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September 2008 HCV Advocate

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HIV/HCV Coinfection Report from the 2008 International AIDS Conference
Liz Highleyman

Boceprevir Top Line Results
Alan Franciscus, Editor-in-Chief

Genotype 4
Alan Franciscus, Editor-in-Chief

HealthWise: Avoiding Common Medication Errors
Lucinda Porter, RN

Brain Fog Busters
Alan Franciscus, Editor-in-Chief

HCV Advocate Eblast
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HIV/HCV Coinfection Report from the 2008 International AIDS Conference
Liz Highleyman

The XVII International AIDS Conference took place August 3-8 in Mexico City. Drawing more than 20,000 participants, the large biannual conference covered all aspects of HIV/AIDS and its management, including an oral abstract session and numerous poster presentations on HIV/HCV coinfection.

Assessing Fibrosis In Coinfected Patients
Mark Nelson from Chelsea and Westminster Hospital in London (abstract THAB0201) opened the oral session with a review of liver fibrosis in the setting of coinfection. Prior research has shown that HIV positive people with chronic viral hepatitis tend to experience more rapid liver fibrosis progression than HIV negative individuals, perhaps due in part to HIV infecting the hepatic stellate cells that produce liver scar tissue.

Liver biopsies remain the “gold standard” for determining which patients are experiencing disease progression and require prompt interferon-based treatment, and which ones might be able to wait until new directly targeted oral anti-HCV drugs become available. Since frequency biopsies are unpleasant and impractical, various noninvasive tests are under study. In addition to several promising blood biomarker assays, FibroScan (transient elastometry), which uses sound waves to measure liver stiffness, is “very easy and very repeatable,” according to Nelson. However, while these tests can distinguish absent or mild from advanced fibrosis, they are “lacking in accuracy” at intermediate stages.

Nelson recommended considering a biopsy if there is a lack of concordance between biomarker and FibroScan results. He also recommended regular screening for liver cancer and tests for liver necroinflammation. Making an analogy to HIV disease, he suggested that liver inflammation (like HIV viral load) can be likened to the “speed of the train,” while fibrosis stage (like CD4 cell count) is the “distance from the cliff.”

24-Hour Response
Prior research has shown that rapid virological response (RVR) at Week 4 of therapy predicts sustained response in both HIV/HCV coinfected and HCV monoinfected individuals. But according to a poster presented by Natalia Laufer and colleagues from Argentina (abstract WEPDB204), HCV decline during even the first day of treatment predicts long-term response in coinfected people.

The researchers analyzed HCV viral load decay during the first 24 hours of therapy in 11 coinfected patients (eight with HCV genotype 1) receiving pegylated interferon plus weight-based ribavirin. Three participants (27%) achieved RVR at Week 4 and eight (73%) achieved early virological response (EVR) at Week 12. During the first 24 hours, HCV viral load declined by an average of 99% among patients who achieved RVR, and by 85% among those who achieved EVR; among patients who did not achieve either RVR or EVR, however, HCV RNA fell by just 51%. The investigators concluded that very early assessment of viral decline “could be of clinical relevance” in evaluating the risks and benefits of continuing therapy in patients experiencing severe side effects, as well as in resource-limited settings where a cost/benefit approach is warranted.

Post-Treatment Relapse
While it is clear that HIV/HCV coinfected individuals do not respond as well to interferon-based therapy, less is known about post-treatment relapse in this population. Jose Medrano and colleagues, also with the Madrid team (abstract THAB0202), hypothesized that coinfected individuals might be more likely to experience HCV relapse following viral suppression at the end of treatment, but may do so more slowly than HIV negative people. The researchers analyzed 119 HIV positive and 134 HIV negative interferon-naïve patients who completed 48 weeks of Pegasys plus weight-based ribavirin and achieved undetectable HCV RNA (<10 IU/mL) at the end of treatment.

About one-third (30.6%) of the coinfected patients experienced post-treatment relapse, compared with about one-quarter (25.5%) of the HCV monoinfected individuals. Among the 41 coinfected relapsers, 47.8% experienced HCV recurrence between the end of treatment and post-treatment Week 12, 46.3% relapsed between post-treatment Week 12 and Week 24, and 4.9% did so after post-treatment Week 24—that is, after they had achieved SVR, or a presumed “cure.” Among the 30 HCV monoinfected relapsers, the percentages were 53.3%, 30.0%, and 16.7%, respectively. Among the coinfected individuals, those with HCV genotypes 1 or 4 were significantly more likely to experience relapse than those with genotypes 2 or 3. HCV recurrence was detected as late as 105 weeks after completion of treatment. The researchers are conducting genetic analysis to rule out reinfection rather than relapse, but said that some of the relapsers had no risk factors for reinfection.

The investigators concluded the incidence of HCV relapse “does not differ significantly” in HCV monoinfected and HIV/HCV coinfected individuals, although it “tends to be more frequent” in coinfected patients; the timing of relapse also did not differ significantly depending on HIV status. Even though very late relapses “may rarely occur” in both HCV monoinfected and HIV/HCV coinfected patients, the researchers indicated that “24 weeks of follow-up is still warranted to confirm SVR.”

Cardiovascular Disease
Cardiovascular disease is a growing concern for people with HIV and several studies have shown a higher risk for heart disease associated either with the virus itself or with antiretroviral therapy, which can raise blood lipid (cholesterol and triglyceride) levels. Roger Bedimo and colleagues (abstract THAB0205) analyzed data from the Veterans Administration Clinical Case Registry of more than 20,000 HIV positive patients (about one-third of whom were coinfected with HCV) to assess the impact of coinfection on the risk of acute myocardial infarction (heart attack) and cerebrovascular disease (stroke) in the pre-HAART (1980 to 1995) and HAART (1996 to 2004) eras.

Coinfected patients were less likely than HIV monoinfected individuals to have abnormally high blood lipid levels (18% vs. 27% for elevated total cholesterol; 55% vs. 60% for elevated triglycerides) or to be taking lipid-lowering medications. While HIV monoinfected patients had an increased likelihood of having high cholesterol after the advent of HAART, the rate did not change among coinfected patients.

In the pre-HAART era, HIV/HCV coinfection was associated with about a 40% higher risk of both acute myocardial infarction and stroke. In the HAART era, acute myocardial infarction rates were 3.36 per 1,000 person-years (PY) for HIV monoinfected individuals compared with 4.19 per 1,000 PY for coinfected patients; this represented a 25% increase in risk for the coinfected group, but did not reach statistical significance. Rates of stroke in the HAART era were 11.12 and 12.47 per 1,000 PY, respectively, for HIV monoinfected and coinfected individuals; this represented a 20% increased risk for the latter group, which in this case was statistically significant. The researchers concluded that “adjustment for HCV status is indicated” when assessing cardiovascular disease risk in people with HIV.

HCV Transmission
In recent years researchers have reported outbreaks of apparently sexually transmitted acute hepatitis C in several European cities, primarily among HIV positive men who have sex with men (MSM). Anouk Urbanus and colleagues (abstract THPDC203) provided further details about a cluster of cases in Amsterdam. In May and November 2007 and in April 2008, the investigators interviewed 3,124 clients at a large sexually transmitted disease clinic and screened them for HIV and HCV antibodies; HIV positive patients received HCV RNA tests regardless of HCV antibody status. 

Among the 2,435 heterosexual men and women, just 0.3% were infected with HCV, and among the 532 HIV negative men, the HCV prevalence rate was similar at 0.4%. But among the 157 HIV positive MSM, 17.8% were coinfected with HCV. The rate of HCV infection among HIV positive MSM rose over time, from 14.6% in May 2007 to 16.7% in November 2007 to 20.9% in April 2008. About one-third of these men were HCV RNA positive but HCV antibody negative, indicating possible acute infection.

Five of the coinfected men (17.9%) reported ever injecting drugs. Along with HIV positive status and injection drug use, fisting was also significantly associated with HCV infection, and fisting was strongly correlated with use of sex toys, group sex, bleeding during sex, and use of gamma hydroxybutyrate (GHB). Phylogenetic analysis revealed a high degree of clustering within this population, suggesting transmission within sexual networks. The researchers concluded that, “Targeted interventions including raising awareness are needed to stop the further spread among HIV-infected MSM, and a possible spill over to HIV negative MSM.”

Looking at mother-to-child HCV transmission, A. Mazus, I. Simonova, and colleagues (abstract WEPE0176) assessed 1,887 HIV positive pregnant women, 43% of whom were HCV coinfected, enrolled at the Moscow Centre for AIDS between 1995 and 2007; infants were monitored from birth through 18 months. While 7% of HIV monoinfected mothers transmitted HIV to their babies, this rose to 11% for HIV/HCV coinfected women. Among the coinfected mothers, 9% also transmitted HCV, and 4% transmitted both viruses. The researchers also reported that infants cleared their mothers’ HCV antibodies sooner than HIV antibodies. This study confirms prior findings showing that HIV positive pregnant women are more likely to transmit HCV.

Conference abstracts and selected Powerpoint slide presentations are available via the conference web site at www.aids2008.org. The hepatitis coinfection oral session can be found at www.aids2008.org/Pag/PSession.aspx?s=236.


HIV And HIV/HCV Resources

HCV Advocate

• HIV/HCV Coinfection Facts
• HIV/HCV Coinfection Poster
• HIV/HCV Coinfection Poster (Spanish)

• Easy C - A Guide to HIV and Hep C Coinfection
/easyfacts /Easy Coinfec GD.pdf

• Frequently Asked Questions about HIV & Hepatitis C

• HIV/HCV Coinfection: Pegasys plus Copegus
factsheets_pdf/Pegasys and Copegus.pdf

• HIV/HCV Coinfection: What You Need to Know


Project Inform:
Hotline:  800-822-7422

San Francisco AIDS Foundation:
Hotline 900-367-2437

National AIDS Treatment
Advocacy Project:


HIV and Hepatitis.Com

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Boceprevir Top Line Results
Alan Franciscus, Editor-in-Chief

On August 4, 2008, Schering-Plough released the top-line results from their phase II clinical study of boceprevir, an HCV protease inhibitor, in combination with PegInterferon plus ribavirin in HCV genotype 1 treatment-naïve patients.  The treatment arms and response rates are listed below.

This study included 595 patients divided into 6 treatment arms*:
Arm 1:  107 patients – triple therapy with no lead-in phase.  Triple therapy = PegIntron (1.5 mcg/kg) plus ribavirin 800-1400 mg daily (based on body weight), and boceprevir 800 mg three times a day. Total treatment duration = 28 weeks.
SVR 24 = 55%

Arm 2:  103 patients – 4 week lead-in phase of PegIntron (1.5 mcg/kg) plus ribavirin 800-1400 mg daily (based on body weight) followed by an additional 24 weeks of triple therapy.    Triple therapy = PegIntron (1.5 mcg/kg) plus ribavirin 800-1400 mg daily (based on body weight), boceprevir 800 mg three times a day. Total treatment duration = 28 weeks.
SVR 24 = 56%

Arm 3:  103 patients – triple therapy with no lead-in phase. Triple therapy = PegIntron (1.5 mcg/kg) plus ribavirin 400-1400 mg daily (based on body weight) boceprevir 800 mg three times a day.  Total treatment duration = 48 weeks.
SVR 12 = 66%

Arm 4:  103 patients – 4 week lead-in phase with PegIntron (1.5 mcg/kg) plus ribavirin 800-1400 mg daily (based on body weight) followed by an additional 44 weeks of triple therapy.  Triple therapy = PegIntron (1.5 mcg/kg) plus ribavirin 400-1400 mg daily (based on body weight), boceprevir 800 mg three times a day.  Total treatment duration = 48 weeks.
SVR 12 = 74%

Arm 5 (Control Arm):  104 patients – combination therapy =  PegIntron (1.5 mcg/kg) plus ribavirin 400-1400 mg daily (based on body weight). Total treatment duration = 48 weeks.
SVR 12 = 38%

*There was another arm that was added to the study that didn’t start enrollment until after the other arms had begun enrollment.  In the new arm, patients received boceprevir in combination with low-dose ribavirin plus PegIntron for a treatment duration of 48 weeks. These results are expected later in the year.  

The most common adverse events (side effects) reported in the boceprevir arms were fatigue, anemia, nausea and headache.  The press release noted that there were no increases in dermatological (skin) adverse events (rash and itching) that are usually seen in patients treated with PegIntron plus ribavirin.  The treatment discontinuations due to adverse events were between 9 and 19% in the boceprevir arms vs. 8% in the control arm (without boceprevir).
The results of this study are encouraging, but they should be interpreted with a bit of caution.   First, the results reported here are top-line numbers so there will be much more information released later in the year at the American Association for the Study of Liver Diseases (AASLD) conference about the patient characteristics, dose reductions (if any), and side effects.  Secondly, this is a small phase II study that included five treatment arms ranging from 103 to 107 patients in each arm.  A small sample size of patients doesn’t give us a clear picture of the effectiveness or side effect profile of a study drug.  Finally, some of these results are SVR12 so there is a possibility that the SVR 24 rates could be a bit lower than listed here.  Schering began recruitment into a phase III study of boceprevir in combination with PegIntron plus ribavirin earlier this year and that study will include many more patients – which should give us a better understanding of the patient population, drug effectiveness, side effect profile and other important issues. 

Source:  Company press release 

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Genotype 4
Alan Franciscus, Editor-in-Chief

There are 6 major genotypes of hepatitis C distributed throughout the world.  It is estimated that about 4 million Americans have been infected with hepatitis C and of those about 70% are infected with HCV genotype 1, and about 30% are infected with HCV genotype 2 & 3.  The remaining HCV genotypes – 4, 5, & 6 are also found in this country but at a much lower prevalence.  It is estimated that there are about 40,000 Americans infected with HCV genotype 4.  Unfortunately, there has been relatively little information available about HCV genotype 4 to enable us to understand the similarities and differences between genotype 4 and the other genotypes, as well as to help patients make informed healthcare decisions.  A review article titled “Hepatitis C Genotype 4:  What We Know and What We Don’t Know Yet,” by  Sanaa M. Kamal and Imad A. Nasser, which was published in the April 2008 issue of the journal Hepatology, however, will greatly add to the body of knowledge about the history, epidemiology, disease progression and treatment outcomes of people infected with HCV genotype 4. 

Origins and Prevalence
It is difficult to nail down the exact origin of any genotype, but genotype 4 is a little easier to track because until recent years it has been mostly confined to the continent of Africa.  In general, the genetic make-up of an HCV genotype varies by about 1/3 between the different genotypes.  Interestingly, the genetic variance between genotype 1 and genotype 4 is closer than the variances between the other genotypes.  This may be one of the reasons why treatment response rates are somewhat similar between genotypes 1 and 4.  When looking at the HCV genotype 4 genetic makeup it is found that the variances are less diverse within genotype 4 compared to the other genotypes, but that it has more subtypes – 18 (4a through 4u) – compared to the other genotypes.  The identification of the subtypes makes it easier to theorize where genotype 4 originated.  Based on various studies it is believed that genotype 4 originated in Central Africa – most likely in Cameroon before spreading to other parts of Africa.  Since HCV is spread by blood-to-blood contact it is difficult to explain the spread of HCV in Africa prior to blood transfusions and legal and illegal injection drug use. But some common indigenous practices such as scarification, male and female circumcision and other blood practices could explain some of the transmissions.  Although sexual transmission is a low risk factor, it could also help to explain the persistence of HCV before the more common risk factors existed.    However, the spread of HCV genotype 4 to other areas of Africa is believed to have occurred  between 1920 and 1960 as the result of unsafe needle practices during mass campaigns to treat trypanosomiasis (African Sleeping Sickness, spread by the tsetse fly) and mass inoculations to protect against other diseases.  At the time, the only available needles were glass syringes, which are notoriously difficult to clean or sterilize before re-using the needle on another person.

Worldwide, Egypt has the highest prevalence of HCV – estimated at about 15% of the population, which accounts for 20% of the estimated 170 million persons worldwide infected with hepatitis C.  Genotype 4 accounts for 90% of the HCV infections in Egypt.  Due to the genetic diversity of HCV genotype 4 found in Egypt, it is estimated that genotype 4 infection within the Egyptian population is a more recent occurrence than those found in Central and West Africa.  The high prevalence in Egypt coincides with a mass campaign in the 1960’s through the 1980’s to control schistosomiasis infection (caused by a parasite transferred by snails to humans in water) using glass syringes for inoculations.  Additional risk factors that may account for the recent high incidence of HCV infections in Egypt are blood transfusions or the use of blood products before 1993, and injection drug use.  Less likely but still possible transmission routes in Egypt include circumcision, dentistry, and complete removal of a body part or organ performed by local informal health providers and centers.   Genotype 4 also accounts for the majority of HCV infections in:

  • Gabon (90% of HCV infections)
  • Central African Republic (100%)
  • Democratic Republic of Congo (100%)
  • Liberia (100%)
  • Uganda (100%)
  • Rwanda (100%).

African countries that have a lower prevalence of HCV genotype 4 in the HCV population include:

  • Cameroon (36%)
  • Tanzania (50%)
  • Tunisia (11%)
  • Sudan (5%)

Genotype 4 infections have also recently spread to Europe where the HCV genotype 4 prevalence in the hepatitis C population is Greece (13.2%), France (4-10%), Spain (3-10%), and Italy (8.3%).   In Europe recent infections are mostly attributed to sharing HCV-infected needles and works among injection drug users since this route is the most commonly reported route for newly acquired infections.   

Natural History
In the studies conducted to date, spontaneous (natural) clearance of acute HCV genotype 4 is between 20-50%, which is similar to the spontaneous clearance of the other genotypes.  People who are infected with HIV and Schistosoma mansoni (parasite) typically have very low rates of spontaneous clearance. 

The rate and degree of HCV disease progression in people with HCV genotype 4 appears to be similar compared to the other genotypes, but there is some evidence that coinfection with Schistosomiasis or HIV accelerates HCV genotype 4 disease progression.  The amount of steatosis (fatty liver) seems similar to the levels found in people with HCV genotype 1, but lower than those seen in people with genotype 3.  The similarities of steatosis percentages in people with genotype 1 seems to indicate that steatosis seen in people with genotype 4 is caused by metabolic conditions rather than the virus-induced steatosis that is seen with HCV genotype 3. 

There is some evidence that there are higher rates of liver cancer in people infected with HCV genotype 4 compared to the incidence of liver cancer in the other genotypes.  It was noted that liver cancer accounts for 13% of all cancers in Egypt and 65% of liver cancer patients in Egypt are infected with HCV genotype 4.  However, more studies are needed to confirm these observations and it is not clear if the higher rates of liver cancer are due to genotype 4 or if they are the result of coinfection with schistosomiasis or contamination of food by aflatoxin.  Aflatoxin is a substance produced by molds that grow in rice and peanuts and it is one of the largest contributors to liver cancer in Africa and parts of Asia.   

There is some evidence that people with HCV genotype 4 do not do as well post transplant – due to more severe fibrosis and faster disease progression.  The authors noted that there are not enough studies to draw concrete conclusions, but two studies found a worse outcome after liver transplantation in people with HCV genotype 4 compared to people who were infected with another HCV genotype:  

  • Zekry et al. found that people with HCV genotype 4 had a worse outcome, more complications and higher death rates. 
  • Wali et al. reported that more HCV genotype 4 patients had severe fibrosis following liver transplantation compared to non-genotype 4 patients—26.3% vs. 6.7%. 

The authors also recommended more studies to confirm these observations and the implementation of strategies to prevent or limit post-transplant complications.

Schistosomiasis is a chronic disease caused by a family of parasites that is most commonly seen in Asia, Africa, and South America.  It is estimated that there are 207 million people worldwide who are infected with some form of schistosomiasis.  The most common transmission occurs from wading or swimming in fresh water that contains the snails infected with the parasite.  The parasites on the snail drop into the water, attach themselves to humans who are wading or swimming in the fresh water.  Once the parasites are attached to human skin they go through various developmental stages while they travel through the body via the lungs, liver and intestines.  There is no vaccine to protect against schistosomiasis but the drug Praziquantel in a single dose is effective in curing the condition.’’

In the past when conventional interferon was the standard of care, it was believed that HCV genotype 4 was one of the most difficult to treat, however treatment with pegylated interferon plus ribavirin has led to dramatic improvements in treatment outcomes.   In a meta-analysis of clinical trials using pegylated interferon plus ribavirin the SVR rates were 55% in people treated with pegylated interferon plus ribavirin compared to 30% in people treated with conventional interferon plus ribavirin. 

There has also been some controversy about the duration of treatment that has not been completely resolved, but the studies to date have indicated that a 48 week treatment duration for people with HCV genotype 4 high viral load (≥ 2 million copies/mL or ≥ 800,000 IU/mL) and 36 weeks for people with HCV genotype 4 low viral load (≤ 2 million copies/mL or £ 800,000 IU/mL) are best, but more studies are needed to really determine the exact duration of treatment.

The same factors that influence successful treatment outcomes in patients with other HCV genotypes are also factors that affect treatment outcome in HCV genotype 4 people – baseline viral load, early and rapid virological response, liver histology or health, and treatment duration. 

Kamal, S.M & Nasser, IA., Hepatitis C:  Genotype 4:  What We Know and What We Don’t Yet Know. Hepatology 2008; 47: 1371-1383.

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HealthWise: Avoiding Common Medication Errors
Lucinda Porter, RN

Last month’s Healthwise discussed medical errors and how to reduce exposure to them.  This month’s column addresses common medication mistakes that patients make.  Like our medical team, we are susceptible to human error.  Unlike our medical team, we are amateurs.  Since we take medication when we are sick or avoiding illness, taking medication is on-the-job training at inopportune moments.

Medication is an essential part of health.  Taken incorrectly, drugs will not do their job.  Although true for current hepatitis C (HCV) treatment it will be more critical as some of the newer HCV antivirals come to market.  Adhering to treatment is not as easy as it looks.  Under the influence of interferon and ribavirin, my brain was as efficient as tapioca.  I could swallow some ribavirin and a minute later not remember if I took my pills.  I needed a strategy in order to take my HCV drugs. 

Medication management begins before the prescription is filled.  It begins before you have even seen your medical practitioner.  It starts with knowing your medical history.  Before your appointment, write down the following and bring a copy with you:

  • Allergies to all drugs, foods and other substances
  • Medications you are taking – include dose, frequency, time of day and reason for taking it
  • All dietary supplements and drugs that you are taking or have taken recently.  Include prescription, over-the-counter, etc. 
  • All medical conditions you have, especially if you have cirrhosis, diabetes or kidney disease
  • The name and phone number of your preferred pharmacy

Good communication between your doctor, nurse and pharmacist is key.  If your doctor prescribes a drug, confirm the instructions for taking it.  Ask if you are supposed to take all of your prescription.  For instance, unless told otherwise, always take the entire antibiotic prescription even if you feel better.

If you are given a paper prescription, compare it to what your doctor told you.  Don’t assume anything.  If you can’t read the prescription, the pharmacist might not be able to either.  Ask for a legible prescription.

Always use the same pharmacy, preferably one that provides information about your medication.  By using the same pharmacy, there is a better chance that drug interactions are caught.  When you pick up your medication, confirm that the name and instructions match those that your doctor told you.  Clear up discrepancies before you take the drug. 

If you fill a prescription and it looks different from the last time you took it, talk to your pharmacist to make sure there has not been an error.  Before taking a medication, check the label two or three times.  If interrupted when about to take a drug, compare the pill in your hand with the one in the bottle and check the label again before taking it. 

Know the medication’s side effects before you start taking it.  Read the literature that comes with the medication.  Check drug interactions of all supplements, prescriptions, and over-the counter drugs at www.drugs.com/drug_interactions.html.

Take the minimum effective prescribed dose unless advised otherwise.  Never take extra medication unless under medical orders.  Do not use someone else’s medication or give your medication to anyone else.  If you have taken the wrong medication or amount, call your medical practitioner or 911 if the mistake is an emergency. 

Never break, crush, or dissolve a pill, tablet, or capsule without making sure this is all right to do.  Some medications need to be intact so stomach acids do not destroy them.  If swallowing pills is difficult for you, tell your medical provider.  When taking liquid medications, use standard measuring spoons rather than eating utensils. 

Take extra precautions when you are stressed, depressed, fatigued, in pain, or under the influence of another medication or mood-altering substance.  Do not take medication in the dark or without your glasses if you need them to read the label.  If you have poor eyesight, ask your pharmacist to use large-print labels.  If you have two medications that could be confused, color-code or mark the containers. 

Recently, a friend told me about a medication incident.  His physician prescribed a drug that looked like his thyroid pill.  He confused the two pills and for several months he had under-medicated his thyroid, leading to serious fatigue.  Fortunately, he discovered his error.  To avoid future mistakes, he created a sample case that contains a one day supply of medication.  He puts together a week’s worth of pills, then checks these against the sample to make sure he included everything. 

Try to take medications on time.  The best way to manage medications is to develop a system and stick to it.  It can help to link taking your medication with another task, such as brushing your teeth.  For example, if you have to take medication on an empty stomach three times a day, you might put 3 pills in a plastic case.  Put the bottle someplace that will catch your eye, such as in your pocket, near your car keys or computer mouse. 

Other handy tools are to set reminders on your wireless phone, computer, or alarm clock.  Daily pill cases can be helpful.  If a drug needs special storage, such as refrigeration, put a note in the case, removing the note after you have taken the medication.  You might use a checklist.  Every week, make a chart with the times you need to take your drugs.  Check off what you take after you take it.  If you have trouble remembering to take medication, ask a pharmacist, nurse, or other health provider for tips. 

Store medications as directed and out of reach of children.  Never expose drugs to extreme temperatures, such as in a car.  Do not take a medication that has expired, smells or looks odd to you.  This is especially important for liquid medications.  Regularly clean out your medicine chest and properly discard expired medications.  For safe medication disposal, visit www.samhsa.gov/rxsafety

If hospitalized or in a position where someone else gives you your medication, look at what you are taking before you take it.  If something does not look right, ask  “What is this and why am I taking it?”  Have the nurse double-check any medications you have questions about.  Keep a copy of your medication instructions at the bedside. 

The good news is that taking medication is essentially an exercise in being careful and using tools to maximize the chances of reaping the medication’s benefits.  Fortunately, we practice being careful and using tools all the time – when we drive, cook, operate machinery, etc.  In short, we already have the skills for good medication management.  We just have to apply them.

Further Information:
Food and Drug Administration’s Consumer Education: What You Need to Know to Use Medicine Safely.  /www.fda.gov/Drugs/ResourcesForYou/

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Vote Health!
Health is a political issue.  Politics intersects many aspects of health – Medicare, health insurance, stem cell research, job protection during illness, malpractice issues, clean air, nurse to patient ratio, etc.  Your vote influences the future of health.  Are you registered to vote?  If not, you can register online.  The U.S.  Election Assistance Commission provides a form www.eac.gov/voter_resources/

A few states don’t accept this form, so you may need to contact your state or county registrar of voters.

Organ and Tissue Donation: Minnesota
  Occasionally an urban legend circulates on the Internet about black market organs.  The gist is that an out-of-town business man orders a drink which happens to be laced with a knock-out drug.  He wakes up in a bathtub filled with ice along with a note instructing him to call 911.  The dramatic ending is that his kidneys were removed by black market bandits.  This story is completely false.  It is illegal to buy or sell organs or tissue in the U.S.  Every transplant is rigorously reviewed by a team.

Residents of Minnesota can help each other by expressing their willingness to be organ and tissue donors.  It is easy to do.  Minnesotans may register at www.donatelifemn.org , call 1-888.5.DONATE, or indicate their wishes on their driver’s license or state I.D.  card.

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Brain Fog Busters
Alan Franciscus, Editor-in-Chief

“Where are my keys?”  What did I do with that book?”  What time was I supposed to meet John?”  Almost every one – including people living with hepatitis C – forgets where they place things or has missed a meeting because they forgot the day or time of the appointment.  Brain fog is loosely defined as a constellation of symptoms, including difficulty concentrating, memory loss, trouble with retaining information, and a whole range of other cognitive problems.  Along with fatigue, brain fog is one of the most common symptoms people with hepatitis C experience.   

The exact cause of brain fog in people with hepatitis C is poorly understood but there have been some theories put forth that may explain the higher incidence of brain fog in the hepatitis C population.  One theory is that since the hepatitis C virus crosses the blood-brain barrier there may be some low levels of inflammation in the brain that would affect cognitive function. Other experts speculate that the cause of brain fog may be due to the fact that the immune system is over stimulated trying to fight the hepatitis C virus.  This process involves the immune system’s activation of the body’s innate defense system that produces killer cells, and a certain protein called interferon.  The result of the natural production of interferon is that the body goes into an attack mode and this process produces side effects such as fatigue, muscle and joint pain as well as general cognitive dysfunction – this is the same process that occurs when someone catches the common cold or the flu. 

Regardless of the reason, brain fog can affect almost every area of life.  On a personal note, the symptoms of fatigue and brain fog are the symptoms of hepatitis C that eventually led me to seek medical care that resulted in a diagnosis of hepatitis C.   

The ten steps listed below are a variety of measures both scientifically proven and from personal experience that have helped me manage brain fog.  I have found that combining various strategies has greatly improved my memory and reduced the stress of having hepatitis C-related brain fog.  

1. Get a Check Up:  Brain fog can be caused by many conditions, such as depression, acute and chronic pain, diabetes, thyroid disease and many other medical conditions.  Talk with a medical provider to make sure that there is no other mental or physical condition that is causing the brain fog.   

2. Physical Exercise:  One of the best strategies to combat brain fog is exercise. Exercise has been proven to increase blood flow in the brain and aid in the replication of brain cells.  Exercise will also help to reduce the build up of plaque in the blood vessels including those in the brain.  There are many types of exercise to choose from, such as walking, jogging, swimming, etc.; but always talk with a medical provider before beginning any new vigorous exercise program.

3. Exercise the Brain:  Do mental activities that stimulate the brain such as crossword puzzles, reading a book, putting together a jigsaw puzzle, playing memory games, solving mathematical problems, playing chess or any other activity that challenges the brain.   

4. Diet:  It is not surprising that a healthy diet affects every area of the body, including the brain.  A poor diet can lead to obesity, diabetes, increased levels of ‘bad’ cholesterol, as well as many other conditions that can affect the health of the body.  A poor diet can lead to build up of plaque in the veins, and poor circulation. Recently, some studies have suggested that uncontrolled diabetes may contribute to Alzheimer’s.   More studies are needed to confirm the findings, but the link between poor diet and the development of cognitive dysfunction appears to be very solid. 

5. Sleep:  Insomnia can lead to many problems, including brain fog.  It is recommended that people try to get between 8 and 10 hours of sleep every night.   

6. Visualize: This is a very good strategy that has worked well for me.  For instance, when you park your car visualize where you parked it as well as the nearest cross streets.  Another example would be that when you put an item in a certain place, visualize that place.  

7. Permanent Location:  Find a permanent location for things like keys, loose change, or any other item so that they can always be located.  I try to put my keys in the same location in the kitchen so that if I am running out of the door I know exactly where to look without wasting time and becoming frustrated trying to find them.     

8. Daily Planner: Write down every appointment in a spiral bound notebook, daily planner or on a computer and use it to refer to when making appointments.  Every morning after my coffee I check the daily planner so that I am aware of and can plan my daily activities accordingly.  Remember not to overbook and also try to write in time between appointments to rest.    

9. Stress Reduction:  Stress is a killer and nothing will make you more confused and forgetful than being stressed out.  Find activities that help to reduce the stress like walking, meditating, reading a good book, listening to music.  Build these types of activities into your daily routine.    

10. Laugh:  Having brain fog is not funny and it can get the better of you and ruin your life.  If you miss an appointment – apologize and move on.  There is no point in self recriminations especially if you are making every effort to cut down on mistakes.  You will find that life is much easier and enjoyable if you can laugh at your very human mistakes. 

CDC Physical Activity for Everyone

The Original Memory Gym

USDA MyPyramid.gov


HCSP Fact Sheets:

HCV Wellness: Sleep

HCV Wellness: Stress Reduction

The Liver: Stress and the Liver

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