November 13, 2013

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PLOS ONE

RESEARCH ARTICLE

He Huang, Rongyan Kang, Zhendong Zhao

Published: Nov 12, 2013  DOI: 10.1371/journal.pone.0081305

Abstract

Background/Aims

Several studies analyzed the association between hepatitis C virus (HCV) infection and the risk of stroke or cerebrovascular death, but their findings were inconsistent. Up to date, no systematic review about the association between HCV infection and stroke was performed. We conducted a meta-analysis to examine whether HCV infection dose increase stroke risk in comparison to the population without HCV infection.

Methods

We followed standard guidelines for performance of meta-analysis. Two independent investigators identified eligible studies through structured keyword searches in several databases. Random-effects and fixed-effects models were used to synthesize the data. Heterogeneity between studies and publication bias were also accessed.

Results

Combining the data from the eligible studies, we calculated the pooled multi-factor adjusted Odds Ratio (OR) with 95% confidence interval (CI). Upon the heterogeneity found between studies, the result was 1.58 (0.86, 2.30) by random-effects model. However, after omitting the study which induced heterogeneity, the pooled OR with 95% CI was 1.97 (1.64, 2.30).

Conclusions

This meta-analysis suggested that HCV infection increased the risk of stroke. More prospective cohort studies will be needed to confirm this association with underlying biological mechanisms in the future.


Citation: He Huang, Kang R, Zhao Z (2013) Hepatitis C Virus Infection and Risk of Stroke: A Systematic Review and Meta-Analysis. PLoS ONE 8(11): e81305. doi:10.1371/journal.pone.0081305

Editor: Vincent Wai-Sun Wong, The Chinese University of Hong Kong, Hong Kong

Received: August 29, 2013; Accepted: October 11, 2013; Published: November 12, 2013

Copyright: © 2013 Huang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The authors have no support or funding to report.

Competing interests: The authors have declared that no competing interests exist.


Introduction

Hepatitis C virus (HCV) has infected more than 170 million people worldwide (approximately 3% of the world’s population) [1]. In up to 80% of infected patients, HCV established persistent infection, often leading to liver cirrhosis and hepatocellular carcinoma [2,3]. Additionally, HCV infection can induce non-hepatic diseases such as type II diabetes [4]. Current therapy is carried out with peg-interferon plus ribavirin, but only a portion of patients can eliminate the virus, and the outcome of treatment is dependent on the viral genotype [5].

Stroke is the second leading cause of death worldwide [6-8]. It is becoming a great health burden in most industrialized countries in future decades. Conventional risk factors for stroke include cardiac diseases, hypertension, diabetes, smoking, alcohol consumption, unhealthy diet, abdominal obesity, lack of exercise, psychosocial stress and depression[8]. Increased evidence indicates that acute and various chronic infectious diseases are important triggers of or risk factors for stroke (reviewed in 9 ). However, the association of HCV infection and stroke is not well established.

Several epidemiological studies have demonstrated that chronic HCV infection is an independent risk factor of stroke or cerebrovascular death [10-15]. However, Younossi et al. did not find an association between HCV and stroke [16]. Until present, there has been no systematic analysis performed yet. We therefore decided to conduct a meta-analysis of published case-control and cohort studies, which permitted to evaluate the role of HCV infection in stroke. In addition to providing a greater understanding about the association between HCV infection and stroke, the finding of the meta-analysis might also give suggestion for future research and help inform clinical practice guidelines.

Methods

Eligibility criteria

The published guidelines for the conduct and reporting of meta-analyses were followed [17]. We did not have a registered protocol. All published epidemiologic studies providing an estimate of risk of stroke among HCV infected people compared to normal population or an estimate of risk of HCV infection among people with stroke compared to without stroke were considered in this meta-analysis.

Studies were excluded if: the exposed and unexposed groups came from different geographically and temporally defined underlying population; the studies included children, post-transplant recipients, or pregnant women; the studies did not provide risk estimates or data necessary to calculated them; the studies were not published in English. If different overlapping studies used the same study population, only the largest or most recent eligible report was included.

Two investigators (He Huang and Rongyan Kang) independently reviewed all identified titles, abstracts and manuscripts to determine if a study was suitable for the meta-analysis. If disagreements appeared, a third investigator will help to resolve the problem.

Search strategy

To identify all potentially eligible studies, two investigators independently conducted searches in selected databases including Embase, Medline, Conference Proceedings Citation Index-Science (CPCI-S), and Cochrane library. Besides, Google scholar was searched to find additional studies. Searches included the combinations of the keywords “hepatitis c”, “hepatitis c virus”, “hepatitis non A non B”, “HCV”, “stroke”, “cerebrovascular event” and “cerebrovascular disease”. In addition, we reviewed the references from all retrieve articles and relevant reviews to find the studies not captured by the search. Searches were updated as of August 21, 2013.

Data abstraction

Two investigators (He Huang and Rongyan Kang) independently extracted data from eligible studies. Data were abstracted and entered into a structured database. The following data were extracted from each study: the first author’s last name, publication year, country where the study conducted, study design, number of subjects, Hazard Ratio (HR), Rate Ratio (RR), or Odds Ratio (OR) with corresponding 95% Confidence interval (95%CI), and confounders adjusted for in multivariate analysis. Meanwhile, the study quality was evaluated using the 9-star Newcastle-Ottawa Scale[18], a validated technique for assessing the quality of non-randomized studies in meta-analysis.

Statistical analysis

We retrieved unadjusted and adjusted risk estimates presented in original studies. If not available, unadjusted risk estimates will be calculated with crude data extracted from the studies. We examined heterogeneity in results across studies by using I2 statistics[19]. The null hypothesis that the studies are homogeneous was rejected if the p value for heterogeneity was p<0.10 or I2>50%. Random-effects model were applied using the DerSimonian-Laird method [20] if heterogeneity was found, otherwise fixed-effects model was used. All meta-analyses were presented as forest plots with risk estimates for all individual studies as well as the overall pooled estimator. The weight of all individual studies was also provided. If heterogeneity was found, sensitive analysis would be performed to indentify potential source of heterogeneity. Publication bias was assessed with Begg’s and Egger’s tests [19,21] and Begg’s funnel plot was presented in this study. The meta-analysis was performed using STATA 10.0 software (StataCorp LP, USA).

Results

Searches

The flow diagram of study identification was shown in Figure 1. The searches retrieved a total of 348 records. After deleting duplicated studies, 311 reports were pooled. After initial review of the abstracts, 9 potentially relevant studies [10-16,22,23] were identified and full-text was retrieved for detailed evaluation. The study, Lee (2010) [11], was excluded because only cerebrovasular death was investigated in this study. Vinikoor (2013) did not provide data on stroke and HCV[22]. Restivo (2013) was a repeated report of Adinolfi (2013) [13,23]. The other 6 studies met the criteria and data was collected [10,12-16].

journal.pone.0081305.g001

Figure 1. Flow diagram of study identification.

Study characteristics

The main characteristics of the six identified studies were shown in Table 1 and Table 2. Of the six studies, five were retrospective studies and one was prospective study. Two studies reported HRs with 95% CI, three studies reported ORs with 95% CI, and the other one reported RR with 95% CI. Five studies were population-based studies and the other one was performed in hospital. All studies were conducted in developed areas.

Meta-analysis

Because stroke was a relatively rare outcome in the population (<3%) studied in Forssen (2009) [10], the distinctions between RR and OR could be ignored [24]. Therefore, the reported RR could be seen as OR and combined with ORs reported by other three studies [13,14,16]. However, the other two studies reporting HRs could not be included in the analysis [12,15].

Because heterogeneity was found between the four included studies (p=0.030, I2=66.5%), random-effects model was used to calculate the pooled risk estimator. By combining data form the four studies, the pooled OR (95% CI) for stroke risk with HCV was 1.58 (0.86, 2.30) (Figure 2). Publication bias was not suggested by Egger’s test (p=0.978) and Begg’s funnel plot (Figure 3).

journal.pone.0081305.g002

Figure 2. Forest plot for meta-analysis comparing risk of stroke in HCV infected patients compared to that in non-infected controls.

Four studies reporting ORs and RR were included. Adjusted ORs from included studies and the pooled OR was shown. Dimension of shaded OR for individual studies is proportional to their total weight in calculation of the pooled estimator.

journal.pone.0081305.g003

Figure 3. Begg’s funnel plot (with pseudo 95% confidence intervals) to detect any publication bias.

Sources of heterogeneity and sensitive analysis

Because the inclusion of studies which induce heterogeneity may causes bias to the final conclusion, we decided to perform the sensitive analysis to explore the heterogeneity among studies. A sensitivity analysis omitting one study at a time and calculating the pooled ORs for the remainder of the studies showed that the study by Younossi et al. might be the key contributor to the between-study heterogeneity. No heterogeneity was observed after excluding this study (p=0.510, I2=0.00%) as shown in Figure 4. The pooled OR (95% CI) for stroke risk with HCV was 1.97 (1.64, 2.30). Publication bias was not suggest by Egger’s test (p=0.491) and Begg’s funnel plot (not shown).

journal.pone.0081305.g004

Figure 4. Forest plot for meta-analysis comparing risk of stroke in HCV infected patients compared to that in non-infected controls.

After omitting the study which induced heterogeneity, adjusted ORs from the other three studies and the pooled OR was shown. Dimension of shaded OR for individual studies is proportional to their total weight in calculation of the pooled estimator.

Discussion

As we know that the result of a single research may be affected by many factors, in order to reduce the bias and increase the efficiency of the small sample study of statistics, meta-analysis was performed to further explore the relationship between stroke and HCV infection. Six studies estimated the risk of stroke in HCV infected population were identified [10,12-16]. The final analysis suggested that HCV infection increased the risk of stroke with statistical significance. To our knowledge, this was the first to attempt to synthesize the existing world literature to evaluate the effect of HCV infection on stroke.

The mechanism(s) by which HCV may favor stroke is not known. Increasing evidence has showed that chronic HCV infection increased the risk of ultrasonographically defined carotid intima-media thickness and or plaque [25-27], which are predictors of cerebrovascular disease [28]. It is well-known that chronic inflammation plays an important role in the instability of plaque [29]. It was also found that HCV replicated with carotid plaque [30]. Beyond, HCV infection also increased the risk of metabolism diseases, such as type II diabetes[4]. All of these events potentially increased the risk of stroke. Thus, it is believed that there is potential association between HCV infection and stroke. However, studies from several groups provided conflicting results. Our meta-analysis consisted of more than 22171 HCV infected individuals and more than 87418 controls and might allow a much greater possibility of reaching reasonably strong conclusions.

The results of combing the four eligible studies suggested that HCV infection was not associated with stroke (Figure 2). However, a substantial heterogeneity among the studies included was found, which can influence the validity and reliability of the results of meta-analysis. Thus, sensitivity analysis was performed to identify the potential sources of between-study heterogeneity and to reduce heterogeneity [31]. Our analyses found that the study by Younossi et al. [16] was a major contributor to the heterogeneity. Inadequate adjusting variables used might induce bias and could be an important source of heterogeneity. We noted that several cofounders, such as race, gender, and hypertension, were significantly different between HCV+ and control in this study [16]. However, these factors were not involved in the adjustment. The differences in HCV positive criteria used might be another source of heterogeneity. After omitting this study, heterogeneity was reduced and the results suggested that HCV infection significantly increased the risk of stroke (Figure 4).

Some limitation in this meta-analysis should be demonstrated in the discussion of the results. Firstly, our search was limited to studies published in English. However, we found no evidence of publication bias, although the statistical tests for detecting this had limited power[32], especially for relatively small numbers of studies. Secondly, we should noted that the number of included studies in this analysis was relatively low (4 studies). Two of the studies were published only in abstract form on conferences[10,14] and the study by Adinolfi et al.[13] was the only one published article in the final analysis (Figure 4). This limitation might induce bias, although publication bias was not found in our analysis. Thirdly, HCV positive criteria and cofounder for adjusting ORs were different between the included studies, which might induce bias in our study. Fourthly, all the included studies were retrospective studies and the inherent limitations of such studies may influence our findings. More studies with prospective design will be needed. Fifthly, the studies were restricted to United States and Italy, so it was uncertain whether these results were generalizable to other populations. The other two studies excluded in the final analysis were performed in Taiwan [12,15]. However, they reported HRs which could not be combined with ORs. Never the less, the results form these two studies both supported our conclusion. Due to the limitations mentioned above, the results of this meta-analysis should be interpreted with care.

In conclusion, our meta-analysis revealed that  HCV infection significantly increased the risk of stroke. Due to the limitations mentioned above, more population-based well-designed cohort studies will be needed to confirm our results. Furthermore, future studies may evaluate the impacts of different genotypes of HCV infection on stroke. The updating of this meta-analysis will give us more information and may help inform clinical practice guidelines in the future.

Checklist S1. PRISMA Checklist for this meta-analysis.

Author Contributions

Conceived and designed the experiments: ZZ. Performed the experiments: RK HH. Analyzed the data: HH. Wrote the manuscript: HH.

References

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                                            23.Restivo L, Iuliano N, Nevola R, Amelia A, Fascione MC et al. (2013) Chronic HCV infection and extrahepatic diseases: Ischemic stroke and ischemic heart disease. Dig Liver Dis 45: S13. doi:. doi: 10.1016/S1590-8658(13)60039-0.

                                              24.Greenland S (1987) Quantitative methods in the review of epidemiologic literature. Epidemiol Rev 9: 1-30. PubMed: 3678409.

                                                25.Fukui M, Kitagawa Y, Nakamura N, Yoshikawa T (2003) Hepatitis C virus and atherosclerosis in patients with type 2 diabetes. JAMA 289: 1245-1246. doi:. PubMed:12633185. doi: 10.1001/jama.289.10.1245-a.

                                                  26.Ishizaka N, Ishizaka Y, Takahashi E, Toda E, Hashimoto H et al. (2002) Increased prevalence of carotid atherosclerosis in hepatitis B virus carriers. Circulation 105: 1028-1030. doi:. PubMed: 11877348. doi: 10.1161/hc0902.105718.

                                                    27.Ishizaka N, Ishizaka Y, Takahashi E, Tooda Ei, Hashimoto H et al. (2002) Association between hepatitis C virus seropositivity, carotid-artery plaque, and intima-media thickening. Lancet 359: 133-135. doi:. PubMed: 11809259. doi: 10.1016/S0140-6736(02)07339-7.

                                                      28.O'Leary DH, Polak JF, Kronmal RA, Manolio TA, Burke GL et al. (1999) Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. Cardiovascular Health Study Collaborative Research Group. N Engl J Med 340: 14-22. doi:. PubMed: 9878640. doi: 10.1056/NEJM199901073400103.

                                                        29.Libby P, Ridker PM, Maseri A (2002) Inflammation and atherosclerosis. Circulation 105: 1135-1143. doi:. PubMed: 11877368. doi: 10.1161/hc0902.104353.

                                                          30.Boddi M, Abbate R, Chellini B, Giusti B, Giannini C et al. (2010) Hepatitis C virus RNA localization in human carotid plaques. J Clin Virol 47: 72-75. doi:. PubMed: 19896417. doi: 10.1016/j.jcv.2009.10.005.

                                                            31.Patsopoulos NA, Evangelou E, Ioannidis JP (2008) Sensitivity of between-study heterogeneity in meta-analysis: proposed metrics and empirical evaluation. Int J Epidemiol 37: 1148-1157. doi:. PubMed: 18424475. doi: 10.1093/ije/dyn065.

                                                              32.Hartemink N, Boshuizen HC, Nagelkerke NJ, Jacobs MA, van Houwelingen HC (2006) Combining risk estimates from observational studies with different exposure cutpoints: a meta-analysis on body mass index and diabetes type 2. Am J Epidemiol 163: 1042-1052. doi:. PubMed: 16611666. doi: 10.1093/aje/kwj141.

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                                                              Drug Pipeline Activity: Hepatitis C

                                                              Randi Hernandez, MS, Associate Editor/Online
                                                              Published Online: Wednesday, November 13, 2013

                                                              We will see a new wave of oral antiviral hepatitis C medicines hitting the market towards the end of this year and the beginning of next year, noted Aimee Tharaldson, PharmD, senior clinical consultant, Emerging Therapeutics, Express Scripts.

                                                               
                                                              This video was shot at the 2013 Academy of Managed Care Pharmacy Nexus meeting in San Antonio, Texas. BONUS: For more information about HCV therapies, read this article on simeprevir and check out the below graph on sofosbuvir SVR rates:
                                                               
                                                              SOFOSBUVIR2

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                                                              Government-run blood banks run out of stocks of HIV, Hepatitis-B and Hepatitis-C diagnostic kits

                                                              Vidya Krishnan

                                                              BloodBank_5C_--621x414

                                                              In India, access to safe blood is mandated by law and is the primary responsibility of the National AIDS Control Organisation. Photo: Mint

                                                              New Delhi: India’s government blood banks will not be able to guarantee safe blood for the next 90 days because they have run out of stocks of HIV, Hepatitis-B and Hepatitis-C diagnostic kits, and the result could be a scramble for safe blood.

                                                              In India, access to safe blood is mandated by law and is the primary responsibility of the National AIDS Control Organisation (NACO). The organization is charged with the task of providing diagnostic kits to 1,137 government blood banks in the country that test each unit of blood for infections before use.

                                                              In the absence of the kits, they will not be able to approve the use of blood.

                                                              The situation has arisen due to the failure to procure testing kits in time.

                                                              In the absence of centrally procured diagnostic kits, NACO has authorized local purchase by blood banks, which officials maintain would help in uninterrupted supplies.

                                                              “We are aware of the flaws in the system and are already working on correcting them,” said Shobini Rajan, assistant director general, NACO, accepting that there is currently a blind spot when it comes to tracking stock of kits.

                                                              “There is a lack of uniformity (across the banks) as poorer states tend to see more stock out. We are toying with the idea of decentralizing this (procurement) slowly. It would be better for state governments to take more ownership, do their own stock-taking, and obtain facility level insight. Meanwhile, orders have been placed and supplies are likely to resume by the end of January,” Rajan added.

                                                              his isn’t the first time blood banks have run out of testing kits.

                                                              The problem was most acute in January this year, when government-run blood banks in India were completely stocked out, resulting in NACO authorizing local purchase of the diagnostic kits using funds generated by blood banks.

                                                              Nor is NACO the only agency to have woken up late to a health problem, highlighting one of the most significant, yet common problems ailing the government’s healthcare initiatives. There are similar problems in combating malaria and tuberculosis (TB).

                                                              All three of India’s largest health interventions have seen stock-outs this year, said an expert.

                                                              “We have seen TB, and malaria (medicines) and HIV (testing kits) stock-outs. All national programmes had to resort to emergency procurement after normal channels failed,” said Leena Menghaney, a lawyer and activist with international medical humanitarian aid organization Médecins Sans Frontières, or Doctors Without Borders. She added that healthcare systems need to have reporting mechanisms built into them, ensuring that every facility-level stock-out can be mapped, with community-based organizations being able report shortage of stocks. “We welcome that the government has made emergency purchase orders to deal with the current crisis of diagnostics, drugs and other health products,” Menghaney said.

                                                              The failure to procure medicines in time is crippling the national malaria programme in the north-eastern states and Odisha that see a high incidence of malaria. To be sure, with the onset of winter, the incidence of malaria declines across the country.

                                                              With tenders failing for procurement of malaria drugs, the health ministry has directed state governments to make their own purchases for the World Health Organization-recommended artemisinin-based combination therapy. According to the World Health Organization’s World Malaria Report 2012, India sees the most cases of malaria, an estimated 24 million a year.

                                                              The malaria control programme comes under the National Vector Borne Disease Control Programme (NVBDCP). According to officials familiar with the development who did not want to be identified, the north-eastern states and Odisha suffered the shortfall all through the peak malaria season, May to September.

                                                              Anshu Prakash, joint secretary, ministry of health, said the state governments have been authorized to purchase drugs. “We had a single tender, and the bidder had quoted unreasonably high prices, so the tender has failed. We have allowed state governments to purchase medicines locally.”

                                                              “We have received reports of stock-outs from Odisha and the North-East,” said A.C. Dhariwal, director, NVBDCP. “We changed the policy for NE (North-East) states and now they are supposed to procure their own medicines. For other states like Odisha, we have been tiding over crisis situations like stock-outs by diverting supply from other states where there is a surplus.”

                                                              Dhariwal’s reference is to an April decision by the ministry to change the anti-malarial medicine used in the seven north-eastern states, a decision that some activist groups claim was not communicated to the local governments. Mint couldn’t independently verify this.

                                                              Meanwhile, fresh reports of stock-outs in TB drugs are coming in the backdrop of the health ministry’s failure to procure essential tuberculosis drugs since 2012. TB drug stock-outs were reported as early as May, after which emergency tenders were floated and drugs were procured.

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                                                              Bristol-Myers Files in Japan for New Hepatitis C Drug

                                                              Provided by The Motley Fool

                                                              By Todd Campbell | More Articles
                                                              November 13, 2013

                                                              In the multibillion-dollar race to bring oral hepatitis C treatments to market, Bristol-Myers Squibb  (NYSE: BMY ) is leapfrogging Gilead Sciences  (NASDAQ: GILD ) andJohnson & Johnson (NYSE: JNJ ) by filing for approval for daclatasvir with Japan's Pharmaceutical and Medical Devices Agency.

                                                              The daclatasvir and asunaprevir combo therapy is the first all-oral treatment to be filed for approval,  eliminating side-effect-riddled interferon and ribavirin. Bristol's strategic move to go for a Japan launch rather than battle Gilead's sofosbuvir and J&J's simeprevir in the United States is a dramatic shift for the industry and may mark a shift in global drug development toward Japan -- a country in the midst of redefining itself as R&D friendly.

                                                              Why Japan?
                                                              Japan has long been known for launch delay. Stringent approval processes, understaffed agencies, and a pricing scheme that punishes new therapies have all kept drug makers and biotech companies focused on developing drugs in the U.S. and European Union instead.

                                                              But, that launch-delay stigma may disappear as Japan embraces a much more R&D friendly stance that includes exemptions for some drugs to its biennial price cuts and the ability to prescribe drugs approved in other countries -- but not yet in Japan -- for the toughest to treat cases. 

                                                              The pressure to bring innovative drug treatments to Japan more quickly is driven by Japan's rapidly aging population. The country's birthrate has been declining steadily since the 1970s, and 24% of its population is over the age of 65.

                                                              That older population, coupled with Japan's wealthy nation status, makes the country very attractive demographically for drug companies. Last year, only the U.S. spent more on drugs than Japan, and Japan represents 10% of the global market.

                                                              Japan's hep-C challenge
                                                              The market for hepatitis C treatment may not be as big in Japan as it is in the United States, but the number of patients infected still totals some 1.2 million. And 350,000 new hepatitis C cases are diagnosed in Japan each year, far more than the 150,000 in America.

                                                              Bristol's focus on Japan is an intriguing shift away from the U.S. and Europe-centric way that most drugs are brought through clinic. The opportunity for daclatasvir to capture share and generate revenue is big, given that as many as 70% of the country's hepatitis C patients are infected with the genotype 1b version of the disease, which has a reputation of being tough to treat.

                                                              In Japanese patients, the daclatasvir and asunaprevir combo therapy produced an 84.7% cure rate at 24 weeks -- during phase 3 trials. Those impressive results and the significant unmet need are likely to help speed a decision from Japan's regulatory agency, which is expected to issue a final "yes" or "no" next year.

                                                              However, even with the head start in Japan, competitors Gilead, J&J, and AbbVie (NYSE:ABBV ) won't be far behind. 

                                                              Gilead is currently studying sofosbuvir in a phase 3 trials for Japanese patients. And J&J gained Japanese approval for its simeprevir in September. However, both Gilead's and J&J's first forays are likely to be combination therapies with interferon and/or ribavirin, and that gives Bristol a substantial advantage -- for now. 

                                                              Both Gilead and J&J have interferon- and ribavirin-free trials ongoing.  In Gilead's Lonestar phase 2 study,100% of  patients treated with sofosbuvir and ledipasvir were cured in 12 weeks, without the help of ribavirin.    In another mid stage phase 2a study called COSMOS, Gilead and J&J teamed up for a non-interferon and ribavirin therapy using a combination of simeprivir and sofosbuvir. That study showed promising results, with SVR8 of 93%.

                                                              Bristol, Gilead and J&J are also looking over their shoulders at AbbVie. The company expects to report phase 3 trial data for its hepatitis C treatment later this year. AbbVie also has an interferon- and ribavirin-free phase 2b trial ongoing for genotype 1b patients. In that study, AbbVie is evaluating ABT-450 in combination with ABT-267 in 82 treatment-naive patients.  

                                                              The Foolish final take
                                                              If Bristol's daclatasvir does get the nod, it gives the company a chance to build market share and insulate itself against Gilead's and J&J's more high profile drugs.  It also gives it running room ahead of AbbVie. It's unlikely the advantage will last, given that Gilead, J&J and AbbVie all have promising drugs in mid- and late-stage trials. But with a large unmet need, all four of the companies may find they've developed blockbusters.


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                                                              Todd Campbell has no position in any stocks mentioned. Todd owns E.B. Capital Markets, LLC, an institutional research firm. E.B. Capital's client may or may not own shares in the companies mentioned. Todd also owns Gundalow Advisors, LLC, a high net worth advisory focused on ETFs. Gundalow's clients do not own shares in the companies mentioned. The Motley Fool recommends Gilead Sciences and Johnson & Johnson. The Motley Fool owns shares of Johnson & Johnson. Try any of our Foolish newsletter services free for 30 days. We Fools may not all hold the same opinions, but we all believe that considering a diverse range of insights makes us better investors. The Motley Fool has a disclosure policy.

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                                                              Also See: BMS Submits First All-Oral, Interferon-Free and Ribavirin-Free Treatment Regimen for Regulatory Review in Japan for Patients with Chronic Hepatitis C Infection

                                                              Costs for Hepatitis C Treatment Skyrocket

                                                              Medscape Medical News > Conference News

                                                              Miriam E. Tucker

                                                              November 13, 2013

                                                              WASHINGTON, DC — The expense of telaprevir-based triple therapy for hepatitis C — including adverse event management — is $189,000 per sustained viral response, report investigators.

                                                              "Our findings indicate that the benefit-cost ratio is lower than projected, based on results of the registration trials," lead investigator Andrea Branch, MD, from the Icahn School of Medicine at Mount Sinai in New York City.

                                                              Kian Bichoupan, MBS, who is Dr. Branch's first-year PhD clinical research student, presented the results here at The Liver Meeting 2013.

                                                              The number seemed to alarm session comoderator Sammy Saab, MD, from the David Geffen School of Medicine at UCLA, who called it "very surprising." It is "at least double what we think the cost is. I didn't know the cost of actually curing someone was so high," he said.

                                                              It is expected that 2 new direct-acting antiviral agents for the treatment of hepatitis C, simeprevir and sofosbuvir, will be approved by the US Food and Drug Administration (FDA) on December 8. Both have far better adverse-event profiles than telaprevir-based regimens, but the degree to which the cost-effectiveness calculation will change depends on their price, which hasn't yet been announced, Dr. Saab explained.

                                                              The benefit-cost ratio is lower than projected.

                                                              Before telaprevir received FDA approval in May 2011, the standard of care for genotype 1 hepatitis C was 48 weeks of pegylated interferon and ribavirin. With that regimen, the sustained viral response ranged from 40% to 50%. With the addition of telaprevir to the peginterferon and ribavirin regimen, response rates increased to 64% to 75%, but adverse events and costs also rose.

                                                              Previous studies have shown that peginterferon and ribavirin dual therapy costs $70,364 per sustained viral response in patients with genotype 1 hepatitis C. Data from phase 3 registration trials suggest that telaprevir-based triple therapy is cost-effective, but real-world data have been unavailable until now, Bichoupan said.

                                                              The researchers evaluated 147 patients who initiated telaprevir-based triple therapy at Mount Sinai. The mean age of the cohort was 56 years, and 68% of the cohort was male, 19% was black, 46% did not respond to previous hepatitis C treatment, and 35% had advanced fibrosis or cirrhosis.

                                                              They calculated the cost of the therapy itself and the management of adverse events from Medicare, the Agency for Healthcare Research and Quality, and other sources.

                                                              Sustained viral response was achieved by 44% of patients. At 48 weeks, the cost of telaprevir was $55,273, of peginterferon was $30,418, and of ribavirin for $4926. Telaprevir accounted for 61% of the $90,617 total, Bichoupan noted.

                                                              Adverse events, primarily anemia, accounted for 8% of the total cost; 48% of the patients required treatment with epoetin alpha, 9% needed blood transfusions, 8% were treated with granulocyte colony-stimulating factor (G-CSF), 13% required hospitalization, and 10% made emergency department visits.

                                                              Total costs were $664,083 for epoetin alfa, $29,007 for G-CSF, and $12,644 for transfusions.

                                                              The total cost of treating hepatitis C was higher for the 65 patients who achieved sustained viral response than for the 82 who did not ($6.33 vs $5.24 million).

                                                              The median cost per patient was $83,509. The researchers multiplied that by the reciprocal of the 44% sustained viral response (2.27), and arrived at $188,859 per response.

                                                              The cost per sustained viral response was lower for treatment-naïve than for previously treated patients ($158,403 vs $199,134). For patients with advanced liver fibrosis, the cost was $185,484. For those with less severe fibrosis, the cost jumped to $256,977, Bichoupan reported.

                                                              He pointed out that this study started when telaprevir had just reached the market, and that outcomes might improve over time with better strategies for preventing adverse events.

                                                              Dr. Branch told Medscape Medical News that these data can't determine whether nearly $200,000 per sustained viral response is cost-effective, because not enough is known about the cost savings associated with such a response.

                                                              Better Options

                                                              Other investigators have compared health costs for patients who achieve a sustained viral response with costs for patients with chronic hepatitis C infection. However, "this is not the best way to do the analysis because patients who achieve a sustained viral response may be healthier than patients who do not," Dr. Branch noted.

                                                              Dr. Saab said he agrees that the cost figures are likely to improve as experience with the drugs increases. However, he noted that telaprevir will likely disappear soon after the expected FDA approval of simeprevir and sofosbuvir.

                                                              Dr. Branch echoed this opinion. Telaprevir-based regimens "are only appropriate for patients who cannot wait even a few months for newer regimens to complete the FDA review and approval process," she said.

                                                              This study was supported in part by Gilead Sciences, the National Institute of Drug Abuse, and the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Saab is a consultant to Bristol-Myers Squibb.

                                                              The Liver Meeting 2013: American Association for the Study of Liver Diseases (AASLD). Abstract 244. Presented on November 5, 2013.

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                                                              Congress Passes HIV Organ Policy Equity Act (HOPE Act)

                                                              Legislation will lead to increases in life-saving donor organs and vital research in the area of HIV organ donation and transplantation

                                                              November 13, 2013 09:02 AM Eastern Standard Time

                                                              WASHINGTON--(BUSINESS WIRE)--The American Society of Transplantation (AST), representing the majority of professionals engaged in the field of organ transplantation, applauded yesterday's action by the U.S. House of Representatives to bring the HIV Organ Policy Equity Act (HOPE Act) one step closer to being signed into law. The legislation, which has bipartisan support, has now passed in both the House of Representatives and Senate and will be sent to the President for final signature into law.

                                                              “AST and its patient and physician constituencies applaud Congress for taking this important step toward ensuring that our laws reflect and keep pace with the latest life saving techniques and medical research available”

                                                              The HOPE Act amends the Public Health Service Act to establish safeguards and standards of quality for research of organs infected with human immunodeficiency virus (HIV). Once signed into law, it will expand the supply of life-saving organs available for transplantation to the more than 118,000 individuals currently languishing on the organ wait list.

                                                              “The HOPE Act is a common sense policy proposal that will improve the lives of many patients in need of organ transplants,” said Dr. Dan Salomon, President of the American Society of Transplantation. “The nation's transplant community is grateful that the House of Representatives and Senate have now both passed this vital legislation. The AST and its thousands of professionals worldwide strongly support this legislative proposal allowing for greater use of life saving donor organs and much needed research in the area of HIV organ donation and transplantation."

                                                              Passage of the HOPE Act in the House and Senate was championed by dozens of key leaders in Washington and led by Representatives Lois Capps (D-CA), Michael Burgess, M.D. (R-TX), Andy Harris, M.D. (R-MD) and Senators Tom Coburn (R-OK) and Barbara Boxer (D-CA).

                                                              “AST and its patient and physician constituencies applaud Congress for taking this important step toward ensuring that our laws reflect and keep pace with the latest life saving techniques and medical research available,” continued Salomon. “Given the current political landscape, it is refreshing to see such bipartisan and bicameral efforts taking a common sense approach to improving and saving lives.”

                                                              About The American Society of Transplantation (AST)

                                                              The American Society of Transplantation (AST) is an international organization of transplant professionals who are dedicated to advancing the field of transplantation and improving patient care by promoting research, education, advocacy, and organ donation. The Society comprises more than 3,100 transplant physicians, surgeons, scientists and allied health professionals. For more information about the Society, go to www.myast.org.

                                                              Contacts

                                                              American Society of Transplantation (AST)
                                                              Sean Carney, 215-735-3470 Ext. 108
                                                              scarney@brownsteingroup.com

                                                              Source

                                                              Treating Hepatitis C Virus: How the Standard of Care is Evolving

                                                              Provided by MPR

                                                              Batya Swift Yasgur MA, LMSW

                                                              November 13, 2013

                                                              hepatitis_490148

                                                              Treating Hepatitis C Virus: How the Standard of Care is Evolving

                                                              Hepatitis C virus (HCV), a major epidemic affecting an estimated 150 million people worldwide, is responsible for more than 350,000 annual deaths from HCV-related liver diseases.1

                                                              Since 1982, the incidence of acute HCV infection in the United States has declined,2due primarily to HCV screening in transfusion centers and universal health care precautions in health care settings.2However, the number of patients with complications of chronic HCV is increasing—a trend that is expected to continue.2

                                                              RELATED: Infectious Diseases Resource Center

                                                              HCV differs from other viral infections in that it can be cured with antiviral therapy because HCV nucleic acids are not integrated into the host genome, nor is there a viral latency phase.2 Current anti-HCV approaches seek to cure the infection, thereby preventing HCV-related complications and potential contagion to others.

                                                              The Evolving Standard of Care

                                                              In the 1990s, interferon (IFN) alpha-2a, IFN alpha-2b, and IFN alfacon-1 were the foundation of HCV treatment. A significant breakthrough occurred in 1998 when ribavirin (RBV), a synthetic guanosine analogue, was approved, used in combination with IFN, and found to significantly improve sustained virologic response (SVR).3

                                                              A further development, pegylated interferon (PegIFN), prolonged the IFN half-life, allowing for once-weekly dosing and improved pharmacokinetic profiles.3 Combination of ribavirin with once-weekly injectable PegIFN over a 24- to 48-week period yielded significant increase in genotype nonspecific  SVR (approximately 55%)3—a dramatic improvement over previous regimens—and became the standard of care.2

                                                              However, this regimen was deficient in several areas. It yielded a low SVR in genotype 1 and poor response rates in certain subpopulations, and patients experienced side effects.2

                                                              In 2011, two direct-acting antivirals (DAAs)—telaprevir and boceprevir—were approved for treatment of HCV, to be used in conjunction with RVC and PegIFN-alpha. This triple therapy "ushered in a new era of HCV treatment."4 These agents target specific genomic pathways that interfere with HCV infection and replication.2

                                                              Telaprevir is a selective inhibitor of NS3/4A protease, a serine protease cofactor that plays an important role in HCV replication.5 Boceprevir is a "potent ketoamide inhibitor of HCV NS3 serine protease."5 Triple therapy has been shown to significantly raise SVR rates.5

                                                              Underuse of Triple Therapy

                                                              Despite its documented efficacy, triple therapy is underused in clinical practice.

                                                              Chen et al4 performed a retrospective cross-sectional study of 487 patients with HCV genotype 1 infection to compare features of patients treated with triple therapy to those who deferred it, over a nine-month period, shortly after the FDA's approval of boceprevir and telaprevir.

                                                              The majority of patients were 50 to 60 years old, male, non-Hispanic white, and married. About half the patients were treatment-naïve, while the other half had been previously treated. The majority had advanced fibrosis, with close to 20% displaying complications of liver disease.

                                                              Only 91 patients (18.7%) began treatment with triple therapy, and 396 patients remained untreated. The low number of patients initiating therapy remained constant throughout the study period.

                                                              The researchers suggested several provider- and patient-specific reasons for treatment deferral. Most of the patients had relative contraindications to treatments, such as complications of liver disease and medical comorbidities. A history of significant side effects during previous treatment was the third most common contraindication.

                                                              Additionally, more than 15% of patients had mild liver disease, suggesting that potent therapy might be unnecessary or premature. A tenth of patients (of whom 76% had at least moderate liver fibrosis) were recommended to wait for future treatment options.

                                                              Lastly, more than one-fifth of patients declined treatment because of concerns about side effects, limited success rates, financial issues, or inability to commit time for treatment.4

                                                              Of those who deferred and then started triple therapy, more than 30% were prior relapsers, while the majority of patients who deferred were treatment-naïve. However, the authors add, there was no difference in HCV RNA viral load, genotype 1 subtypes, or IL28B genotyping.

                                                              Twenty-one percent (19 patients) of those treated with triple therapy discontinued within 12 weeks of therapy—15% due to adverse events. Other reasons included nonadherence and nonresponse to DAA therapy.

                                                              The authors observed that the combined treatment rate of 18.8% was "nearly identical to the reported treatment rates during the dual therapy era." They commented, "The disappointingly low use of the new therapies . . . suggests that several concerns are at play: the continued requirement of IFN, the safety profile, the low predicted response rates in prior nonresponders, coupled with the suggestion of further major improvements, such as IFN-free therapies, likely colored the thinking of physicians and patients alike in this setting."

                                                              Conclusion

                                                              Several current agents under investigation are second-generation HCV NS3/N4A oral protease inhibitors: HCV NS5A and NS5B inhibitors, and iIFN-sparing regimens5 The authors state that they expect that these new agents, once approved, "will be applied in the treatment of HCV-infected patients and that they will have more potent efficacy and less adverse events."

                                                              References

                                                              1. World Health Organization. Hepatitis C: Fact sheet N°164. (July, 2013) Available at:http://www.who.int/mediacentre/factsheets/fs164/en/. Accessed: August 7, 2013.

                                                              2. Poordad F, Dieterich D. Treating hepatitis C: current standard of care and emerging direct-acting antiviral agents. J Viral Hepat. 2012;19(7):449-464.

                                                              3. Chan J. Treatment of chronic hepatitis C: The new standard of care for the future.

                                                              4. Chen EY, Sclair SN, Czul F, et al. A small percentage of patients with hepatitis C receive triple therapy with boceprevir or telaprevir. Clin Gastroenterol Hepatol. 2013;11(8):1014-1020.e2.

                                                              5. Kanda T, Yokosuka O, Omata M. Treatment of hepatitis C virus infection in the future. Clin Transl Med. 2013;2(1):9.

                                                              6. Formulary. August 1, 2011. Available at: http://formularyjournal.modernmedicine.com/formulary-journal/news/clinical/clinical-pharmacology/treatment-chronic-hepatitis-c-new-standard-car. Accessed: August 7, 2013.

                                                              7. Pol S, Ghalib RH, Rustgi VK, et al. Daclatasvir for previously untreated chronic hepatitis C genotype-1 infection: a randomised, parallel-group, double-blind, placebo-controlled, dose-finding, phase 2a trial. Lancet Infect Dis. 2012;12(9):671-677.

                                                              Source

                                                              Uneven gains in AIDS/HIV in different populations

                                                              Kathryn Roethel
                                                              Published 3:52 pm, Tuesday, November 12, 2013

                                                              A quarter century ago, when the AIDS epidemic was at its peak in the United States, HIV was the No. 1 killer of Americans ages 25 to 44. Now, with new treatment options, it's the sixth-leading cause of death for that group, and the number of new diagnoses each year is less than half of what it once was.

                                                              But, as a new report on AIDS in America points out, certain populations have not made as many gains over the disease.

                                                              The good news: The nation's AIDS awareness is high. About 82 percent of Americans who have HIV today have been formally diagnosed, according to the Kaiser Family Foundation, a nonprofit health research organization that published an analysis of AIDS in the United States this year.

                                                              Antiretroviral therapy drugs are very effective in stopping HIV progression and extending lives, but patients must take multiple pills at precise times each day and receive regular medical care. As a result, only 1 in 4 patients is adhering to a treatment regimen closely enough to suppress the virus.

                                                              Blacks and Latinos have rates of HIV diagnosis that far surpass rates among whites, and they are less likely to get the recommended treatment. Many Southern states and the District of Columbia have rates many times above the national average.

                                                              These numbers paint a picture of the United States' successes and challenges in the battle with AIDS.

                                                              50,000
                                                              The number of new HIV infections diagnosed each year in the United States. That number has remained relatively stable for the past decade. The first case of AIDS in this country was diagnosed in 1981, and by the late 1980s, diagnoses peaked at 130,000 a year.

                                                              63%
                                                              The percentage of new HIV infections resulting from male-to-male sexual contact in 2010. Heterosexual contact is responsible for 25 percent of new diagnoses.

                                                              20%
                                                              The percentage of new HIV infections in 2010 among women. Black women accounted for nearly two-thirds of those.

                                                              8
                                                              The rate of new HIV infections in black men and women was eight times higher than that of white men and women. The rate among Latinos was three times higher than among whites.

                                                              11.9%
                                                              The percentage of the nation's 2011 HIV diagnoses that were in California. That year's 5,965 diagnoses were the most of any state. But California isn't in the nation's top 10 when it comes to HIV cases as a percentage of the state's population. Seven of the top 10 are in the South, and Washington, D.C., has the highest rate - 177.9 HIV cases for every 100,000 people, or nine times the national rate.

                                                              For the full Kaiser Family Foundation HIV/AIDS Report: http://bit.ly/175gsiI

                                                              Source

                                                              Ask the Pharmacist: Are You at Risk for Hep C?

                                                              11.11.13  |   John Fowler

                                                              HepC_150x150

                                                              What do Mickey Mantle, Evel Knievel, Naomi Judd, Pamela Anderson, Jim Nabors and Keith Richards have in common? They all faced hepatitis C.

                                                              About 3.2 million Americans have chronic hepatitis C. It claims the lives of more people each year than HIV/AIDS and is the leading cause of liver transplants in the U.S.

                                                              As specialist pharmacists with disease-specific expertise in hepatitis C, my team and I flag drug interactions and provide support to patients for their therapy and side effects.

                                                              Understanding the Disease

                                                              Hepatitis C is a contagious liver disease that ranges in severity from a mild illness lasting a few weeks to one that is serious and lifelong. For a lucky few, their body is able to clear the virus. However, with most people, the initial infection leads to a long-lasting, chronic infection.

                                                              The disease is much more common among baby boomers. Many individuals were infected between 1970 and 1990, before universal screenings of the blood supply were adopted. The Centers for Disease Control and Prevention recommend that all baby boomers be tested, and Medicare will cover the cost of screening if you are at high risk or symptomatic.

                                                              Managing the Condition

                                                              Hepatitis C treatment can be difficult to tolerate and the side effects are often severe, including fatigue and flu-like symptoms. This can make adherence a challenge. And unfortunately, nonadherence can cause therapy failure and lead to liver failure. Despite this, nearly 40% of hepatitis C patients are nonadherent.

                                                              Understanding a few key things about your medication regimen can lead to better health outcomes:

                                                              • Be adherent: Being adherent to a medication’s dosing regimen is key for the best health outcomes. People with hepatitis C often must follow a medication regimen that demands multiple doses of three separate medications each day. Talk with your doctor or specialist pharmacist if you need support with your schedule or are struggling with adherence.
                                                              • Read the fine print: Many hepatitis C medications provide specific instructions to help minimize side effects. For example, one commonly prescribed medication may cause flu-like symptoms, so some patients take the dose at night or the day before a day off work. Taking an ibuprofen at the same time can also lessen side effects.
                                                              • Follow specific instructions: Some of the newest medications for hepatitis C are oral medications. While oral medications are more convenient, they must be taken at precisely spaced intervals throughout the day and with food to ensure adequate absorption. In fact, some medications specify the nutritional content requirements of the food.
                                                              • Stay well-hydrated: Consuming enough fluids is very important. A great rule of thumb is to determine your body weight (in pounds) and strive to drink half that number (in ounces) per day. For example, if you weigh 200 pounds, you should drink 100 ounces of fluid each day.
                                                              • Delay pregnancy: Some drugs that treat hepatitis C can harm an unborn child, so women should avoid getting pregnant while on therapy and for up to six months after completion of therapy. Men undergoing hepatitis C treatment should also practice safe sex during the same time period.
                                                              • Document the side effects: Report all side effects and other concerns to your physician and your specialist pharmacist so they can be resolved quickly before symptoms worsen.

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