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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.

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World Hepatitis Day 2012 in Cairns, Queensland, Australia

WHD 2012 Cairns: Hep Day Out friends - Yvonne, Rhondda, Murph & Allana

A personal reflection on WHD events from Guest Blogger Yvonne Drazic

WHD was again promoted and celebrated in style in Cairns with lots of dedicated people making it a great success. The key organizers were Rhondda, the Viral Hepatitis Health Practitioner from the Cairns Sexual Health Service, and Alanna and Julie from the Queensland Injectors’ Health Network (QuIHN). At present, the bulk of hepatitis B health promotion and patient support is done through these organizations as part of hepatitis C and HIV services because sufficient separate government funding for hepatitis B is not yet forthcoming.

Last year, Rhondda organized a fabulous free lecture about hepatitis B which, while aimed at health care professionals and medical staff, was open to the public and especially to people affected by or living with hepatitis B. The speaker was Dr. Benjamin Cowie, an infectious diseases physician from Melbourne with a special interest in hepatitis B. His passionate and compelling presentation evoked great feedback from the audience, many stating it was a real eye-opener. This year’s lecture was presented by Dr. Joshua Davis who spoke equally engaging about his efforts to address hepatitis B in Indigenous communities in the Northern Territory. The talk attracted an audience of more than 100 people. As an add-on to the lecture, Aboriginal and Torres Straits Islander health workers could move on to an event/workshop called Yarnin up HepB where they were able to discuss anything hepB – and get expert advice – from Dr. Davis. This was very well received although many participants were quite disturbed about the statistics of hep B in Aboriginal and Torres Strait Islander people.

This year the open day at Cairns Sexual Health Service was called “Hep Day Out”. It was designed to be fun with funky, colourful posters (created by the talented Murph) and a music jam session. Like last year, the day featured tours of the premises with screening opportunities, as well as the famous QuIHN van offering information, a scrumptious lunch and fun activities. Every visitor who took the tour and completed a short quiz received a cool t-shirt courtesy of Hepatitis Queensland (see photos) and a health pack. In addition, the resident psychologist was on site for people who wanted a chat and I was available for brain-picking for everyone who wanted to know more about hepatitis B. Invitations were distributed to migrant services and communities but unfortunately did not attract any visitors from these groups. Possibly the time was unsuitable due to work commitments but it could also be due to fear of stigmatization which may be increased in these populations. I am currently conducting research to explore barriers and other issues that may keep people from engaging in health-protective actions such as screening and monitoring. It will also help to find more effective ways of engaging with migrant communities and get a better turnout for next year’s WHD.

Overall, plenty of awareness was raised, many people were educated about viral hepatitis, and a fun time was had by all.

Hepatitis B Advocacy

Dreams on Hold – A personal story of an aspiring medical student

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The summer before starting medical school, most of my friends traveled and had fun. But I could not.

The months of June and July marked 60 days of complete horror—the lowest point in my life. First, my sister suffered 
a near-death medical complication. Then, for the first time in my life, I experienced discrimination due to an unexpected medical diagnosis.

My discrimination story started on June 20, 2011. The director of admissions at (X) Medical School notified me that
I had been accepted into their program and offered a generous scholarship to attend. Because of this scholarship and the potential to obtain in-state residence, I dropped the other medical school I had been considering, including a $2,500 enrollment deposit.

I began the grueling paperwork to matriculate to (X) Medical School. It took nearly a week to schedule doctor appointments, fill out health forms, get required blood work done, look for apartments, and apply for financial aid. The following week, I traveled across the country to finalize an apartment lease. I returned home less than 24 hours later, exhausted but having successfully signed a lease.

Then my doctor called and said, “You have hepatitis B.” The nightmare began after that call.

The next day, (X) Medical School’s Student Health Services demanded that I have further blood tests within three days; otherwise, their committee would not be able to review my file before the start of classes.

I completed all of the tests, and the results were sent to the committee within a week. I pleaded with the committee 
to keep me enrolled, and I even agreed
 to drop out of medical school if the antivirals did not work.

The response from (X) Medical School came one week before orientation started: I was deferred until next year.
 In addition, my scholarship was revoked. They demanded that I sign a contract accepting deferment with conditions, including no guarantee of readmission and I had to sign within a week of receiving this devastating news.

At that moment I had to juggle not only my new medical diagnosis, but also the fact that I had a lease that could not be cancelled or sublet, a full year without any plans, and uncertainties about my future.

The nightmare still lingers. However, 
I am slowly getting back on my feet. The antivirals are lowering my viral load. I am working in public health and reapplying to medical schools. My future is still uncertain.

Note: This story is one of the four cases that galvanized the Hepatitis B Foundation into action. At a June 2011 meeting convened by the CDC, the HBF and other national thought leaders worked with the CDC to update their 1991 hepatitis B recommendations for health care workers and students, which were just updated, July 2012. It is hoped that the newly Updated CDC Recommendations for the Management of Hepatitis B virus- Infected Health Care Providers and Students  guidelines and advocacy efforts of HBF and others will make a dent in hepatitis B based discrimination.  Please note that these newly revised guidelines strongly state that hepatitis B is not a condition that should prevent anyone from entering or practicing in health care.

Hepatitis B Diagnosis & Monitoring

World Hepatitis Day Reflection: Asian Institute of Medical Sciences, Hyderabad Pakistan

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Thank you to Prof., Dr. Muhammad Sadik Memon, MBBS, FCPS (Gastro), FCPS (Med), MACP, MAGA,  for his personal reflection from World Hepatitis Day, 2012 events in Pakistan.

In order to raise awareness on World Hepatitis  Day, Saturday, 28th of July 2012, the Department of Gastroenterology and Hepatology of the Asian Institute Of Medical Sciences, organized a public awareness and open discussion seminar.

Gastroenterologists, family physicians, GPs, postgraduate students and para- medical staff all participated in the open discussion.

The program was started in the name of “Almighty Allah” and a recitation from the Holy Quran.

Dr Iqbal Haroon, Director of Hajiyani Hospital, was the moderator of the open discussion.

“It  is closer than you think” was the theme of this year’s World Hepatitis Day, and the open discussion focused on raising awareness on the different forms of viral  hepatitis: what they are, how they are transmitted, who is at risk, and the various methods of prevention and treatment.

Professor, Dr. Sadik  Memon, organizer of this event,  said that in Pakistan, many patients have lost their lives at the hands of quacks, so Pakistan needs the strictest possible laws to fight against these quacks, and must eradicate these deadly liver diseases.

Dr. Sadik Memon further described how in Pakistan millions of people are infected with HBV . He added that every 10th to 12th individual in the Pakistani population is infected with hepatitis B or C ,which far exceeds the numbers from the last big earthquake  in Pakistan. It is essential that Pakistani doctors unite to save human lives and spare them of these deadly diseases.

The most important aspects of prevention are hepatitis B vaccination, the screening of blood products, sterilized equipments and better hygiene standards in barber shops.

Dr. Waqar, focal person of the Government Hepatitis Program, discussed the efforts of the Sindh government regarding the hepatitis program.  He said that thousands of peoples from Sindh are receiving free interferon and anti- viral therapy from Zakat and Bait-ul-mal funds.

Before the end of open discussion Dr. Aamir Ghouri gave thanks to the audience, the guests of honor, and also the Roche Pharmaceutical company for sponsoring such a wonderful event in this blessed Month of Razman.

After completing the open discussion, DUA, (prayer) was performed for patients who are suffering from liver diseases by the Asian  Institute of Medical Sciences staff. Another open discussion was followed by Iftaar dinner. It was a memorable World Hepatitis Day.

Liver Cancer, Living with Hepatitis B

Dr. Tom London – Hepatitis B and Liver Cancer

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Hep B Talk is pleased to introduce Guest Blogger W.Thomas London, MD. Dr. London is internationally renowned for his many decades of work on hepatitis B and liver cancer, which started with his joining the research team  that discovered the hepatitis B virus. Dr. London has been at the forefront of liver cancer prevention and has written extensively about hepatitis B from the perspective of an epidemiologist, a clinician and a virologist. As founder and director of the Liver Cancer Disease Prevention Division at Fox Chase Cancer Center in Philadelphia, PA, he  developed one of the first successful community-based strategies to help people reduce their cancer risk through the early detection of chronic HBV infection. Dr. London has received the Distinguished Interdisciplinary Research Award  from the American Cancer Society and the Distinguished Scientist Award from the Hepatitis B Foundation where he currently serves as Vice-Chair of the Board and as the Senior Medical Advisor.  

Liver cancer, hepatocellular carcinoma (HCC), is the 3rd most common cause of death in the world.  Little attention was paid to HCC in the United States until recently because it was thought to be rare, but now it is one of the few cancer types that is rising in incidence (number of new cases per year). It is now the most rapidly increasing cancer in men in the US. The prognosis of HCC is poor; one year survival in the United States from the time of diagnosis is only 50%.  Detection of tumors when they are very small, less than 2 cm in diameter, and can be removed surgically is the best chance for cure.  Liver transplantation is often done if there is more than 1 tumor and the cancers are less than 3 cm in diameter.  Unfortunately, most HCCs are diagnosed when they are too large for successful surgical resection or transplantation.

Chemotherapy for HCC has been disappointing. Recently, the drug, Sorafenib (Nexavar), has been shown to be active against HCC, but it only extended survival time by a few months.  Thousands of drugs have been developed by the pharmaceutical industry for a great variety of conditions.  Of these, 983 have approved by the FDA.  That is they were tested in clinical trials, found to be safe and were beneficial for the purposes that they were approved

Scientists at the Hepatitis B Foundation and elsewhere have raised the question, are there drugs on the currently approved FDA list that are used for other purposes that might have a role in the treatment or prevention of HCC?  Recent publications suggest 2 candidates.  One is metformin (Glucophage), which is derived from the French lilac, and has been used in Europe since 1958 to treat Type 2 diabetes and in the United States since 1995. The other is propranalol, which is used to treat patients with cirrhosis who have varicose veins in the lower end of their esophagus (esophageal varices).

Diabetes is a recognized risk factor for HCC, particularly in persons who are obese and have a fatty liver. (Diabetics are also at increased risk of acquiring hepatitis B). Because patients with diabetes are often treated with metformin, investigators in China and France have looked at whether treatment with metformin lowers the risk of developing HCC.  By examining the records of diabetic patients who were treated with metformin or not, they observed that the risk of HCC was lower in the treated patients.  Furthermore, an experimental study of liver cancer in mice showed that metformin reduced the number and size of liver tumors.

Propranolol is used to lower the pressure in the portal vein and thereby in esophageal varices.  A group of physicians in France looked at the occurrence of HCC in patients with hepatitis C and esophageal varices who received propranolol treatment and those who did not.  There was about a 75% reduction in the incidence of HCCs in the propranolol treated patients.  Propranolol blocks receptors for epinephrine (adrenalin) and nor-epinephrine on cells in the body.  Such receptors are particularly rich on the surface of tumor cells, including HCCs. Experimentally propranolol has been effective in reducing the size and number of  several different kinds of tumors.

The studies that have been done so far are intriguing, but they are not conclusive.  Neither drug has been studied in a clinical trial to either treat established HCCs or to prevent HCC from occurring in the first place.  Such studies are in the planning stages.  Keep watching for progress on this front.

 

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Raising awareness and Enabling Protective Action in an Affected Community in Australia: A work in progress…

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Welcome Guest Blogger Yvonne Drazic. She is a PhD candidate at James Cook University in Cairns, Far North Queensland, Australia. Her research focus is on reducing the rate of undiagnosed and untreated chronic hepatitis B, in migrant communities from endemic areas, particularly the local Hmong community. Yvonne lives with chronic hepatitis B, and feels privileged to be one of the less than 3% of hepatitis B cases treated in Australia. She gives back in so many ways, and is also a list parent on the HB-List, an online patient forum. 

As a research student from tropical Far North Queensland in Australia, I am grateful that today’s technology allows me to be part of the global hepatitis B community. My goal is to help our local Hmong community of about 700 people to prevent future repercussions of undetected and untreated chronic hepatitis B (CHB). Having CHB myself, I was amazed to learn how many people miss out on vital medical care because they are unaware of their infection, or of its potential consequences. At present, the incidence of hepatitis B-related liver cancer is rising in Australia because undiagnosed CHB is doing much more harm than newly acquired infections in adults. The majority of affected people in Australia are migrants from endemic areas and Aboriginal and Torres Straits Islander people who were mostly infected at birth or in early childhood. Yet, less than 3% of cases are currently receiving antiviral therapy (Carville & Cowie, 2012).

I chose to focus on the Hmong community because studies in the U.S. show a particularly high CHB prevalence (~15%) in this population (Kowdley, Wang, Welch, Roberts, & Brosgart, 2011). And sure enough, when talking to members of the community, I heard sad stories of family members getting sick or dying from liver disease. Hepatitis B as a threat to public health has long been neglected in Australia, compared to the attention given to HIV and hepatitis C. However, based on a National Hepatitis B Needs assessment (Wallace, McNally, & Richmond, 2008) and other reports that showed an urgent need for a co-ordinated public health response, the first National Hepatitis B Strategy was finally released in 2010. The strategy highlights priority action areas such as raising awareness in patients and doctors, improving screening and diagnosis practices, and removing barriers in culturally and linguistically diverse (CALD) populations.

In Australia, pregnant women are routinely screened for hepatitis B. However, research suggests that many who test positive during pregnancy do not receive adequate follow-up care (Guirgis, Zekry, Yan, Bu, & Lee, 2009). In addition, recent studies indicate that CHB awareness is still low in Australian general practitioners (GPs), and that many patients are not managed according to guidelines (Dev, Nguyen, Munafo, Hardie, & Iacono, 2011; Guirgis, Yan, Bu, & Zekry, 2011). Therefore, in order to achieve improvements in early detection and timely referral for treatment, increasing GP involvement is a priority.

My project comprises (1) an assessment of knowledge, current practice, awareness of resources and educational preferences of local GPs; (2) assessments (pre- and post) and an appropriate intervention in the Hmong community (all based on behavioural theory); and (3) an assessment of pregnant women and new mothers. At the time of writing, data collection from GPs is under way.

Community engagement is, of course, an ongoing process. The project has the support of a community leader who is providing invaluable information about what may and may not work in his community. Initial information about the project was recently distributed. Building trust and showing that my motives are genuine takes time and it is important to let things develop instead of pushing ahead too fast. The fact that I have CHB myself may help to convey the message that it is okay and even necessary to talk about hepatitis B. Normalization assists in the removal of stigma.

More of my work to be shared in another blog. A big thank you to the special people who have been inspiring and encouraging me to do this work and keep offering tremendous, ongoing support.

Yvonne

References:

Carville, K. S., & Cowie, B. C. (2012). Recognising the role of infection: preventing liver cancer in special populations. Cancer Forum, 36(1), 21-24.

Dev, A., Nguyen, J., Munafo, L., Hardie, E., & Iacono, L. (2011). Chronic hepatitis B: A clinical audit of GP management. Australian Family Physician, 40(7), 533-537.

Guirgis, M., Yan, K., Bu, Y. M., & Zekry, A. (2011). A study into general practitioners’ knowledge and management of viral hepatitis in the migrant population. Internal Medicine Journal, Accepted article. doi: 10.1111/j.1445-5994.2011.02440.x

Guirgis, M., Zekry, A., Yan, K., Bu, Y. M., & Lee, A. (2009). Chronic hepatitis B infection in an Australian antenatal population: Seroprevalence and opportunities for better outcomes. Journal of Gastroenterology and Hepatology, 24(6), 998-1001. doi: 10.1111/j.1440-1746.2009.05841.x

Kowdley, K., Wang, C., Welch, S., Roberts, H., & Brosgart, C. (2011). Prevalence of chronic hepatitis B among foreign-born persons living in the United States by country of origin. Hepatology, Accepted preprint.

Wallace, J., McNally, S., & Richmond, J. (2008). National hepatitis B needs assessment. Melbourne: Australian Research Centre in Sex, Health, and Society, La Trobe University.

 

 

Baruch S. Blumberg Institute