Sleep Disorders in Cirrhotics; How can we detect?

Liver Int. 2014 Feb 10. doi: 10.1111/liv.12485. [Epub ahead of print]

Gencdal G¹, Gunsar F, Meral CE, Salman E, Gürsel B, Oruç N, Karasu Z, Ersöz G, Akarca US.

Abstract

INTRODUCTION: Sleep disorders (SDs) are common in cirrhotics and are often associated with hepatic encephalopathy. SDs negatively affect patients' daily activities and work efficiency. For this reason, early diognosis is important. The methods used for diagnosis of SDs are not practical and need longer periods of application and evaluation. In this study we aimed to investigate sleep disorders and related clinical parameters in liver cirrhosis and also want to investigate the using of Sleep Timing and Sleep Quality Screening questionnaire (STSQS), a simple form with a short application time, for diagnosis of SDs and its correlation with Pittsburg Sleep Quality Index (PSQI) form.

METHODS: Cirrhotic patients and age-matched healthy volunteers were enrolled. Patients were excluded from the study if they had neuropsychiatric disease or used excessive alcohol or drugs known to affect sleep. Both groups completed validated Turkish form of PSQI and STSQS. SD was defined as PSQI score (0-21) of >5 or STSQS≥5.

RESULTS: 131 cirrhotic patients and 18 healthy volunteers were enrolled. SDs in cirrhotics and control group were detected 56.5% and 27.8% by PSQI, 49.6% and 16.7% by STSQS respectively, SDs is the most frequent in the Child C patients, and the least frequent in the Child A patients (p>0,05). No correlation was found between the MELD score and SDs. SDs were more common in cirrhotic patients with hypoalbuminemia and low hemoglobin levels. In addition, the patients with decompensated cirrhosis had more frequently SDs than the patients with compensated cirrhosis. In the patient group, sleep latency and total sleep time, sleep parameters were correlated with SDs. STSQS had statistical significant correlation with PSQI for diagnosis of SDs.

CONCLUSION: SDs are common in cirrhotics and STSQS could be an appropriate and practical method for diagnosis of SDS in these patients. We can use it in cirrhotic patients at outpatient clinics. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

KEYWORDS: PSQI , STSQS , Liver Cirrhosis, Sleep, Sleep Disorders

PMID: 24512086 [PubMed - as supplied by publisher]

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No Risk of Worse Outcomes in Liver Transplantation With Hepatitis C-Positive Organs

Source: DGNews 

Presented at CEOT

By Nancy A. Melville

CHANDLER, Arizona -- February 18, 2014 -- The use of organs positive for hepatitis C virus (HCV) carries no increased risk of poorer outcomes among recipients who are also positive for HCV, according to research presented here at the American Society of Transplantation’s 2nd Annual Cutting Edge of Transplantation (CEOT) Meeting.

“Using the United Network for Organ Sharing (UNOS) and Scientific Registry of Transplant Recipients databases, we were able to demonstrate that since the introduction of the new organ allocation system in 2002 [Model for End-Stage Liver Disease or MELD system], HCV-positive recipients and the HCV serostatus of the donor do not have any impact on overall patient or graft survival,” said Martin Montenovo, MD, University of Washington, Seattle, Washington, on February 14.

For the study, Dr. Montenovo and colleagues evaluated 59,899 liver-transplant recipients aged ≥18 years in the UNOS database from 2002 to 2013.

Among the patients, 1,695 (2.8%) were HCV-positive recipients who had received HCV-positive allografts.

An analysis of differences in patient characteristics between recipients of HCV-positive and HCV-negative organs, as well as graft survival, showed that HCV-positive patients who received HCV-negative grafts were more likely to be hospitalised, in the intensive care unit, and on a ventilator and to have higher MELD scores and higher bilirubin.

Whereas patient and graft survival rates at 1, 5, and 10 years among HCV-positive recipients were inferior to HCV-negative recipients, there were no survival differences between HCV-positive patients who received HCV-positive or HCV-negative grafts.

“As far as we know, this is the first report looking at the effect of HCV donor status on HCV-positive recipients since the introduction of the MELD system,” Dr. Montenovo said. “All previous studies have shown some disparities in the results regarding the impact of the HCV donor status on patient and graft survival.”

The findings offer important evidence that the use of HCV-positive organs does not necessarily compromise outcomes, added Dr. Montenovo .

“The utilisation rate of this pool of donors has not changed over the years since the introduction of the MELD score allocation system,” he said.

“With the increasing number of HCV-positive recipients waiting for an organ in an era of significant organ shortage, more interest should be placed on HCV-positive donors who are often disregarded due to concerns of long-term outcomes,” Dr. Montenovo concluded. “Further large studies are needed to assess the impact, if any, of HCV-RNA donor status on outcomes.”

[Presentation title: The Clinical Impact of Hepatitis C-Positive Donors in Liver Transplantation: Patient Protection or Lost Opportunities? Abstract P-27]

Source

Cure of Hepatitis C Virus Infection Without Interferon Alfa: Scientific Basis and Current Clinical Evidence

Topics in Antiviral Medicine Volume 21 Issue 5 December 2013/January 2014

Perspective

Cure of hepatitis C virus (HCV) infection is achievable without interferon alfa through the use of new direct-acting antiviral (DAA) drugs. In this era of interferon alfa–sparing therapy, however, interferon alfa sensitivity still matters, even as it turns out, if interferon alfa is not used. Inclusion of ribavirin in the treatment regimen remains a factor in treatment response, as does duration of treatment. HCV genotype and subtype remain relevant considerations in choosing a treatment regimen, and viral resistance may emerge when treatment fails. The potency and barrier to resistance of new DAAs and the use of appropriately designed interferon alfa–sparing combinations can overcome obstacles to cure posed by HCV resistance, interferon alfa resistance, and differences in response based on HCV genotype and subtype. Studies demonstrating the use of new DAAs to overcome these obstacles are discussed. This article summarizes a presentation by David L. Thomas, MD, MPH, at the IAS–USA continuing education program held in New York, New York, in June 2013.

Keywords: HCV, hepatitis C, treatment, interferon, sparing, interferon alfa–sparing, direct-acting antivirals, DAAs, genotype, protease inhibitor, NS5A, NS5B, resistance, sofosbuvir, simeprevir

The first hepatitis C virus (HCV)-infected patients were cured in 1984 and 1985, before it was known that a virus was causing their disease. In studies at the National Institutes of Health (NIH), Hoofnagle and colleagues used interferon alfa to treat individuals with non-A or non-B hepatitis and observed a normalization of liver enzymes in these individuals.1 After the virus was identified, it became clear that eradication of HCV had also been achieved. Since then, interferon alfa has been the mainstay in the treatment and cure of HCV infection. Regimens that include interferon alfa have been associated with marked improvement in important therapeutic outcomes, including reductions in mortality, liver cancer, and other serious liver-related events. However, interferon alfa–based treatments are not always successful and have been associated with considerable toxicity and morbidity. Now, a new era of interferon alfa–sparing HCV treatment has begun, and soon it will be possible to achieve cure for most patients with as little as one pill once a day.

The Context

There are viral replication foci in approximately 10% to 20% of hepatocytes distributed throughout an HCVinfected liver. Approximately 1 to 50 viruses can be detected at any one time in a single hepatocyte, but there are places in the liver with no detectable HCV RNA. Thus, to be effective, HCV treatment must reach all sites in the liver that harbor infected hepatocytes. Further, in an HCV-infected liver, there are approximately 1 trillion viruses produced every day. If an environment becomes inhibitory for one variant, another will quickly take its place. To be successful, HCV treatment must also overcome the genetic and phenotypic heterogeneity of HCV. The ongoing host immune response to the virus sometimes clears infection. When it does not, those patients with chronic infection seem to have 1 of 2 different states. One state is characterized by inflammation and the upregulation of interferon-stimulated genes (ISGs). The HCV infections of persons with this high-ISG state are less responsive to exogenous interferon alfa, and these individuals often have a haplotype around the genes for the lambda interferons. In particular, the commercially available IL28B test to determine specific genotype indicates that individuals with a high-ISG state HCV infection have what is called the unfavorable IL28B T allele genotype. Persons with the other state have low expression of ISGs, and their HCV infections remain responsive to exogenous alpha-interferon. They are much more likely to have different genotypes near IL28B, and in particular, the favorable IL28B C allele genotype. Interestingly, persons in these 2 states of differing interferon sensitivity and the associated IL28B genotypes continue to have different susceptibilities to interferonsparing treatments, reflecting their intrinsic tendency to eradicate infection.

The context of infection can also be important when liver tissue is markedly distorted by cirrhosis. Patients with cirrhosis are harder to treat effectively, even with new interferon alfa–sparing regimens, possibly because the distorted tissue inhibits drug penetration or because of factors such as changes in portal pressure.

The Tools

Almost all of the major steps in the HCV life cycle are potential targets for inhibiting viral replication, including entry, endosomal release and internal ribosome entry site (IRES)-dependent translation, protease cleavages, membranous web formation and lipoprotein assembly linked to nonstructural protein (NS) 5A (NS5A), and NS5B RNAdependent RNA polymerase (RdRp) activity. Investigational drugs have been developed to target nearly all of these steps but several drugs are further along in development.

Currently, the 3 main groups of HCV drugs are protease inhibitors (PIs; ie, telaprevir and boceprevir), NS5Aacting agents, and nucleos(t)ide RdRp inhibitors. HCV PIs are potent, can affect a variable range of HCV genotypes, and have a variable barrier to resistance, especially with HCV genotype 1a compared with genotype 1b. Nucleos(t)ide polymerase inhibitors are characterized by high potency, can affect a wide range of HCV genotypes, and have a high barrier to resistance. NS5A-targeting drugs also have high potency, but their barrier to resistance has been problematic.

In formulating approaches to combination therapy, the strategy is to exploit the beneficial properties of the different drug groups and also to include a drug with a high barrier to resistance. In some cases, the investigation of drug combinations is limited by the practicalities of drug development, with drug companies developing combinations of their own products. Thus, some of the most obvious drug combinations for HCV therapy are not being tested in phase III trials.

Interferon Alfa–Sparing Treatment

Although there are data to show that HCV can be cured with investigational treatments that do not include interferon alfa, sensitivity to interferon alfa may still be a factor in treatment response and resistance may emerge when a treatment is unsuccessful. HCV genotype and subtype, ribavirin use, and duration of treatment may also be factors in the efficacy of HCV therapy. However, a drug’s potency or its barrier to resistance can trump these other factors.

Figure 1. Design of a trial evaluating the use of the investigational drugs faldaprevir and deleobuvir, with or without ribavirin, in 362 treatment-naive patients with genotype IL28B (CC or non-CC) and hepatitis C virus (HCV) genotype 1 (subtype 1a or 1b) infection. Thirty-three patients enrolled in the trial had compensated cirrhosis. BID indicates twice daily; QD, once daily; TID, thrice daily. Adapted with permission from Zeuzem et al.2

A study assessing the use of the investigational HCV PI faldaprevir (once daily) combined with the investigational nonnucleoside (nn) NS5B inhibitor deleobuvir (formerly BI 207127; twice or thrice daily), with or without ribavirin, for various treatment durations in treatment-naive patients with HCV genotype 1 infection illustrates many of these points (Figure 1).2,3 Substantial rates of sustained virologic response (SVR) 12 weeks after cessation of treatment (SVR12), considered to constitute cure, were observed with all regimens, indicating that cure of HCV infection is indeed possible without the use of interferon alfa (Figure 2).2 SVR12 rates were higher in the groups that received ribavirin, indicating that ribavirin may still impact the efficacy of HCV treatment. In the same study, IL28B genotype and interferon alfa sensitivity were still factors in treatment response, as shown by the higher SVR12 rates seen in patients with the IL28B CC genotype, regardless of which regimen they received (Figure 3, top).2 Furthermore, HCV subtype remained a factor, as shown by the higher SVR12 rates in patients with HCV genotype 1b versus genotype 1a infection, again regardless of which regimen they received (Figure 3, bottom).2 Several PIs show marked differences in their ability to eradicate genotype 1a virus compared with genotype 1b virus. In this study, the SVR12 rate in patients with HCV genotype 1a infection whose regimens did not include ribavirin was only 11%.2 Faldaprevir may be indicated for use only in patients with HCV genotype 1b infection.

Figure 2. Sustained virologic response (SVR) rates, by treatment group, in a trial evaluating the use of the investigational drugs faldaprevir and deleobuvir, with or without ribavirin, in treatment-naive patients with hepatitis C virus (HCV) genotype 1 infection. BID indicates twice daily; QD, once daily; SVR12, SVR 12 weeks after cessation of treatment; TID, thrice daily. Adapted with permission from Zeuzem et al.2

Figure 3. Sustained virologic response (SVR) rates, by treatment group, in a trial evaluating the use of the investigational drugs faldaprevir and deleobuvir, with or without ribavirin, in treatment-naive patients with genotype IL28B (CC or non-CC) and hepatitis C virus (HCV) genotype 1 (subtype 1a or 1b) infection, stratified by patient genotype (top) and HCV subtype (bottom). BID indicates twice daily; QD, once daily; SVR12, SVR 12 weeks after cessation of treatment; TID, thrice daily. Adapted with permission from Zeuzem et al.2

In another study, 19 treatmentnaive patients with HCV genotype 1 infection received a 12-week regimen of the ritonavir-boosted investigational PI ABT-450, the investigational nnNS5B inhibitor ABT-333, and ribavirin.4 Of these 19 patients, 47% had IL28B T genotype and 89% had HCV genotype 1a infection. All 19 patients achieved virologic suppression; SVR12 was achieved in 18 patients (95%), with 1 patient withdrawing from the study due to elevated levels of alanine transaminase. However, when the same regimen was given to 17 of the study patients whose previous regimen of interferon alfa and ribavirin had failed (all patients had IL28B T genotype and 94% of patients had HCV genotype 1a infection), SVR12 was achieved in only 8 patients (47%), 6 experienced breakthrough viremia, and 3 relapsed. Of the latter 9 patients, viral resistance developed in all but 1.

In a separate study, the same regimen was fortified with the investigational NS5A inhibitor ABT-267, which is highly potent but does not have a high barrier to resistance.5,6 As shown in Figure 4, SVR rates in patients with prior nonresponse to interferon alfa were 89% to 98% when ABT-267 was added to their regimen, with very few patients experiencing breakthrough or relapse. This study demonstrates that the addition of another drug can dramatically improve response rates by overcoming resistance to interferon alfa in those with prior nonresponse.

(Click to view larger image)

Figure 4. Sustained virologic response (SVR) rates, by treatment group, in a trial evaluating the use of the ritonavir-boosted (/r) investigational protease inhibitor ABT-450, the investigational nonstructural protein (NS) 5A (NS5A) inhibitor ABT-267, the investigational nonnucleoside NS5B inhibitor ABT-333, and ribavirin in 438 hepatitis C virus (HCV)-infected, treatment-naive patients and in 133 HCV-infected patients with prior nonresponse to interferon alfa. SVR12 indicates SVR 12 weeks after cessation of treatment; SVR24, SVR 24 weeks after cessation of treatment. Adapted with permission from Kowdley et al.6

Similar principles of treatment may be observed when a nucleotide inhibitor (ie, sofosbuvir) with broad genotypic activity is used with or without ribavirin in individuals with HCV genotype 2 or 3 infection. Sofosbuvir has been approved by the US Food and Drug Administration (FDA) since the June presentation summarized here.

In an initial study of sofosbuvir given with or without ribavirin to treatment-naive patients with HCV genotype 2 or 3 infection, the SVR24 rate was 100% (10 of 10) in patients who received sofosbuvir and ribavirin and 60% (6 of 10) in patients who received sofosbuvir monotherapy.7,8 Likewise, in 25 treatmentnaive patients with HCV genotype 1 infection who received a combination of sofosbuvir and ribavirin, the SVR24 rate was 84%. However, SVR24 was achieved in only 1 of 10 HCV genotype 1–infected patients with prior nonresponse to interferon alfa. Therefore, the use of sofosbuvir and ribavirin can achieve high SVR rates in treatment- naive patients who are relatively sensitive to interferon alfa, whether they have HCV genotype 1, 2, or 3 infection. However, as represented in patients with prior nonresponse, resistance to interferon alfa still plays a role and, as discussed below, it can be overcome.

A study of sofosbuvir and ribavirin in 201 patients with prior nonresponse and HCV genotype 2 or 3 infection demonstrated that genotype and duration of treatment were factors in achieving SVR.7 Among patients with HCV genotype 2 infection, SVR was achieved in 94% of those who received 16 weeks of treatment and in 86% of those who received 12 weeks of treatment. Among patients with HCV genotype 3 infection, SVR rates were lower but still reflected a benefit with longer treatment duration: SVR was achieved in 62% of the 16-week treatment group and 30% of the 12-week treatment group. Longer duration of treatment was also beneficial to patients with cirrhosis: SVR was achieved in 66% of the 16-week treatment group and 31% of the 12-week treatment group.9

In another study, the addition of the investigational NS5A-acting agent ledipasvir to a 12-week regimen of sofosbuvir and ribavirin produced SVR in 100% (9 of 9) of HCV genotype 1–infected patients with prior nonresponse and in 100% (25 of 25) of treatment- naive, HCV genotype 1–infected patients.10 Sofosbuvir and ledipasvir, coformulated as a single, once-daily pill, taken with or without ribavirin for a 12- or 16-week treatment period is currently being assessed in phase III trials.

Early phase studies have evaluated investigational HCV drugs from 2 different pharmaceutical companies. Although combination forms of these drugs do not seem destined for FDA approval anytime soon, there is some preliminary evidence that the treatments are effective. FDA approval of some of these individual drugs may offer clinicians the possibility of devising interferon alfa–sparing regimens in the very near future and prior to FDA approval of combination regimens.

For instance, simeprevir was recently approved by the FDA for use in combination with ribavirin and interferon alfa in HCV genotype 1–infected patients with compensated liver disease, including cirrhosis. And an early phase study has shown that the investigational combination of the PI simeprevir and the nucleotide inhibitor sofosbuvir, with or without ribavirin, produced SVR in more than 90% of HCV genotype 1–infected patients with prior nonresponse.11 Similarly, the combination of the investigational NS5A-acting agent daclatasvir and the nucleotide inhibitor sofosbuvir, with or without the addition of ribavirin, produced an SVR rate of nearly 100% in a study of 41 patients whose prior treatment with telaprevir, boceprevir, and interferon alfa plus ribavirin had failed.12

Conclusion

Interferon alfa–sparing treatment for HCV infection is coming. Presently, many practitioners are faced with the decision of whether to treat their patients with currently available drugs or to wait until new drugs are available. As availability of the newer options approaches, many practitioners are choosing to wait or are enrolling their patients in clinical trials that evaluate new treatments.

With the recent approval by the FDA of sofosbuvir in combination with ribavirin for patients with HCV genotype 2 or 3 infection and in triple therapy with interferon alfa and ribavirin for treatment-naive patients with HCV genotype 1 or 4 infection, waiting to begin treatment may no longer be necessary for some patients. The recent FDA approval of simeprevir to be used with peginterferon alfa and ribavirin for patients with HCV genotype 1 infection also makes possible the use of sofosbuvir in combination with simeprevir, but this combination is investigational and not approved by the FDA at this time. The combination was effective for some patients in the COSMOS (Combination of Simeprevir and Sofosbuvir in HCV Genotype 1 Infected Patients) study.11 In 2014, approvals of additional medications, including interferon alfa–sparing combination regimens for HCV genotype 1, are likely.

More data are needed to determine the best ways to use new treatments for HIV/HCV-coinfected patients and other special populations. Substantial drugdrug interactions between sofosbuvir and most antiretroviral drugs have not been observed, and sofosbuvir and ribavirin regimens are already being studied in HIV/HCV-coinfected patients.

Interferon alfa may still be used to treat HCV infection for the foreseeable future in settings where new treatments may initially be too expensive. However, the widespread use of interferon alfa–sparing treatment options for all HCV-infected patients, whether in resource-rich or resource-poor locales, can be envisioned.

Presented by Dr Thomas in June 2013. First draft prepared from transcripts by Matthew Stenger. Reviewed and edited by Dr Thomas in December 2013.

Financial Affiliations: Dr Thomas has received grants awarded to his institution from Gilead Sciences, Inc, and Merck & Co, Inc.

Additional Suggested Reading

Lawitz E, Mangia A, Wyles D, et al. Sofosbuvir for previously untreated chronic hepatitis C infection. N Eng J Med. 2013;368(20):1878-1887.

References

1. Hoofnagle JH, Mullen KD, Jones DB, et al. Treatment of chronic non-A, non-B hepatitis with recombinant human alpha interferon. A preliminary report. N Engl J Med. 1986;315(25):1575-1578.

2. Zeuzem S, Soriano V, Asselah T, et al. Interferon (IFN)-free combination treatment with the HCV NS3/4A protease inhibitor BI 201335 and the non-nucleoside NS5B inhibitor BI 207127 +/- ribavirin (R): final results of the SOUND-C2 and predictors of response [Abstract 232]. 63rd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD). November 9-13, 2012; Boston, Massachusetts.

3. Zeuzem S, Soriano V, Asselah T, et al. Faldaprevir and deleobuvir for HCV genotype 1 infection. N Engl J Med. 2013;369(7):630-639.

4. Poordad F, Lawitz E, Kowdley KV, et al. Exploratory study of oral combination antiviral therapy for hepatitis C. N Engl J Med. 2013;368(1):45-53.

5. Kowdley K, Lawitz E, Poordad F, et al. A 12- week interferon-free treatment regimen with ABT-450/r, ABT-267, ABT-333 and ribavirin achieves SVR12 rates (observed data) of 99% in treatment-naive patients and 93% in prior null responders with HCV genotype 1 infection. 63rd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD). November 9-13, 2012; Boston, Massachusetts.

6. Kowdley K, Lawitz E, Poordad F, et al. Safety and efficacy of interferon-free regimens of ABT-450/r, ABT-267, ABT-333 +/- ribavirin in patients with chronic HCV GT1 infection: results from the AVIATOR study. 48th Annual Meeting of the European Association for the Study of the Liver. April 24-28, 2013; Amsterdam, The Netherlands.

7. Gane EJ, Stedman CA, Hyland RH, et al. Nucleotide polymerase inhibitor sofosbuvir plus ribavirin for hepatitis C. N Engl J Med. 2013;368(1):34-44.

8. Gane E, Stedman C, Anderson J, et al. 100% Rapid virologic response for PSI- 7977 + ribavirin in genotype 1 null responders (ELECTRON): early viral decline similar to that observed in genotype 1 and genotype 2/3 treatment-naive patients. 19th Conference on Retroviruses and Opportunistic Infections (CROI). March 5-8, 2012; Seattle, WA.

9. Jacobson IM, Gordon SC, Kowdley KV, et al. Sofosbuvir for hepatitis C genotype 2 or 3 in patients without treatment options. N Engl J Med. 2013;368(20):1867- 1877.

10. Gane E, Hyland R, Ding X, et al. ELECTRON: 100% suppression of viral load through 4 weeks post-treatment for sofosbuvir + ledipasvir (GS-5885) + ribavirin for 12 weeks in treatment-naive and -experienced hepatitis C virus GT1 patients [Abstract 41LB]. 20th Conference on Retroviruses and Opportunistic Infections (CROI). March 3-6, 2013; Atlanta, Georgia.

11. Lawitz E, Ghalib R, Rodriguez-Torres M, et al. Suppression of viral load through 4 weeks post-treatment results of a oncedaily regimen of simeprevir + sofosbuvir virus GT1 null responders [Abstract 155LB]. 20th Conference on Retroviruses and Opportunistic Infections (CROI). March 3-6, 2013; Atlanta, Georgia.

12. Sulkowski M, Gardiner DF, Rodriguez- Torres M, et al. Sustained virologic response with daclatasvir plus sofosbuvir ± ribavirin (RBV) in chronic HCV genotype (GT) 1–infected patients who previously failed telaprevir (TVR) or boceprevir (BOC). 20th Conference on Retroviruses and Opportunistic Infections (CROI). April 24-28, 2013; Amsterdam, The Netherlands.

Top Antivir Med. 2014;21(5):152-156
©2014, IAS–USA. All rights reserved

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The beginning of the end: What is the future of interferon therapy for chronic hepatitis C?

Antiviral Res. 2014 Feb 15. pii: S0166-3542(14)00039-4. doi: 10.1016/j.antiviral.2014.02.005. [Epub ahead of print]

Feld JJ.

Abstract

Interferon has been the backbone of therapy for hepatitis C virus (HCV) infection for over 20 years. Initial response rates were poor, but slowly but steadily improved, such that with the addition of the nucleotide analogue ribavirin and the pegylation of interferon, over 50% of infected individuals could be cured with a course of therapy. However, interferon therapy is not ideal, requiring up to a year of weekly injections and associated with numerous systemic side effects. Advances in understanding of the HCV lifecycle have led to the development of numerous highly effective, well-tolerated oral direct acting antivirals. Although the first DAAs were combined with peginterferon and ribavirin, with the rapid progress in the field, it is likely that interferon-free therapy will be available for most patients in the relatively near future. In the short term, peginterferon will be required with either the protease inhibitor simeprevir, or the nucleotide analogue polymerase inhibitor, sofosbuvir, for the treatment of genotype 1 infection. Peginterferon also appears to be a useful adjunct to sofosbuvir and ribavirin for patients with genotype 3 infection, particularly those with cirrhosis. In the future, once combination DAA therapies are available, peginterferon will serve a smaller and smaller role. Peginterferon may be useful as part of QUAD therapy with 2 DAAs and ribavirin in prior null responders or in patients who fail DAA regimens with multi-drug resistant HCV. Peginterferon may also have a role in resource-limited regions to reduce the number and/or duration of DAAs required. Ultimately, although peginterferon will remain a salvage therapy, its days as a mainstay of therapy are definitely numbered.

Copyright © 2014. Published by Elsevier B.V.

PMID: 24548815 [PubMed - as supplied by publisher]

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Mortality among Persons in Care with Hepatitis C Virus Infection -- The Chronic Hepatitis Cohort Study (CHeCS), 2006-2010: liver disease deaths 12 times higher

Provided by NATAP

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"The age-adjusted mortality rate for liver disease in CHeCS was twelve times higher than the MCOD rate......mean age of death was 59 years, 15 years younger than MCOD deaths......only 19% of all CHeCS decedents and only 30% of those with recorded liver disease had HCV listed on their death certificates.....This effect was seen with extra-hepatic causes as well"

Reena Mahajan1, Jian Xing1, Stephen J. Liu1, Kathleen N. Ly1, Anne C. Moorman1, Loralee Rupp2, Fujie Xu1, Scott D. Holmberg1, for the Chronic Hepatitis Cohort Study (CHeCS) Investigators*
1Centers for Disease Control and Prevention, Atlanta, Georgia
2Henry Ford Health System, Detroit, Michigan, USA

Summary: Using US health system data from an observational cohort study, HCV is under-documented on death certificates. Only 19% of those with known HCV infection had HCV listed on their death certificate although two-thirds had pre-mortem indications of chronic liver disease......Disease-specific, liver- and non-liver-related, mortality for HCV-infected patients in an observational cohort study, the Chronic Hepatitis Cohort Study (CHeCS) at four US health care systems, were compared with Multiple Cause of Death (MCOD) data in 12 million death certificates in 2006-2010......The age-adjusted mortality rate for liver disease in CHeCS was twelve times higher than the MCOD rate......only 19% of all CHeCS decedents and only 30% of those with recorded liver disease had HCV listed on their death certificates.

"In Table 4 just below you can see a 15 year difference in age at death between those in this study with HCV & the general population 59 vs 74 yrs old......The mortality rate estimated from this analysis was twelve times higher than the general population; this is much higher than the two-to-five times higher mortality rates in HCV-infected vs uninfected persons seen in other studies...... This effect was seen with extra-hepatic causes as well.....In summary, our analysis of a known HCV-infected cohort demonstrates that less than one-fifth of deaths in HCV-infected persons are coded as having HCV; this indicates a significant underestimation of the number of deaths among people with HCV and the true medical and public health impact of HCV. In this analysis, we have tried to be clear about the difference between dying with HCV and dying from HCV, but both represent a substantial public health burden. For purposes of public health, policy planning, disease modeling, and medical care, this is a huge burden that should be reported and hopefully spur public health action as curative, all-oral therapies are becoming available to treat HCV. Addressing the true impact of HCV, including of those chronically infected with HCV who are not utilizing health services, will be essential to appropriately respond to this epidemic. 35"

"whether the death was considered HCV or non-HCV-related, mean age of death in HCV-infected persons (59 years) was 15 years younger than for all cause mortality in the general population (74 years), a finding similar to previous research. 28......Despite confirmed chronic HCV infection, only 19% (306/1,590) had HCV infection listed on the death certificate."

---------------------------------------
Mortality among Persons in Care with Hepatitis C Virus Infection--The Chronic Hepatitis Cohort Study (CHeCS), 2006-2010

Abstract

Background. Numbers of deaths in hepatitis C virus (HCV)-infected persons recorded on US death certificates have been increasing, but actual rates and causes of death in them have not been well elucidated.

Methods. Disease-specific, liver- and non-liver-related, mortality for HCV-infected patients in an observational cohort study, the Chronic Hepatitis Cohort Study (CHeCS) at four US health care systems, were compared with Multiple Cause of Death (MCOD) data in 12 million death certificates in 2006-2010. Pre-mortem diagnoses, liver biopsies, and FIB-4 scores (a non-invasive measure of liver damage) were examined.

Results. Of 2,143,369 adult patients seen at CHeCS sites in 2006-2010, 11,703 (0.5%) had diagnosed chronic HCV infection, and 1,590 (14%) died. CHeCS decedents were born from 1945-1965 (75%), white (50%), and male (68%); mean age of death was 59 years, 15 years younger than MCOD deaths. The age-adjusted mortality rate for liver disease in CHeCS was twelve times higher than the MCOD rate. Before death, 63% had medical record evidence of chronic liver disease, 76% had elevated FIB-4 scores, and of those biopsied 70% had moderate or worse liver fibrosis. However, only 19% of all CHeCS decedents and only 30% of those with recorded liver disease had HCV listed on their death certificates. Conclusions. HCV infection is greatly under-documented on death certificates. The 16,622 persons with HCV listed in 2010 may represent only one-fifth of about 80,000 HCV-infected persons dying that year, at least two-thirds of whom (53,000 patients) would have pre-mortem indications of chronic liver disease.

Excerpts

Of deaths from 1999-2007 with HCV infection listed as a primary or underlying cause of death, 57% had chronic liver disease as a cause 2 but many also had extra-hepatic manifestations.4 Presence of HCV may potentially accelerate the disease process in heart disease, 5-7 diabetes, 8,9 various malignancies, 10,11 and genitourinary conditions. 12,13

In this study, we looked at hepatic and extra-hepatic causes of death for a cohort of hepatitis C-infected patients in care in the United States.

The age-adjusted CHeCS mortality rate in these HCV-infected patients was 12,854 per 100,000 persons compared to the MCOD mortality rate of 1,046 per 100,000 persons.\

The age-adjusted CHeCS mortality rate in these HCV-infected patients was 12,854 per 100,000 persons compared to the MCOD mortality rate of 1,046 per 100,000 persons. The age-adjusted mortality rate for all liver disease categories in CHeCS was higher than the national MCOD rate; for example, alcohol-related liver disease was 6 times greater while other hepatitis was 86 times higher than the national rate (Table 2). The most frequently cited cause of death was non-alcohol related liver disease; it was listed for 32% of all deaths (513 /1,590). The CHeCS mortality rate among persons with non-alcohol related liver disease was 669 vs. 51 per 100,000 for alcohol-related liver disease. In addition, all age adjusted death rates from extra-hepatic causes were higher than the national MCOD rates; the highest rates were seen with genitourinary causes, mental/behavioral disorders, and diabetes (Table 2). Of 1,590 deaths, only 12 (1%) were due to intentional self-harm, 93 (6%) due to sepsis due to any cause, and none were due to overdose/poisonings.

Despite confirmed chronic HCV infection, only 19% (306/1,590) had HCV infection listed on the death certificate. HCV was not listed for the majority of deaths across disease categories whether liver or non-liver related. The total number of deaths listed as liver-related was 47% (752/1,590), but of these, only 41% (306/752) had HCV listed as a cause of death. By type of liver-related death, HCV was listed for 36% (183/513) of those with non-alcohol related liver disease, 27% (13/49) of those with alcohol-related liver disease, 31% (53/169) of those with liver cancer, and only 9% (6/70) of those with ÒotherÓ hepatitis (Figure; Table 3). Even among 156 (10%) of decedents who had a liver transplant before death, HCV was only listed on 46 (29%) of death certificates.

Discussion:

Data from this study suggests a much greater role of HCV on mortality in the United States than has been previously understood based on analyses of death certificate data. The data in this paper document and contradict prevalent views that, perhaps because of its long incubation period (30 years), HCV infection is an indolent infection that is not of urgent concern. Originally intended as a study of causes of death in approximately 1,600 well characterized decedent HCV patients in the CHeCS, we found that only 19% had HCV listed on their death certificates, and only in 30% of death certificates in which liver disease had been noted. Even among the 156 HCV-infected CHeCS patients who had a liver transplant before death, only 46 (29%) had had HCV noted on their death certificate. As there were 16,622 death certificates in the US listing HCV as an underlying or contributing cause of death in 2010, we extrapolate that only one-fifth of those with HCV who die are having HCV recorded on their death certificates. Thus, our analysis suggests that at least 80,000 persons with HCV may have actually died in 2010. Given that 63% of the well-characterized CHeCS patients had medical records (ICD 9 codes) indicating pre-mortem liver disease--and 76% had FIB4 scores indicative of substantial or more liver damage-this suggests that total US deaths contributed to by HCV total at least 53,000.

Our results may be a conservative estimate as recent studies indicate that only about half of all HCV-infected persons have been diagnosed with the infection. 20-22 Further, approximately 50% of all deaths in those with known HCV had liver disease listed on their death certificates. Thus, even if we exclude other diseases associated with HCV infection such as diabetes and non-Hodgkin lymphoma, 23-26 it appears that most are dying not just with HCV but in possibly from HCV. These considerations are especially important because identifying and treating HCV patients in an era of rapidly evolving and effective, curative therapies could have a major public health impact.

Often, the high mortality and burden from HCV infection are minimized because other non-HCVrelated causes of death are considered to be more proximal or immediate reasons. For example, in a recent survey of New York resident physicians, over-documentation of cardiopulmonary causes of death and other inaccuracies-- both knowing and unavoidable--were reported; those surveyed believe that the current cause-of-death reporting system is generally inaccurate.27 This study also indicates that in the HCV-infected population over 70% had pre-mortem liver disease by ICD-9-CM electronic hospital record coding, liver biopsy, or FIB-4 score. So, in addition to under-recording HCV infection, even verified pre-mortem liver disease is also under-recorded, Further, whether the death was considered HCV or non-HCV-related, mean age of death in HCV-infected persons (59 years) was 15 years younger than for all cause mortality in the general population (74 years), a finding similar to previous research. 28

The mortality rate estimated from this analysis was twelve times higher than the general population; this is much higher than the two-to-five times higher mortality rates in HCV-infected vs uninfected persons seen in other studies. 29-32 Even with significant underreporting, persons who died in our cohort with non-alcohol related liver disease had 24 times the risk of death and those with liver cancer had almost 29 times the risk of death compared to over 12 million deaths in the age-matched general population. This effect was seen with extra-hepatic causes as well: compared to the general population, cases had three times the rate of injuries and genitourinary causes of death, ten times the rate of HIV, and twice the rate of mental/behavioral disorders. Other researchers have attributed higher rates of injuries/trauma as well as mental/behavioral disorders to lifestyle factors, including a previous history of substance abuse. 7,33 However, results from our death certificate data show that only 1% of CHeCS patients had suicide listed, 6% had sepsis, and none died of overdose or poisoning.

Our data represent findings from four health care systems in the United States and thus have a number of limitations. While two sites have transplant centers associated with them, we cannot measure how many patients are ÒattractedÓ to these medical centers because they have tertiary care facilities vs the fact that they are in the catchment area of these large integrated health systems. However, as only a minority (10%) of the CHECS decedents were seen at the transplant centers, these patients do not affect the overall picture. Level of care provided at a particular site should not affect the low rate of death certificate recordings of HCV (29%). Due to the variability in the definition of ICD-10 mortality codes used for chronic liver disease, we compared the codes that we used for our definition of chronic liver disease with a previously established definition. We found that for both definitions, 46% of cases were identified as having liver-related causes of death.34 This concordance further substantiates our findings.

An additional limitation is the use of the FIB-4 index as a measure of chronic liver disease; although validated, changes to liver enzymes and platelet count may be affected by non-liver related conditions such as infection or malignancy. However, the overlap between liver disease defined by ICD-9-CM codes and FIB-4 scores correlates with the findings using the ICD-10 mortality codes indicating that there is truly underlying liver disease in patients dying with and from HCV.

In summary, our analysis of a known HCV-infected cohort demonstrates that less than one-fifth of deaths in HCV-infected persons are coded as having HCV; this indicates a significant underestimation of the number of deaths among people with HCV and the true medical and public health impact of HCV. In this analysis, we have tried to be clear about the difference between dying with HCV and dying from HCV, but both represent a substantial public health burden. For purposes of public health, policy planning, disease modeling, and medical care, this is a huge burden that should be reported and hopefully spur public health action as curative, all-oral therapies are becoming available to treat HCV. Addressing the true impact of HCV, including of those chronically infected with HCV who are not utilizing health services, will be essential to appropriately respond to this epidemic. 35

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HCV Genotype 3

Provided by NATAP

Written by Jules Levin

You are asking if Sovaldi (sofosbuvir) is effective for patients with genotype 3 with compensated cirrhosis???

Here is the data below from studies showing 83%+ SVR rates with Sovaldi+Peg/Rbv having better results than Sovaldi+Rbv without Peg/INF. Small phase 2 study in genotype 3 patients with & without cirrhosis have been conducted with daclatasvir+Sovaldi with good SVR rates but a smaller number of patients who were non-cirrhotic & treatment-naive, just starting is a study in genotype 3, here are links to this data......

Bottom lime Sovaldi+Peg/Rbv appears to provide more effective results for patients with cirrhosis & gt3 than Sovaldi+Rbv, and that is FDA approved with 83% SVR but the number of patients in the study is small, see links & pics below.\

ALSO, in development is Gilead's GS-5816 for genotype 3, it's in earlier stage of development, data from early phase 2 studies show it to be potent, studies are ongoing:

AASLD: Deep Sequencing of HCV NS5A From a 3-Day Study of GS-5816 Monotherapy Confirms the Potency of GS-5816 Against Pre-Existing Genotype 1-3 NS5A Resistance-Associated Variants - (11/05/13)

AASLD: GS-5816, a Once-Daily NS5A Inhibitor, Demonstrates Potent Antiviral Activity in Patients With Genotype 1-4 HCV Infection in a 3 Day Monotherapy Study - (11/04/13)

The New HCV Guidelines/Recommendations from AASLD/IDSA were released Feb 1, 2014. Several days after that BMS announced the start of several phase 3 studies of daclatasvir+sofosbuvir (Sovaldi) including a study for genotype 3 patients. The Guidelines for genotype 3 are below and discuss Sofosbuvir+Peg/Rbv and Sofosbuvir+Ribavirin in treatment-naives & prior nonresponders, below are links and pics of the results from studies in genotype 3 patients using sofosvuvir+Peg/Rbv and sofosbuvir+Rbv.

Here is a link to the phase 3 study of daclatasvir+sofosbuvir (IFN/Rbv free): Phase III Daclatasvir and Sofosbuvir for Genotype 3 Chronic HCV

And here is link to the study results from the small phase 2 study conducted with daclatasvir+sofosbuvir in genotypes 1, 2 and 3"

EASL/2012: Potent Viral Suppression With the All-Oral Combination of Daclatasvir (NS5A Inhibitor) and GS-7977 (Nucleotide NS5B Inhibitor), +/- Ribavirin, in Treatment-Naive Patients With Chronic HCV GT1, 2, or 3 (100% SVR gt1, 91% gt2) - (04/19/12)

Here is a link to study of daclatasvir+Sovaldi in patients who failed boceprevir+telaprevir, some patients had more advanced fibrosis:

EASL: Sustained Virologic Response With Daclatasvir Plus Sofosbuvir ± Ribavirin (RBV) in Chronic HCV Genotype (GT) 1-Infected Patients Who Previously Failed Telaprevir (TVR) or Boceprevir (BOC) - (04/27/13)

The daclatasvir+Sovaldi (IFN/Rbv free) regimen is not FDA approved, the data from their studies:

AASLD: Sofosbuvir in Combination With PegIFN and Ribavirin for 12 Weeks Provides High SVR Rates in HCV-Infected Genotype 2 or 3 Treatment- Experienced Patients with and without Compensated Cirrhosis: Results from the LONESTAR-2 Study - (11/05/13)

The LONESTAR-2 study aimed to:
- Evaluate the efficacy of a 12-week SOF + PEG/RBV regimen in treatment-experienced patients with GT 2 or 3 infection, including those with cirrhosis-

AASLD: Sofosbuvir + Ribavirin for 12 or 24 Weeks for Patients With HCV Genotype 2 or 3: the VALENCE Trial - (11/04/13)

VALENCE (NCT01682720) is a Phase 3 study conducted in Europe assessing safety and efficacy of SOF+RBV administered for:
- 12 weeks in patients with HCV GT 2
- 24 weeks in patients with HCV GT 3
Treatment-naïve or -experienced patients with HCV GT 2 or 3 were originally randomized 4:1 to receive SOF+RBV for 12 weeks or matching placebo

CONCLUSIONS:
- SOF + RBV for 24 weeks demonstrated SVR rates >90% in treatment-naïve HCV GT 3 patients
- In treatment-experienced HCV GT 3 patients, SVR rates were 60% and 87% in those with and without cirrhosis, respectively
- GT 2 patients had high SVR rates following treatment with SOF+RBV for 12 weeks
- No resistance detected in any patient with relapse SOF+RBV for 12 or 24 weeks was well tolerated
- Safety profile consistent with that of RBV
- No additional adverse events when treatment was extended to 24 weeks

These are the recommendations from the new HCV Guidelines for patients who have been previously treated, non responders......

Link to New HCV Guidelines:

New Recommendations for Testing, Managing, and Treating Hepatitis C from AASLD/IDSA Panel. And newer developments in HCV therapy - (01/31/14)

The phase 3 FUSION trial compared 12 weeks (n=103) with 16 weeks (n=98) of daily sofosbuvir (400 mg) and weight-based RBV (1000 mg to 1200 mg) in genotype 2 or 3 HCV-infected patients in whom previous PEG/RBV therapy had failed. Of patients, 63% had genotype 3; 34% of all patients had cirrhosis. Because persons who had experienced prior relapses to IFN-based therapy accounted for 75% of patients, the number of patients with a prior nonresponse in the study was limited. The SVR rate for genotype 3 patients in the 12-week arm was 30% (19% among patients with cirrhosis and 37% among those without cirrhosis). Extending therapy to 16 weeks increased the SVR rate among genotype 3 patients to 62% (61% among patients with and 63% in those without cirrhosis).

Based on results from FUSION, the phase 3 multicenter, randomized placebo-controlled VALENCE trial was amended to evaluate the effect of extending sofosbuvir plus RBV therapy to 24 weeks in all patients with HCV genotype 3. As with the FUSION study, most (65%) treatment-experienced patients had relapsed. The SVR12 rates after 24 weeks of therapy for treatment-experienced patients with genotype 3 was 79% (60% among patients with and 87% in those without cirrhosis). The increased efficacy with 24 weeks of sofosbuvir plus RBV therapy across all fibrosis stages combined with a favorable safety and tolerability profile supports the recommendation to use 24 weeks of sofosbuvir plus RBV in all genotype 3 patients despite the minimal number of patients studied to date. The response rate for HCV genotype 3-infected patients with cirrhosis treated for 24 weeks in the VALENCE trial (60%) was similar to that observed after 16 weeks of treatment in the FUSION trial (61%). Although longer treatment duration with a well-tolerated regimen may potentially be more successful in these more difficult-to-treat patients, data remain limited. Either duration of treatment is considered acceptable at this time (see below).

Choice of specific regimen may be influenced by previous or anticipated tolerance to PEG or the presence of advanced fibrosis or cirrhosis. For most patients, the ease of administration and tolerability of sofosbuvir plus RBV will outweigh any potential benefit associated with the addition of PEG. However, for HCV genotype 3-infected patients who have cirrhosis, responses to sofosbuvir and RBV alone for 24 weeks were suboptimal.

In the LONESTAR-2 study, adding 12 weeks of PEG to the sofosbuvir and RBV regimen resulted in numerically higher response rates among persons with HCV genotype 3 than those obtained with sofosbuvir and RBV for 24 weeks. Of HCV genotype 3-infected patients with and without cirrhosis, 10 (83%) of 12 achieved SVR. Given the limited number of patients in this demographic in both the VALENCE and LONESTAR-2 studies, these differences in response rates should be interpreted with caution.

No HCV protease inhibitors have been approved or are indicated for the treatment of genotype 3 HCV infection. Although PEG/RBV has been the mainstay of treatment of genotype 3 HCV, it is less efficacious and has more adverse effects than the recommended regimens.

--------------------------

Genotype 3

The VALENCE study assessed the efficacy and safety of sofosbuvir (400 mg daily) plus RBV for 24 weeks in 250 treatment-naive (42%) and treatment-experienced (58%) subjects with HCV genotype 3 infection. The overall SVR12 was 84% and was higher among treatment-naive than treatment-experienced patients (93% versus 77%, respectively). These results suggest higher response rates can be achieved with a 24-week duration of sofosbuvir plus RBV than those reported for the 12- or 16-week durations studied in the FISSION (Lawitz, 2013b) (12 weeks, SVR12: 63%), POSITRON, (Jacobson, 2013c) (12 weeks, SVR 12: 61%) and FUSION (12 weeks, SVR12: 30%, 16 weeks, SVR12: 62%) trials. The primary reason for the higher SVR with extended therapy among treatment-naive patients was a reduction in the relapse rate from 40% to 5%. In sub-analysis, response rates were similarly high among those with (n=45) and without (n=100) cirrhosis (92% and 93%, respectively).

The combination of sofosbuvir plus PEG/RBV has been evaluated in patients with genotype 3 infection. In 2 phase 2 clinical trials, PROTON and ELECTRON, 38 of 39 (97%) treatment-naive patients with genotype 3 infection achieved SVR with sofosbuvir plus PEG (4 to 12 weeks of therapy)/RBV. (Gane, 2013b) For many patients with genotype 3, the adverse effects and increased monitoring requirements of PEG make this less acceptable than the recommended regimen of sofosbuvir plus weight-based RBV.

Although the combination of PEG/RBV is an FDA-approved regimen for HCV genotype 3, its less acceptable adverse effect profile, requirement for more intensive monitoring, and overall lower efficacy make it less desirable than the recommended regimen.

Because of their limited in vitro and in vivo activity against genotype 3, boceprevir, telaprevir, and simeprevir should not be used as therapy for patients with HCV genotype 3 infection.

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Lambda Legal Files Federal Lawsuit Against Louisiana Insurers for Dumping People with HIV

Provided by Lambda Legal Blog

by Lambda Legal
February 20, 2014

Lambda Legal today filed a federal class action discrimination lawsuit in U.S. District Court for the Middle District of Louisiana against BlueCross BlueShield of Louisiana (BCBS), which will no longer accept the federally-funded premium subsidies that enable low-income Louisianans living with HIV to purchase health insurance. Two other insurers included as defendants—Louisiana Health Cooperative and Vantage Health Plan—are also following the lead of Louisiana’s largest insurer, BCBS.  Lambda Legal is seeking an emergency injunction to force all three defendants to accept the premium payments and to provide health insurance until the lawsuit is heard.

Scott Schoettes, HIV Project Director at Lambda Legal, said:

The situation is urgent. Refusing federal funds that provide life-saving care to people living with HIV could potentially affect thousands of low-income Louisiana residents. This discriminatory policy keeps low-income people living with HIV off of BlueCross BlueShield’s insurance rolls, perpetuating the deliberate insurance industry practice of denying coverage to those living with HIV that the Affordable Care Act was designed to reverse. Continuous coverage is critical for people living with HIV.  The health care crisis these insurers have created must be stopped.

Lambda Legal filed today’s lawsuit on behalf of John East, a part-time worker in the hospitality industry, and other low-income Louisianans living with HIV. East, a 59-year-old New Orleans man insured by BCBS for nearly 30 years, learned in mid-January that BCBS would no longer accept the federal Ryan White subsidies for which he qualifies. Without the subsidies, East will not be able to afford his medical care and HIV medications. Lambda Legal’s lawsuit follows earlier efforts—including complaints filed with the U.S. Department of Health and Human Services Office of Civil Rights—to persuade the insurers to continue accepting federal Ryan White premium subsidies. The New Orleans AIDS Task Force is assisting in this advocacy.

Lambda Legal client John East said:

I couldn’t believe it when I was told BCBS would no longer accept my Ryan White insurance subsidies. What am I supposed to do now? I’ve been with BCBS for 29 years. I paid my premiums that whole time, and now they are finding a way to dump me just because I’m living with HIV. I need these medications to stay healthy, so that I can continue to work and contribute to my community.

The Louisiana Ryan White Health Insurance Program is a federally-funded program that functions as the payer of last resort, helping low-income individuals living with HIV purchase health insurance they could not otherwise afford. Beginning this month, BCBS of Louisiana abruptly stopped accepting Ryan White premium subsidies, from current policyholders and new enrollees alike.

Lambda Legal sent a letter to BCBS of Louisiana on January 27, 2014, asking that the insurance provider reverse its policy change and resume accepting Ryan White premium subsidies or explain the rationale for its abrupt and harmful policy shift. Lambda Legal requested a response by January 30, 2014, but BCBS of Louisiana never responded.

Read the complaint.

Read the press release.

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Hepatitis C- An emerging epidemic: HepCoN

Morung Express News | February 22, 2014

Dimapur: Hepatitis Coalition of Nagaland (HepCoN) expressing its concern on the HCV disease burden in Nagaland, stated that “if Hepatitis C (HCV) is not addressed with a collaborated effort, then the day is not far when the epidemic proportion may go beyond control.”

Alarming number of HCV reported cases in Wokha, Phek and Kohima

Highlighting the need of prevention through mass awareness campaign at all levels as the key to containing the Hepatitis C Virus in the state, HepCoN and NUN in partnership with IDS, FDS TDUN, TUN conducted a one day sensitization meeting at Tuensang Town Hall on February 21.

Total 80 representatives from NGOs and various Health Service Centers including Grace Chapel, ART center, DAN, and some participants from Tuensang OST Center participated in the meeting.

A press release stated that the resource persons Abou and Ketho of HepCoN, spoke on various subject matter regarding the alarming number of HCV reported cases in the context of Wokha, Phek and Kohima district. Topics for the programme also include basics of Hepatitis and its types including HCV, its routes of transmission, prevention, and treatment services in Nagaland.

The programme started with keynote address by Ketho with a slide presentation of some available data, which highlighted a high HCV prevalence rate (IBBA, R-2) in Wokha with 20.8% and Phek district with 8.7% and a general population data of Naga Hospital Authority Kohima (NHAK) of 1.8% prevalence rate.

He described the different existing types of Hepatitis Virus such a HAV, HBV, HCV, HDV, HEV and HGV. On describing these kinds of Viruses, He mentioned where the viruses are found, how it is transmitted, how it is not transmitted and how it can be prevented. Special concentration was given on discussing the nature of Hepatitis C virus by explaining on the presence of the virus in the Human Blood, while small amount can be found in the semen and the vaginal secretions during sex. The routes of transmission explained were through the sharing of infected Needles and syringes and drug injecting Paraphernalia, sharing of tattoo equipments, personal care items like toothbrush, comb or even razors.

He also mentioned as to how the virus is not transmitted such as shaking hands, sharing of glass and utensils, using public toilets. He also spoke on its preventive measures such as using clean needles and syringes, not sharing personal equipments like razors, combs, Tattooing needle and inkwells, always practicing safer sexual practices.

Abou Mere spoke on the types of diagnostic test, which are Antibody test followed by confirmatory test through Viral Load and Genotyping test. He also mentioned the symptoms while also of the drugs that are used to treat HCV with a combination therapy of Pegylated interferon and Ribavirin of 24 and 48 weeks depending on the genotype. He announced that the drug is available but because of the high price many are not able to initiate on their treatment and people on treatment also undergoes some side effects like Insomnia, fever, Joint pains etc. He stressed on adopting a positive lifestyle if one is tested positive for HCV like avoiding fatty food, fast foods, doing light exercise, avoiding or minimizing alcohol and drugs consumption and following up with doctor six monthly for monitoring.

A member from HepCoN shared his experience as a person living with Hepatitis C. He shared that recently through HepCoN, he came to know more of HCV and went to NHAK for testing. He was tested antibody reactive but not disheartened. He encouraged the participants to always practice safe methods and to spread awareness at their own organizational level. Earlier, Thapli Lama of TDUN delivered the welcome address and Imsii Pongen, Program Officer NERO-DAC, pronounced vote of thanks.

HepCoN has conducted similar programme in Dimapur, Kohima, Wokha, Peren, and Zunheboto district. HepCoN aims to reach out to all the remaining five districts within the next few months. HepCoN also informed that one could avail free HCV testing facilities at NHAK, FPAI in Kohima and Dimapur Civil Hospital.

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