor at the University of Washington, recalls a bit of friction in that regard. “We talked to him about coming back, and he wasn’t going to do that,” he said.

Dr. Beasley arranged independent funding for his research project, married a co-researcher and settled down in Taiwan, where he would spend the next 14 years. But he kept his affiliation with the University of Washington, which lasted nearly two decades.

With exacting attention to detail, Dr. Beasley and his colleagues designed long-term studies that would follow more than 22,000 Taiwanese government workers for decades, in the process proving that the hepatitis B virus is a main cause of liver cancer — at the time a controversial theory — and that childbirth can transmit the virus from a mother to her baby, who becomes a carrier and much more likely to develop liver cancer.

Dr. Beasley found that a shot of immune globulin at birth protected babies; later, his work helped push the World Health Organization to include the hepatitis B vaccine in routine vaccination programs.

For his work, Dr. Beasley was awarded the King Faisal International Prize in Medicine, the Charles S. Mott Prize, the Maxwell Finland Award for Scientific Achievement and the 2010 Distinguished Scientist Award by the Hepatitis B Foundation.

“There are at least a million people alive today who otherwise would not be here if not for Dr. Beasley’s pioneering research in hepatitis B,” Nobel laureate Baruch Blumberg said at the award ceremony, according to the foundation.

Robert Palmer Beasley was born in Glendale, Calif. He received a degree in philosophy from Dartmouth College in 1958, a medical degree from Harvard University in 1962 and a master’s degree in preventive medicine from the University of Washington in 1969.

Early in his career, he worked as an epidemic investigator for what is now the Centers for Disease Control and Prevention in Atlanta from 1963 to 1965, including an assignment to find a sample of plague in Bolivia.

Riding in trucks and on burros, he and his colleague James Gale tracked down plague in a tiny village on the east side of the Andes, said Gale, now an emeritus professor of epidemiology at the University of Washington. Because the disease had killed nearly all those in the village, they had to exhume a body, cut off a finger and get it back to the capital city, where the material containing the plague was injected into a guinea pig, which promptly died.

Assured that the pathogen was still viable, the two doctors packed it up in dry ice for shipment to a secure lab in Maryland.

From 1987 to 2005, Dr. Beasley was dean of the University of Texas School of Public Health.

His first marriage, to Sonia Garon, ended in divorce. Survivors include his wife of 32 years, Dr. Lu-Yu Hwang of Houston, an epidemiologist who collaborated with him on his research; two children from his first marriage, Monica Payson of Seattle and Fletcher Beasley of Los Angeles; a daughter from his second marriage, Bernice Hwang Beasley of Seattle; a brother; and two grandchildren.

Baruch S. Blumberg Institute