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In This Issue:
Why We Should Test: Editorial
Alan Franciscus, Editor-in-Chief
Lucinda K. Porter, RN
Liver Transplantation: HCV Recurrence and Treatment
HealthWise: Humor, Health, and Hepatitis C
Lucinda K. Porter, RN
HCV Advocate Eblast
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Why We Should Test: Editorial
—Alan Franciscus, Editor-in-Chief
I have received many inquiries lately asking for my opinion on testing for hepatitis C (HCV). This is a hotly debated topic because many of the people who might be tested do not have access to medical care. I think the renewed interest in mass testing is because of the newly approved OraQuick HCV Antibody Test (finger prick and whole blood has been approved—we are all waiting, waiting, waiting for the oral swab to be approved and used). Another reason for the increased interest is the pending approval of the new triple combination therapy of an HCV protease inhibitor and pegylated interferon plus ribavirin which promises increased cure rates and a shorter treatment duration for some.
You should know, however, that I have a bias about this issue. I believe that everyone should be tested for hepatitis C regardless of access to medical care. When I mean everyone I don’t mean the entire population: I am referring to various models such as the aged-based testing model—that is, to test everyone at a certain age (more about the aged-based model in a future article).
Testing everyone for HCV regardless of medical coverage is a very contentious issue and I want to acknowledge the very real concerns about testing everyone. I really do get it: We may be causing more harm than actually providing benefit. This would definitely be the case if people were not offered some help after the initial positive (or negative) test results. At the point of time when a person has been given the tests results there are many things we can provide the newly diagnosed person with that will ultimately benefit them and that far outweigh the potential harm. For this article I am only going to talk about people who are given positive test results.
If someone is diagnosed one of the first pieces of information should be prevention strategies. This information (to me) is reason enough to offer testing to everyone at risk. How can we stop the transmission of hepatitis C if people don’t know they have it? Another aspect of prevention measures is protecting the person who is diagnosed from getting another type of infection. This provides protection for the person and the community at large.
At the time of diagnosis with an HCV antibody test we have to remember to counsel patients that there is a chance that about 1 in 4 people will have cleared the virus naturally. We tell people to live like they have hepatitis C until they find out otherwise. An additional benefit for the person who tests antibody positive, but HCV RNA (viral load) negative is preventing a future infection with HCV.
A measure to prevent panic when someone is newly diagnosed is to explain to him or her that having the hepatitis C virus is not a death sentence. Further clarification should include information about why it is so important to make certain lifestyle changes and seek medical care to prevent further disease progression.
There are many additional support strategies we can use to help keep people healthy until the time that they can get medical care. These include:
We can protect people from harm by providing the hepatitis A and hepatitis B vaccine if they have not already been infected. Being infected with two liver infections could lead to more serious and potentially deadly consequences.
We can advise the person that they should not eat raw or undercooked shellfish (oysters, clams, etc.) and should avoid swimming or wading in warm brackish water (such as the Gulf of Mexico) because of the risk of contracting vibrio vulnificus a potentially lethal bacterial infection that attacks the liver. Contracting vibrio can cause harm to anyone, but it is especially dangerous for people with an existing liver disease such as hepatitis C.
We should also educate and encourage the newly diagnosed person about lifestyle changes that can keep them healthy until they can get medical care:
- Avoid alcohol or greatly reduce the amount of alcohol they are drinking. Drinking alcohol can cause additional damage to the liver. If people can’t stop, try to get them to cut back on the amount of alcohol consumed with the ultimate goal of avoiding alcohol altogether. It is important to remember that alcohol is an addictive substance so the newly diagnosed person may have trouble with complete abstinence. There are many rehabilitation programs for people who are addicted to substances—this would be a good time to try to help the newly diagnosed person explore some of these options. In fact, it is probably one of the best things that people can do to keep their liver and whole body healthier.
- Avoid smoking cigarettes or cut down on the amount that they smoke. Smoking cigarettes has been linked to a whole array of health problems as well as to liver cancer. Cigarettes are one of the most addictive substances known so it is good to plant the seed of eventually stopping.
- Although there is very little research data on the effects of taking street drugs on hepatitis C there are some issues that should be discussed with the newly diagnosed person such as what substances were used to cut the drug with that could add to the overall harm caused to the liver.
- The newly diagnosed person should try to get their medical provider to evaluate any prescription, over-the-counter medications, herbs and supplements they are taking to make sure the liver is not being harmed. When in doubt, stop taking anything unless it is first screened by a medical provider.
- Drink a lot of clear fluids like water to stay as well-hydrated as much as possible. This is good for overall health maintenance.
- Try to eat a healthy and well-balanced diet. This is not easy for many people especially those who have little or no income, but there are options that do not cost a lot of money—like water, vegetables, and fruits. Stay away from foods that contain a lot salt, sugar or if the food is overly processed.
- Another piece of information that needs to be discussed is HCV treatment. Very soon, we will have the new HCV protease inhibitor combination therapy that will greatly increase the response rates. It is never too early to work toward getting a person’s overall health stabilized, getting adequate medical insurance and putting together a support network to prepare for the eventual time when the person will go on HCV therapy. At the time when someone is ready to seek HCV therapy all of these various issues will hopefully be resolved, and this will mean that treatment will be easier to start and stay on and hopefully lead to a better treatment outcome—cure! In another 5-7 years many experts believe that an interferon-free regime will be available that will approach a 100% success rate. Interferon-free therapy and the higher cure rates will allow almost everyone with chronic hepatitis C to seek treatment with antiviral medications.
A person who is newly diagnosed will have a lot of questions. Try to provide them with verbal and written information to reduce fear and to start the education process. A basic resource list can be given to the person that lists where to go for free or low cost services.
If there is a support group in your area, try to get them to attend at least one meeting. Most people get information about HCV and other important information from support group members. Also check to see if there is a clinical social worker that you can refer the newly diagnosed person to so they could begin the process of applying for public assistance if needed or help them to take advantage of other low-cost or free services.
Another referral would be to clinical trials. Clinical trials may be a way to cover the costs of medical visits, drugs, lab work, etc. In some ways, a person who enters into a clinical trial can receive even better medical care compared to a private practice because there is a medical person assigned—a clinical trial coordinator who oversees the patient’s care. There are many clinical trials for treatment-naïve (never been treated) or treatment-experienced patients. You can help the person by showing them the process of finding clinical trials by going to www.clinicaltrials.gov
As a person who was diagnosed in 1996, I believe I would have greatly benefited physically and emotionally by knowing my HCV status earlier on. I feel like I had years of needless worry about my physical symptoms like fatigue, muscle and joint pain, night sweats, and declining cognitive issues that would have been easier to take if I had only known I had hepatitis C. AND if I had known earlier I could have developed strategies to manage the symptoms and made lifestyle changes that would have helped my long-term health.
Finally, I am not sure why we are even making this decision for the person being tested—shouldn’t the ultimate decision about testing be left up to the person who is being offered the test? We can provide a realistic picture of the potential benefits and risks of being tested and let the person make the decision. This approach is probably too simple, but it certainly works for me!
I would be very interested to hear from our readers about what they think about this issue. Email me at firstname.lastname@example.org
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—Lucinda K. Porter, RN
Article: Silibinin Monotherapy Prevents Graft Infection after Orthotopic Liver Transplantation in A Patient with Chronic Hepatitis C—Sandra Beinhardt, Susanne Rasoul-Rockenschaub, Thomas Matthias Scherzer, Peter Ferenci
Source: Journal of Hepatology March 2011; Vol. 54, Issue 3, pages 591-592
Silibinin is one of the active ingredients found in milk thistle, an herb believed to have properties that help the liver. One of the investigators in this study, Peter Ferenci demonstrated silibinin’s anti-viral properties in previous studies when used intravenously (IV) in patients infected with hepatitis C virus (HCV). In this research, IV silibinin was given to a patient following liver transplantation. Typically HCV is active despite liver transplantation, so researchers are looking for ways to suppress or eliminate HCV in order to protect the transplanted organ.
After continual silibinin infusions, the patient had undetectable HCV on day 22 following transplantation. Silibinin was stopped on day 25 and the patient remained HCV-negative at the 5-month follow-up visit.
The Bottom Line: In one post-transplant patient, silibinin showed remarkable potential as a treatment choice for chronic HCV infection.
Editorial Comment: A case study involving one patient does not provide enough evidence to change the standard of care, but this is still an exciting finding. It is wonderful to see solid research on the use of milk-thistle derivatives. This case study raises the possibility of alternatives for those who can’t tolerate or don’t want to take the combination therapy of peginterferon with ribavirin.
Article: Use of Surveillance for Hepatocellular Carcinoma among Patients with Cirrhosis in the United States—Jessica Davila, Robert Morgan, Peter Richardson, Xianglin Du, Katherine McGlynn, Hashem El-Serag
Source: Hepatology July 2010; Volume 52, Issue I, Pages 132-141
People with alcoholic liver disease, hepatitis B or late-stage hepatitis C are at risk for liver cancer, specifically hepatocellular carcinoma (HCC). HCC rates have doubled in the past two decades and are expected to triple in the next two decades. Late stage HCC has a poor prognosis, but is often treatable with early detection. Clinical practice guidelines were developed to help identify those at risk for HCC.
In this population-based study of Medicare-enrolled patients of 65 and older, 1873 patients with HCC were enrolled; all had a prior diagnosis of cirrhosis during 1994-2002. Researchers learned that adequate HCC screening (ultrasound and AFP testing) occurred in 17% of those at risk. Inadequate screening was performed on 38% of those at risk (only ultrasound or AFP testing). Patients with higher incomes or living in urban areas were more likely to be adequately screened for HCC. Patients who received medical care from a gastroenterologist or hepatologist were 4.5 times more likely to be screened for HCC compared to those seen by primary care physicians. Other patients who were more likely to be screened were younger, Asian, women, or diagnosed in recent years. Those receiving health care from providers associated with medical schools were more likely to be screened.
The Bottom Line: Screening for liver cancer is inadequately performed in the U.S.
Editorial Comment: If you have any risk factors for HCC, such as hepatitis B, alcoholic liver disease, cirrhosis or even stage 3 fibrosis, you should be screened every 6 months for liver cancer. These simple tests are covered by insurance.
Article: Enhanced Efficacy of Pegylated Interferon Alpha-2a over Pegylated Interferon and Ribavirin in Chronic Hepatitis C Genotype 4A Randomized Trial and Quality of Life Analysis— Sanaa M. Kamal, Amany Ahmed, Sara Mahmoud, Leila Nabegh, Iman El Gohary, Isi Obadan, Tamer Hafez, Dahlia Ghoraba, Ahmed A. Aziz, Mona Metaoei
Source: Liver International March 2011 Volume 31, Issue 3, pages 401–411
This was a randomized, prospective, parallel-group clinical trial based on the premise that treatment for genotype 4 HCV patients is not optimal. Subjects were randomized to one of two arms: weekly 180 µg pegylated interferon a-2a (PEG-IFN a-2a), or weekly 1.5 µg/kg pegylated interferon a-2b (PEG-IFN a-2b). Both groups received a daily dose of ribavirin (1000–1200 mg) for 48 weeks with 24 weeks post-treatment follow-up. Safety, efficacy, and quality of life were measured; 219 subjects were enrolled.
Overall results were a 60% sustained virologic response (SVR) rate. Patients in the PEG-IFN a-2a had a significantly higher SVR at 70.6% versus 54.6% for PEG-IFN a-2b group. Quality of life was low during HCV treatment but significantly improved after successful treatment.
The Bottom Line: In this study, PEG-IFN a-2a with ribavirin had much better SVR’s compared to PEG-IFNαa-2b with ribavirin.
Editorial Comment: There have been a number of studies comparing PEG-IFN αa-2a and PEG-IFN a-2b. The results are mixed, with no clear “winner.” Although this study seems better designed than most, it is small; a larger study would be the next logical step.
Article: IL28B Genomic-based Treatment Paradigms for Patients with Chronic Hepatitis C Infection: the Future of Personalized HCV Therapies— Paul Clark, Alex Thompson, John McHutchison
Source: American Journal of Gastroenterology. January 2011, pages 38-45
One of the most exciting developments in hepatitis C research has been the discovery that genetic variations may predict how well patients are likely to respond to treatment. Genotype 1 patients who have a particular genetic coding in the IL28B gene—C/C genotype—are twice as likely to respond to HCV treatment. IL28B C/C genotype is associated with spontaneous clearance of HCV. Also, IL28B genotype varied among ethnic groups, providing a possible explanation for the differences between treatment response rates between Caucasians, African Americans and Asians.
The Bottom Line: The presence of IL28B gene variations may play a huge role in determining treatment regimens for HCV patients. This knowledge may allow medical providers to tailor treatment for specific genetic variations, thus maximizing patients’ chances of obtaining an SVR.
Editorial Comment: Just a little over 20 years ago, HCV didn’t have a specific name. Shortly after, we learned that certain genotypes were more resistant to treatment. Now the body of knowledge has been further refined, and with each discovery, solutions seem to follow. The role of IL28B to predict treatment response in an HCV protease inhibitor containing therapy has yet to be completely elucidated. Hopefully, more information will be available in the near future.
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Liver Transplantation: HCV Recurrence and Treatment
Hepatitis C is the leading indication for liver transplantation in the U.S. As described in the March HCV Advocate, advances in surgical techniques and medical management have improved transplant outcomes, but people with hepatitis C virus (HCV) still do not fare as well as patients receiving new livers for other reasons.
In most cases HCV infects the donor liver graft, usually soon after surgery. Just as it did in the original liver, the virus—or more precisely, the body’s response to the virus—can lead to fibrosis, cirrhosis, and hepatocellular carcinoma.
Research has shown that disease progression is more rapid, on average, among liver transplant recipients. An estimated 25% to 30% of HCV-infected transplant recipients develop cirrhosis within five to ten years, a process that typically takes decades in people with their original livers. Some transplant patients, however, do not experience aggressive disease progression.
A number of virus and host factors are associated with rapid fibrosis progression, including HCV genotypes 1 or 4 (versus 2 or 3), non-white race/ethnicity, older donor and recipient age, and longer ischemia time (how long the graft goes without oxygen between removal from the donor and insertion into the recipient).
In the August 30, 2010, Journal of Experimental Medicine, French researchers reported that only the most efficient pre-transplant HCV strains could evade immune defenses and re-infect the new liver. Another team reported in the July 2010 issue of Virology that patients with less HCV genetic diversity were more likely to experience poor post-transplant outcomes.
Recent research finds that host genetic factors also play a role. A study presented at the 2010 American Association for the Study of Liver Diseases (AASLD) Liver Meeting showed that variations in the IL28B gene¾which has been linked to spontaneous HCV clearance and response to interferon-based therapy¾also influences the timing of HCV recurrence after liver transplantation. M. Charlton and colleagues from the Mayo Clinic found that transplant recipients with the protective rs12979860 C/C pattern had later recurrence.
Immunosuppressive medications used to prevent organ rejection can impair immune response to HCV, resulting in higher viral load and faster fibrosis progression. But studies have produced conflicting findings about which immunosuppressive drugs have the most detrimental effects and which are the safest for transplant recipients with hepatitis C.
Liver transplant patients with hepatitis B virus (HBV) can take antiviral drugs, immune globulin (antibodies), and the hepatitis B vaccine to prevent the virus from attacking their new liver graft. Unfortunately, such measures do not work well for people with hepatitis C. There is no effective HCV immune globulin product or vaccine, and anti-HCV therapy has only limited success. As a consequence, recurrent HCV is a leading cause of graft failure and death among liver transplant recipients.
The optimal time to start interferon-based therapy for patients undergoing liver transplantation remains unclear. People with advanced liver damage awaiting transplants have lower sustained virological response (SVR) rates and often have difficulty tolerating the side effects of interferon and ribavirin, but this group has the most pressing need for effective treatment.
Antiviral therapy has traditionally been considered contraindicated for individuals with decompensated cirrhosis, but several studies have shown that it can be successful with careful monitoring.
At the 2008 Digestive Disease Week conference, A. Retana and J. Wong reported findings from a systematic review of studies looking at the risks and benefits of pre-transplant interferon-based therapy for hepatitis C patients with decompensated cirrhosis. Among 255 total participants, the overall SVR rate was 23%. Although 30% of patients required dose reductions due to adverse effects and 24% discontinued treatment, those who remained untreated fared worse, with a higher likelihood of adverse outcomes and a two-fold higher mortality rate.
Some studies find that patients who achieve SVR while awaiting liver transplantation may have a reduced risk of post-transplant HCV recurrence. In an August 2005 review article in Hepatology, for example, G. Everson from the University of Colorado estimated that successful pre-transplant treatment prevents HCV recurrence in as many as 25% of cases.
But most apparent sustained responders with “undetectable” HCV RNA still experience recurrence after transplantation, indicating that some virus remains in the body waiting for an opportunity to attack the new liver. Several studies have shown that people with unmeasurable post-treatment viral load using standard PCR tests can have residual detectable HCV RNA using more sensitive assays.
Even though low-level HCV remains in the body, however, pre-transplant treatment responders have less severe recurrence on average, with lower viral loads and less rapid fibrosis progression compared with nonresponders. While tolerability of therapy remains a serious concern, Everson advised that it is often worth pursuing since pre-transplant treatment can improve post-transplant outcomes.
After transplantation patients may either start preemptive antiviral therapy right away in an effort to prevent HCV recurrence and liver damage, or else wait until liver disease progression has started to occur.
As noted, interferon-based therapy does not really act as post-exposure prophylaxis to prevent HCV from infecting the liver graft, as antiviral drugs do in the case of HBV. Nevertheless, interferon-based treatment after transplantation has been shown to improve outcomes in numerous studies. The new direct-acting anti-HCV drugs have not yet been tested in people with decompensated cirrhosis or liver transplant recipients.
Thinking that treatment might work best if started early—while HCV RNA levels are still low and damage to the new liver has not yet occurred—researchers have studied preemptive interferon-based therapy within the first few weeks after transplantation. Results have been disappointing, however, since transplant recipients at this stage often have blood cell deficiencies, kidney dysfunction, and increased susceptibility to infection, making it hard to tolerate the side effects of interferon and ribavirin. A 2007 review of randomized trials of preemptive therapy found SVR rates ranging from about 10% to about 30%.
Based on a more recent systematic review of medical literature and conference presentations published in the January 2011 issue of Alimentary Pharmacology and Therapeutics, P. Guillouche and C. Feray concluded that while antiviral therapy “must be considered” before liver transplantation, it is “poorly tolerated and has poor results in patients with cirrhosis and end-stage liver disease or hepatocellular carcinoma.”
For this reason, many experts recommend a “watch and wait” strategy, deferring therapy until liver biopsies and other tests indicate disease progression. The advantage of this approach is that transplant recipients who will never experience serious recurrent liver damage can avoid unnecessary treatment.
Looking at post-transplant interferon-based therapy for patients who do experience disease progression, most studies have observed SVR rates around 30% to 40% for patients with a mix of HCV genotypes — considerably lower than sustained response rates for non-transplant patients. Reduced response is attributable in part to inability to use adequate doses of interferon and ribavirin for a long enough period of time.
For example, the PROTECT study, reported at the 2010 annual meeting of the European Association for the Study of the Liver (EASL), evaluated the safety and efficacy of pegylated interferon plus weight-adjusted ribavirin in 125 U.S. transplant recipients. SVR rates were 24% for patients with HCV genotype 1 and 55% for genotypes 2 or 3. Among participants who completed therapy, however, sustained response rates rose to 51% and 69%, respectively. But more than half the patients required dose reductions and 30% discontinued treatment due to adverse events.
As reported in the August 2008 Journal of Hepatology, M. Berenguer and colleagues performed a systematic review of published studies of pegylated interferon plus ribavirin in patients with recurrent liver disease after transplantation. They identified 19 studies published between 2004 and 2007 that included a total of 611 patients (86% with HCV genotype 1). Participants started treatment an average of two years after transplantation, at which point most had mild to moderate liver disease.
The overall average SVR rate was 30%, rising to 60% or higher for patients with non-1 genotypes. But about three-quarters of participants required dose reductions and about 25% discontinued treatment due to side effects. Guillouche and Feray’s review likewise found combination therapy response rates of up to 30% in patients with post-transplant HCV recurrence.
In Charlton’s study, the protective IL28B C/C pattern was more
common in donor livers than in recipients, meaning some patients got a liver graft with a more favorable pattern. The post-transplant SVR rate was 86% if both the recipient and donor had the C/C pattern, 50% if only the donor liver had the favorable pattern, 42% if only the recipient had the C/C pattern, and just 16% if neither had the favorable pattern. A Spanish study likewise found that favorable patterns at both the rs12979860 and rs8099917 gene locations led to better treatment response. Four patients who did not carry protective IL28B patterns themselves went from being pre-treatment nonresponders to post-treatment responders after receiving donor livers with more favorable patterns.
Both research teams suggested that donor livers with favorable IL28B patterns might be preferentially allocated to hepatitis C patients, since this group stood to benefit more than individuals receiving transplants for other reasons.
Sustained response to interferon-based therapy not only suppresses viral load in transplant patients, but also leads to clinical benefits.
Several studies have demonstrated that sustained response slows or halts fibrosis progression. Berenguer’s review, for example, found that liver biopsies of treatment responders generally showed lack of progression or even improvement in histological activity.
Similarly, a 30-person study by A. Kornberg and colleagues, published in the August 15, 2008, issue of Transplantation, found that none of the one-third of recipients who achieved sustained response to interferon/ribavirin experienced fibrosis progression, while all nonresponders did so.
At the 2007 EASL meeting Spanish researchers reported findings from a study in which transplant recipients with mild (F0-F2) or severe (F3-F4) recurrent liver fibrosis were treated with pegylated interferon/ribavirin. People who achieved SVR had a reduced fibrosis progression rate, and patients with stable or improved fibrosis also experienced stabilized or reduced hepatic vein pressure, an indicator of liver decompensation. These results, the researchers concluded, “support a less restrictive indication” for antiviral therapy in transplant patients with advanced liver disease.
At the 2010 AASLD meeting M. Rendina and colleagues reported that successful post-transplant treatment also reduces mortality. An analysis of medical records from 448 Italian transplant patients with recurrent HCV over 20 years showed that 35% achieved SVR. Sustained response was “highly protective” against liver-related death, the researchers found. In fact, all but one of the patients who died¾73% of them due to HCV-related causes¾ had been unable to achieve SVR.
Taken together, these findings show that liver transplant recipients are considerably less likely to respond to interferon-based therapy, but those who do have reduced fibrosis, fewer negative clinical outcomes, and lower mortality. Further studies are needed to determine whether new direct-acting antiviral drugs will improve response rates in this difficult-to-treat population.
Berenguer M. Systematic review of the treatment of established recurrent hepatitis C with pegylated interferon in combination with ribavirin. Journal of Hepatology 49(2): 274-287. August 2008.
Charlton M et al. IL28B polymorphisms are associated with histological recurrence and treatment response following liver transplantation in patients with HCV with HCV Infection. 61st Annual Meeting of the American Association for the Study of Liver Diseases. Boston, October 29-November 2, 2010. Abstract 1.
Coto-Llerena M et al. IL28B polymorphisms may improve response to hepatitis C therapy after liver transplantation. 61st Annual Meeting of the American Association for the Study of Liver Diseases. Boston, October 29-November 2, 2010. Abstract 1140.
Everson GT et al. Treatment of advanced hepatitis C with a low accelerating dosage regimen of antiviral therapy. Hepatology 42(2): 255-262. August 2005.
Fafi-Kremer S et al. Viral entry and escape from antibody-mediated neutralization influence hepatitis C virus reinfection in liver transplantation. Journal of Experimental Medicine 207(9): 2019-2031. August 30, 2010.
Gordon F et al. Peginterferon alfa-2b and ribavirin for hepatitis C recurrence post orthotopic liver transplantation (OLT): final results from the PROTECT Study. 45th Annual Meeting of the European Association for the Study of the Liver. Vienna, Austria. April 14-18, 2010.
Guillouche P and Feray C. Systematic review: anti-viral therapy of recurrent hepatitis C after liver transplantation. Alimentary Pharmacology and Therapeutics 33(2):163-174. January 2011.
LiH et al. Genetic diversity of hepatitis C virus predicts recurrent disease after liver transplantation. Virology 402(2): 248-255. July 5, 2010.
Rendina M et al. SVR to antiviral therapy is highly protective against liver-related death in patients with HCV recurrence on the graft after liver transplantation (LT). 61st Annual Meeting of the American Association for the Study of Liver Diseases. Boston, October 29-November 2, 2010. Abstract 4.
Retana A and Wong J. Pre-transplant antiviral treatment of hepatitis C with decompensated cirrhosis: a systematic review of risks and benefits. Digestive Disease Week 2008. San Diego, CA. May 17-22, 2008. Abstract S1011.
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HEALTHWISE: Humor, Health, and Hepatitis C
—Lucinda K. Porter, RN
Regular Healthwise readers know that my April column leans towards humor, in honor of April Fool’s Day. I’ve long been interested in the therapeutic side of humor, so when I write, I try to amuse as well as inform. Let’s face it, chronic hepatitis C virus (HCV) is a heavy topic and it needs lightening up. However, I will start on a serious note.
A slogan that I state repeatedly is that although HCV is a serious, potentially fatal condition, the majority of us will die with, not of this virus. That may sound like good news, but it is tempered with the reality that we are at the threshold of a problem; HCV-related complications are expected to increase in the next two decades. At the 2009 meeting for the American Association for the Study of Liver Diseases (AASLD), Gary Davis and colleagues presented data1 arguing that 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 peaking at 1 million people in 2020.2 They estimate that the severest form of cirrhosis (decompensation) will rise until 2022. HCV-related liver cancer will peak in 2019 with 14,000 cases annually.
Despite this projected burden, good news is on the horizon. New treatments with excellent results are in the pipeline; two treatments are being reviewed by the FDA, and news about these should be out soon. The other good news is that you can have HCV and still be happy. Stick with me for a moment, especially if you are rolling your eyes or grabbing a barf bag.
I believe that happiness is product of attitude, and not the result of how my body feels. Granted, if I am in pain, my attitude is unlikely to be doing cartwheels. Depression, fatigue, HCV treatment, and other medical conditions would probably make Pollyanna turn into Eminem. Even the remarkable physicist, Stephen Hawking, who has lived with Lou Gehrig’s disease (also known as ALS) since the 1960’s, has suffered a couple bouts of depression.
Although attitude adjustment leads to happiness, I am not suggesting that the cure for the doldrums is something like Julie Andrews singing “My Favorite Things” in The Sound of Music. I can’t imagine Stephen Hawkings prancing around with his respirator belting out “Raindrops on roses and whiskers on kittens.”
The elements that help me keep my spirits up are acceptance, patience, intention, and humor. Acceptance means that I accept my reality. If I am feeling like excrement, then I need to accept that fact. (Note: as a nurse, I can sneak technical terms such as excrement past my editor, but I am sure you know what I really meant to say.) Accepting the truth means that I don’t pretend that everything is rosy when it is not. Patience helps me get through the scatological stage.3 Patience is the ability to endure discomfort; it is that deep inner knowing that this mood or circumstance will pass. Intention is my commitment to changing my present circumstance or feeling about it. Humor is what I use to endure the unendurable.
The therapeutic effects of humor have been studied scientifically for at least 50 years. William Fry, psychiatrist and professor emeritus at Stanford University Medical Center, studied the biology of humor beginning in the early 1960’s. His research showed the therapeutic benefits of laughter, particularly on the immune system. Laughter also improves mood and the ability to manage pain.
Norman Cousins increased our awareness about the potential of humor to heal with an article published in the New England Journal of Medicine. (Anatomy of an Illness as Perceived by the Patient N Engl J Med 1976; 295(26):1458–63) Cousins confronted two life-threatening illnesses and credited his recovery to the fact that he prescribed a marathon of comedies for himself. Cousins turned his personal experience into a lifelong avocation.
Cousins’ experience is not science. I cannot argue that because one man watched Candid Camera reruns and got well twice, that humor is a cure-all. What I can say with certainty is that humor seems like a much better way to endure anything, regardless of the outcome. So, if I don’t feel well, I have nothing to lose by using humor. It’s not going to harm anything unless I had mouth or stomach surgery and it hurts to laugh.
If you are looking for evidence about humor and HCV, you aren’t going to find it because it hasn’t been done. Although more than 9000 results showed up searching Google Scholar using the words hepatitis C and humor, the articles either discussed patients’ lack of humor as a symptom of depression or aqueous humor, which is fluid in the eye. However, if you aren’t laughing because research hasn’t shown that it improves HCV, then perhaps you are depressed. If I wasn’t laughing because I needed a scientific reason to, I’d be swimming in some serious excrement and I hope I’d get some help.
So, I think it is time for a new slogan to replace “The majority of us will die with, not of HCV.” How about this: “All of us are going to die of something, so we might as well laugh as much as we can until then.”
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 National Health and Nutrition Examination Survey (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. Scatological refers to the study of fecal matter and people who do this are scatologists. Can you imagine meeting someone at a party and asking them what they do for a living and they reply, “I am a scatologist.” The opportunities for witty replies are endless. If the guy’s name is John, it would be a too much for me to bear.
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