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September 2013 HCV Advocate

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In This Issue:

Drugs in Development: Phase 3 – Genotype 1 - DAA plus PEG/RBV
Alan Franciscus, Editor-in-Chief

Snapshots
Lucinda K. Porter, RN

HEALTHWISE: Hepatitis C and Your DNA
Lucinda K. Porter, RN


HCV and Correctional Centers: A Missed Population
Sonya Becker & Juliana Chan, Pharm.D.

The Other Forgotten Hepatitis B Minority—African-Americans
Christine M. Kukka


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Drugs in Development: Phase 3 – Genotype 1 - DAA plus PEG/RBV
—Alan Franciscus, Editor-in-Chief

There are many new drugs that are being developed to treat chronic hepatitis C.  In fact, there are a couple of new combination therapies that are currently being evaluated by the Food and Drug Administration (FDA) for marketing approval.  This article will provide a short recap of the major therapies in Phase 3 studies to treat people with HCV genotype 1 using different types of direct acting antivirals (DAAs) plus pegylated interferon and ribavirin (PEG/RBV).

Standard of Care
For people with genotype 1 the standard of care (SOC) is the combination of an HCV protease inhibitor (boceprevir or telaprevir) plus pegylated interferon plus ribavirin (PEG/RBV).  Standard treatment duration is up to 48 weeks, but some people can be treated for a shorter period of time.  Cure rates are up to 80% across all groups.  But the current  HCV protease inhibitor combination therapies also have significant side effects which have prevented some people from seeking treatment. 

For those who can wait there are many medications in development that hold the promise of higher viral cure rates and less side effects. 

Next Standard of Care
There are four Phase 3 studies that combine DAA’s plus PEG/RBV:

  • Janssen’s simeprevir (QD) plus PEG/RBV,

  • Gilead’s sofosbuvir (QD) plus PEG/RBV,

  • Boehringer Ingelheim’s faldaprevir plus PEG/RBV,

  • BMS’s daclatasvir plus asunaprevir plus PEG/RBV

Simeprevir (QD—once daily) plus PEG/RBV:
Simeprevir is an HCV protease inhibitor that that is being studied in combination PEG/RBV. 

Cure rates:  In two late stage studies it was reported that in people who had never been treated (treatment naïve) 80 to 81% of people achieved a viral cure.  In another trial of simeprevir, but this time in people who had relapsed (viral load negative on treatment but the viral load returned after treatment was completed), 79% of people achieved a viral cure. 

Treatment duration: The treatment duration was based on how quickly or slowly HCV viral loads decreased:  Eighty-five to 91% per cent of the people in the treatment-naïve and 93% in the treatment-experienced group were able to shorten their treatment durations to 24 weeks.  

Side effects:  The side effects reported in the studies were similar between the simeprevir group plus PEG/RBV and the group that received PEG/RBV without simeprevir, except there was a higher incidence of mild rash and photosensitivity (sensitivity to sunlight) with PEG/RBV.  What this means is that there are fewer side effects than with the current HCV protease plus PEG/RBV therapies.

There is also an on-going clinical trial of simeprevir PEG/RBV in treatment-experienced patients.  

FDA approval:  End of 2013 or early 2014.

Sofosbuvir (QD) plus PEG/RBV:
In another late stage study, sofosbuvir (HCV polymerase inhibitor) plus PEG/RBV was tested for the treatment of HCV genotypes 1, 4, 5, and 6—treatment naïve and treatment experienced. 

Cure rates:  Treatment naïve—89% of the people in the study were genotype 1.  Overall 91% of patients achieved a viral cure—89% genotype 1; 96% genotype 4; all of the patients in the remaining patients were cured (one patient with HCV genotype 5 and 6 patients with genotype 6).  Similar cure rates were seen in a study of treatment-experienced patients.

What is important about the Gilead studies is that even in people who usually don’t respond well to current treatment—cirrhosis, high viral load, unfavorable gene variations—as a group, in this study, at least 80% achieved a viral cure.  

Treatment Duration: 8 weeks to 12 weeks.

Side effects:  The side effects were similar between the sofosbuvir group plus PEG/RBV and the group that received PEG/RBV (without sofosbuvir), which means that this combination therapy has less side effects than the current HCV protease combination inhibitor therapies.

FDA approval:   End of 2013 or early 2014.

Faldaprevir (QD) plus PEG/RBV:
Faldaprevir is another late stage study of an HCV protease inhibitor plus PEG/RBV. 

Cure rates:  Reported cure rates were 79% and 80%.  Faldaprevir has been found to work better in HCV genotype 1b than in 1a. 

Treatment duration:  In the study people were given different doses of faldaprevir with PEG/RBV.  Faldaprevir plus PEG/RBV was given for 12 or 24 weeks and the patients were continued on PEG/RBV for a total of 24 or 48 weeks depending on how quickly they responded to treatment.  Most (88%) were able to complete treatment at week 24.

Side effects:  The addition of faldaprevir to PEG/RBV did not seem to add many additional side effects to HCV protease inhibitor combination therapy except there were higher rates of rash, gastrointestinal distress and elevated bilirubin levels.

FDA Approval:  The application for FDA approval has not been submitted, but it is expected that the application will be filed soon with a possible approval by mid-2014 to the end of 2014.

Daclatasvir (QD), Asunaprevir PEG/RBV:
There are many different clinical trials of BMS’s direct-acting antivirals daclatasvir (NS5A inhibitor) and asunaprevir (protease inhibitor) used in combination with PEG/RBV.

Cure rates:  There is limited data released on the quad therapy trials, but some reports have found high viral cure rates—one study of prior treatment null responders reported a viral cure rate of 93%.  

Side Effects:  The reported side effect that was higher in the trial was headache. 

FDA Approval: There is no information on the status of the Phase 3 clinical trials, but if BMS files for marketing approval it is likely to occur this year and approval would be expected by the end of mid-2014 to late-2014. 


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Snapshots
—Lucinda K. Porter, RN

Article: Hepatitis C-Associated B-Cell Non-Hodgkin Lymphomas: Epidemiology, Molecular Signature and Clinical Management – J. Peveling-Oberhag, et al.
  Source: Journal of Hepatology July 2013

Clinical evidence shows an association between chronic hepatitis C virus (HCV) infection and B-cell non-Hodgkin lymphoma (B-NHL). Data suggests a causal relationship between the two, notably because B-NHL occurrence is reduced in those who have a sustained response (SVR) to HCV treatment. This article was a review of the data on the epidemiology, interventional studies, and molecular mechanisms of HCV-associated B-NHL.

The Bottom Line:  HCV patients have a moderately increased risk of B-cell non-Hodgkin lymphoma. Patients who are in remission from B-NHL, should be considered for HCV treatment in order to prevent B-NHL recurrence. The authors of this article encourage the inclusion of patients with B-NHL in HCV studies.

Editorial Comment: I chose this paper because it is a sharp reminder that HCV patients are at increased risk of other comorbidities, and these risks are yet another reason to consider HCV treatment.

Article: A Diagnostic Score for the Prediction of Spontaneous Resolution of Acute Hepatitis C Virus Infection – Sandra Beinhardt, et al.
  Source: Journal of Hepatology July 2013 published online 11 July 2013

Around 20 – 40% of those who contract hepatitis C viral infection (HCV) are able to clear it on their own without treatment. However, the best time to treat acute HCV is in the first six months. Many have wondered if delaying HCV treatment impairs treatment response, and if there is a way to predict who might be most likely to clear HCV spontaneously, and therefore avoid treatment. 

The goal of this retrospective Austrian study was to develop a score enabling identification of patients who might be more likely to spontaneously clear HCV versus those more likely to develop chronic HCV, and be candidates for early antiviral treatment. Data from 136 HCV patients was analyzed. Factors associated with spontaneous clearance were IL28B C/C-genotype (see “Healthwise,” in this issue), detectability of HCV-specific CD4(+)Th1 cells and serum IP-10 levels (a protein found in humans) at time of diagnosis.

Other factors associated with spontaneous clearance included bilirubin levels, HCV-RNA decline until week 4 after diagnosis, and younger age at infection. The average subject age was 35 ±15 years and those who had spontaneously clearance were younger (31±13 vs. 37±16 years). Gender, genotype, and ALT levels were not associated with spontaneous clearance.

The Bottom Line: Researchers developed a simple score to differentiate patients with high probability for spontaneous clearing of HCV from those in need of early antiviral treatment.

Editorial Comment: This study is small, but exciting. Here we are on the threshold of curing HCV with easier to tolerate medications, simultaneously evaluating the possibility of identifying those who might not need HCV treatment at all.

Article: Predictive Factors of Risk of Hepatocellular Carcinoma in Chronic Hepatitis C – Juan Carlos Gavilán, et al.
  Source: European Journal of Internal Medicine published online 12 July 2013

While patients weigh the decision to treat HCV now or wait for approval of new treatments, they need to monitor the progression of HCV. Researchers devised a risk score that may help assess HCV patients’ risk for developing liver cancer (hepatocellular carcinoma or HCC).

This study enrolled 863 HCV patients, following them for an average of nearly seven years, of which 58 patients developed HCC (7%). Researchers constructed a risk score formula based on four factors associated with HCC risk: age, alpha-fetoprotein level, gammaglobulin level and platelet count (<150,000/ml). The formula had three levels of HCC risk: low (annual incidence of 0.05%), intermediate (annual incidence of 0.6%) or high (annual incidence 2.6%). Subjects were assessed every 6 months for the development of HCC using serum alpha-fetoprotein (AFP) levels and ultrasound imaging to detect new lesions.

The Bottom Line: The score was more accurate at predicting HCC than was the commonly used fibrosis index.

Editorial Comment: This is a small, but important study.  These findings were published online two days after an article stating that liver cancer deaths have doubled over last 20 years (The State of US Health, 1990-2010 Burden of Diseases, Injuries, and Risk Factors; the Journal of the American Medical Association’s (JAMA) July 10, 2013).  Also of note were preliminary findings showing that the noninvasive Fibroscan may predict liver disease progression better than the liver biopsy does. (Abstract TUABO104 International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention). In short, HCV-related medical assessments are improving.

Article: Renal Impairment Is Frequent in Chronic Hepatitis C Patients under Triple Therapy with Telaprevir or Boceprevir – Stefan Mauss, et al.
  Source: Hepatology published online July 2013

It has been slightly more than two years since triple therapy using telparevir or boceprevir has been on the market, and we are still collecting information about adverse events. Researchers evaluated 895 HCV patients with genotype 1 who received at least 12 weeks of therapy (575 using telaprevir-based triple therapy, 211 using boceprevir, 109 on dual therapy);  and 591 who received 24 weeks or more (398 telaprevir, 113 boceprevir and 80 on dual therapy). The goal was to measure the impact of HCV treatment on the kidneys. 

The Bottom Line: HCV triple therapy using either boceprevir or telaprevir was associated with an increased risk of renal impairment that typically resolved after switching to dual therapy.  There was more anemia, and thus reduction of ribavirin dose in those with renal impairment. This risk was associated with increased risk for those who were older, or had arterial hypertension or diabetes.

Editorial Comment: Patients on HCV treatment should be monitored for kidney function during HCV treatment.

Article: The Safety of Chemotherapy for Breast Cancer Patients with Hepatitis C Virus Infection – Yuji Miura, et al.
  Source: Journal of Cancer July 2013

There is little data about the relationship between HCV, cancer and chemotherapy; even less about breast tumors. Using a sample that was representative of the total population, 23 HCV-positive women with breast cancer participated in this Japanese study; ten underwent chemotherapy. Liver function, breast cancer characteristics, various laboratory safety markers, and HCV viral load during chemotherapy were retrospectively evaluated.

The Bottom Line: Chemotherapy for HCV patients with breast cancer infection is feasible. Neutropenia (low white blood cell count) risk is increased and growth factors may be considered.

Editorial Comment: This is a small, but long overdue study.  Although more research is needed, I have a fantasy that with improved HCV treatment around the corner, perhaps we can cure HCV so we won’t need to study patients with comorbidities.


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HEALTHWISE: Hepatitis C and Your DNA
—Lucinda K. Porter, RN

If you were a geneticist and had never met me, you’d know that my eyes are blue, my hair is straight, and that I can tolerate lactose. If you knew I had hepatitis C and had been through interferon-based treatment twice, you could look at my DNA, and despite not knowing my hepatitis C genotype, you would guess that I didn’t respond to treatment. You might also predict that my platelets would drop dramatically from interferon, and that my odds of developing ribavirin-induced anemia are typical.  You would be right on all accounts.

“Your genome knows much more about your medical history than you do,” said scientist Danny Hillis. Many of us who live with chronic hepatitis C virus infection (HCV) can tell you what our HCV genotype is, liver disease stage, and viral load, but when it comes to knowledge about our own DNA, we draw a blank. Isn’t DNA testing for paternity suits and TV crime shows?

Actually, any adult can have genetic testing, and you don’t need a doctor’s order to have it done. Many genetic testing companies offer a wide range of services, and I chose 23andMe. I received a lengthy report on potential health risks, ancestry, traits, and drug-response information.  It cost me $99 ($79 for additional kits) and some saliva. I had the results in less than six weeks.

I did this because I wanted the drug-response information. Generally, we look at factors such as HCV genotype, HIV status and presence of cirrhosis when trying to predict response to HCV treatment. However, each of us carries another predictor of response to medication, and this information is located in our genes.

Let’s start with a simple explanation of genetics. We inherit copies of genes from each parent. Most genes are the same in all people. In fact, less than 1 percent of our genes vary among people. These small differences contribute to each person’s features, and their capacity to respond to certain drugs as well as their ability to resist certain diseases.

One of the inherited factors is the interleukin-28B (IL28B) gene. The IL28B gene is involved in the immune response to certain viruses, including hepatitis C. There are three IL28B subtypes: CC, CT, and TT. These subtypes are sometimes referred to as genotypes. To clarify, this is your genotype; your virus has its own genotype. People with the CC genotype have a stronger immune response to HCV infection than people with the CT or TT genotypes (called non-CC genotypes). People who have a CC genotype are more likely to clear HCV without treatment within six months of becoming infected. 

People who have a CC genotype are also two to three times more likely to be cured by HCV treatment using peginterferon. When considering my own HCV treatment choices, I wanted to know my IL28B genotype. Since I still had HCV despite two treatments, it was no surprise that my results showed moderately lower odds of responding to interferon-based therapy. It was also no surprise that I did not have the least favorable genetic type, since I did respond to HCV treatment, just not permanently.

The IL28B genotype may explain the differences in response rates among various ethnic groups.

The IL28B CC genotype is substantially more common in European than African populations, which may explain why those of European ancestry have a significantly higher probability of being cured than those of African ancestry. Fortunately, genome isn’t destiny, as many HCV-positive people of African descent have been cured. Conversely, if you look at my web page photo, you might wonder how I ended up sharing a genetic polymorphism with my darker-skinned companions with HCV.

A recent study showed that IL28B testing may be useful for those who are HIV/HCV co-infected.  In this study of genotype 1 and 4 patients, those who received peginterferon/ribavirin (PEG-IFN/RBV) showed a higher response rate than those with the IL28B-CC genotype. Those with TT were less likely to respond to HCV treatment; those with the CT type had the lowest response rates. However, only 14% of participants had the genetic profile associated with the best outcomes.1

Use of IL28B testing has been making its way into HCV testing in recent years, particularly in HCV clinical trials. Some medical providers are ordering IL28B tests for their patients.  However, there is another HCV treatment-related genetic marker that is less known, and it has to do with side effects.

On the ITPA gene, two markers may predict a person’s risk for anemia or thrombocytopenia (low platelets) from HCV treatment using PEG-IFN/RBV. The data are small and considered preliminary.

Note: The CC genotype on the ITPA markers are not the same as the CC genotype on the IL28B gene.

Looking at HCV treatment using ribavirin, researchers compared 231 subjects of Japanese descent who experienced anemia while being treated with PEG-IFN/RBV to 463 individuals who were treated but did not experience anemia. Those with the AA or AC genotype on one location of the ITPA gene had about 33 times lower odds of having anemia in response to PEG-IFN/RBV therapy, compared to individuals with the ITPA CC genotype. A European study found that those with the AA or AC genotypes maintained stable levels of hemoglobin while taking PEG-IFN/RBV, while those with the CC genotype experienced a decrease in hemoglobin levels. 2

Looking at treatment-induced thrombocytopenia, researchers compared 282 subjects of Japanese descent who had low platelets during PEG-IFN/RBV treatment. They compared these to 412 subjects without thrombocytopenia. Those with the CT or CC genotype at a marker near the ITPA gene had about 3.9 times higher odds of developing thrombocytopenia in response to PEG-IFN/RBV therapy, compared to individuals with the TT genotype. Genetic variants in ITPA may also be associated with ribavirin-induced anemia and hemoglobin levels in European populations.3

While all this may sound like alphabet soup, the real story is what it means for us. The Human Genome Project ushered in a new technology that may shape medical practice. Instead of one-size fits all, medicine may be tailored to our genetic variations. Before prescribing Coumadin or Plavix, your medical provider might want to know if your genetic make-up predisposes you to be overly sensitive to these medications. 

Although this all sounds good, there are some risks involved with genetic testing. I recently spoke to a woman who agreed to genetic testing to see if she carried a marker for a disease that her niece had. Although she did not have the disease, she had the marker. Her long-term insurance carrier dropped her like the proverbial hot potato. In short, if others can access your test results, you may have an insurability issue.

Although beginning in January 2014, health insurance companies will no longer be able to deny coverage to those with preexisting conditions per the Affordable Care Act (ACA), companies can still deny applications for long-term care, disability or life insurance. In fact, according to benefits expert and HCV Advocate contributor Jacques Chambers, ACA does not even affect Medicare Supplement (Medigap) policies.

Another risk of genetic testing is that the information might be unsettling. How would it feel to learn that you had an increased risk of Alzheimer’s or Parkinson’s disease? A marker does not mean you are necessarily going to get a disease, and the absence of a marker doesn’t mean you won’t get a disease. If you are prone to worrying about your health, then genetic testing might produce anxiety rather than reassurance. The bottom line is to know your risks before submitting your saliva. 

It is a risk I am glad I took. As V. Utt from Estonia posted, “The best book that has ever been written is in us and nowadays we have an opportunity to read it.” I think genetic testing is one of the most interesting advances in medicine. Our DNA tells our story, a story that makes us who and what we are.

Further Information

Lucinda K. Porter, RN, is a long-time contributor to the HCV Advocate and author of Free from Hepatitis C and Hepatitis C One Step at a Time (September 2013) Her blog is http://lucindaporterrn.com

Endnotes
1 Neukam K et al. Variations in multiple genes improve interleukin 28b genotype predictive capacity for response to therapy against hepatitis C genotype 1 or 4 infection. AIDS 27, online edition, doi: 10.1097/01.aids.0000432459.36970.a9, 2013
2 Tanaka Y et al. Genome-wide association study identified ITPA/DDRGK1 variants reflecting thrombocytopenia in pegylated interferon and ribavirin therapy for chronic hepatitis C. Hum Mol Genet 2011; 20(17):3507-16;
  Ochi H et al. ITPA polymorphism affects ribavirin-induced anemia and outcomes of therapy--a genome-wide study of Japanese HCV virus patients. Gastroenterology 2010;139(4):1190-7;
  Fellay J et al. ITPA gene variants protect against anemia in patients treated for chronic hepatitis C. Nature 2010 464(7287):405-8
3 Tanaka Y et al.


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HCV and Correctional Centers: A Missed Population
—Sonya Becker & Juliana Chan, Pharm.D.

Hepatitis C
Hepatitis C is a global phenomenon that affects approximately 150 million people worldwide and from which more than 350,000 people die annually.1 Currently in the United States, it is estimated that 2.7 million Americans, or 1% to 1.5% of the population has been infected with the hepatitis C virus (HCV).2-3 Most individuals with HCV have no idea they have been infected because more than 70% of people are asymptomatic. However, those who do have symptoms may complain of fatigue, which could result in poor quality of life.  In more severe cases, HCV may progress from a mild liver disease to cirrhosis or even liver cancer—making it the leading cause for liver transplantation.4

HCV is primarily transmitted through exposure from tainted blood. Because of this, people who inject drugs (PWID) who share syringes, needles, and other drug paraphernalia account for up to 60% of newly acquired HCV cases in the general population.5 Additionally, individuals who received blood transfusions, clotting factors, or organ transplantation before 1992 were also at a greater risk of acquiring HCV.4 With safer medical practices and blood products now screened, the risk of acquiring HCV is less than 0.001%.6  High-risk sexual behavior, such as HIV positive men who have sex with men (MSM), multiple sexual partners, and co-infection with sexually transmitted diseases (STDs) represents a low risk of viral transmission.5  Other lower risk exposures include hemodialysis, tattoos, being born to an HCV-infected mother, and occupational contact through contaminated materials (e.g., by health care workers). In addition, individuals born between the years 1945-1965 share an increased likelihood of exposure through high-risk behaviors conducted decades prior to the identification and elucidation of HCV transmission.4 This baby boomer generation now represents 75% of all people in the US living with chronic HCV disease.

A disproportionately large number of HCV-infected people pass through the prison system on a yearly basis.  In 1996, it was estimated that almost 1/3 of all people infected with HCV in the US served time in a correctional facility that year.7  This turnover rate indicates that millions of people in the general public are exposed to a population that has high rates of HCV infection and are unaware of the potential risk exposure.  Because of this, correctional facilities represent an under-utilized opportunity to screen, treat, and educate a high-risk population.  

Hepatitis C in the Prison Population
The burden of HCV in the imprisoned community is 9-10 times greater than in the general US population, with an estimated 12% to 35% of prisoners having chronic HCV.3, 7 Prison systems tend to condense a population that participates in high-risk behaviors placing them at risk for infection.  Intravenous drug use remains the most significant risk factor for transmission of HCV, with rates ranging between 72% to 86% among this high risk population.7  Although the risk of HCV increases with prolonged drug use, over 30% of PWIDs acquire HCV within 2 years after the first injection.5

The high HCV prevalence in the prison community can be attributed to the rising rate of incarcerations among PWIDs.  Over the past two decades, drug-related offenses have increased from 40,000 to 450,000 with drug offenders making up almost half of the entire prison population.8-9 One-third of all prisoners were abusing illegal substances at the time of their incarceration, yet imprisonment has a minimal effect on drug abuse rehabilitation.10 It is estimated that one quarter of PWIDs have abused drugs while incarcerated, with longer prison terms associated with increased likelihood of abuse.11

The prevalence of HCV is greater among PWIDs in the general community compared to continuously incarcerated inmates. This suggests that most inmates return to drug abuse once they make parole or are released back into society.11 Individuals with a history of recent incarceration are at a greater risk of contracting HCV, as witnessed by the high rates of drug overdose and deaths upon release.

Furthermore, there is a surge in the number of young incarcerated individuals who also abuse drugs. It has been noted that incarceration rates from substance abuse violations for juveniles from 1990 to 1999 had increased by 132%.5 Because age is associated with length of drug abuse, the younger generation is at an increased risk of contracting HCV. It is estimated that 590,000 young adults aged 18–29 have used IV drugs and as many as 45% of that population is infected with HCV.13

Despite segregation from society and close supervision, inmates still manage to obtain and abuse illicit drugs.  Although the number of people abusing IV drugs is substantially lower compared to the general community, the risk of HCV infection may be much greater.11 Poor sanitation as well as high rates of sharing injection equipment may lead to contamination and a greater potential to spread HCV.  In addition, IVDU may place prisoners at an increased risk for other infections such as HIV and STDs. 

Next to IVDU, getting a tattoo in prison has been implicated as being the largest risk factor for acquiring HCV.12 The art of tattooing requires needles to be exposed to skin, blood, and potentially other bodily fluids.14 This may be a source of viral transmission if equipment is not sterilized properly, as puncturing the skin with improper technique may increase the risk of bleeding and HCV infections.  Almost two-thirds of inmates have been tattooed, and approximately 45% of inmates reported reusing and sharing needles, which are oftentimes crafted out of any available sharp object.12-14 Receiving a tattoo in prison is a concern for increased risk of HCV transmission, but additional studies are still needed to validate this implication. 

It is estimated that 20% of people in the general prison population had reported sexual exposures as a source of HCV transmission (i.e., MSM, or multiple partners) in the absence of other high-risk behaviors.15 Even though all states have laws prohibiting sex between residents in a correctional setting, sexual activity is not uncommon.4, 17 Additionally, it has been reported that individuals who are in and out of the penal system engage in high risk sexual behaviors defined as having unprotected anal sex, inserting fingers into rectum, and men engaging in rough sexual practices.11, 16 These practices may cause bleeding in the anal canal, increasing one’s risk of acquiring viral infections. It is estimated that 4% to 65% of adult males engage in unprotected consensual homosexual activities while incarcerated.11 Additionally, about 4.5% of adult inmates and 9.5% of juveniles have been victimized by  unwanted sexual advances within the past year, a preventable, but a potential contributory risk factor for viral transmission.17 Male sexual activity within the prison system coupled with the lack of condoms may put inmates at greater risk of acquiring HCV or STDs within correctional facilities compared to the general population.

The transmission rate of HCV due to altercations involving exchange of blood between parties is unknown, yet two reported cases have been identified documenting the successful transfer of HCV during confrontations.18-19 An estimated 7% of jail inmates reported injuries due to a fight since admission, an increased risk which is closely associated with the length of time served.20 HCV’s increased prevalence, spontaneous fights, and riots involving many inmates are all dangers that place prisoners at an increased risk of acquiring HCV through bloody altercations.

HCV Prevention and Treatment
HCV is a disease that causes inflammation of the liver. It is important to note that the progression of liver damage is usually slow and takes decades before significant changes occur, including cirrhosis.  However, the use of alcohol or ingestion of other liver toxic substances, as well as co-infection with HIV or hepatitis B, have all been directly associated with increased rates of liver disease progression.  Abstinence from alcohol use in addition to receiving hepatitis A and hepatitis B vaccines is highly recommended to reduce the progression of disease and preserve liver function.4, 21

If a patient has been diagnosed with HCV, it is important to seek medical attention to determine if treatment is necessary. At present, current HCV treatment regimens may result in cure rates ranging from 50% to 70%.20, 21 All suitable candidates for HCV treatment will receive an injection medication given once a week (pegylated interferon) and ribavirin to be taken twice daily.  Depending on the patient’s genotype (type of hepatitis C), the patient may receive another class of medications known as protease inhibitors (i.e., telaprevir or boceprevir).22 People with HCV genotype 1 who receive only pegylated interferon and ribavirin  have lower cure rates and thus require ‘triple therapy,’ which includes the addition of a protease inhibitor. Adverse effects from HCV therapy can be unpleasant and sometimes serious, leading to dose reductions or discontinuation of treatment.21-22 Not all people experience the same side effects—which may include skin rashes, anemia, mental and psychiatric symptoms, vision or eye problems, and/or increased risk of infections.  Even if HCV treatment may not offer a cure, the medications may still be beneficial in preventing long-term health complications including liver cirrhosis and liver cancer.4

Because no vaccine exists for HCV, prevention education should be directed towards the disease, routes of transmission, risk factors, and disease outcomes.4 Behavioral interventions, such as drug rehabilitation programs, must focus on educating those at high risk for HCV exposure.  It is noted that inmates who are paroled and continue to participate in health-related programs in the general community are less likely to commit future crimes. Inmates participating in residential drug abuse treatment programs were on average 16% less likely to commit crimes and 15% less likely to relapse.23 Increased employment rates, increased independent living, and decreased homelessness rates indicate that people who seek drug treatment are more likely to maintain health-conscious behavior.

Conclusion
The high prevalence of infectious disease in the incarcerated population should now be recognized as a public health concern.  Not only does this population have a disproportionately high burden of HCV, but they also have an increased prevalence of other infectious disease such as HIV and other sexually transmitted diseases.  Correctional facilities are critical settings in which to instill interventions such as the prevention and treatment of such infections.  Most inmates return to the general community after incarceration, representing a potential source of disease transmission to the public.  By targeting this high-risk population in the correctional setting, it benefits not only the inmates and their families, but also the public health of the communities to which these inmates return.

Authors
Sonya Becker, Pharm.D. Candidate
College of Pharmacy
University of Illinois at Chicago

Juliana Chan, Pharm.D., BCACP
Clinical Associate Professor
Clinical Pharmacist – Gastroenterology/Hepatology and Illinois Department of Corrections HCV Telemedicine Clinic, Departments of Pharmacy Practice and Medicine, Colleges of Pharmacy and Medicine Sections of Hepatology, Digestive Diseases and Nutrition

References:

  1. Hepatitis C. World Health Organization. [Online] Available at: http://www.who.int/mediacentre/factsheets/fs164/en/index.html. Last accessed: July 2, 2013.

  2. Kim WR. The burden of hepatitis C in the United States. Hepatology. 2002 Nov;36(5 Suppl 1):S30-4.

  3. Viral Hepatitis Specific Settings: Correction Facilities and Viral Hepatitis. Centers for Disease Control and Prevention. http://www.cdc.gov/hepatitis/Settings/corrections.htm. Last accessed July 3, 2013.

  4. Moyer VA; on behalf of the U.S. Preventive Services Task Force. Screening for Hepatitis C Virus Infection in Adults: U.S. Preventive Services Task Force Recommendation Statement. Ann Intern Med. 2013 Jun 25. doi: 10.7326/0003-4819-159-5-201309030-00672.

  5. Weinbaum C, Lyerla R, Margolis HS; Centers for Disease Control and Prevention. Prevention and control of infections with hepatitis viruses in correctional settings. Centers for Disease Control and Prevention. MMWR Recomm Rep. 2003 Jan 24;52(RR-1):1-36.

  6. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. Centers for Disease Control and Prevention. MMWR Recomm Rep. 1998 Oct 16;47(RR-19):1-39.

  7. National Commission on Correctional Health Care. In: The Health Status of Soon-to-Be-Released Inmates: A Report to Congress. Vol. 2. Chicago; March 2002. https://www.ncjrs.gov/pdffiles1/nij/grants/189736.pdf. Last accessed July 3, 2013.

  8. Boutwell AE, Allen SA, Rich JD. Opportunities to address the hepatitis C epidemic in the correctional setting. Clin Infect Dis. 2005 Apr 15;40 Suppl 5:S367-72.

  9. Quick facts about the bureau of prisons. Updated June  29, 2013.  http://www.bop.gov/news/quick.jsp#4. Last accessed July 13, 2013.

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The Other Forgotten Hepatitis B Minority—African-Americans
—Christine M. Kukka

Which racial/ethnic group in the United States had the highest rate of acute (new) hepatitis B infections in 2010?

You might assume Asian-Americans who have high chronic infection rates had this distinction, but think of another racial group facing similar cultural and economic barriers to health care—African-Americans.

According to a study by University of Pennsylvania researchers, African-Americans make up the largest percentage of people who are newly infected with hepatitis B today.

In 2010, African-Americans had the highest rate of acute HBV infection with 1.7 cases per 100,000 people. In contrast, Asian-Americans had an acute infection rate of 0.6 per 100,000. Asian-Americans may have a higher rate of chronic infection due to infection at birth, but most of the new infections occurring in the United States today happen to African-Americans.

In America, being black means you have a 3.9-fold chance of being infected with hepatitis B, compared to whites.

According to the study, published in the August issue of the Journal of Clinical Gastroenterology and Hepatology, African-Americans tend to be infected with HBV genotype A (84%), which is associated with a 4-  to 5-fold increase in liver cancer compared to other genotypes. In contrast, Asian-Americans are often infected with less virulent genotypes B and C.

To make matters worse, the few hepatitis B studies that have been performed in African-Americans and immigrants from Africa found that liver cancer occurs at a younger age in these populations than in other ethnic groups. African-Americans may have genetic risk factors that predispose them to developing chronic hepatitis B following exposure to the virus that other ethnic groups do not face. Yet, few doctors know to screen their African-American clients for hepatitis B.

If little is known about the progression of liver disease in HBV-infected African-Americans, even less is known about the effectiveness of treatment.

A long-term follow-up study of patients treated with interferon found that African American patients were "much more likely to respond to therapy," researchers wrote. "Of note, all African American responders not only cleared the hepatitis B "e" antigen and (achieved undetectable) HBV DNA ... but all cleared HBsAg, a relatively rare milestone with HBV therapy that (usually) occurs in (only) 7.8% of patients on therapy."

Unfortunately, this was a small study and no additional research into African-Americans' remarkable ability to reportedly clear hepatitis B infection after interferon treatment has been repeated to verify these results.

When it comes to the effectiveness of antivirals in African-Americans, few clinical trials have examined their impact in this population. "There are inadequate data about the efficacy and safety of these agents in African American patients with chronic HBV infection," researchers added.

As with Asian-Americans, few African-Americans who qualify for treatment ever receive it. A small study that included patients from an urban medical center found that only 7% of a predominantly African-American and Hispanic population had been initiated on therapy.

The study cited lack of health insurance, failure to take medication as prescribed and ongoing drug and alcohol use as possible reasons for poor access to treatment. Not surprising, access to liver transplants was also far lower among African-Americans than whites.

"Continued research is needed to identify and address areas of disparity in chronic HBV infection and treatment, and an improvement in enrollment of African-Americans in clinical trials is essential for achievement of this goal," the researchers noted.

Source: http://www.ncbi.nlm.nih.gov/pubmed/23811241



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