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March 2010 HCV Advocate

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In This Issue:

HBV and HCV Coinfection
Alan Franciscus, Editor-in-Chief

HealthWise: Aging Gracefully with Hepatitis C
Lucinda Porter, RN

How Does Smoking Affect Hepatitis C Progression?
Liz Highleyman

Predictors of Disease Progression
Alan Franciscus, Editor-in-Chief

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HBV and HCV Coinfection
—Alan Franciscus, Editor-in-Chief

There are many similarities between the hepatitis B virus (HBV) and the hepatitis C virus (HCV).  Both viruses mainly attack and damage the liver.  The viruses are transmitted similarly via blood exposure and the groups that are at highest risk are somewhat similar.  International studies have found that the rate of coinfection with chronic HBV and HCV ranges anywhere from 10 to 15%.  Little is known, however, about the rate of coinfection of chronic HBV and HCV infection in America because there have been few studies conducted to date.  A new study recently released in Hepatology titled “Hepatitis B Virus Infection among American patients with Chronic Hepatitis C Virus Infection:  Prevalence, Racial/Ethnic Differences, and Viral Interactions”1 will give us a better understanding of the prevalence of chronic HBV and HCV coinfection in the U.S. and of those factors that increase the likelihood of being infected with both viruses. 

The Study
This was a prospective study conducted at the Veterans Administration (VA) New York Harbor Healthcare System and Bellevue Hospital Center located in New York City.  The study was conducted between September 1998 and July 2004.  Patients were excluded from the study if they were HIV positive or were previously treated for HBV or HCV.  A total of 1,257 patients with chronic HCV were included in the study.  Most of the study participants were male and the people included in the study were racially and ethnically diverse.  As expected, the most common risk factor for HCV infection was prior injection drug use.  About half of the study participants reported more than 25 lifetime sexual partners and the majority of the participants were infected with HCV genotype 1. 

All of the study participants were tested for HBV—the testing included viral and antibody markers for previous infection, current infection and resolved infection.   Seven-hundred, seventy-three people (61.5%) were found to have markers of prior HBV infection, but the HBV infection was resolved and 73 people (5.8%) were found to be coinfected with chronic HBV and HCV. 

Factors that increased the likelihood of chronic HBV and HCV coinfection included age less than 40 years, Asian race, injection drug use and a greater number of lifetime sexual partners. 

Liver biopsies were performed in 26 chronic HBV and HCV coinfection patients and 658 chronic HCV-monoinfected patients—people who were coinfected with chronic HBV and HCV were found to have more severe disease progression and were more likely to develop a faster rate of fibrosis/cirrhosis progression, more severe steatosis and were at increased risk for developing liver cancer. 

The obvious limitations of the study were that the population was primarily men and conducted in the same geographic area (New York City). 

There are clear guidelines in place for people with hepatitis C to be screened for HBV and vaccinated if needed.  It is somewhat surprising that so many HCV positive individuals were found to be infected with hepatitis B especially in the Veteran’s Administration where the standard of care for testing, care and treatment is better than in the general population.   

The authors acknowledged that “HBV infection is a major public health problem and is an important cause of liver disease in Americans with chronic HCV Infection,” and that there are no guidelines for the management and treatment of chronic HBV and HCV Coinfection.

The authors made the following recommendations:

  • Public and physician awareness is needed in order to identify, evaluate, and treat people at high risk for chronic HBV and HCV coinfection
  • More studies are needed to evaluate the prevalence of chronic HBV and HCV coinfection in America
  • Additional research is needed to better understand how the viruses interact and affect one another

The authors also suggested that chronic HBV and HCV coinfected individuals should be offered a liver biopsy, aggressive treatment of the virus that is most dominant and be screened for liver cancer. 

1Edmund J. Bini and Ponni V. Perumalswami, Hepatology, Vol 51, No. 1, 2010.

Similarities and Differences between HBV and HCV:

HBV:  The hepatitis B virus is mainly transmitted by blood and by contact with bodily fluids such as semen and vaginal secretions.  Factors that increase the risk of transmission of HBV and populations that are at high-risk for HBV include: 

  • Babies born to HBV-infected mothers
  • Having sex with an HBV-infected individual
  • Unsafe tattoo and piercing; services provided at a personal care salon (where blood is present)
  • Sharing HBV-infected needles and works (cottons, cooker, water, etc.)
  • Sharing HBV-infected personal hygiene items (razors, toothbrushes)
  • Blood exposure and needle stick accidents (healthcare workers)
  • Biting and scratching among children
  • Hemodialysis (filtering blood)
  • Breast feeding is considered safe and recommended—if a mother is HBV-positive and the baby is started on the infant HBV vaccine within 12 hours of birth, it is still considered safe to breast feed the baby

The hepatitis B virus can live outside the body for at least 7 days.

HCV:  Hepatitis C is mainly transmitted by blood.  The most common risk factors include:

  • Sharing HCV-infected needles and works. 
  • Receiving a blood transfusion or solid organ transplant prior to 1992
  • Receiving clotting factors before 1987
  • Babies born to HCV-infected mothers
  • Unsafe tattoo or piercing; services at personal care salons (where blood is present)
  • Having rough or bloody sex with an HCV-infected person
  • Healthcare workers who have blood exposure or needle stick incidents 
  • Breast feeding is considered safe and recommended

The hepatitis C virus can live outside the body for at least 16 hours, but no longer than 4 days.

Hepatitis B and C can be prevented by standard blood-borne pathogen prevention measures, and safer sex practices.  Vaccination against hepatitis B is one of the most effective HBV prevention strategies.   There is currently no vaccine to protect against HCV.  All persons with HCV should be tested and vaccinated against HBV if they are susceptible.

  • HBV:  The rate of acute to chronic HBV infection in adults is 5 to 6%. 
  • HCV:  The rate of acute to chronic hepatitis C infection in adults is up to ~ 80%.

Mother to Child
HBV:  Mother-to-child transmission of chronic HBV can occur in 90% of babies born to chronic HBV-infected mothers, but the rate of chronicity can be reduced to ~10% by giving the baby immune globulin and starting on the HBV infant vaccine series within 12 hours of birth.  Every pregnant woman in the U.S. should be tested for hepatitis B.  There have been relatively few studies that have looked at treating HBV pregnant women with HBV medications to reduce the risk of transmission to the baby.

HCV:  The rate of mother-to-child transmission of HCV is estimated at 5-6% and there are no known medications or procedures to reduce the risk of transmission to the baby.  Pregnant women with HCV cannot take treatment with current HCV medications because of the potentially high risk of birth defects.

Disease Progression
HBV:  In the United States it is estimated that 3,000 to 4,000 people with chronic hepatitis B die each year of complications from HBV—70% of the deaths from chronic HBV are due to liver cancer.  Progression of chronic HBV to serious disease progression that can include cirrhosis, liver failure or liver cancer occurs in about 15 to 25% of people.  Factors that are believed to increase the likelihood of a more severe HBV disease progression include male gender, advanced age, alcohol use, and tobacco smoking.  Other factors include persistently high HBV DNA (viral load), coinfection with HIV or HDV, and severity and frequency of ALT elevations.  Coinfection with HIV also increases the risk of HBV disease progression. 

HCV:  In the United States it is estimated that 10,000 people die each year from complications of chronic hepatitis C.  There are many factors that increase the likelihood of a more severe HCV disease progression – see the article “Predictors of  Disease Progression” in this issue.

HBV:  Treatment of chronic hepatitis B is a complicated process that takes into consideration many factors such as HBV DNA (viral load), degree of liver damage and HBV genotype.  The current medications include tenofovir, entecavir, pegylated interferon (Pegasys), lamivudine, adefovir, telbivudine.  Certain drugs are more effective and produce lower rates of drug resistance—tenofovir, entecavir, pegylated interferon—and are recommended as first line treatment drugs.  The side effects of HBV medications (excluding pegylated interferon) are mild in nature. The drugs are taken for either short- or long-term use depending on treatment response or the development of drug resistance.  

HCV:  Treatment of chronic hepatitis C is based on several factors including stage of liver disease and predictors of treatment response.  HCV medications include interferon, pegylated interferon, and ribavirin (only given with interferon).  The current standard of care is pegylated interferon plus ribavirin therapy.  Treatment duration is generally 48 weeks for HCV genotype 1, and 24 weeks for genotypes 2 and 3.  The current medications to treat hepatitis C do not become resistant.   The side effects of interferon and ribavirin are well-documented.  The most common side effects include muscle and joint pain, insomnia, fatigue, loss of appetite, headaches, gastrointestinal distress, depression, and anxiety.

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Aging Gracefully with Hepatitis C
—Lucinda K. Porter, RN

On a recent trip, I popped into a fast-food establishment for a cup of coffee and free Internet access.  Armed with my iPod and laptop, I was feeling very cool and techno-savvy.  That is, until I was charged the senior rate for the coffee.  To set the record straight, I am 56 years old and completely unprepared to be seen as a geezer by a whippersnapper wearing a red hat.  I was relieved to learn that one merely needs to be over 50 to qualify for this 40-cent bargain.  In the end, my pride was soothed by the extra money in my pocket. 

I thought I was proud about aging, but apparently I am fine with being old just as long as I don’t look it.  That may be a problem since officially I look like a senior citizen to at least one person.  As time passes, there will be more incidents like this since I am not getting younger.  However, the real issue here is not my vanity but my attitude.  What is wrong with looking or being old? And, what does that have to do with hepatitis C (HCV)?

Lets start with the second question.  At the 2009 meeting for the American Association for the Study of Liver Diseases (AASLD), Gary Davis and colleagues presented an abstract about the aging HCV population.1  Analyzing existing data from National Health and Nutrition Examination Survey (NHANES)2, the prevalence of HCV peaked in 2001, but the burden of HCV is still ahead.  With the likelihood of HCV-related cirrhosis occurring between ages 60 to 80, Davis et al., project that cirrhosis will increase dramatically for 20 years peaking at 1 million cases in 2020.  They estimate that those with the severest form of cirrhosis (decompensation) will rise until 2022.  HCV-related liver cancer will peak in 2019 at 14,000 cases annually.  Davis and colleagues conclude that due to the long durations patients have had HCV, the next two decades will experience a burden of HCV-related complications.  The researchers suggest that this impact could be reduced if more people are successfully treated for HCV.  In short, we Baby Boomers are becoming Senior Boomers with HCV.  Those of us who are lucky enough to live long may also need to come to terms with having had HCV for a long time.

This leads me to the first question, what is wrong with looking or being old? Philosophically, there is nothing wrong with it.  As Maurice Chevalier put it, “Old age is not so bad when you consider the alternatives.”  However, medically it is a challenge.  The body and mind aren’t working as well and there are many more opportunities to visit with one’s medical provider.  Heck, those colonoscopies alone aren’t exactly a highlight of the golden years.

I believe there is another problem, a bigger issue, an attitude problem.  My reaction when confronted with the truth about my age is an example.  But the problem is more than this—it’s stereotyping or ageism.  It’s when we put people in a box by making assumptions about them, assumptions that may injure them. 

According to a report published by the Alliance for Aging Research, healthcare in the U.S. is plagued with prejudice against its oldest citizens.  In Ageism: How Healthcare Fails the Elderly,3 a long list of problems is identified.

  • Medical professionals do not receive adequate training for working with older adults, with a mere 10% of medical schools requiring geriatric coursework.
  • Older adults are less likely than younger adults to receive preventive medical care, such as immunizations.
  • Health screening and testing is not conducted as frequently in older patients as it is in younger ones.
  • Older patients are less likely to be offered medical treatment with proven medical interventions.  Conversely, they may endure extremely invasive treatments that are not necessarily appropriate.
  • Clinical drug trials often exclude older subjects. 

An example of age-related bias is reflected in the fact that 9 out of 10 adults over age 65 are not adequately screened for diseases.4 Simple tests and interventions for heart disease, colorectal cancer, diabetes, melanoma, osteoporosis and the flu are insufficiently recommended.  HIV and substance abuse may be overlooked simply because some medical providers don’t consider older patients to be at risk. 

I observed and participated in some of this unintended bias as a nurse working in a liver disease clinic.  I never questioned the fact that older patients were excluded from clinical drug trials.  I accepted the practice of not offering HCV treatment to older patients.  Generally, patients were treated as individuals, but there was an underlying assumption that most patients over the age of 65 would not be offered HCV medications unless they were very healthy and youthful.

Decay and disease are not inevitable consequences of aging.  We have the power to prevent various diseases when we employ good health habits.  Often we try magic bullets, such as vitamins and other supplements.  Although these may provide some benefit, they are unproven, compared to health advice that has been around for ages.  Yes, taking ginseng is easier than exercising and may go down better than Brussels sprouts, but expecting a pill to replace a healthy lifestyle is like hoping your car can run on fuel without an engine.

Getting old is not just weak bladder and wrinkles.  Its about wisdom and appreciation for life.  Many times I’ve heard or said, I wouldn’t trade being my age for being young again.  Sure, it would be nice not to have hair growing out of unwanted places, but not in exchange for what I have gained along the way.  Granted, saying this while I am healthy and a mere 56 may be easier said than done.  I hope to live long enough to be really old, regardless of the possible issues. 

“Advancing age is one of the greatest challenges we face, but it brings with it a lifetime of honed skills involving coping, growth, and resiliency, and these qualities are more powerful than disease,” comments Samuel Appel, MD, a Geriatric Psychiatrist at Highline Medical Center in Washington.  Note the word resiliency.  Merriam-Webster defines resilience as the ability to recover from or adjust easily to misfortune or change.5 (Resiliency is the topic of next months Healthwise.) Until then, consider this advice from former Chief Justice of the U.S.  Supreme Court, Earl Warren, “Don’t complain about growing old—many, many people do not have that privilege.” 



  1. Aging of Hepatitis C Infected Persons in the United States: A Multiple Cohort Model of HCV Prevalence and Disease Progression. G.  L.  Davis; M.  J.  Alter; H.  B.  El-Serag; T.  Poynard; L.  W.  Jennings.  2009 American Association for the Study of Liver Diseases Meeting.  Abstract #1613
  2. Many HCV statistics are gleaned from the NHANES data.  Some experts believe that the NHANES estimates are low because certain populations with a high incidence of HCV were not counted, such as prisoners, homeless, military and those in institutions.  Therefore, the number of those projected to experience HCV-related complications is likely to be significantly higher.
  3. Ageism:  How Healthcare Fails the Elderly.  Alliance for Aging Research; 2003 www.agingresearch.org/content/article
  4. Healthy Aging for Older Adults, Centers for Disease Control and Prevention 2003
  5. www.merriam-webster.com

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How Does Smoking  Affect Hepatitis C Progression?
—Liz Highleyman

By now, everyone knows that tobacco smoking is a health hazard.  But for people with hepatitis C, there is even more reason to quit, because smoking has been linked to liver disease progression and possibly poorer response to treatment.

Smoking contributes to an estimated one in five deaths in the U.S. – including leading killers such as heart disease and cancer.  By far the leading preventable cause of death, cigarette smoking kills more Americans than motor vehicle accidents, HIV/AIDS, homicide, and suicide combined, according to the American Cancer Society.

Smoking and Disease Progression
One of the liver’s primary functions is to process and detoxify chemicals that enter the body.  Some harmful effects of cigarettes are caused by nicotine itself, while others are due to carbon monoxide, tars, and other toxins in smoke.

Cigarette smoking affects the entire body.  It is linked to inflammation, which is increasingly implicated in a host of chronic progressive conditions including cardiovascular disease and neurocognitive impairment.

In the liver, smoking has been shown to increase necroinflammatory or histological activity, an indicator of ongoing injury.  Alanine transaminase (ALT) is the classic biomarker of liver inflammation.  One French study found that the likelihood of ALT elevation in people with chronic hepatitis C rose with both the number of cigarettes smoked per day, and the number of years a person smoked.

Smoking also appears to promote fibrosis, the buildup of fibrous scar tissue as the liver tries to repair itself.  Further, animal and human studies have shown that smoking is linked to liver steatosis, or fat accumulation. 

Overall, smokers experience worse liver disease progression than nonsmokers, whether due to chronic hepatitis C or B, alcoholic cirrhosis, non-alcoholic fatty liver disease (NAFLD), or other causes.  But specific study data are inconsistent and sometimes conflicting.  A recent study published in the Scandinavian Journal of Gastroenterology, for example, found that smoking was associated with severe fibrosis and steatosis in people with chronic hepatitis C but not hepatitis B.

The mechanisms by which smoking promotes liver damage are not fully understood, but oxidative stress and changes in levels of cytokines (chemical messengers) appear to play a role.  For example, smoking leads to increased production of the pro-inflammatory cytokines interleukin 1 (IL-1), IL-6, and tumor necrosis factor-alpha, as well as activation of T-cells.

In 2006, A. Dev and colleagues reported that in a study of 170 chronic hepatitis C patients, smokers had significantly more fibrosis than nonsmokers; 21% of smokers had Metavir scores of F3 or F4 (indicating advanced fibrosis or cirrhosis), compared with 14% of nonsmokers.  The researchers hypothesized that low oxygen levels due to smoking might lead to increased expression of the cytokines vascular endothelial growth factor (VEGF) and VEGF-D and their receptors.  In a multivariate analysis, elevated VEGF-D was indeed an independent predictor of more severe fibrosis.

Tobacco smoke is also carcinogenic, or cancer-causing.  This may be due to a combination of direct toxicity to cells, interference with tumor suppressor genes, and inhibition of T-cells responsible for surveillance and removal of malignant cells.  Though most commonly linked to lung cancer, numerous studies indicate that smoking also increases the risk of primary liver cancer. 

In people with HCV, smoking and chronic viral infection appear to have a synergistic effect in promoting hepatocellular carcinoma (HCC).  According to a recent study by M. Hassan and colleagues, regular cigarette smoking (though not chewing tobacco, snuff, or cigar or pipe smoking) was associated with HCC in men.  Furthermore, cigarette smoking interacted synergistically with chronic HCV in men, leading to a 136-fold increase in risk.  A related study by S. Franceschi and colleagues in Italy found that tobacco smoking was unrelated to HCC risk overall, but seemed to increase its likelihood among people with viral hepatitis.

Smoking may be even more detrimental for people with end-stage liver disease and liver transplant recipients.  A study by J. Leithead and colleagues found that while one-year post-transplant survival rates for smokers and nonsmokers were equal at 94%, they diverged over time, with ten-year rates of 54% for smokers versus 77% for lifetime nonsmokers.  The researchers attributed the added risk to higher rates of cardiovascular disease and sepsis.

In contrast, a study of more than 2,000 patients by D. Lee and colleagues found that smoking was not associated with increased risk of mortality in patients evaluated for or receiving liver transplants.  While this certainly should not encourage anyone to smoke, it does suggest that transplant centers and insurance companies may not be justified in denying liver transplants for tobacco smokers.

Some research suggests that tobacco smoking is associated with lower rates of sustained virological response (SVR) to interferon-based therapy, but here again data are mixed.  In the large WIN-R trial, for example, treatment outcomes were similar for smokers and nonsmokers with HCV genotype 1, but response rates were lower for smokers compared to nonsmokers with genotypes 2 or 3. 

Studies of treatment response may be confounded by the fact that smokers tend to have more advanced liver disease, which itself is a predictor of diminished response.  It is more clear that smoking can exacerbate side effects of treatment  or of chronic HCV infection itself  including depression.

If not motivated by concern for one’s own health, second-hand smoke has been shown to contribute to cardiovascular disease, cancer, and other conditions in people who do not smoke themselves.  A study published in the September 2009 Journal of Hepatology found that second-hand smoke promotes NAFLD by interfering with regulation of fat metabolism.  Even “third-hand smoke” – the toxic residues left on clothing, furniture, and other surfaces – may be carcinogenic, according to a study published last month in the advance online edition of Proceedings of the National Academy of Sciences

Kicking the Habit
While smoking is one of the most hazardous health risks, it does have one advantage: unlike age, sex, or family history, it is a modifiable factor that people can do something to change.

This is not to suggest, however, that quitting smoking is easy.  Most ex-smokers say kicking the habit is one of the hardest things they have ever done.  (Take it from this recent ex-smoker, who quit two years ago after smoking for nearly 30 years!)

For many people, smoking represents not just one dependence, but rather two: addiction to nicotine and the habits surrounding cigarettes.  Smokers find that it can relieve stress, increase alertness, alleviate boredom, and promote social interaction.  Common symptoms of nicotine withdrawal include anxiety, inability to concentrate, and insomnia.  But while it takes only a few days for nicotine to leave the body, the psychological addiction can take much longer to kick. 

Yet the benefits of smoking cessation are undeniable.  According to the American Cancer Society, within 24 hours after quitting, the heart rate drops and carbon monoxide levels in the blood return to normal.  Within a few months, circulatory and respiratory function improves.  By one year, the risk of heart disease is half that of a continuing smoker.  Experts estimate that people who stop smoking at age 35 can extend their lifespan by eight to nine years, but even people who quit in their sixties can add years to their lives.

Many smokers worry about weight gain when they contemplate quitting.  Some quitters do, in fact, gain some weight, in part because smoking speeds up metabolism, but also because it is common to eat as a substitute for smoking.  Typically, however, weight gain is not large (less than ten pounds on average) and is offset by the benefits of not smoking.  Exercise – such as yoga or going to the gym regularly – can help prevent weight gain, relieve anxiety, and replace an unhealthy habit with a healthy one.

People often try to quit by going “cold turkey” on their own, but research shows that most do better with some form of assistance.  This can range from nicotine replacement products (patches, gum, or lozenges), to the prescription medications bupropion (Zyban) or varenicline (Chantix), to alternative therapies such as acupuncture and hypnosis, to support from professional counselors, peer groups, telephone hotlines, or the Internet. 

Studies show that using a combination of methods may produce the best results.  Unfortunately, as T. Chandra and colleagues revealed in the December 21, 2009 World Journal of Gastroenterology, internists and gastroenterologists do not adequately counsel their hepatitis C patients about tobacco and alcohol use.

But even with help, most smokers do not stay off cigarettes permanently on the first try.  Like many things in life, quitting improves with practice.  With each relapse, people learn new strategies and insights, and rates of long-term success increase with subsequent attempts.

Materials from the Hepatitis C Support Project

Selected sources

  • Chandra, T. et al.  Frequency of alcohol and smoking cessation counseling in hepatitis C patients among internists and gastroenterologists.  World Journal of Gastroenterology 15(47): 6010-6001.  December 21, 2009.
  • Dev, A. et al.  Relationship of smoking and fibrosis in patients with chronic hepatitis C.  Clinical Gastroenterology & Hepatology 4(6): 797-801.  June 2006.
  • De Luca, L. et al.  Is smoking a prognostic factor in patients with chronic hepatitis C? Minerva Gastroenterology Dietology 55(2): 139-143.  June 2009. 
  • Hassan, M.  Effect of different types of smoking and synergism with hepatitis C virus on risk of hepatocellular carcinoma in American men and women: case-control study.  International Journal of Cancer 123(8): 1883-1891.  October 15, 2008.
  • Lee, D  et al.  Effects of smoking on survival for patients with end-stage liver disease.  Journal of the American College of Surgeons 208(6): 1077-1084.  June 2009.
  • Tsochatzis, E. et al.  Smoking is associated with steatosis and severe fibrosis in chronic hepatitis C but not B.  Scandinavian Journal of Gastroenterology 44(6): 752-759.  2009.
  • Yuan, H. et al.  Second-hand smoke stimulates lipid accumulation in the liver by modulating AMPK and SREBP-1.  Journal of Hepatology 51(3): 535-547.  September 2009.

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Predictors of Disease Progression
—Alan Franciscus, Editor-in-Chief

Disease progression of hepatitis C (HCV) is highly variable, which means that it is difficult to tell who will and who will not have severe HCV disease progression.  In general about 80% of people with chronic hepatitis C will have a slow rate of disease progression that may not lead to serious complications.  The other 20% of people with chronic hepatitis C will have severe disease progression that could lead to complications such as severe fibrosis, cirrhosis, liver failure, liver cancer and death. 

The question that has vexed us all is why some people with HCV have serious disease progression while others only have mild progression.  Although we are far from completely understanding and answering this important question there is information available about some of the factors that will likely increase the risk for serious HCV disease progression.  This article will discuss the various factors that increase the likelihood of disease progression and steps we can all take to minimize these effects – at least for those factors over which we have some control.

ALT Levels
Alanine aminotransferase or ALT (previously called SGPT) is a chemical produced in the liver.  ALT levels are elevated when liver cells are inflamed, damaged, or destroyed by HCV, HBV, alcohol and certain drugs.  Persistently elevated ALT levels are more of a sign that there is ongoing damage to the liver, and, if elevated over a long period of time, indicate ongoing fibrosis progression.  But it is important to know that people with persistently normal ALT levels can also have fibrosis progression, although the risk is much lower. 

The amount or degree of inflammation in the liver roughly correlates with the development of fibrosis and cirrhosis.  The amount of inflammation can be reduced by taking HCV medical treatment and avoiding any substance that causes harm to the liver, such as alcohol, etc. 

Light, moderate, or severe scarring of the liver (fibrosis) can eventually lead to even more severe scarring of the liver called cirrhosis.  The damage caused by hepatitis C is not linear – this means that once fibrosis and cirrhosis start to develop, the progression of liver disease speeds up.  In other words, it may take 10 years to progress from one degree or stage of liver damage to another, but the next increase in the amount of damage may take less time – say 7 years.  Progression to the next stage may only take 5 years and so forth.  HCV treatment can help to reduce, slow down or stop the disease progression progress especially if HCV treatment is successful.  Lifestyle changes can also help the liver to stay healthy by maintaining a healthy weight, eating a healthy diet, avoiding alcohol and drugs, moderate exercise, stress reduction, etc.

Age plays a critical role in HCV disease progression.  The age at the time that someone acquired HCV plays an important role in disease progression – so the older you are when you acquire HCV the faster the disease progression.  This is because the body’s immune system doesn’t work as well to minimize the damage HCV causes.  On the other hand, if someone acquires HCV at an early age, as they get older the greater the chances of more severe disease progression due to the accumulation of damage over time.  For instance, some studies have found that people over 60 years old have a quicker disease progression and other studies have found that having HCV for 25 years or longer increases the chances of disease progression. (See the Healthwise column in this issue for more on Age and HCV)

Fatty liver or steatosis can contribute to lower HCV treatment response and a faster rate of HCV disease progression.  The cause of steatosis in most people with HCV is a synergistic effect of the virus, poor diet and lack of exercise.  If you are HCV genotype 3, however, steatosis is most likely caused by the hepatitis C virus.  For example, in people with genotype 3 who are successfully treated with HCV medications steatosis has been found to be decreased or eliminated.  This is not true of steatosis in people with HCV non-3 genotype. 

For most people, steatosis can be prevented and even reversed by the simple, but not so easy, methods that we all struggle with – a healthy diet and exercise program.  We recommend that anyone who undertakes a diet and exercise program consult with a medical provider and experts in the field of diet and exercise.  Unfortunately, these tools are not available to everyone; but there are still many avenues and resources open to become even healthier.  On the internet there is a wealth of diet and exercise sites to help.

There have been some studies that have found that regular daily use of marijuana can significantly increase the risk of fibrosis progression.  There is a caveat, however, about the data that has surfaced.  The studies have been self-disclosure studies that are typically extremely difficult to gauge as to how truthful people may answer questions about how much they smoke.  But the most important factor is that it is impossible to measure the concentrations of THC (the active ingredient in marijuana) that the participants were smoking.  Interestingly, the studies that report that daily marijuana causes significant fibrosis progression also report that non-daily use of marijuana did not accelerate fibrosis progression.  The bottom line – more is not better when it comes to many issues including using marijuana. 

I don’t think anyone these days would be surprised to learn that smoking cigarettes causes many health-related problems including increasing the chances of fibrosis progression and liver cancer. (See “How Does Smoking Affect Hepatitis C Progression?” by Liz Highleyman on in this issue.)

Another no-brainer is that alcohol consumption can increase fibrosis and cirrhosis progression.  Excessive alcohol consumption – in and of itself – can lead to cirrhosis, liver failure and liver cancer.  If both of the negative effects, alcohol and HCV, were combined I think it’s easy to see why people with HCV should avoid alcohol.  If someone has trouble stopping, they should cut back on the amount of alcohol they drink and get help to stop.  There are many effective programs to help people stop drinking. 

Metabolic Syndrome
In the last decade the relationship between metabolic disorders and fibrosis progression has been well-documented.  Metabolic disorders are a group of conditions that increase the likelihood for cardiovascular disease and other health problems.  Components of metabolic syndrome include:

  • Abdominal obesity
  • High blood cholesterol and high triglycerides
  • High blood pressure
  • Insulin resistance
  • State of inflammation caused by obesity, insulin resistance, etc.
  • Prothrombotic state – increased platelets

Although there are different components that define metabolic syndrome they are also interconnected especially with obesity.  Obesity and insulin resistance are the two factors that stand out as factors that increase fibrosis progression.  A simple tool to measure insulin resistance is the HOMA-IR – the higher the score, the higher the degree of insulin resistance.  The higher the HOMA-IR score, the more rapid fibrosis progression is. 

Many of the factors of metabolic syndrome can be treated with lifestyle changes (diet, exercise, stress reduction) and medications to control diabetes, high blood pressure, cholesterol, etc. 


For More on HCV Disease Progression go to:


HCV Disease Progression
PDF Acute Hepatitis C
PDF Cirrhosis

PDF Fibrosis
PDF Steatosis
PDF Liver Transplantation
PDF Symptoms and Complications of Cirrhosis


Treatment Issues
PDF A Guide to Hepatitis C: Making Treatment Decisions
PDF A Guide to Hepatitis C: Preparing for Treatment
PDF A Guide to Hepatitis C: Treatment Side Effect Management
PDF After HCV Treatment: An HCSP Guide
PDF HCV Negative: A Guide for Healthy Living without HCV

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