Back to Newsletters
Download printable version
In This Issue:
HCV Protease Inhibitor—TMC435: Phase 3 Studies
Alan Franciscus, Editor-in-Chief
Hepatitis C in Egypt
Alan Franciscus, Editor-in-Chief
Lucinda K. Porter, RN
Liver Transplantation: An Overview
HealthWise: The Power Is in Our Hands
Lucinda K. Porter, RN
HCV Advocate Eblast
Stay informed on the latest news ..click here to register for email alerts
Back to top
HCV Protease Inhibitor—TMC435: Phase 3 Studies
—Alan Franciscus, Editor-in-Chief
On February 18, 2011, Tibotec Pharmaceuticals announced that they will begin three different phase 3 studies of their investigational drug TMC435—a once-a-day HCV protease inhibitor (tablet) taken in combination with pegylated interferon and ribavirin. The studies will be guided by type of on-treatment response—12 weeks of triple combination of TMC435/Pegylated interferon/ribavirin followed by an additional 12 or 36 weeks of the combination of pegylated interferon/ribavirin (without TMC435). The pegylated interferon used in the trials will be Pegasys except where noted.
- QUEST-1 (TMC435-C208): Treatment-naïve (never been treated) patients will receive either TMC435 (100 mg) QD (once-a-day) or placebo
- QUEST-2 (TMC435-C216): Treatment-naïve patients will receive either TMC435 QD (150 mg) or placebo. In this trial different treatment arms use either Pegasys or PegIntron
- PROMISE (TMC435-C3007): Patients who had been previously treated with interferon-based therapy, but who relapsed (the viral load becomes undetectable, then detectable) during therapy will receive TMC435 QD (100 mg) or placebo
Tibotec expects to enroll 1,125 HCV genotype 1 patients in 24 countries with a total of 160 clinical trial sites worldwide.
On February 22, 2011 interim results from a phase 2 study were released and 278 patients results were made available:
For HCV genotype 1 treatment-naïve patients using TMC435 QD (75 or 150 mg) the sustained virological response (SVR) rates were 76 to 84% in the groups that received TMC435. The study was response guided with 83% of patients being able to stop all therapy at 24 weeks.
Interim results from another phase 2 study of 462 HCV Genotype 1 patients who had not achieved an SVR with a previous course of interferon plus ribavirin therapy were released late last year. The patients in the study received either TMC435 QD 100 or 150 mg plus pegylated interferon/ribavirin for a period of either 12, 24 or 48 weeks. All of the patients in the trial received TMC435, but some took TMC435 for a shorter period of time; however, all of the patients in the trial continued on with pegylated interferon plus ribavirin, but without TMC435. The 24-week interim results found that 94% of relapsers, 86% of partial responders, and 78% of null responders were HCV RNA undetectable at week 24.
In both trials the side effect profile was similar between all treatment arms and consistent with side effects seen with pegylated interferon plus ribavirin therapy.
To find a clinical trial in your area go to www.clinicaltrials.gov, type in “HCV” and drill down to find the enrollment criteria and location of the trial sites.
Source: Company press release / www.clinicaltrials.gov
Back to top
Hepatitis C in Egypt
—Alan Franciscus, Editor-in-Chief
The world has recently focused on the extraordinary events that have taken place in Egypt that will hopefully lead to the implementation of a truly democratic form of government. There is, however, another important crisis in Egypt that has been largely ignored by the government—hepatitis C infection.
Worldwide, Egypt has the highest prevalence of HCV of any country—estimated at up to 13% of the population, and about 90% of these are HCV genotype 4.
Hepatitis C is spread by blood-to-blood contact. In Egypt the transmission routes are believed to be from sharing needles and works for injection drug use (medical, traditional practices and recreational use), receiving a blood transfusion or an organ transplant when blood and organs are not screened, dental practices, circumcision, and medical care from local informal health providers and centers. But the most likely transmission route for the majority of the infected population is the result of a mass campaign in the 1960’s though the 1980’s to control schistosomiasis infection—a parasite transferred by snails to humans in water. At that time schistosomiasis was treated with injections of a medication called tartar emetic using unsterilized syringes. Yes, you read that correctly – dirty needles.
In general, HCV disease progression in people with genotype 4 is the same as the other genotypes. In Egypt, however, coinfection with schistosomiasis accelerates HCV disease progression because the parasite can live for years in the body and is constantly replicating and infecting the liver.
Regarding treatment with pegylated interferon plus ribavirin therapy to treat people with HCV genotype 4 the sustained virological response (SVR) ranges from 50 to 79%, which is higher than SVR rates seen in people with HCV genotype 1 but generally lower than SVR rates seen in people with HCV genotype 2 and 3. Various studies of pegylated interferon plus ribavirin found that people with a low viral load could be treated for 24 weeks and achieve similar SVR rates to those treated for 48 weeks regardless of viral load. Based on additional studies using on-treatment response guided-criteria it was found that treatment duration and success could be tailored to 24, 36 or 48 weeks. An investigational drug, nitazoxanide, added to pegylated interferon plus ribavirin is being studied that could possibly increase SVR rates and shorten the treatment period to 24 or 36 weeks.
In people with genotype 1 the approval of the new HCV protease inhibitors (PI’s) are expected in May 2011. There have been few studies of the new HCV PI’s in people infected with HCV genotype 4 so it is not known what the effect of these PI’s will be on the genotype 4 population inside and outside of Egypt. The potential use of PI’s in Egypt is further complicated by the lack of studies in the Egyptian population with genotype 4, the limited resources, lack of health care insurance and services available to the masses, and the projected increase in cost of the PI’s mean that few Egyptians will have access to the new PI’s.
Hopefully, the newly elected democratic government will translate into a booming economy that will allow for more government intervention to tackle the hepatitis C epidemic in Egypt.
Back to top
—Lucinda K. Porter, RN
This month’s HCV Snapshots features articles that appeared in Liver International’s Supplement Issue published for the 4th Paris Hepatitis Conference in January 2011.
Article: The Role of Triple Therapy with Protease Inhibitors in Hepatitis C Virus Genotype 1 Naïve Patients – David R. Nelson.
Source: Liver International January 2011; Volume 31, Supplement Issue, pages 53 - 57.
With protease inhibitors poised for FDA-review, Dr. Nelson discusses the potential impact and issues related to these new medications for treatment of chronic hepatitis C virus (HCV) infection. In the pipeline are telaprevir and boceprevir and either are used with peginterferon and ribavirin as triple therapy.
Research results of triple therapy using telaprevir or boceprevir yielded higher cure rates for all test groups and shorter treatment lengths for some patients. Genotype 1 patients without prior treatment who were treated with triple therapy had significantly higher cure rates compared to those treated with peginterferon and ribavirin. The really exciting feature of triple therapy is the concept of response guided therapy (RGT). This means that patients who responded quickly to the medications (non-detectable virus after 4 weeks of medications) were eligible for shorter lengths of treatment—sometimes as little as 24 weeks rather than 48 weeks for genotype 1 patients. This quick and early response is called a rapid virological response (RVR).
The downsides of triple therapy are more side effects and a new problem—drug resistance. Rash, itching and anemia were more common with telaprevir use. Patients using boceprevir had a significantly higher incidence of anemia and taste perversion (dysgeusia). It is noteworthy that the boceprevir studies allowed the use of growth factors (erythropoietin) to manage treatment-induced anemia, whereas the telaprevir studies restricted the use of erythropoietin, so presumably anemia can be managed better if growth factors are used.
The Bottom Line: The future of HCV treatment looks even more promising. Let’s see what the FDA decides.
Editorial Comment: David Nelson, the author of this paper, commented that the use of response-guided therapy for triple therapy using boceprevir was unclear. I found the study design and results for the boceprevir studies hard to decipher. With two protease inhibitors in the pipeline, it would serve consumers better if we could make side-by-side comparisons.
Article: The Role of Triple Therapy with Protease Inhibitors in HCV Genotype 1-Experienced Patients – Michael W. Fried.
Source: Liver International January 2011; Volume 31, Supplement Issue, pages 58 - 61.
Up to now, patients who have failed HCV treatment have had few options. In this paper, Michael Fried presents reasons for optimism—triple therapy—telaprevir or boceprevir used with peginterferon and ribavirin.
Non-responders (60%) and relapsers (40%) were enrolled in the phase II PROVE 3 study using telaprevir with peginterferon and ribavirin. Patients who had an RVR (non-detectable HCV after 4 weeks of treatment) were allowed to continue. Relapsers had a sustained virologic response (SVR) of 76% after 48 total weeks of therapy (24 weeks of triple therapy followed by 24 weeks of combination therapy); non-responders had an SVR of 40%. A shorter treatment arm of 12 weeks of triple therapy followed by 12 weeks of combination therapy yielded 69% SVRs for relapsers who had prior HCV treatment.
Fried mentioned results of the phase 3 REALIZE study that were announced in a press release: 12 weeks of triple therapy using telaprevir followed by peginterferon and ribavirin for a total of 48 weeks—non-responders had an 86% SVR. Looking at the use of boceprevir in combination with peginterferon and ribavirin, the phase III RESPOND-2 study used response-guided treatment. SVR for prior relapsers after 48 weeks of triple therapy was 75%; 52% for prior non-responders.
The Bottom Line: The addition of protease inhibitors in combination with peginterferon and ribavirin is yielding better cure rates for HCV.
Editorial Comment: The latest advances in HCV treatment are exciting, but it is important to temper this excitement with the need for more evidence. Patients may soon have choices to make about treatment options, and we will need clear guidelines to help us make intelligent choices.
Article: Role of Insulin Resistance and Hepatic Steatosis in the Progression of Fibrosis and Response to Treatment in Hepatitis C – Arun J. Sanyal.
Source: Liver International January 2011; Volume 31, Supplement Issue, pages 23 - 28.
In this article, Arun Sanyal discusses the association of HCV, hepatic steatosis (fat accumulation in the liver cells), and insulin resistance (a pre-diabetic or diabetic condition). Approximately 20 to 30% of those with HCV have hepatic steatosis. Genotype 3 patients are at a higher risk of hepatic steatosis, and it appears to be directly related to genotype. Genotype 1 hepatic steatosis seems to be related to higher body mass index (BMI) and the presence of type 2 diabetes or metabolic syndrome.
Increased fibrosis correlates with a reduced response to HCV treatment. Fibrosis severity appears to be related to longer HCV infection, higher BMI, advanced steatosis and menopause. Fibrosis severity is lower for women receiving menopause-related hormone replacement therapy.
The Bottom Line: HCV, hepatic steatosis and insulin resistance present a trio of potential medical complications, particularly when it comes to treating HCV.
Editorial Comment: Insulin resistance and fatty liver are related to lifestyle and are largely preventable conditions. Even patients with HCV-genotype 3, who are at risk for fatty liver disease, can control lifestyle-related risk factors that influence the future of their health. Results from studies using protease inhibitors for those with advanced fibrosis or cirrhosis are encouraging, leaving me to believe that when these drugs are approved, patients will have improved response rates to treatment using triple therapy.
Article: The Impact of Human Immunodeficiency Virus on Viral Hepatitis – Vincent Mallet, Anaïs Vallet-Pichard and Stanislas Pol.
Source: Liver International January 2011; Volume 31, Supplement Issue, pages 135 - 139.
Among those with HIV, liver disease is one of the main causes of non-AIDS-related deaths. HCV is a contributing factor, as 25% of those with HIV are also coinfected with HCV. Current recommendations are to treat HCV before beginning anti-retroviral treatment when at all possible. Treatment for those with HIV/HCV coinfection is similar to those with HCV monoinfection, but SVR rates are much lower. SVR is associated with improved fibrosis and prognosis.
The Bottom Line: Researchers are hoping that new therapies, such as protease inhibitors will offer improved treatment outcomes for HIV/HCV-coinfected patients. In the interim, HCV screening and early treatment may improve treatment responses.
Editorial Comment: Patients who are harder to treat because of comorbidities (the presence of more than one medical condition) often have to wait before research investigates their particular circumstance. This is not personal. Science looks at as few factors as possible, and tries to benefit the most people as possible. That said, some HIV/HCV treatment studies using triple therapy are being conducted.
Back to top
Liver Transplantation: An Overview
Over years or decades, chronic hepatitis C virus (HCV) infection can progress to severe liver problems including cirrhosis and hepatocellular carcinoma (HCC). When the liver is no longer able to perform its vital functions, whether due to acute liver failure or advanced end-stage liver disease, a transplant may be the only option.
Liver damage due to hepatitis C is the most common reason for liver transplants in the U.S., accounting for about 30% of cases. In comparison, hepatitis B is responsible for less than 10% of transplants, largely thanks to an effective vaccine. Other reasons include alcoholic liver disease and acute liver toxicity (for example due to acetaminophen overdose or poisonous mushrooms).
Advances in surgical techniques and medical management have led to improvements in liver transplant outcomes in recent decades. Today the overall one-year survival rate is approximately 90%—up from about 30% in the 1970s—and the five-year survival rate is in the range of 70% to 80%. But patients with hepatitis C, on average, do not fare as well as people receiving transplants for other causes.
Liver Transplant Procedures
The most common transplant procedure is orthotopic liver transplantation (OLT), in which the damaged liver is removed and replaced with a new one (known as an allograft), usually from a recently deceased donor, and the major blood vessels and bile ducts are connected to the new organ.
Unfortunately, the supply of donor livers does not come close to meeting the demand, meaning most people who require a transplant are put on a waiting list. In the U.S., livers are allocated on a regional basis by the United Network for Organ Sharing (UNOS).
In 2002 UNOS adopted a system called MELD (Model for End-Stage Liver Disease) that uses three lab tests–bilirubin, creatinine, and prothrombin time (a measuring of blood clotting)–to predict how likely patients are to die. The system is intended to give priority to people who need new livers most urgently, but are still well enough to benefit, rather than those who have been waiting longest.
According to a study published in 2004, the number of liver transplants increased by 10% and deaths on the waiting list fell by nearly 4% after MELD was adopted. But the system has required some adjustment so it does not favor certain groups, such as people with liver cancer. While the current method has reduced the disparity between white and black patients, a study presented at the 2010 meeting of the European Association for the Study of the Liver (EASL) found that women are more likely than men to die while awaiting a new liver.
However they are allocated, there are not enough good quality deceased donor livers to meet the existing need. In 2008, according to the U.S. Organ Procurement and Transplantation Network (OPTN), approximately 6,000 liver transplants were performed, nearly 1,800 patients died while awaiting a donor liver, and there were about 16,000 people on the liver waiting list at the end of the year.
To address the shortage of deceased donor livers, alternative methods have been developed to increase the liver supply:
• Split Liver Transplant: Thanks to the liver’s ability to regenerate itself, a deceased donor liver can be split into two pieces and transplanted into two recipients, with each piece growing into a fully functioning organ. Split liver transplants produce the best results when the larger right lobe is given to an adult and the smaller left lobe to a child. An Italian study presented at the 2008 EASL meeting found that over a ten-year period split-liver transplant outcomes were comparable to those of whole-liver procedures, leading the researchers to concluded that, “all livers meeting suitability criteria should be used as split-liver transplants to increase the availability of grafts for transplantation.”
• Living Donor Transplant: A living donor transplant uses a liver segment from a live person, usually a relative (although livers do not require close genetic matching like some other organs). The procedure, which was developed in the late 1980s, accounted for nearly 10% of transplants in 2001, but the proportion decreased to about 4% by 2010. Once hailed as a way to dramatically increase the supply of livers, the procedure has somewhat fallen out of favor due to the risk of complications, including death, for the donor.
• Lower Quality Livers: Transplants produce the best outcomes when using infection-free livers from young donors, with a short cold ischemic time (amount of time kept on ice, without a supply of oxygen, after removal from the donor). A study published in 2005, for example, found that the five-year graft survival rate was 72% when the liver came from a donor younger than 60 years, compared with 35% when the donor was age 60 or older. Under some circumstances, however, a poorer quality allograft is preferable to no new liver at all. In particular, a liver from a donor with hepatitis B or C may be given to a recipient who already has the same infection(s). Researchers reported at the 2009 American Association for the Study of Liver Diseases (AASLD) Liver Meeting that hepatitis C patients who received liver grafts infected with HCV or both HBV and HCV had survival rates similar to those of people who received uninfected livers.
Although the number of liver transplants has decreased slightly from its peak in 2006, it is expected to remain high as people infected with HCV decades ago reach the stage of advanced liver disease. Some advocates have called for implementation of a “presumed consent” system, like those in some European countries, that considers everyone a potential organ donor unless they explicitly opt out. Researchers are also studying transplants using animal livers and human liver cells grown in a laboratory, as well as various artificial liver dialysis methods.
Liver transplant recipients may experience a number of complications following surgery, including graft rejection, increased risk for infection, and blood vessel or bile duct leakage. Rejection, infection, and recurrence of the original disease—for example hepatitis C or liver cancer—are the leading causes of post-transplant mortality.
Liver graft rejection may occur either as an acute episode soon after transplantation (usually within the first two weeks) or gradual worsening over a longer period. Signs and symptoms of graft rejection may resemble those of viral hepatitis, including fever, fatigue, weakness, abdominal pain, jaundice, and elevated liver enzymes. Sometimes chronic rejection does not cause symptoms initially but can damage the new liver over time.
Transplant recipients must take immunosuppressive drugs to prevent the immune system from attacking the foreign organ. These agents generally work by altering T-cell activity and cytokine production.
The most commonly used medications include corticosteroids, azathioprine, cyclosporine, mycophenolate, sirolimus (also known as rapamycin), and tacrolimus. These and other drugs are typically used in combination regimens, and the mix may change over time. Acute rejection is usually managed with a high dose of steroids. Studies have shown that many patients can safely reduce and eventually stop steroids after the first few months without significantly increasing their risk of organ rejection.
Because their immune function is suppressed, transplant recipients are at increased risk for infection. During the first weeks or months after surgery, when the strongest immunosuppressive regimens are used, patients are prone to develop bacterial infections, viral, and fungal infections.
Transplant patients are susceptible to some of the same opportunistic illnesses affecting people with AIDS, including cytomegalovirus (a virus in the herpes family), pneumocystis pneumonia, toxoplasmosis, and persistent yeast infections. Immune suppression also increases the risk of developing certain cancers. Some of these infections can be prevented by using prophylactic drugs, and most can be successfully treated. In addition to using antibiotics and other specific medications, doses of immunosuppressive drugs may need to be reduced.
Transplant recipients who do not experience overt organ rejection or develop opportunistic infections may still experience detrimental effects over the long term.
As described in the December 2009 issue of Liver Transplantation, for example, transplant patients are more likely to develop metabolic syndrome—characterized by excess abdominal fat, abnormal blood cholesterol and glucose levels, and high blood pressure—which increases the risk of cardiovascular disease, heart attacks, and stroke. And in the May 2010 issue of Liver Transplantation, British researchers reported that transplant recipients showed signs of premature T-cell aging or senescence, losing the ability to proliferate in response to invaders.
Liver transplant patients with hepatitis C face additional challenges. HCV almost always recurs and can cause fibrosis, cirrhosis, and ultimately failure of the liver graft. Post-transplant HCV recurrence will be discussed in the next issue of the HCV Advocate.
Fortunately, successful hepatitis C treatment with sustained virological response can control the virus and halt liver disease progression. Novel direct-acting anti-HCV drugs,—the first of which are expected to be approved this year,—will improve the likelihood of curing hepatitis C and preventing damage to the new liver after transplantation.
De Feo, T. et al. Results of a 10-year multicenter experience in split-liver transplantation in an Italian transplant program. 43rd Annual Meeting of the European Association for the Study of the Liver. Milan, Italy. April 23-27, 2008.
Gelson, W. et al. Features of immune senescence in liver transplant recipients with established grafts. Liver Transplantation 16(5): 577-587. May 2010.
Moylan, A. et al. Disparities in liver transplantation before and after introduction of the MELD score. Journal of the American Medical Association 300(20): 2371-2318. November 26, 2008.
Myers, R. et al. Increased mortality on the liver transplant waiting list in females under the MELD allocation system: utility of revised meld incorporating estimated glomerular filtration rate. 45th Annual Meeting of the European Association for the Study of the Liver. Vienna, Austria. April 14-18, 2010. Abstract 52.
Pagadala, M et al. Posttransplant metabolic syndrome: an epidemic waiting to happen. Liver Transplantation 15(12): 1662-1670. December 2009.
Sreenivasan, P et al. Use of combined HCV and Hepatitis B core antibody positive liver grafts in HCV recipients. Impact on graft and patient survival. 60th Annual Meeting of the American Association for the Study of Liver Diseases. Boston. October 30-November 1, 2009. Abstract 615.
Back to top
HEALTHWISE: The Power Is in Our Hands
—Lucinda K. Porter, RN
Science can dazzle us with stories about its progress; from cloning to the manufacture of body parts, the stories that are the stuff of science fiction novels are becoming reality. Despite all the amazing developments, science has yet to cure one of the most prevalent illnesses—the common cold.
Fortunately, we have at our disposal, a powerful tool that provides some protection against many diseases, including colds. There is nothing newfangled, complicated or expensive about this tool, and it is available to everyone, although not necessarily all the time. It is hand washing.
The benefits of hand washing have been well-documented. Done properly, hand washing reduces the transmission of microscopic pathogens (disease-producing particles, such as viruses and bacteria). This is particularly true for pathogens that are passed by direct contact or by a fecal-oral route. Hand washing does not completely protect us from catching colds because the cold virus is an airborne virus. Sneezing, coughing, and spitting will propel the virus into the air and if we are in harm’s way, then we are at risk. However, hand washing provides some protection, because there are many opportunities to come into contact with the virus. For instance, using the ATM key pad or shaking hands with someone who just coughed may put you in contact with a pathogen.
One question that is frequently asked is, will hand washing reduce the transmission of hepatitis C virus (HCV)? The answer is “sort of.” HCV isn’t passed casually, meaning that generally it isn’t passed via hand contact. However, we do know that good hand washing helps to prevent the spread of other viruses, such as hepatitis A, so theoretically hand washing extends to HCV. Hand washing is definitely recommended after cleaning up blood, and before and after tending to a cut or wound. Always wear disposable gloves when there is the potential for blood contact.
Hand washing is much like flossing our teeth; we know it is good for us, but many of us don’t practice it as diligently as we should—or at all. The American Society of Microbiology and the American Cleaning Institute have been tracking our hand washing behavior since 1996, and published their latest findings in A Survey of Handwashing. In telephone interviews, 96% of Americans say that they always wash their hands after using the public restroom. However, when observed in public bathrooms, only about 85% of people washed their hands before leaving the facility. The good news is that this is the highest incidence of hand washing since 1996—up from 77% in 2007.
Even those of us who are regular hand washers may not do so properly. Here is the correct way:
- Start by rinsing your hands with water, pointing your hands downward towards the drain. The goal is to rinse dirt away from you and not have it run back up your arms.
- Using soap, lather, rub, and scrub your hands for 20 seconds. Friction is key.
- Remember to get the back of the hands, between the fingers, under the nails and around rings.
- Rinse well.
- Dry well with a clean towel. Wet hands are susceptible to germs.
- Turn off the tap with the towel and if the door to the bathroom opens inward, use the towel to turn the handle and discard the towel after you leave.
Believe it or not, there is even more to be said on the topic of hand washing. Here are a few more tips:
- Most of us don’t wash for the full 20 seconds. To help gauge the time, imagine singing the Happy Birthday song twice. Note that I said imagine singing it. If you sing Happy Birthday out loud in a public restroom, you will look ridiculous, especially if you sing it twice.
- Make sure you use soap. Used alone, water doesn’t get the job done. Liquid soap is probably better than bar soap, as there is evidence that microbes live on the bar soap.
- Plain soap is just as effective as antibacterial soap for cleaning the hands.
- Warm water is better than cold water. It doesn’t kill pathogens, but warm water is better at removing oil and grime from the hands.
- From a hygienic point of view, but not from an environmental one, paper or clean towels are better for drying than electric dryers are. However, there are some better electric dryers on the market now, and it will be interesting to see how these compare to towel-drying.
What about hand sanitizers? Specifically, are they better than washing with soap and water? The research on this is a bit conflicting; some say they are better, some say not. These products disinfect the hands rather than cleanse them. They are a good alternative, except for the fact that they don’t remove visible dirt. If you have soiled hands and aren’t around water, you are much better off using a hand sanitizer rather than nothing. Also, alcohol-based hand sanitizers are more effective than anti-microbial wipes, but again, you are better off using them than using nothing.
Since both techniques get the job done, I use soap and water when I can and sanitizer as a back-up. I carry hand sanitizer with me, particularly when I travel. To use properly, squirt some in your hand and rub your hands together until your hands are dry. Don’t forget to rub between your fingers and the backs of your hands.
When should you wash your hands? The following recommendations are from the Centers for Disease Control and Prevention’s Handwashing: Clean Hands Save Lives (www.cdc.gov/handwashing):
- Before, during, and after preparing food
- Before eating food
- After using the toilet
- After changing diapers or cleaning up a child who has used the toilet
- Before and after caring for someone who is sick
- After blowing your nose, coughing, or sneezing
- After touching an animal or animal waste
- After touching garbage
- Before and after treating a cut or wound
At the risk of sounding like the obsessive-compulsive private investigator on Monk, when I am around children I increase my hand washing, particularly if they are showing symptoms of an illness. I also wash my hands before putting in a contact lens and after handling money or if I’ve done a lot of hand shaking.
One issue that bothers people about hand washing is that it dries out the skin. Keep hand cream near your sink so you can apply this immediately after washing your hands. A scent-free cream or lotion is more suitable for both men and women or those bothered by perfumes.
In these high-tech times, it is reassuring to know that we have power over our health. That power is in our own hands. Hand washing is cheap, simple and easy to practice—all we have to do is do it.
Centers for Disease Control and Prevention www.cdc.gov/handwashing
HCSP Fact Sheet HCV Wellness - Hand Washing: A Primer www.hcvadvocate.org/hepatitis
Back to top
Back to Newsletters