Activists dressed as Gilead butchers greeted participants at the European Conference on HIV and Hepatitis Coinfection

ACTIVISTS CHARGE HEP C CONFERENCE DEMANDING ACCESS TO MEDICATION

On the morning of Thursday 10th December 2015, a public action targeted specifically at big pharma profiteering from the lives of people with hepatitis C happened in central London. Activists dressed as Gilead butchers greeted participants as they arrived at the European Conference on HIV and Hepatitis Coinfection

The ACT UP LONDON (2) activists were demanding Gilead and other drug companies drop the prices of the new medicines which can cure hepatitis C. The companies are charging extortionate prices – tens of thousands of pounds for pills that cost just a few hundred pounds to make (3).

Gilead were revealed last week by US congress to have sent internal emails saying “let’s hold our price higher regardless of the uproar.” Kevin Young, Gilead’s executive vice president for commercial operations, wrote to colleagues in November 2013 …”Two sincere requests…Let’s not fold to advocacy pressure in 2014. Let’s hold our position whatever competitors do or whatever the headlines” (4).

Read more here....

December Updates

Reducing the cost of new hepatitis C drugs
An index of articles pointing the reader to the current controversy over the high price of Sovaldi, Harvoni (ledipasvir/sofosbuvir) and AbbVie Viekira Pak.

Also See
Sovaldi Investigation Finds Revenue-Driven Pricing Strategy Behind $84,000 Hepatitis Drug
Dec 1 2015
A report released Tuesday by US Senators Ron Wyden and Charles Grassley claims that Gilead Sciences priced the hepatitis C treatments Sovaldi (sofosbuvir) and Harvoni (ledipasvir/sofosbuvir) with the sole goal of maximising revenue. The report was based on an investigation of 20 000 pages of internal company documents, dozens of interviews with health care experts and data from Medicaid programmes in all 50 states and the District of Columbia.
“Gilead pursued a calculated scheme for pricing and marketing its Hepatitis C drug based on one primary goal, maximizing revenue, regardless of the human consequences. There was no concrete evidence in emails, meeting minutes or presentations that basic financial matters such as R&D costs or the multi-billion dollar acquisition of Pharmasset, the drug’s first developer, factored into how Gilead set the price....

Sudden drop-off in VA hepatitis C treatments alarms veterans community

Sudden drop-off in VA hepatitis C treatments alarms veterans community
By Diane Zumatto

Despite the fact that Congress appropriates VA’s medical services account a full year in advance precisely to avoid a slowdown in VA services and treatment should there be any fiscal uncertainty with the rest of the government at the start of a new fiscal year, VA’s treatment of veterans with HCV dropped astoundingly to less than 400 for the first week of October, and has remained alarmingly low since then.

Continue reading....

Senate Hearings To Investigate Rising Price Of Medications

European Physicians Report Strong but Variable Uptake of All-Oral Interferon-Free Hepatitis C Virus Regimens Across EU5 Countries

BURLINGTON, Mass., Dec. 8, 2015 /PRNewswire/ -- Decision Resources Group finds that surveyed EU5 physicians report that more than half of their hepatitis C virus (HCV) patients were being treated with interferon (IFN)-free regimens. Factors such as regulatory approval date and pricing and reimbursement negotiations contributed to wide variation in the uptake dynamics of novel HCV therapies. Differences between EU5 markets were most apparent in the treatment of non-cirrhotic patients with lower liver fibrosis scores, who are typically deprioritized for access to IFN-free therapies. This effect is exemplified in the United Kingdom, where 45 percent of non-cirrhotic treatment-naive genotype-1 patients were being treated with IFN dual therapy or first generation protease inhibitor triple therapy, according to survey results, though this will change rapidly with the recent approval of new direct acting antivirals in the UK in late 2015.

Other key findings from the special report entitled "TreatmentTrends: Hepatitis C Virus 2015 (EU)":

• Surveyed EU5 physicians report that nearly two-thirds of their genotype-1 and -2/3 HCV patients are non-cirrhotic and thus are not prioritized for treatment. However, only one-quarter of treatment-naive non-cirrhotic HCV patients in the EU5 are being actively warehoused, down from 30 percent a year ago, suggesting EU5 countries are increasingly treating HCV-infected patients regardless of liver disease stage.
• Across EU5 countries, Gilead's Harvoni and a combination of Gilead's Sovaldi and Bristol-Myers Squibb's Daklinza are the leading regimens for treatment-experienced cirrhotic patients with genotype-1 and -2/3 infection, respectively. Uptake of these agents in the EU5 was primarily driven by France and Germany. Surveyed EU5 physicians rate both regimens highly on overall safety, efficacy in both compensated and decompensated cirrhotic patients, as well as efficacy in HCV genotype-1 and -3 infections.
• Surveyed EU5 physicians indicate the need for novel therapies with pan-genotypic activity, regimens with treatment duration under 12 weeks and for increased patient access to efficacious but costly therapies. In addition, physicians expect Merck & Co.'s grazoprevir/elbasvir to bring the most immediate benefit to their patients, likely due to improved treatment efficacy in difficult-to-treat populations, such as patients with renal impairment.

Comments from Decision Resources Business Insights Analyst James T. Heeres, Ph.D.:

• "Although EU5 physicians rate Gilead's Harvoni and Bristol-Myers Squibb's Daklinza highly on efficacy, they are clearly critical of the cost of these therapies. However, according to our research, cost issues may recede in the near future as some EU5 countries work to lift access barriers. This still leaves the door open for emerging therapies to compete on efficacy in niche populations and, to some degree, on cost."
• "As our primary research had predicted, drug treatment rates and patient shares for Harvoni, Abbvie's Viekirax, and Daklinza have grown in the EU5, largely in response to lowering of market access barriers. However, the potential approval of several pan-genotypic regimens (e.g. Gilead's Sovaldi + velpatasvir) and regimens targeting niche populations (e.g. Merck & Co.'s grazoprevir/elbasvir) will likely kick-start another round of pricing negotiations. Alternatively, currently approved regimens may retain market share if physician preference and cost present substantial market access barriers for emerging therapies."

For more information on purchasing this report, please email questions@teamdrg.com.

About Decision Resources GroupDecision Resources Group offers best-in-class, high-value data, analytics and insights products and services to the healthcare industry, delivered by more than 900 employees across 14 global locations. DRG provides the pharmaceutical, biotech, medical device, financial services and payer industries with the tools, insights and advice they need to compete and thrive in an increasingly complex and value-based marketplace. DecisionResourcesGroup.com.

Media contact:

SHIFT CommunicationsTheresa Masnik
617.779.1871
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NEW DELHI - Hetero gets DCGI approval to market Gilead's Harvoni Hepatitis C drug

Hetero gets DCGI approval to market Hepatitis C drug  

NEW DELHI: Drug maker Hetero has received approval from DCGI to market generic version of Gilead's Harvoni, a drug used in the treatment of Hepatitis C, in the country.

Hetero is the first company in India to receive the approval for the fixed-dose combination Ledipasvir-Sofosbuvir (90mg/400mg) from Drug Controller General of India (DCGI), the company said in a statement.

Read more at:
http://economictimes.indiatimes.com/articleshow/50092074.cms?utm_source=contentofinterest&utm_medium=text&utm_campaign=cppst

HCV genotype 3: a wolf in sheep’s clothing

Journal: Expert Review of Anti-infective Therapy
Editorials

HCV genotype 3: a wolf in sheep’s clothing

DOI:10.1586/14787210.2016.1127757

José-R. Blancoa* & Antonio Rivero-Juarez
1a Infectious Diseases Area. Hospital San Pedro - Center for Biomedical Research of La Rioja (CIBIR) . Piqueras 98, 26006 Logroño , La Rioja ( Spain ).
2b Infectious Diseases Unit. Instituto Maimonides de Investigación Biomédica de Córdoba (IMIBIC) . Hospital Universitario Reina Sofía de Córdoba. Universidad de Córdoba . Avda. Menendez Pidal s/n, 14004 Córdoba , Córdoba ( Spain ).

Publishing models and article dates explained

Received: 16 Sep 2015
Accepted: 30 Nov 2015
Accepted author version posted online: 03 Dec 2015

Keywords: Hepatitis C, Genotype 3, Metabolic syndrome, Hepatocellular carcinoma

Download as PDF or Interactive PDF

HCV genotype 3: a wolf in sheep’s clothing

"All truths are easy to understand once they are discovered; the point is to discover them". Galileo Galilei"

At present, the hepatitis C virus (HCV) is a major cause of morbidity and mortality affecting over 185 million people worldwide,[1] equivalent to a global prevalence of about 2.5% in 2015. Genotype 3 (HCV G3) is one of the seven recognized genotypes.[2] HCV G3 is the second most common genotype overall and is estimated to account for 54.3 million cases throughout the world (30.1%).[1] Although three-quarters of them occur in South Asia where it is endemic, the 3a subtype is an “epidemic subtype“ widely distributed geographically, probably associated with injecting drug use.[3]

 In the last two years, the history of HCV infection has changed radically with the appearance of the new direct-acting antiviral agents (DAAs).[4] Although HCV G3 was one of those genotypes who achieved a better sustained viral response (SVR) using pegylated interferon and ribavirin (PEG-IFN/Rbv) therapy,[5] the current effectiveness of the new DAAs against HCV G3 leaves a lot to be desired compared with the results obtained with other genotypes.[6] This is a major problem since, compared to other genotypes, HCV G3 is associated with faster progression of fibrosis,[7,8] a greater risk for hepatocellular carcinoma (HCC),[8-10] and a higher mortality.[11] Why is it so pathogenic and resistant to treatment? The reasons for this “aggressiveness” are without doubt multiple, complex and not well known.

First, it is important to remember that the host immune response plays an important role in HCV G3 infection because of its potential to contribute to viral clearance. So, acutely HCV-infected patients are much more likely to spontaneously clear HCV if they are infected with HCV G3 than HCV G1.[12] Indeed, chronically infected HCV G3 patients had higher SVR rates after shorter treatment with PEG-IFN/Rbv therapy when compared to those with chronic HCV G1 infection.[13] One of the possible reasons could be that in monocytic cell and plasmacytoid dendritic cell lines and in macrophages differentiated from monocytes with macrophage colony-stimulating factor, HCV G3 induces greater interferon transcription than either genotype 1a or 1b.[14] However, this apparent benefit may backfire because of the increased rate of fibrosis progression of HCV G3, probably due to the higher non-parenchymal cell transcription of IFN genes following intracellular HCV G3 sensing.[14]

It has been reported previously that HCV G3 is associated with a significantly increased risk of developing cirrhosis and HCC compared to HCV G1, and association that is independent of the patients’ age, diabetes, body mass index, or antiviral treatment.[8] The high viremia observed in HCV G3-infected patients may be a marker of rapid disease damage, reflecting either the inability of the immune system to control the infection or the existence of some escape mechanisms in HCV G3 which prevents the immune system response from being effective.[15]

Secondly, another problem that is not well understood is the interaction between HCV and lipid metabolism.[16] So, HCV G3 selectively interferes with the late cholesterol synthesis pathway,[17] although this interference is resolved after the SVR. Other mechanisms that alter lipid metabolism are increased the novo lipogenesis and the inhibition of mitochondrial fatty acid degradation.[18] At what level of lipid metabolism does HCV G3 work? Is the damage the consequence of the virus or of its proteins in infected hepatocytes? Given that, in previous studies, the variables independently associated with SVR were high LDL levels,[19,20] low HDL levels [19] and statin use,[19] one might think that statins would be a useful option for such patients. Nonetheless, this is not actually the case with HCV G3. In one analysis of patients with HCV 1-3 genotypes who received combination therapy with PEG-IFN/Rbv, the significant impact of statin use was only observed among the HCV G1 patients.[20] Similar findings were reported by Selic Kurincic et al.[21]

Steatosis is a common histologic finding in patients infected by HCV G3, independently of the presence of fibrosis, diabetes, hepatic inflammation, ongoing alcohol abuse, higher body mass index, and older age.[22] Indeed, steatosis in HCV G3 infected patients is not the result of overexpression of genes involved in lipogenesis.[23] The higher rates of hepatic steatosis in HCV G3 patients, even in absence of other metabolic complications, suggest that some specific viral sequences may be involved in the etiology of steatosis.[18] In fact, after reaching SVR, hepatic steatosis in these patients had disappeared.[24,25] Another possible explanation for the high presence of steatosis could be that HCV G3 steatosis induces the liberation of proinflammatory chemokines that increase the recruitment of inflammatory cells to the liver.[14] In support of this idea, the depletion of liver Kupffer cells prevents the development of diet-induced hepatic steatosis and insulin resistance.[26]

It is important to bear in mind that there is a significant correlation between the steatosis score and the titer of intrahepatic HCV RNA in patients with HCV G3, providing virological and some clinical evidence that steatosis is the morphological expression of a viral cytopathic effect in patients infected with this genotype.[27] This finding has important implications, such as lower SVR rates or higher relapse rates after HCV treatment.[28,29] Is steatosis a marker of rapid progression or bad prognosis in HCV G3 infected patients?

Non-alcoholic fatty liver disease (steatosis/steatohepatitis) is similarly recognized as the hepatic manifestation of metabolic syndrome (MS). HCV virus genotype 3 infection increases the risk of insulin resistance and diabetes, probably due to the direct effect of the virus on intracellular insulin signaling.[30] This situation not only increases the cardiovascular risk but also reduces the likelihood of achieving a SVR.[31] Another common manifestation of MS is obesity, a problem that also increases the expression of some inflammatory cytokines and activates several signaling pathways involved in the pathogenesis of insulin resistance.[32] The inflammation may also contribute to the pathogenesis of liver damage.[33] Obesity has also been correlated with a lower SVR rate.[34] Once again, this opens up an interesting way to research the mechanisms involving MS and SVR in these patients. Are insulin resistance and/or obesity indicators of the the existence of an established liver damage, even though we are unable to diagnose it? Is there some symbiotic relationship between the adipocytes and HCV G3 that reduces the efficacy of the DAAs? In view of the higher rates of SVR using the new DAAs, is the presence of MS still important in chronic HCV infection?.[35] Probably not, but there is as yet no concrete answer for this question and so the controversy about steatosis and HCV remains. Valenti et al also reported that the rs738409 genotype, a polymorphism that influences liver fat without affecting insulin resistance and body composition, was associated with severe hepatic steatosis in patients infected with a non-3 HCV genotype, and also with fibrosis stage and cirrhosis (OR = 1.47; P = 0.002).[36] Similarly, Cai et al [37] reported that rs738409 was associated with an increased risk of steatosis in patients infected with a non-3 HCV genotype. These results suggest distinct pathogenic mechanisms in the 3 and non-3 genotypes.

Moving on to the third point, and so concluding this topic, it is necessary to understand the clinical implications of the different HCV G3 subtypes (in other words, immunity, inflammation, prognosis, response to DAAs). This is something we already known for HCV G1a and 1b.[38] At least 10 HCV G3 subtypes have been described so far.[39] Are some of these HCV G3 subtypes able to evade the immune response? Can we expect the same SVR for different subtypes? The correct identification of HCV G3 subtypes would probably be necessary because they are crucial in clinical trials evaluating the new DAAs. No data have so far stratified the response of HCV G3 to the new DAAs, which could be an essential issue that requires further investigation.

In summary, given the aggressiveness of HCV G3, it is increasingly necessary to initiate antiviral treatment as soon as possible in all patients, including those with steatosis and/or MS. In these patients, even those with SVR, continued surveillance is necessary, paying careful attention to patients with cirrhosis. There is no doubt that better knowledge of HCV G3 should be a priority for us all.

Financial & competing interests disclosure
JR Blanco has carried out consulting work for Abbvie, Bristol-Myers Squibb, Gilead Sciences, Janssen, Merck, and ViiV Healthcare; has received compensation for lectures from Abbvie, Bristol-Myers Squibb, Gilead Sciences, Janssen, Merck, and ViiV Healthcare, as well as grants and payments for the development of educational presentations for Gilead Sciences and BristolMyers Squibb. A Rivero-Juarez is the recipient of a Postdoctoral Perfection Grant from Fundación Progreso y Salud, Consejería de Salud y Políticas Sociales, Junta de Andalucia (0024-RH-2013). He has received compensation for lectures from Bristol-Myers Squibb, Janssen, Merck, and ViiV Healthcare.The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. 

References
1. Mohd Hanafiah K, Groeger J, Flaxman AD, Wiersma ST. Global epidemiology of hepatitis C virus infection: new estimates of age-specific antibody to HCV seroprevalence. Hepatology. 2013;57(4):1333-1342.
2. Smith DB, Bukh J, Kuiken C, Muerhoff AS, Rice CM, Stapleton JT, et al. Expanded classification of hepatitis C virus into 7 genotypes and 67 subtypes: updated criteria and genotype assignment web resource. Hepatology. 2014;59(1):318-327.
3. Pybus OG, Cochrane A, Holmes EC, Simmonds P. The hepatitis C virus epidemic among injecting drug users. Infect. Genet. Evol. 2005;5(2):131- 139.
4. Gentile I, Buonomo AR, Zappulo E, Borgia G. Interferon-free therapies for chronic hepatitis C: toward a hepatitis C virus-free world? Expert. Rev. Anti. Infect. Ther. 2014;12(7):763-773.
5. Hoofnagle JH, Seeff LB. Peginterferon and ribavirin for chronic hepatitis C. N. Engl. J. Med. 2006;355(23):2444-2451.
6. AASLD/IDSA HCV Guidance Panel Hepatitis C guidance: AASLD-IDSA recommendations for testing, managing, and treating adults infected with hepatitis C virus. Hepatology. 2015;62(3):932-54.
7. Probst A, Dang T, Bochud M, Egger M, Negro F, Bochud PY. Role of hepatitis C virus genotype 3 in liver fibrosis progression--a systematic review and meta-analysis. J. Viral Hepat. 2011;18(11):745-759.
8. Kanwal F, Kramer JR, Ilyas J, Duan Z, El-Serag HB. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98- 105.
9. Nkontchou G, Ziol M, Aout M, Lhabadie M, Baazia Y, Mahmoudi A, et al. HCV genotype 3 is associated with a higher hepatocellular carcinoma incidence in patients with ongoing viral C cirrhosis. J. Viral Hepat. 2011;18(10):e516-522.
10. McCombs J, Matsuda T, Tonnu-Mihara I, Saab S, Hines P, L'italien G, et al. The risk of long-term morbidity and mortality in patients with chronic hepatitis C: results from an analysis of data from a Department of Veterans Affairs Clinical Registry. JAMA Intern. Med. 2014;174(2):204-212.
11. van der Meer AJ, Veldt BJ, Feld JJ, Wedemeyer H, Dufour JF, Lammert F, et al. Association between sustained virological response and all-cause mortality among patients with chronic hepatitis C and advanced hepatic fibrosis. JAMA. 2012;308(24):2584-2593.
12. Lehmann M, Meyer MF, Monazahian M, Tillmann HL, Manns MP, Wedemeyer H. High rate of spontaneous clearance of acute hepatitis C virus genotype 3 infection. J. Med. Virol. 2004;73(3):387-391.
13. Hadziyannis SJ, Sette H Jr, Morgan TR, Balan V, Diago M, Marcellin P, et al. Peginterferon-alpha2a and ribavirin combination therapy in chronic hepatitis C: a randomized study of treatment duration and ribavirin dose. Ann. Intern. Med. 2004;140(5):346-355.
14. Mitchell AM, Stone AE, Cheng L, Ballinger K, Edwards MG, Stoddard M, et al. Transmitted/founder hepatitis C viruses induce cell-type- and genotypespecific differences in innate signaling within the liver. MBio. 2015;6(2):e02510.
15. Buti M, Esteban R. Hepatitis C virus genotype 3: a genotype that is not 'easy-to-treat'. Expert Rev. Gastroenterol. Hepatol. 2015;9(3):375-385.
16. Clement S, Peyrou M, Sanchez-Pareja A, Bourgoin L, Ramadori P, Suter D, et al. Down-regulation of phosphatase and tensin homolog by hepatitis C virus core 3a in hepatocytes triggers the formation of large lipid droplets. Hepatology. 2011;54(1):38-49.
17. Clark PJ, Thompson AJ, Vock DM, Kratz LE, Tolun AA, Muir AJ, et al. Hepatitis C virus selectively perturbs the distal cholesterol synthesis pathway in a genotype-specific manner. Hepatology 2012;56(1):49-56.
18. Negro F. Hepatitis C virus-induced steatosis: an overview. Dig Dis. 2010;28(1):294-299.
19. Harrison SA, Rossaro L, Hu KQ, Patel K, Tillmann H, Dhaliwal S, et al. Serum cholesterol and statin use predict virological response to peginterferon and ribavirin therapy. Hepatology 2010;52(3):864-874.
20. Pandya P, Rzouq F, Oni O. Sustained virologic response and other potential genotype-specific roles of statins among patients with hepatitis Crelated chronic liver diseases. Clin. Res. Hepatol. Gastroenterol. 2015;39(5):555-565.
21. Selic Kurincic T, Lesnicar G, Poljak M, Meglic Volkar J, Rajter M, Prah J, et al. Impact of added fluvastatin to standard-of-care treatment on sustained virological response in naive chronic hepatitis C patients infected with genotypes 1 and 3. Intervirology. 2014;57(1):23-30.
22. Leandro G, Mangia A, Hui J, Fabris P, Rubbia-Brandt L, Colloredo G, et al. Relationship between steatosis, inflammation, and fibrosis in chronic hepatitis C: a meta-analysis of individual patient data. Gastroenterology, 2006;130(6):1636-1642. Downloaded by [68.43.174.156] at 12:46 07 December 2015
23. Ryan MC, Desmond PV, Slavin JL, Congiu M. Expression of genes involved in lipogenesis is not increased in patients with HCV genotype 3 in human liver. J. Viral Hepat. 2011;18(1):53-60.
24. Poynard T, Ratziu V, McHutchison J, Manns M, Goodman Z, Zeuzem S, et al. Effect of treatment with peginterferon or interferon alfa-2b and ribavirin on steatosis in patients infected with hepatitis C. Hepatology. 2003;38(1):75-85.
25. Kumar D, Farrell GC, Fung C, George J. Hepatitis C virus genotype 3 is cytopathic to hepatocytes: Reversal of hepatic steatosis after sustained therapeutic response. Hepatology 2002;36(5):1266-1272.
26. Huang W, Metlakunta A, Dedousis N, Zhang P, Sipula I, Dube JJ, et al. Depletion of liver Kupffer cells prevents the development of diet-induced hepatic steatosis and insulin resistance. Diabetes 2010;59(2):347-357.
27. Rubbia-Brandt L, Quadri R, Abid K, Giostra E, Malé PJ, Mentha G, et al. Hepatocyte steatosis is a cytopathic effect of hepatitis C virus genotype 3. J. Hepatol. 2000;33(1):106-115.
28. Aziz H, Gill U, Raza A, Gill ML. Metabolic syndrome is associated with poor treatment response to antiviral therapy in chronic hepatitis C genotype 3 patients. Eur. J. Gastroenterol. Hepatol. 2014;26(5):538-543.
29. Restivo L, Zampino R, Guerrera B, Ruggiero L, Adinolfi LE. Steatosis is the predictor of relapse in HCV genotype 3- but not 2-infected patients treated with 12 weeks of pegylated interferon-alpha-2a plus ribavirin and RVR. J. Viral Hepat. 2012;19(5):346-352.
30. Kawaguchi T, Yoshida T, Harada M, Hisamoto T, Nagao Y, Ide T, et al. Hepatitis C virus down-regulates insulin receptor substrates 1 and 2 through up-regulation of suppressor of cytokine signaling 31. Am. J. Pathol. 2004;165(5):1499-1508. 31. Poustchi H, Negro F, Hui J, Cua IH, Brandt LR, Kench JG, et al. Insulin resistance and response to therapy in patients infected with chronic hepatitis C virus genotypes 2 and 3. J. Hepatol. 2008;48(1):28-34.
32. Chen L, Chen R, Wang H, Liang F. Mechanisms linking inflammation to insulin resistance. Int. J. Endocrinol. 2015;2015:508409.
33. Szabo G, Petrasek J. Inflammasome activation and function in liver disease. Nat. Rev. Gastroenterol. Hepatol. 2015;12(7):387-400.

"

All truths are easy to understand once they are discovered

; the point is to

discover them

"

.

Galileo Galilei

St. Louis VA says it’s not turning away any patients with Hepatitis C seeking expensive prescriptions

St. Louis VA Supplying an Expensive Cure to Hep C

December 7, 2015 8:16 AM

The new drug, Sofosbuvir, can cost the VA $42,000 for each patient’s 12-week treatment.
Complaints are reported elsewhere about VA patients being put on a waiting list, but in St. Louis Dr. Leela Nyak, a liver specialist at the John Cochran Medical Center says the cost isn’t forcing them to turn people away.

Read more... 

The Impact Of New Hepatitis C Drugs On National Health Spending

The Impact Of New Hepatitis C Drugs On National Health Spending

Charles Roehrig

Those who follow Altarum Institute’s monthly health sector briefs and trend reports are well aware that the five-year run of record low growth rates in national health spending (from 2009 through 2013) has come to an end, or at least been interrupted. According to data just released by the Centers for Medicare & Medicaid Services (CMS), health spending grew by 5.3 percent in 2014, compared to 2.9 percent in 2013 and roughly 4 percent from 2009 through 2012. Our estimates for the first eight months of 2015 show growth of 6.2 percent, though on a downward path, indicating that the year could finish at around 6 percent growth.

Many analysts had predicted well in advance an increased health spending growth rate for 2014 due to the implementation of the Patient Protection and Affordable Care Act (ACA). The expanded coverage provisions of the ACA were expected to increase the number of persons with health insurance and hence health spending (Note 1).

However, the huge jump in prescription drug spending that occurred in 2014 was unforeseen. In 2013, spending on prescription drugs grew by only 2.4 percent, but in 2014, it skyrocketed to 12.2 percent. Some of this increase in spending on prescription drugs is due to expanded coverage, and some is due to the acceleration in prescription drug prices.

A major source of this growth was the introduction of Sovaldi in December 2013, and Harvoni in October 2014. Both are very expensive breakthrough drugs for the treatment of hepatitis C (a disease of the liver, affecting approximately 3 million Americans). The new hepatitis C drugs have had a significant impact on growth rates in spending on prescription drugs and on national health spending.
Company Sales Of New Hepatitis C Drugs

I use company reports to track quarterly U.S. sales of the four bestselling new prescription drugs for the treatment of hepatitis C: Harvoni and Sovaldi (Gilead Sciences, Inc.), Viekira Pak (AbbVie), and Olysio (Janssen Pharmaceutical Companies of Johnson & Johnson). While these sales figures are not identical to the final sales captured in health spending, they provide a basic sense of the impact of hepatitis C drugs on overall health spending growth rates (Note 2).

The quarterly sales are shown in Figure 1. Combined sales were $100 million in Q4 2013, jumping to $2.4 billion and $3.8 billion in Q1 and Q2 2014. In Q3, sales of the existing drugs fell to $2.9 billion, presumably due to the expected release of a more appealing drug, Harvoni, in October. Starting in Q4 2014, sales moved back to $3.5 billion and have stayed in that range during the first three quarters of 2015.

Source: Altarum Center for Sustainable Health Spending, computed from Gilead, AbbVie, and Johnson & Johnson Company reports.

Impact On 2014 Growth In Health Spending

National health spending in 2013 was about $2.9 trillion. In 2014, company sales of the new hepatitis C drugs were $12.3 billion higher than in 2013. This represents 0.4 percent of total health expenditures in 2013, and suggests that the new hepatitis C drugs added 0.4 percentage points to the 2014 health spending growth rate. In the absence of these new drugs, national health spending would have grown by about 4.9 percent rather than 5.3 percent.

Prescription drug spending in 2013 was $265 billion. Similar math suggests that the new hepatitis C drugs added about 4.6 percentage points to the growth in prescription drug spending in 2014. The total growth rate in prescription drug spending in 2014 was 12.2 percent, so we estimate that it would have been 7.6 percent in the absence of the new hepatitis C drugs. That latter would still have been a large increase relative to the 2.6 percent growth seen in 2013 for prescription drugs and is likely due to a combination of expanded coverage and accelerated price growth.
Likely Impact On 2015 Growth In Health Spending

While spending on hepatitis C drugs in 2015 remains very high ($14.4 billion is a reasonable estimate, assuming $3.5 billion in Q4), it represents a much smaller increase ($1.9 billion) than experienced in 2014 ($12.3 billion). This means that in 2015, hepatitis C drugs will have added less than 0.1 percentage points to the growth rate in national health expenditures and 0.6 percentage points to the growth rate in prescription drug spending.

To put it another way, the relatively small increase in hepatitis C spending in 2015 should reduce the overall rate of growth in national health expenditures by more than 0.3 percentage points compared to the growth rate in 2014. For prescription drugs, it should bring the growth rate down by about 4 percentage points (Note 3).

Our November health sector spending brief shows that the growth rate in spending on prescription drugs has indeed been falling in 2015 and, as of September, was at 8.4 percent, year over year. This is 3.8 percentage points below the growth rate in 2014, and we attribute much of the decline to the leveling off in spending on hepatitis C (Note 4).

The decline in the prescription drug spending growth rate in 2015 has been more than offset by a higher rate of growth in spending on health care services so that, in September, the health spending growth rate of 5.5 percent was actually higher than the rate for 2014. In the absence of the prescription drug spending slowdown, the September growth rate would have been about 5.9 percent.
Implications For 2016 And Beyond

I conclude with speculation about the future using rough estimates that I believe nonetheless provide some useful information. U.S. sales of hepatitis C drugs seem to have stabilized at about $14 billion per year, which equates to about 150,000 persons treated per year (at a rate of $90,000 per person treated).

The number of new cases per year is about 30,000 so our current rate of spending should be sufficient to reduce prevalence by about 120,000 per year. There are about 3 million people with hepatitis C in the U.S., so our current rate of spending could continue for many years before we run out of cases to treat. (Because hepatitis C is spread by those already infected, the number of new cases should dwindle toward zero as the overall prevalence falls toward zero.)

Of course, the amount we actually spend per year over the next few years could be higher or lower than what we spent in 2015. Recent recommendations argue for treatment of nearly all diagnosed cases, yet many states and other payers continue to prioritize candidates for treatment based on severity of illness and other factors. This means that the near-term rate of spending is quite unpredictable and depends upon how much effort is put toward identifying and treating existing cases, how much resistance there is to approving treatment, and what competition might do to reduce drug prices. In the longer term, the curative powers of these drugs should drive hepatitis C prevalence, and therefore spending, to very low levels.
Note 1

Estimates from the American Community Survey show that the percentage of the population with health insurance grew by 2.8 percentage points between 2013 and 2014.
Note 2

One difference is the lag between when the sale (to an intermediary) is recorded by the company and when the final sale is made to the consumer. Another is that retail markups are included in health spending but not in company sales. Finally, prescription drug sales in the national health accounts refer only to retail sales, while company sales include sales to hospitals and physicians for drugs administered during the health encounter and whose costs are embedded in the hospital or physician bill.The vast majority of hepatitis C drugs are sold at retail.
Note 3

For further analysis of prescription drug spending, see: R. Kamal and G. Claxton, October 30, 2015, “Recent trends in prescription drug spending and what to look out for in coming years,” Peterson-Kaiser Health System Tracker.
Note 4

The leveling off we observe in company sales in 2015 runs counter to a recent report stating that Medicare spending on these drugs grew by $4.5 billion in 2015. Some of this may be due to lags between company sales to intermediaries and the subsequent sales to Medicare patients. We have not built lags into our analysis, and this could mean we have somewhat overstated the 2014 impact and understated the 2015 impact.
tags: harvoni, hepatitis c, prescription drugs, sovaldi, spending growth

Source

http://healthaffairs.org/blog/2015/12/07/the-impact-of-new-hepatitis-c-drugs-on-national-health-spending/