February 13, 2012

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Journal of Hepatology Feb 12 2012

Christophe Moreno, Thomas Berg, Tawesak Tanwandee, Satawat Thongsawat, Hans Van Vlierberghe, Stefan Zeuzem, Oliver Lenz, Monika Peeters, Vanitha Sekar, Goedele De Smedt

1Department of Gastroenterology and Hepatopancreatology, Hopital Erasme, Universite Libre de Bruxelles, Brussels, Belgium
2Department of Hepatology, Clinic of Gastroenterology and Rheumatology, University Clinic Leipzig, Leipzig, Germany
3Department of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand 4Chiang Mai University, Chiang Mai, Thailand
5Department of Gastroenterology and Hepatology, Ghent University Hospital, Ghent, Belgium
6Department of Medicine I, J.W. Goethe University Hospital, Frankfurt, Germany
7Tibotec, Beerse, Belgium

"Novel agents for the treatment of genotypes 4 to 6 would be advantageous as SVR rates are low [17,31], and together with genotype 1 these groups are considered 'difficult to treat'. Antiviral activity against genotypes 4 to 6 observed in this study suggests that TMC435 could provide a clinical benefit, particularly for patients infected with genotypes 4 and 6. For genotype 5, the mean decline in HCV RNA from baseline over the 7 day monotherapy period was slightly lower compared to genotypes 4 and 6, suggesting that the TMC435 activity was somewhat lower in this group. Due to SVR rates of ≥70% in genotype 2 and 3 patients following treatment with PegIFN/RBV, there is perhaps a less urgent need for novel agents to treat infection with these genotypes, though patients who do not respond to treatment could benefit from regimens including novel DAAs. TMC435 showed antiviral activity in 3/6 patients infected with genotype 2, and no activity against genotype 3. Of note, given the high sequence variability between the different genotypes and subtypes, further work is ongoing to investigate the role of naturally occurring baseline polymorphism in variation 1 in virologic response, and to fully characterise viral variants observed in patients with viral breakthrough."

"In spite of study limitations outlined above, the results of this phase IIa study in 37 treatment-naïve patients suggest that this investigational agent may be a future candidate for treatment of infection with HCV genotypes 4, 5 and 6, and potentially particular subtypes of genotype 2."

Abstract

Background & Aims

TMC435 is an investigational, once-daily, oral NS3/4A protease inhibitor currently in phase III development for the treatment of hepatitis C virus (HCV) infection. Phase I and II studies in patients infected with HCV genotype 1 have demonstrated that TMC435 is generally well tolerated, has a pharmacokinetic profile that supports once daily dosing, and demonstrates potent antiviral activity. This phase IIa study (TMC435-C202; NCT00812331) was conducted to investigate the antiviral activity, safety, tolerability, and pharmacokinetics of TMC435 in treatment-naïve patients infected with HCV genotypes 2 to 6.

Methods

The study consisted of 7 days of monotherapy with TMC435 (200 mg once daily). Patients could begin treatment with pegylated interferon/ribavirin from Day 8 with a follow-up period up to Days 37-42.

Results

Thirty-seven patients were enrolled in Germany, Belgium and Thailand. For the primary endpoint at Day 8, the mean (±standard error) change in plasma HCV ribonucleic acid (log10 IU/mL) from baseline was greatest for genotypes 6 (-4.35±0.29) and 4 (-3.52±0.43), followed by genotypes 2 (-2.73±0.71) and 5 (-2.19±0.39). No antiviral activity was evident for genotype 3. Viral breakthrough occurred in six patients during the monotherapy phase and in six additional patients during PegIFN/RBV-only period. All adverse events were mild or moderate and there were no discontinuations during the TMC435 monotherapy period.

Conclusions

The results of this phase IIa proof-of-concept trial provide evidence that TMC435 has a spectrum of activity against multiple HCV genotypes, except for genotype 3. In this study, TMC435 was generally safe and well tolerated.

Introduction

The hepatitis C virus (HCV) is a single-stranded RNA virus and one of the leading causes of chronic liver disease worldwide [1]. It is estimated that 130-170 million people are infected with HCV, constituting 2.2-3.0% of the global population [2]. HCV can be classified into six major genotypes based on sequence divergence of 30% [3]. Genotype 1 has a broad global distribution [4-10]. Genotype 2 is prevalent in North America, Europe and Japan (subtypes 2a and 2b), Northern Italy (2c) [11], and Western Africa [12]. Genotype 3 is noted for its wide distribution among intravenous drug users in a number of countries [13-15], and is also predominant in India and Pakistan [16]. Genotype 4 is responsible for >90% of HCV infections in Egypt, where it is associated with the re-use of needles during mass administration of parenteral antischistosomal therapy until the 1980s, and is also prevalent in other regions of the Middle East and sub-Saharan Africa [3,17-19]. In Europe, its prevalence has recently increased due to immigration and transmission between intravenous drug users [17]. Genotype 5 is found most commonly in South Africa, as well as in four regions in France, Spain, Syria and Belgium [3,17]. Genotype 6 is found in South East Asia and surrounding regions where overall HCV prevalence is high [3,20,21]. Recommended treatment for patients infected with non-genotype 1 HCV is pegylated interferon and ribavirin (PegIFN/RBV). Treatment for different genotypes differs slightly, with PegIFN alpha (α) plus weight-based RBV for 48 weeks recommended for genotypes 1, 4 and 6, and PegIFNα plus low-dose RBV (800 mg) for 24 weeks for genotypes 2 and 3 [22-27]. Of note, given the recent approval of the HCV NS3/4A protease inhibitors boceprevir and telaprevir [28,29] the standard of care for genotype 1 is expected to change [27,30].

Sustained virologic resp 1 onse (SVR, undetectable HCV RNA in patient plasma 24 weeks after treatment end) is achieved in approximately 75% of patients infected with genotypes 2 and 3 [31]. Rates with genotypes 4, 5 or 6 are 43-70% [17]. Furthermore, PegIFN/RBV therapy is poorly tolerated in some patients. In randomised trials of PegIFNα/RBV, influenza-like and neuropsychiatric symptoms occurred in up to 24-64% of patients [22,32], adverse events (AEs) led to study discontinuation in 14-32% and dose reduction in 11-42% [22,32], and anemia or neutropenia led to dose reduction in 9-22% and 18-20%, respectively [22,32].

It is, therefore, clear that novel direct-acting antivirals (DAAs) are required to address issues of sub-optimal efficacy, poor tolerability and compliance failures, and to reduce treatment duration.Boceprevir and telaprevir have demonstrated significantly improved virologic outcomes in both treatment-naïve and -experienced genotype 1 patients [28,29]. However, their thrice daily dosing schedule (with food) and increased rates of AEs including anemia and rash, in comparison to PegIFN/RBV, suggest that there is still room for improvement. Furthermore, activity in other genotypes has not been extensively investigated.

TMC435 is an investigational, once-daily oral NS3/4A protease inhibitor currently in phase III clinical development for the treatment of HCV infection. Phase I and II trials in patients infected with HCV genotype 1 have demonstrated that TMC435 is generally well tolerated, has a pharmacokinetic profile that supports once daily (q.d.) dosing, and demonstrates potent antiviral activity and efficacy [33-36]. Given sub-optimal responses to existing treatment options and the worldwide distribution of genotype 1, this genotype is the current focus of the TMC435 clinical development program. A phase IIa study (TMC435-C202; NCT00812331) was also performed in patients infected 1 with genotypes 2 to 6 to assess the antiviral activity of TMC435 against these genotypes. Data from biochemical protease assays available before the study start indicated that TMC435 is a potent NS3/4A protease inhibitor in genotypes 2, 4, 5 and 6, with a medium inhibitory concentration (IC50) of <13 nM for all HCV NS3/4A enzymes tested [37]. IC50 for genotype 3 was 37 nM [37]. This study assessed antiviral activity, safety, tolerability and pharmacokinetics of TMC435 (200 mg q.d. administered for 7 days as monotherapy) in treatment-naïve patients infected with HCV genotypes 2 to 6.

Results

Patient demographics and baseline characteristics

The trial was conducted from 3 March to 18 November 2009. A total of 37 patients were enrolled (Fig. 1) across Germany, Belgium and Thailand. No major differences in demographics and baseline disease characteristics were observed, except that all patients with genotype 6 were Asian, and median age of patients with genotype 5 was higher compared with other genotype cohorts (Supplementary Table 1). Overall, 11% of patients in the study had cirrhosis (Metavir score F4), including patients infected with genotype 2 (n=1), genotype 3 (n=1) and genotype 5 (n=2). Multiple subtypes were included in cohorts for genotype 2 (2b, 2c, 2i, 2k), genotype 4 (4, 4c, 4d) and genotype 6 (6a, 6c-l, 6j, 6n) (Table 1).

Following the 7-day TMC435 treatment period, all patients started PegIFN/RBV therapy. Thirty-one patients began PegIFN/RBV on Day 8 or 9, whereas one patient with genotype 3 and five with genotype 6 began PegIFN/RBV after Day 9.
Antiviral activity

Change in plasma HCV RNA from baseline

An initial rapid decline in HCV RNA from baseline at Day 3 of TMC435 monotherapy was evident for all patients infected with HCV genotypes 4 to 6, and for three out of six patients with genotype 2 (Figs 2 and 3). Of these three patients, those who responded were infected with subtypes 2b and 2c.

At Day 3, the mean (±standard error [SE]) change from baseline in plasma HCV RNA (log10 IU/mL) was greatest for genotypes 6 (-3.57±0.197) and 4 (-3.43±0.167), followed by genotypes 5 (2.71±0.335) and 2 (-2.02±0.625). For the primary endpoint at Day 8, the mean (±SE) change from baseline was greatest for genotypes 6 (-4.35±0.29) and 4 (-3.52±0.43) cohorts, followed by genotypes 2 (-2.73±0.71) and 5 (-2.19±0.39) (Figs 1 and 2). However, no clear antiviral activity was evident for patients with genotype 3 (change from baseline at day 3 and 8; Figs 2 and 3). At Day 8, four patients (two patients with genotype 4 and two with genotype 6) achieved HCV RNA levels of <25 IU/mL detectable. No patients achieved HCV RNA levels of <25 IU/mL undetectable at Day 8.

From Day 8 to the end of follow-up 2 (Days 37-42), when patients had been treated with PegIFN/RBV only for up to 35 days, mean HCV RNA declined in all genotypes, with the exception of genotype 4 where mean HCV RNA began to increase (Fig. 2). By the end of follow-up 2, HCV RNA change from baseline was -5.19±0.37 for genotype 2, -4.96±0.37 for genotype 3, -3.26±0.77 for genotype 4, -3.89±0.60 for genotype 5 and -5.46±0.32 for genotype 6. HCV RNA was <25 IU/mL detectable for 5/6 (83%), 6/8 (75%), 5/8 (63%), 2/7 (29%) and 7/8 (88%) of patients with genotypes 2, 3, 4, 5 and 6, respectively. HCV RNA <25 IU/mL undetectable was achieved by 5/6 (83%), 3/8 (38%), 5/8 (63%), 1/7 (14%) and 6/8 (75%) of patients with genotypes 2, 3, 4, 5 and 6, respectively.

Viral breakthrough

One patient infected with genotype 3, two with genotype 4 and three with genotype 5 experienced viral breakthrough during the TMC435 monotherapy period. In addition, another 6 patients experienced viral breakthrough during the follow-up period, whilst being treated with PegIFN/RBV only, suggesting lack of activity of PegIFN/RBV treatment in these patients: two infected with genotype 2, one with genotype 3, one with genotype 4, and two with genotype 6.

In genotype 2 and 3-infected patients with viral breakthrough, viral sequencing did not reveal emerging mutations. However, for most genotype 4, 5, and 6 patients with viral breakthrough, emerging mutations were detected. The most frequently observed emerging mutations in the NS3 protease domain were R155K, D168E and D168V (data not shown).

Safety and tolerability

The type and incidence of AEs (all Grade 1-2) during the 7-day TMC435 monotherapy period was similar across all cohorts in the study (Table 2) and the most common AEs were influenza-like illness and headache. There were no clinically relevant changes in laboratory parameters, and no clinically significant findings in terms of vital signs, physical examinations or ECG recordings. Mild elevations in bilirubin (total, direct and indirect) levels were observed in all cohorts. Mean change from baseline to Day 8 was 1.38 μmol/L (95% confidence interval [CI] 0.88, 1.87) for direct and 3.06 μmol/L (95% CI 1.51, 4.61) for indirect bilirubin. These returned to baseline value after completion of TMC435 dosing and were not associated with clinical symptoms or elevations in aspartate aminotransferase, alanine aminotransferase or alkaline phosphatase (Supplementary Table 2). On Day 8 (after the 7-day dosing period with TMC435 was completed), one patient experienced an SAE of Grade 1 ileitis not considered related to TMC435 therapy. The patient 1 discontinued from the study and recovered after 4 days. No other discontinuations due to AEs occurred during the trial.

Pharmacokinetics

Steady-state TMC435 C0h, Cmin, Cmax and AUC24h were similar for the genotype 4, 5 and 6 cohorts, though lower values were observed for the genotype 2 and 3 cohorts with the lowest values in the genotype 3 cohort (Supplementary Table 3). Tmax 6 values were generally similar for all genotype cohorts (Supplementary Table 3). Exposure did not differ according to race or cirrhosis (data not shown).

Discussion

The results of this phase IIa proof-of-concept trial provide evidence that TMC435 has a broad spectrum of activity against multiple HCV genotypes, with the exception of genotype 3.

Monotherapy with oral TMC435 200 mg q.d. for 7 days was associated with potent antiviral activity in patients infected with genotypes 2, 4, 5 and 6. The greatest antiviral activity was observed among patients infected with genotypes 4 and 6, followed by genotypes 2 and 5. Of note, potent activity was observed in three patients with genotype 2, with limited activity observed in the other three patients in this cohort. No antiviral activity was seen against genotype 3. Viral breakthrough (protocol defined: plasma HCV RNA increase >1 log10 IU/mL from the lowest reached, or >100 IU/mL in patients whose HCV RNA was previously <25 IU/mL undetectable or detectable) occurred in six patients during the monotherapy phase. Six additional patients had viral breakthrough during the PegIFN/RBV-only period, and could therefore be considered viral rebound after cessation of treatment with TMC435. In this study, TMC435 was generally safe and well tolerated. All AEs were mild to moderate and during the 7-day period of TMC435 monotherapy there were no discontinuations or untoward changes in biochemical parameters. This is the first study in which an HCV protease inhibitor has demonstrated antiviral activity in genotypes 5 and 6. Furthermore, data for genotypes 2, 3 and 4 are limited for other investigational agents. In a phase IIa study, telaprevir combined with PegIFN/RBV showed substantial activity against genotype 2, modest activity against genotype 4 [38] and limited activity against genotype 3 [39]. Of note, unlike nucleotide inhibitors, NS3 protease inhibitors are generally 1 considered to have limited activity in certain genotypes. However, results of this study suggest that the protease inhibitor TMC435 could be efficacious across multiple genotypes, though additional clinical data are required to provide further support.

A limitation of this study relates to the high subtype diversity in genotypes 2, 4 and 6 (such diversity is not observed in genotypes 3 and 5). Not all subtypes were included in this study and the number of patients per subtype was sometimes limited. Importantly, no difference in efficacy between included subtypes was observed in genotypes 4 or 6. The difference in antiviral activity between patients infected with genotype 2 may be caused by the different subtypes, as HCV RNA change from baseline at Day 3 in patients infected with 2b and 2c was -3.19 to -3.61- log10 IU/mL, compared with -0.26 to -0.99 in those infected with 2, 2k and 2i. In addition to this limitation, the sample size in each cohort was relatively small. It should also be noted that a TMC435 dose of 200 mg q.d. was administered in this trial, whereas a dose of 150 mg is currently in phase III development.

The lack of antiviral activity against genotype 3, compared with other genotypes, is consistent with the lower IC50 value of TMC435 against a genotype 3 isolate in an in vitro biochemical assay [37]. It is suggested that this may be due to the presence of a naturally occurring D168Q polymorphism at baseline, which is present in most genotype 3a isolates known to date and was observed in all genotype 3a patients included in this study (data not shown). A D168Q mutation alone has been shown to reduce TMC435 activity in a genotype 1b replicon assay by >700 fold [40]. TMC435 exposure (as indicated by C0h, Cmin, Cmax and AUC24h) was lower in genotypes 2 and 3 than in genotypes 4, 5 and 6, though it is suggested that this may be due to chance due to the small number of patients 1 in this study. Furthermore, as mean AUC values were <3 fold lower in the genotype 3 cohort compared to genotype 6 but in vitro susceptibility of genotype 3 isolates was >700 fold lower, the lower exposure observed in this cohort does not explain the lack of antiviral activity against genotype 3.

In patients infected with HCV genotype 4, mean change from baseline in HCV RNA began to increase after Day 5. Prior to Day 8, this was driven by two patients who experienced viral breakthrough under TMC435 monotherapy. The further increase in HCV RNA after Day 8 is thought to reflect a lack of response to PegIFN/RBV. Novel agents for the treatment of genotypes 4 to 6 would be advantageous as SVR rates are low [17,31], and together with genotype 1 these groups are considered 'difficult to treat'. Antiviral activity against genotypes 4 to 6 observed in this study suggests that TMC435 could provide a clinical benefit, particularly for patients infected with genotypes 4 and 6. For genotype 5, the mean decline in HCV RNA from baseline over the 7 day monotherapy period was slightly lower compared to genotypes 4 and 6, suggesting that the TMC435 activity was somewhat lower in this group. Due to SVR rates of ≥70% in genotype 2 and 3 patients following treatment with PegIFN/RBV, there is perhaps a less urgent need for novel agents to treat infection with these genotypes, though patients who do not respond to treatment could benefit from regimens including novel DAAs. TMC435 showed antiviral activity in 3/6 patients infected with genotype 2, and no activity against genotype 3. Of note, given the high sequence variability between the different genotypes and subtypes, further work is ongoing to investigate the role of naturally occurring baseline polymorphism in variation 1 in virologic response, and to fully characterise viral variants observed in patients with viral breakthrough.

In spite of study limitations outlined above, the results of this phase IIa study in 37 treatment-naïve patients suggest that this investigational agent may be a future candidate for treatment of infection with HCV genotypes 4, 5 and 6, and potentially particular subtypes of genotype 2.

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Ohio_State_Med_Cntr_16_13

By Staff Editor
Feb 13, 2012 - 2:00:01 PM

(HealthNewsDigest.com) - COLUMBUS, Ohio – New research conducted at The Ohio State University’s Wexner Medical Center suggests an alternate form of natural vitamin E delays the progression of disease in patients awaiting liver transplantation, the only definitive therapy that reduces a patient’s morbidity, mortality and improves their quality of life. The study shows, for the first time, successful delivery of the vitamin – administered orally – to vital human organs such as the brain, heart, liver, skin and fatty tissue.

Researchers at Ohio State’s Wexner Medical Center initially sought to measure levels of vitamin E tocopherol (TCP) and vitamin E tocotrienol (TE) in tissue and vital organs of patients with end stage liver disease. The data displayed a significant increase in TE levels in the bloodstream and tissue of study participants who received daily oral supplements of TE.

“This work is the first to show oral supplements of tocotrienol are being transported to the vital organs of patients,” says Chandan K. Sen, associate dean for translational and applied research in The Ohio State University College of Medicine. “This is exciting evidence for patients at high risk for stroke because our previous work identified low levels of TE to be protective against stroke-induced damage to the brain. Findings of this current research are equally excited for patients on the liver transplant list as it increases their chances of receiving a new liver, and therefore survival.”

Earlier research published by Dr. Sen and colleagues at Ohio State’s Medical Center proved tocotrienol a safe and neuroprotective nutrient, which minimizes stroke-related damage to the brain. “We also showed in previous studies that TE can be part of a regular diet and keeps the brain enriched and better prepared to defend itself,” added Sen, also vice chair for research in Ohio State's Department of Surgery.

For this recent study, published in the February issue of Journal of Nutrition, researchers studied blood and tissue samples from 80 participants. One cohort involved healthy patients who received oral TE or TCP supplements. Vitamin E levels found in tissue were measured in healthy participants after 12 weeks of receiving oral supplementation. Healthy adult participants were selected for this study because they could receive oral supplements for a designated period of time, whereas the other cohort was bound by surgery schedules.

In another cohort, adult surgical patients were randomized and received daily oral supplements of either TE or TCP. Concentration levels of both vitamin E sources were measured in vital organs, including: cardiac muscle from heart transplant patients with end stage heart failure; liver from transplant patients with end stage liver disease; abdominal fatty tissue from morbidly obese patients undergoing reconstructive plastic surgery; and brain tissue from epileptic patients.

The results showed oral supplementation of tocotrienol significantly increased the levels of the nutrient found in blood, skin, fatty tissue, the brain, cardiac muscle and the liver. Tocotrienol was delivered to the human brains of study participants at levels found to be neuroprotective in earlier stroke-related research.

Oral administration of tocotrienol also lowered the model for end stage liver disease (MELD) score in 50 percent of the patients who received TE supplements, while only 20 percent of patients who received TCP supplements experienced a reduction in their MELD score. MELD score refers to a clinical scoring system used to determine the severity of chronic liver disease and assess the priority and need for liver transplant allocation.

The tocotrienol form of vitamin E is available as a nutritional supplement in American supermarkets. One of the richest and healthiest food sources for TE is palm oil, which contains an abundance of the nutrient. It contains zero tans fat content and is also a popular component of a typical Southeast Asian diet. Other foods containing TE include rice, bran, oat, barley, and wheat germ.

Sen says he and colleagues are planning a much larger Phase II clinical trial testing the safety and effectiveness of tocotrienol against stroke and end stage liver disease in humans.

Along with Sen, other Ohio State researchers involved in the study were Viren Patel, Cameron Rink, Gayle M.Gordillo, Savita Khanna, Urmila Gnyawali, Sashwati Roy, Bassel Shneker, Kasturi Ganesh, Gary Phillips, J. Layne Moore, Atom Sarkar, Robert Kirkpatrick, Elmahdi A. Elkhammas, Emily Klatte, Michael Miller, Michael S. Firstenberg and E. Antonio Chiocca. Kalanithi Nesaretnam, from the Malaysian Palm Oil Board’s Food Technology and Nutrition Unit, also participated in the research.

The research was supported by a grant awarded by the National Institutes of Health. In addition, the Malaysian Palm Oil Board – an institution of Government of Malaysia – funded the study.

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Larger belly linked to memory problems in people with HIV

Public release date: 13-Feb-2012

Contact: Rachel Seroka
rseroka@aan.com
651-695-2738
American Academy of Neurology

ST. PAUL, Minn. – A larger waistline may be linked to an increased risk of decreased mental functioning in people infected with the AIDS virus HIV, according to research published in the February 14, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology.

"Interestingly, bigger waistlines were linked to decreased mental functioning more than was general obesity," said study author J. Allen McCutchan, MD, MSc, of the University of California, San Diego. "This is important because certain anti-HIV drugs cause weight gain in the center of the body that is most dramatic in the abdomen, neck, chest and breasts."

The study was performed in 130 HIV positive people from six clinics. Participants were around the age of 46 with HIV infection for an average of 13 years. Most participants were taking combinations of anti-HIV drugs called antiretroviral therapy. Impaired mental functions such as poor memory and concentration, called neurocognitive impairment (NCI), was diagnosed in 40 percent of study participants.

People with NCI had waist circumferences of an average of 39 inches, compared to 35 inches for those without memory difficulties. NCI was also linked to older age, a longer time living with HIV and diabetes in people older than 55 years. For example, five times as many people with memory problems also had diabetes compared to those with no memory problems (15 percent compared to 3 percent).

"Avoiding those HIV drugs that cause larger waistlines might protect or help to reverse NCI," said McCutchan. "We don't know if central obesity is causing NCI directly or is just a marker for exposure to a more direct cause such as anti-HIV drugs. People with HIV should talk to their doctors before considering changes in their anti-HIV medications."

###

The study was supported by the National Institutes of Health.

To learn more about cognitive impairment, visit http://www.aan.com/patients.

The American Academy of Neurology, an association of more than 25,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer's disease, stroke, migraine, multiple sclerosis, brain injury, Parkinson's disease and epilepsy.

For more information about the American Academy of Neurology, visit http://www.aan.com or find us on Facebook, Twitter, Google+ and YouTube.

Media Contacts:
Rachel Seroka, rseroka@aan.com, (651) 695-2738
Angela Babb, APR, ababb@aan.com, (651) 695-2789

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Hepatitis Testing Day – May 19

img-cdcLogoHeader

CDC’s Know More Hepatitis campaign was officially announced on World Hepatitis Day, July 28th, 2011 at a special White House event to release the U.S. Department of Health & Human Services’ Combating the Silent Epidemic of Viral Hepatitis: Action Plan for the Prevention, Care & Treatment of Viral Hepatitis. The plan calls for a national education campaign to educate people about viral hepatitis and encourage people to get tested. As part of this educational initiative, May 19th has been designated as a national “Hepatitis Testing Day” in the United States.

The CDC will use the first ever Hepatitis Testing Day on May 19, 2012 as an opportunity to remind health care providers and the public who should be tested for chronic viral hepatitis. Millions of Americans have chronic viral hepatitis; most of them do not know they are infected.

Resources

HHS Plan

Combating the Silent Epidemic of Viral Hepatitis: Action Plan for the Prevention, Care & Treatment of Viral Hepatitis
http://www.hhs.gov/ash/initiatives/hepatitis/actionplan_viralhepatitis2011.pdf  [PDF - 84 pages]

Chronic Hepatitis B

Resources for Health Professionals
http://www.cdc.gov/hepatitis/HBV/TestingChronic.htm

Patient information about testing
http://www.cdc.gov/hepatitis/HBV/PDFs/HepBAtRisk.pdf   [PDF - 2 pages]

Chronic Hepatitis C

Resources for Health Professionals
http://www.cdc.gov/hepatitis/HCV/Management.htm

Patient information about testing
http://www.cdc.gov/hepatitis/HCV/PDFs/HepCTesting-Diagnosis.pdf   [PDF - 2 pages]

Twitter

Twitter: Follow CDC’s Division of Viral Hepatitis @cdchep.
Share information on Twitter about how you’re taking action for Hepatitis Testing Day, use the hashtag #HTD.

Theme Contest

Theme – submit your ideas for this year’s theme to hepatitis@cdc.gov.

Know More Hepatitis Campaign

Learn more about CDC’s upcoming campaign at
http://www.cdc.gov/hepatitis/KnowMoreHepatitis.htm

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