Gastroenterology. 2011 Jul;141(1):119-27. Epub 2011 Mar 24.
Chevaliez S, Hézode C, Soulier A, Costes B, Bouvier-Alias M, Rouanet S, Foucher J, Bronowicki JP, Tran A, Rosa I, Mathurin P, Alric L, Leroy V, Couzigou P, Mallat A, Charaf-Eddine M, Babany G, Pawlotsky JM.
National Reference Center for Viral Hepatitis B, C and delta, Department of Virology, Hôpital Henri Mondor, Université Paris-Est, Créteil, France; INSERM U955, Créteil, France.
Abstract
BACKGROUND & AIMS: In patients with chronic hepatitis C who failed to respond to standard therapy, high-dose pegylated interferon (IFN)-α and/or ribavirin could induce a stronger antiviral response and prevent treatment failure and HCV resistance when combined with direct-acting antivirals. The influence of genetic determinants in this context remains unknown.
METHODS: Eighty-three patients infected with HCV genotype 1 who were nonresponsive to standard therapy received pegylated IFN-α2a (360 μg once per week or 180 μg twice per week) with ribavirin (1.0-1.2 or 1.2-1.6 g/d) for up to 72 weeks. Virological responses were assessed at different time points, and the influence of the IL-28B genotype was studied.
RESULTS: At weeks 12 and 24, respectively, 47 (56.6%) and 50 (60.2%) patients achieved a ≥2-Log(10) decrease of HCV RNA levels; 8 (9.6%) and 21 (25.3%) patients had undetectable HCV RNA after 12 and 24 weeks of treatment, respectively. Patients with a CT IL-28B genotype responded significantly better and earlier than those with a TT genotype. In multivariate analysis, the IL-28B genotype was an independent predictor of the virological responses at weeks 4, 12, and 24.
CONCLUSIONS: High-dose pegylated IFN-α with standard or high doses of ribavirin induces a potent antiviral response in a substantial number of patients who did not respond to standard therapy. The IL-28B genotype is an independent predictor of the antiviral response. High-dose pegylated IFN-α in combination with ribavirin and protease inhibitors appears as an attractive option for future study in this population.
Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.
Source
July 7, 2011
Direct Medical Care Costs Among Pegylated Interferon Plus Ribavirin-Treated and Untreated Chronic Hepatitis C Patients
Dig Dis Sci. 2011 Jun 30. [Epub ahead of print]
Solomon M, Bonafede M, Pan K, Wilson K, Beam C, Chakravarti P, Spiegel B.
Stanford University School of Medicine, Stanford, CA, USA.
Abstract
BACKGROUND: Hepatitis C virus (HCV) is a common and expensive infectious disease. The current standard of care for HCV infection, pegylated interferon with ribavirin (PEG-RBV), is costly and has a significant adverse event profile.
AIM: To quantify the direct economic burden of HCV infection and PEG-RBV treatment for HCV.
METHODS: Using a large administrative claims database, we evaluated the medical and prescription drug costs of patients with HCV from 2002 to 2007. A cohort of patients with PEG-RBV was 1:1 propensity score-matched to a cohort of untreated HCV patients. Multivariate models adjusted for demographic and clinical characteristics in evaluating the effect of PEG-RBV treatment on direct medical expenditure.
RESULTS: The matched analysis included 20,002 patients. PEG-RBV-treated patients had higher total direct medical costs ($28,547 vs. $21,752; P < 0.001), outpatient pharmacy costs ($17,419 vs. $2,900; P < 0.001), and outpatient physician visit costs ($894 vs. $787; P < 0.001), but lower inpatient costs ($3,942 vs. $9,543; P < 0.001) and emergency room costs ($366 vs. $505; P < 0.001). After multivariate adjustment, PEG-RBV use was associated with an additional $9,423 in total direct medical costs and an additional $12,244 in HCV-related total medical costs.
CONCLUSION: Total HCV-related medical costs are higher for treated than untreated patients, driven mostly by higher outpatient pharmacy costs, which outweigh higher HCV-related inpatient costs incurred by untreated patients.
Source
Solomon M, Bonafede M, Pan K, Wilson K, Beam C, Chakravarti P, Spiegel B.
Stanford University School of Medicine, Stanford, CA, USA.
Abstract
BACKGROUND: Hepatitis C virus (HCV) is a common and expensive infectious disease. The current standard of care for HCV infection, pegylated interferon with ribavirin (PEG-RBV), is costly and has a significant adverse event profile.
AIM: To quantify the direct economic burden of HCV infection and PEG-RBV treatment for HCV.
METHODS: Using a large administrative claims database, we evaluated the medical and prescription drug costs of patients with HCV from 2002 to 2007. A cohort of patients with PEG-RBV was 1:1 propensity score-matched to a cohort of untreated HCV patients. Multivariate models adjusted for demographic and clinical characteristics in evaluating the effect of PEG-RBV treatment on direct medical expenditure.
RESULTS: The matched analysis included 20,002 patients. PEG-RBV-treated patients had higher total direct medical costs ($28,547 vs. $21,752; P < 0.001), outpatient pharmacy costs ($17,419 vs. $2,900; P < 0.001), and outpatient physician visit costs ($894 vs. $787; P < 0.001), but lower inpatient costs ($3,942 vs. $9,543; P < 0.001) and emergency room costs ($366 vs. $505; P < 0.001). After multivariate adjustment, PEG-RBV use was associated with an additional $9,423 in total direct medical costs and an additional $12,244 in HCV-related total medical costs.
CONCLUSION: Total HCV-related medical costs are higher for treated than untreated patients, driven mostly by higher outpatient pharmacy costs, which outweigh higher HCV-related inpatient costs incurred by untreated patients.
Source
Impact of insulin resistance on sustained response in HCV patients treated with pegylated interferon and ribavirin: a meta-analysis
J Hepatol. 2011 Apr 13. [Epub ahead of print]
Deltenre P, Louvet A, Lemoine M, Mourad A, Fartoux L, Moreno C, Henrion J, Mathurin P, Serfaty L.
Service d'Hépato-Gastroentérologie, Hôpital Huriez, CHRU Lille, Lille, France; Service d'Hépato-Gastroentérologie, Hôpital de Jolimont, Haine-Saint-Paul, Belgium.
Abstract
BACKGROUND/AIMS: Recent studies suggested that SVR rates might be lower in HCV patients with insulin resistance (IR) than in patients without IR, but the extent of the impact of IR on treatment response has not been established. We aimed to confirm the role of IR assessed by the homoeostasis model assessment (HOMA-IR) on SVR and to assess its magnitude.
METHODS: We performed meta-analysis of studies evaluating the impact of IR in HCV patients treated with pegylated interferon and ribavirin.
RESULTS: Fourteen studies involving 2,732 patients were included. SVR was less frequent in patients with IR than in patients without IR (mean difference: -19.6%, 95% CI: -29.9% to -9.4%, p<0.001). In sensitivity analyses according to HCV-1 patients, patients with IR also less frequently attained a SVR than patients without IR (mean difference: -13.0%, 95% CI: -22.6% to -3.4%, p=0.008). In addition, the baseline HOMA-IR index was lower in responders than in non-responders (mean difference: -0.92, 95% CI: -1.53 to -0.32, p<0.001). In sensitivity analyses restricted to HCV-1 patients, the baseline HOMA-IR index remained lower in responders than in non-responders (mean difference: -0.63, 95% CI: -1.13 to -0.14, p<0.001).
CONCLUSIONS: HCV patients with IR have a 20% lower SVR than patients without IR. The baseline HOMA-IR index is a major determinant of SVR.
Copyright © 2011. Published by Elsevier B.V.
Source
Deltenre P, Louvet A, Lemoine M, Mourad A, Fartoux L, Moreno C, Henrion J, Mathurin P, Serfaty L.
Service d'Hépato-Gastroentérologie, Hôpital Huriez, CHRU Lille, Lille, France; Service d'Hépato-Gastroentérologie, Hôpital de Jolimont, Haine-Saint-Paul, Belgium.
Abstract
BACKGROUND/AIMS: Recent studies suggested that SVR rates might be lower in HCV patients with insulin resistance (IR) than in patients without IR, but the extent of the impact of IR on treatment response has not been established. We aimed to confirm the role of IR assessed by the homoeostasis model assessment (HOMA-IR) on SVR and to assess its magnitude.
METHODS: We performed meta-analysis of studies evaluating the impact of IR in HCV patients treated with pegylated interferon and ribavirin.
RESULTS: Fourteen studies involving 2,732 patients were included. SVR was less frequent in patients with IR than in patients without IR (mean difference: -19.6%, 95% CI: -29.9% to -9.4%, p<0.001). In sensitivity analyses according to HCV-1 patients, patients with IR also less frequently attained a SVR than patients without IR (mean difference: -13.0%, 95% CI: -22.6% to -3.4%, p=0.008). In addition, the baseline HOMA-IR index was lower in responders than in non-responders (mean difference: -0.92, 95% CI: -1.53 to -0.32, p<0.001). In sensitivity analyses restricted to HCV-1 patients, the baseline HOMA-IR index remained lower in responders than in non-responders (mean difference: -0.63, 95% CI: -1.13 to -0.14, p<0.001).
CONCLUSIONS: HCV patients with IR have a 20% lower SVR than patients without IR. The baseline HOMA-IR index is a major determinant of SVR.
Copyright © 2011. Published by Elsevier B.V.
Source
Beneficial IL28B genotype associated with lower frequency of hepatic steatosis in patients with chronic hepatitis C
J Hepatol. 2011 Apr 14. [Epub ahead of print]
Tillmann HL, Patel K, Muir AJ, Guy CD, Li JH, Lao XQ, Thompson A, Clark PJ, Gardner SD, McHutchison JG, McCarthy JJ.
Duke Clinical Research Institute and the Division of Gastroenterology, Duke University Medical Center, Durham, NC, USA.
Abstract
Background IL28B polymorphisms have been associated with both treatment induced and spontaneous clearance of hepatitis C virus (HCV). We previously found that LDL cholesterol levels were higher in chronic hepatitis C (CHC) patients with the CC genotype at the rs12979860 polymorphism, located proximal to the IL28 gene. Here we analyzed the association of steatosis with IL28B genotype in treatment naïve patients with CHC. Methods Two independent cohorts of 145 genotype 1 infected patients from an antifibrotic study and 180 genotype 1 patients from Duke were analyzed for presence and severity of steatosis in relation to the rs12979860 polymorphism at the IL28B locus. TaqMan assay based genotyping classified three groups CC, CT and TT. Results CC genotype was associated with a lower prevalence of steatosis. In the antifibrotic study steatosis was found in 47.6% (50/105) of IL28B non-CC versus 22.5% (9/40; p=0.008) in CC patients. Similarly, steatosis was found in 67.4% (89/132) of non-CC patients compared to only 39.6% (19/48; p=0.001) of CC patients in the Duke cohort. Conclusions IL28B CC genotype is associated with less pronounced disturbances of lipid metabolism, as reflected both in serum lipoprotein levels and hepatic steatosis, in HCV infection.
Copyright © 2011. Published by Elsevier B.V.
Source
Tillmann HL, Patel K, Muir AJ, Guy CD, Li JH, Lao XQ, Thompson A, Clark PJ, Gardner SD, McHutchison JG, McCarthy JJ.
Duke Clinical Research Institute and the Division of Gastroenterology, Duke University Medical Center, Durham, NC, USA.
Abstract
Background IL28B polymorphisms have been associated with both treatment induced and spontaneous clearance of hepatitis C virus (HCV). We previously found that LDL cholesterol levels were higher in chronic hepatitis C (CHC) patients with the CC genotype at the rs12979860 polymorphism, located proximal to the IL28 gene. Here we analyzed the association of steatosis with IL28B genotype in treatment naïve patients with CHC. Methods Two independent cohorts of 145 genotype 1 infected patients from an antifibrotic study and 180 genotype 1 patients from Duke were analyzed for presence and severity of steatosis in relation to the rs12979860 polymorphism at the IL28B locus. TaqMan assay based genotyping classified three groups CC, CT and TT. Results CC genotype was associated with a lower prevalence of steatosis. In the antifibrotic study steatosis was found in 47.6% (50/105) of IL28B non-CC versus 22.5% (9/40; p=0.008) in CC patients. Similarly, steatosis was found in 67.4% (89/132) of non-CC patients compared to only 39.6% (19/48; p=0.001) of CC patients in the Duke cohort. Conclusions IL28B CC genotype is associated with less pronounced disturbances of lipid metabolism, as reflected both in serum lipoprotein levels and hepatic steatosis, in HCV infection.
Copyright © 2011. Published by Elsevier B.V.
Source
Genetic variation in IL28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection
Hepatology. 2011 Jun 30. doi: 10.1002/hep.24503. [Epub ahead of print]
Marabita F, Aghemo A, De Nicola S, Rumi MG, Cheroni C, Scavelli R, Crimi M, Soffredini R, Abrignani S, De Francesco R, Colombo M.
INGM - Istituto Nazionale Genetica Molecolare Milano, Italy.
Abstract
Polymorphisms in the IL28B region are associated with spontaneous and treatment-induced viral clearance in Hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection. Thus, we asked if an association between IL28B polymorphisms and liver fibrosis progression existed. We studied 247 consecutive patients with chronic HCV, an accurate estimate of the date of infection and a liver biopsy performed before any treatment. No patient had a history of alcohol abuse or co-infection with other viruses. We assessed the role of rs8099917 and rs12979860 polymorphisms and the effect of host and environmental factors on fibrosis progression. Blood transfusion (75%) was the main modality of infection. The median age at infection was 21 years and the median interval between infection and liver biopsy was 25 years. 129 patients (52%) were infected by HCV-1, 74 (30%) by HCV-2, 34 (14%) by HCV-3 and 10 (4%) by HCV-4. Bridging fibrosis/cirrhosis (Ishak≥4) was detected in 24% of patients. Age at infection had a marked effect on fibrosis progression by both a linear model and Cox-proportional hazard regression (P<2E-16). A 12.1% increase in the hazard of advanced fibrosis was estimated for each additional year at infection, suggesting that this is the major explanatory variable in this cohort. Male gender (P<0.05), HCV genotype 3 (P<0.001) and steatosis (P<0.05) were also associated to faster fibrosis progression. Conversely, the two IL28B polymorphisms had no impact on fibrosis progression. Conclusions: In HCV patients with known date of infection IL28B genotype was not associated with fibrosis progression rate or with the risk of developing advanced liver fibrosis. (HEPATOLOGY 2011.).
Copyright © 2011 American Association for the Study of Liver Diseases.
Source
Marabita F, Aghemo A, De Nicola S, Rumi MG, Cheroni C, Scavelli R, Crimi M, Soffredini R, Abrignani S, De Francesco R, Colombo M.
INGM - Istituto Nazionale Genetica Molecolare Milano, Italy.
Abstract
Polymorphisms in the IL28B region are associated with spontaneous and treatment-induced viral clearance in Hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection. Thus, we asked if an association between IL28B polymorphisms and liver fibrosis progression existed. We studied 247 consecutive patients with chronic HCV, an accurate estimate of the date of infection and a liver biopsy performed before any treatment. No patient had a history of alcohol abuse or co-infection with other viruses. We assessed the role of rs8099917 and rs12979860 polymorphisms and the effect of host and environmental factors on fibrosis progression. Blood transfusion (75%) was the main modality of infection. The median age at infection was 21 years and the median interval between infection and liver biopsy was 25 years. 129 patients (52%) were infected by HCV-1, 74 (30%) by HCV-2, 34 (14%) by HCV-3 and 10 (4%) by HCV-4. Bridging fibrosis/cirrhosis (Ishak≥4) was detected in 24% of patients. Age at infection had a marked effect on fibrosis progression by both a linear model and Cox-proportional hazard regression (P<2E-16). A 12.1% increase in the hazard of advanced fibrosis was estimated for each additional year at infection, suggesting that this is the major explanatory variable in this cohort. Male gender (P<0.05), HCV genotype 3 (P<0.001) and steatosis (P<0.05) were also associated to faster fibrosis progression. Conversely, the two IL28B polymorphisms had no impact on fibrosis progression. Conclusions: In HCV patients with known date of infection IL28B genotype was not associated with fibrosis progression rate or with the risk of developing advanced liver fibrosis. (HEPATOLOGY 2011.).
Copyright © 2011 American Association for the Study of Liver Diseases.
Source
Differential Efficacy of Protease Inhibitors against HCV Genotype 2a, 3a, 5a, and 6a NS3/4A Protease Recombinant Viruses
Gastroenterology. 2011 Jun 12. [Epub ahead of print]
Gottwein JM, Scheel TK, Jensen TB, Ghanem L, Bukh J.
Copenhagen Hepatitis C Program (CO-HEP), Department of Infectious Diseases and Clinical Research Centre, Copenhagen University Hospital, Hvidovre and Department of International Health, Immunology and Microbiology, Faculty of Health Sciences, University of Copenhagen, Denmark.
Abstract
BACKGROUND & AIMS: The hepatitis C virus (HCV) genotype influences efficacy of interferon (IFN)-based therapy. HCV protease inhibitors are being licensed for treatment of genotype 1 infection. Since there is limited or no data on efficacy against HCV genotypes 2-7, we aimed at developing recombinant infectious cell culture systems expressing genotype specific NS3 protease (NS3P).
METHODS: Viability of J6/JFH1- based recombinants with genotype 1-7 NS3P/NS4A was evaluated in Huh7.5 cells. Adaptive mutations were identified in reverse genetic studies. Efficacy of lead compound linear protease inhibitors VX-950 (telaprevir) and SCH503034 (boceprevir) and macrocyclic inhibitors TMC435350, ITMN-191 (danoprevir), and MK-7009 (vaniprevir) was determined in high-throughput infection assays.
RESULTS: For genotype(isolate) 2a(J6), 3a(S52), 5a(SA13), and 6a(HK6a) we developed culture systems producing supernatant infectivity titers of 3.5-4.0 log(10) FFU/ml. Against 2a(J6), 5a(SA13) and 6a(HK6a) all inhibitors showed similar efficacy; macrocyclic inhibitors had ~10-fold greater potency than linear inhibitors. However, compared to 2a recombinant J6/JFH1 efficacy against 3a(S52) was 16- to 70-fold lower for macrocyclic inhibitors and 2- to 7-fold lower for linear inhibitors. Testing of additional genotype 2a and 3a isolates showed that these differences were genotype specific. The resistance of 3a isolates was similar to J6/JFH1 with engineered resistance mutations originally observed for genotype 1 patients. In contrast, we found similar efficacy of NS5A inhibitor BMS-790052 and interferon-alfa2.
CONCLUSIONS: Novel HCV culture systems with genotype specific NS3P/NS4A revealed similar efficacy of protease inhibitors against genotype 2a, 5a, and 6a and comparatively low but varying efficacy against genotype 3a isolates. These systems will facilitate genotype specific studies of HCV protease inhibitors and of viral resistance.
Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.
Source
Gottwein JM, Scheel TK, Jensen TB, Ghanem L, Bukh J.
Copenhagen Hepatitis C Program (CO-HEP), Department of Infectious Diseases and Clinical Research Centre, Copenhagen University Hospital, Hvidovre and Department of International Health, Immunology and Microbiology, Faculty of Health Sciences, University of Copenhagen, Denmark.
Abstract
BACKGROUND & AIMS: The hepatitis C virus (HCV) genotype influences efficacy of interferon (IFN)-based therapy. HCV protease inhibitors are being licensed for treatment of genotype 1 infection. Since there is limited or no data on efficacy against HCV genotypes 2-7, we aimed at developing recombinant infectious cell culture systems expressing genotype specific NS3 protease (NS3P).
METHODS: Viability of J6/JFH1- based recombinants with genotype 1-7 NS3P/NS4A was evaluated in Huh7.5 cells. Adaptive mutations were identified in reverse genetic studies. Efficacy of lead compound linear protease inhibitors VX-950 (telaprevir) and SCH503034 (boceprevir) and macrocyclic inhibitors TMC435350, ITMN-191 (danoprevir), and MK-7009 (vaniprevir) was determined in high-throughput infection assays.
RESULTS: For genotype(isolate) 2a(J6), 3a(S52), 5a(SA13), and 6a(HK6a) we developed culture systems producing supernatant infectivity titers of 3.5-4.0 log(10) FFU/ml. Against 2a(J6), 5a(SA13) and 6a(HK6a) all inhibitors showed similar efficacy; macrocyclic inhibitors had ~10-fold greater potency than linear inhibitors. However, compared to 2a recombinant J6/JFH1 efficacy against 3a(S52) was 16- to 70-fold lower for macrocyclic inhibitors and 2- to 7-fold lower for linear inhibitors. Testing of additional genotype 2a and 3a isolates showed that these differences were genotype specific. The resistance of 3a isolates was similar to J6/JFH1 with engineered resistance mutations originally observed for genotype 1 patients. In contrast, we found similar efficacy of NS5A inhibitor BMS-790052 and interferon-alfa2.
CONCLUSIONS: Novel HCV culture systems with genotype specific NS3P/NS4A revealed similar efficacy of protease inhibitors against genotype 2a, 5a, and 6a and comparatively low but varying efficacy against genotype 3a isolates. These systems will facilitate genotype specific studies of HCV protease inhibitors and of viral resistance.
Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.
Source
Q&A on Hepatitis C and African Americans With Jonathan McCone, M.D., Victrelis Researcher
By Kellee Terrell
From The Body
July 6, 2011
Recently, the U.S. Food and Drug Administration announced the approval of two drugs for hepatitis C virus (HCV) treatment, Incivek (telaprevir) and Victrelis (boceprevir) -- the first new HCV therapies in 10 years. This news is exciting for many people living with HCV, but especially so for African Americans.
HCV, a blood-borne disease that damages the liver, affects almost 4 million Americans (many of whom are also living with HIV), and African Americans account for almost 22 percent of those cases. Historically, with older HCV therapies, African Americans haven't had much success. But these new drugs appear to significantly increase the odds that treatment will work. For instance, when Victrelis was studied specifically in African Americans, researchers found that the African Americans who took the drug along with standard HCV treatment showed a significant increase in the odds that their HCV infection would be treated and cured.
I spoke with Jonathan McCone, M.D., the lead researcher of the African-American cohort in which Victrelis was studied, about this breakthrough drug and the importance of getting screened for HCV.
Can you explain what HCV is and how one contracts it?
HCV is a disease caused by a virus that infects the liver. Essentially, the liver kills itself. In time, it can lead to permanent liver damage as well as cirrhosis, liver cancer and liver failure.
People who are at risk are people who received blood transfusions before 1992 (because labs were not checking for HCV in the blood before then), people who have gotten stuck with infected needles, intravenous drug users who share infected needles, and people who have received piercings and tattoos with used needles that are infected.
This basically is not a sexually transmitted disease, unless there is blood involved. [Editor's note: Blood can be involved during many types of sex or foreplay, including anal sex and fisting; even a small amount of blood entering a microscopic cut on the body can potentially put a person at risk for infection.] You don't get it by kissing or breathing. It's generally a blood-to-blood illness, but if it's not specially checked for, it's not picked up. That doesn't mean that damage isn't occurring.
Can you tell us a little bit about Victrelis?
Victrelis is the first new medicine in a decade that has been approved in treating HCV. It's a pill that must be taken three times a day along with the other treatment: a once-a-week interferon shot and another twice-a-day pill [whose generic name is ribavirin]. You need all three forms of medicine to reap the benefits of the treatment. Victrelis will not work without the other treatments.
The most important thing to know is that HCV can be cured. Before Victrelis, we were seeing overall cure rates of just 40 percent in Caucasian Americans and only 23 percent cure rates in African Americans. But when we added Victrelis, African Americans who didn't have cirrhosis of the liver improved two-fold.
Why would cirrhosis make a difference in the success of HCV treatment?
If someone has cirrhosis, advanced damage is occurring. The liver tries to fight the virus by releasing cells to attack it. But what ends up happening is that virus kills those cells, and then turns the cells into scar tissue. The more scar tissue, the harder it is for the liver to do what it's supposed to do. The more advanced the disease, the harder it is to treat HCV.
I've seen patients who didn't know they had HCV and for 20 to 30 years their livers were getting worse and worse. If your disease gets really advanced, you might need a liver transplant or end up dying. This is why you have to get tested and treated early.
What are some of the side effects of HCV therapy, including Victrelis?
The most common side effects from HCV treatment are fatigue, anemia, feeling like you have the flu, headache, depression, weight loss and being irritable. But the good thing is that when people begin therapy, doctors check for all of these side effects and know how to modify certain things.
With Victrelis, there have been some complaints about having a metallic taste, but from what we know, it's not an overwhelming taste.
How long does HCV therapy usually last?
Before Victrelis, therapy usually lasted for one year in hopes to achieve a cure. But we have found that when Victrelis was added, for most patients, therapy time was cut down to six months. That's half the time.
Yes, there are a lot of pills and side effects to deal with. But I tell my patients, "You don't have a virus that gives a cold, you have a virus that makes you get a liver transplant and will kill you. Now you only have to take it for six months to reduce your [HCV] viral load and even cure your disease so you can enjoy your life. That's worth it all."
Why have African Americans had such little success with past HCV therapies?
Genetics. People who have good configurations of [a gene called] IL28B have a higher chance of being cured of HCV when on therapy. And what we have found is that African Americans were most likely to have bad configurations of IL28B, so even when they adhered to the therapy and did everything right, the treatment was less likely to be successful.
But when Victrelis was added to the existing therapies, even the people who had bad configurations had a better chance of being cured than without Victrelis. This is why this is such great news for the African-American community.
Is there a vaccine for HCV?
No, there is no vaccine for HCV. There are vaccines for hep A and B, though.
This is why it's important to get tested and get tested early. It's estimated that 75 percent of people who have HCV don't even know they have it. They are walking around, feeling good, but little do they know that damage is being done to their liver.
Also, doctors need to do a better job in making sure that they screen people and stop assuming who they think are the usual HCV suspects. Just like, at the age of 50, people are receiving colonoscopies, baby boomers should be getting routinely checked at 50 [for HCV] too.
This transcript has been edited for clarity.
Kellee Terrell is the news editor for TheBody.com and TheBodyPRO.com.
Source
From The Body
July 6, 2011
Recently, the U.S. Food and Drug Administration announced the approval of two drugs for hepatitis C virus (HCV) treatment, Incivek (telaprevir) and Victrelis (boceprevir) -- the first new HCV therapies in 10 years. This news is exciting for many people living with HCV, but especially so for African Americans.
HCV, a blood-borne disease that damages the liver, affects almost 4 million Americans (many of whom are also living with HIV), and African Americans account for almost 22 percent of those cases. Historically, with older HCV therapies, African Americans haven't had much success. But these new drugs appear to significantly increase the odds that treatment will work. For instance, when Victrelis was studied specifically in African Americans, researchers found that the African Americans who took the drug along with standard HCV treatment showed a significant increase in the odds that their HCV infection would be treated and cured.
I spoke with Jonathan McCone, M.D., the lead researcher of the African-American cohort in which Victrelis was studied, about this breakthrough drug and the importance of getting screened for HCV.
Can you explain what HCV is and how one contracts it?
HCV is a disease caused by a virus that infects the liver. Essentially, the liver kills itself. In time, it can lead to permanent liver damage as well as cirrhosis, liver cancer and liver failure.
People who are at risk are people who received blood transfusions before 1992 (because labs were not checking for HCV in the blood before then), people who have gotten stuck with infected needles, intravenous drug users who share infected needles, and people who have received piercings and tattoos with used needles that are infected.
This basically is not a sexually transmitted disease, unless there is blood involved. [Editor's note: Blood can be involved during many types of sex or foreplay, including anal sex and fisting; even a small amount of blood entering a microscopic cut on the body can potentially put a person at risk for infection.] You don't get it by kissing or breathing. It's generally a blood-to-blood illness, but if it's not specially checked for, it's not picked up. That doesn't mean that damage isn't occurring.
Can you tell us a little bit about Victrelis?
Victrelis is the first new medicine in a decade that has been approved in treating HCV. It's a pill that must be taken three times a day along with the other treatment: a once-a-week interferon shot and another twice-a-day pill [whose generic name is ribavirin]. You need all three forms of medicine to reap the benefits of the treatment. Victrelis will not work without the other treatments.
The most important thing to know is that HCV can be cured. Before Victrelis, we were seeing overall cure rates of just 40 percent in Caucasian Americans and only 23 percent cure rates in African Americans. But when we added Victrelis, African Americans who didn't have cirrhosis of the liver improved two-fold.
Why would cirrhosis make a difference in the success of HCV treatment?
If someone has cirrhosis, advanced damage is occurring. The liver tries to fight the virus by releasing cells to attack it. But what ends up happening is that virus kills those cells, and then turns the cells into scar tissue. The more scar tissue, the harder it is for the liver to do what it's supposed to do. The more advanced the disease, the harder it is to treat HCV.
I've seen patients who didn't know they had HCV and for 20 to 30 years their livers were getting worse and worse. If your disease gets really advanced, you might need a liver transplant or end up dying. This is why you have to get tested and treated early.
What are some of the side effects of HCV therapy, including Victrelis?
The most common side effects from HCV treatment are fatigue, anemia, feeling like you have the flu, headache, depression, weight loss and being irritable. But the good thing is that when people begin therapy, doctors check for all of these side effects and know how to modify certain things.
With Victrelis, there have been some complaints about having a metallic taste, but from what we know, it's not an overwhelming taste.
How long does HCV therapy usually last?
Before Victrelis, therapy usually lasted for one year in hopes to achieve a cure. But we have found that when Victrelis was added, for most patients, therapy time was cut down to six months. That's half the time.
Yes, there are a lot of pills and side effects to deal with. But I tell my patients, "You don't have a virus that gives a cold, you have a virus that makes you get a liver transplant and will kill you. Now you only have to take it for six months to reduce your [HCV] viral load and even cure your disease so you can enjoy your life. That's worth it all."
Why have African Americans had such little success with past HCV therapies?
Genetics. People who have good configurations of [a gene called] IL28B have a higher chance of being cured of HCV when on therapy. And what we have found is that African Americans were most likely to have bad configurations of IL28B, so even when they adhered to the therapy and did everything right, the treatment was less likely to be successful.
But when Victrelis was added to the existing therapies, even the people who had bad configurations had a better chance of being cured than without Victrelis. This is why this is such great news for the African-American community.
Is there a vaccine for HCV?
No, there is no vaccine for HCV. There are vaccines for hep A and B, though.
This is why it's important to get tested and get tested early. It's estimated that 75 percent of people who have HCV don't even know they have it. They are walking around, feeling good, but little do they know that damage is being done to their liver.
Also, doctors need to do a better job in making sure that they screen people and stop assuming who they think are the usual HCV suspects. Just like, at the age of 50, people are receiving colonoscopies, baby boomers should be getting routinely checked at 50 [for HCV] too.
This transcript has been edited for clarity.
Kellee Terrell is the news editor for TheBody.com and TheBodyPRO.com.
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