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Hepatitis C May Increase Deaths from Both Liver-Related and Other Diseases
http://www.idsociety.org/2012_HepC_Death_Increase/
"Researchers found increased mortality from liver- and non-liver-related diseases—including cancers of the esophagus, prostate, and thyroid, as well as circulatory and renal diseases—among those infected with HCV. Mortality was higher in HCV-infected participants with detectable serum levels of HCV RNA, indicating they had active infections; subjects with previous infections who only had HCV antibodies, but not HCV RNA, in their blood did not have increased mortality on follow-up."
On-Chip Ultra-Thin Layer Chromatography and Surface Enhanced Raman Spectroscopy
http://pubs.rsc.org/en/content/articlelanding/2012/lc/c2lc40221a
Preventing The Spread Of Bacteria By Modifying Surfaces (From Medical News Today)
23 Jul 2012
Researchers at the Institute for Agrobiotechnology (a mixed research centre set up by the Public University of Navarre, the CSIC-National Scientific Research Council, and the Government of Navarre) are designing, by means of laser application, nanostructured reliefs on surfaces so that they acquire antibacterial properties and are more resistant to the formation of bacterial biofilms. The authors of the research say that in the preliminary tests carried out so far with the bacteria Staphylococcus aureus a reduction in the region of 65-70% has been confirmed in the adhesion of bacteria.
Apart from selecting the materials that best inhibit the adhesion of bacteria, the research is also looking into other aspects. These include the resistance to disinfectants of the bacteria adhered to nanostructured surfaces, how these surfaces retain their properties during prolonged use, or the behaviour of the bacteria on the surface of biomaterials. Topographical patterns that encourage the adhesion of bacteria will also be identified.
The authors anticipate that the applications coming out of this research will have an impact on a broad field from surgical material treated in advance using laser (prostheses, catheters) to water or aquaculture tanks with surfaces that prevent the adhesion of bacteria.
Preventing the creation of a bacterial biofilm
Bacterial biofilm is created when bacteria grow adhered to a surface and are surrounded by a matrix that they themselves produce and which makes them more resistant. "Bacteria," according to the head researcher Jaione Valle-Turrillas, "stick to any surface; it can be the skin, internal organs, surfaces of materials, etc. and they produce this biofilm, a kind of film that makes them more resistant to antibiotic treatments, disinfectants, etc." Biofilms can be found in nature (bacteria adhered to the surfaces of stones in rivers), in our own bodies (intestinal and buccal flora), in filters and pipes, in water tanks, on farms (milking equipment) and in the clinical ambit (prostheses, surgical catheters), etc.
The Biofilms Microbianos research group of the Institute of Agrobiotechnology is working mainly with two bacteria: S. aureus and Salmonella. Various lines of research focusing on the prevention or elimination of biofilms and ranging from the development of vaccines to research into biofilm dispersants, are being pursued in the laboratory, and right now, research is being done in this project to modify surfaces to prevent the formation of biofilm.
"Thanks to DLIP [Direct Laser Interference Patterning] technology, a surface is interfered with and modified using different laser beams on a nanometric scale," explains Jaione Valle. "You can create different patterns and drawings, of different periodicity, from nanometres to micra. We've already tested different surfaces and have found a material and a pattern that will stop the bacteria from sticking to the surface; it does not eliminate them completely, but the reduction is between 65 and 70%."
First of all, the surface is modified by means of laser and then the bacteria are applied to see how they produce the biofilm and in what quantity. Various materials have been used during the tests, and it has been seen how the number of bacteria and the production of biofilm diminish according to bacteria type and type of structure applied to the surface.
To quantify the reduction in the number of bacteria and the extent to which they remain adhered to the nanostructured surface, the researchers used a reagent (Alamar Blue), which emits fluorescence when it comes into contact with live bacteria. "This reaction is measured in a fluorometer so that the more bacteria there are, the greater the fluorescence that is produced," points out the researcher. The problem is that this technique cannot differentiate when the adhesion differences are small. That is why we are now using another method: we collect all the bacteria that have stuck to the surface, we sow them in a culture medium and count the number of colonies; it's more laborious, but it's also much more reliable."
The project "Development and evaluation of antibacterial properties of surfaces with nanostructured reliefs generated by Direct Laser Interference Patterning (DLIP)" is scheduled to run for three years, and will be brought to a conclusion at the end of December 2013. It is being run in collaboration with the German R+D centre Institut Fraunhofer for Material and Beam Technology, which has provided the laser technology to generate the reliefs on the surfaces. The IdAB-Agrobiotechnology Institute, for its part, is conducting the study and experimental tests. The total budget, funded by the Department of Innovation, Companies and Employment of the Government of Navarre, amounts to 179,800 euros.
References:
Elhuyar Fundazioa
Citations:
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MLA
Elhuyar Fundazioa. "Preventing The Spread Of Bacteria By Modifying Surfaces." Medical News Today. MediLexicon, Intl., 23 Jul. 2012. Web.
24 Jul. 2012. <http://www.medicalnewstoday.com/releases/248130.php>
APA
Elhuyar Fundazioa. (2012, July 23). "Preventing The Spread Of Bacteria By Modifying Surfaces." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/248130.php.
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NIH Leadership at the XIX International AIDS Conference
Posted: 17 Jul 2012 02:30 AM PDT
By Jack Whitescarver, Ph.D., NIH Associate Director for AIDS Research and Director, NIH Office of AIDS Research
Dr. Jack Whitescarver
The hosting of the XIX International AIDS Conference in our nation’s capital, Washington, DC, is a tremendous opportunity to reflect on how AIDS has affected the United States, and how the United States has worked to reduce the impact of the epidemic in the U.S. and around the world.
The first cases of what we would come to know as AIDS were identified here more than thirty years ago. It was soon apparent, however, that AIDS would touch the entire world. The United States was the birthplace of the community-based response to this epidemic, and to activist efforts that helped push HIV/AIDS to the top of the global health agenda.
The United States is also the global leader in supporting research to reduce the epidemic and to make the prospect of an AIDS-free generation a reality. Research at the National Institutes of Health has:
¦Led to the co-discovery of HIV and development of the first blood test for HIV, which has allowed the diagnosis of the infection and essentially eliminated transfusion-related HIV transmission
¦Defined the pathogenesis and structure of HIV, paving the way for effective treatments, prevention tools, and diagnostics
¦Established the scientific basis for effective antiretroviral therapies and drug regimens
¦Demonstrated interventions that significantly reduce the risk of mother-to-child HIV transmission
¦Demonstrated prevention strategies including treatment as prevention, medical male circumcision, syringe exchange, pre-exposure prophylaxis and key behavioral HIV prevention strategies
¦Led to breakthroughs in the search for microbicides and an HIV vaccine
¦Outlined potential strategies to eliminate viral reservoirs in the body, leading, for the first time, to research aimed at a possible AIDS cure.Investments in AIDS research have also led to critical advances that benefit research on the diagnosis, treatment and prevention of dozens of other serious diseases as well, from cancers to Alzheimer’s disease to new strategies to improve maternal and child health.
The results of this national commitment to AIDS research are evident. More than a third of the 3,000-plus abstracts at AIDS 2012 will be presented by researchers supported by the National Institutes of Health.
Research progress against HIV has been inspiring, but the challenges ahead are also significant. Today, NIH is prioritizing critical research to: improve existing HIV prevention tools and develop new prevention technologies, including a vaccine and microbicide; develop better, less toxic treatments for HIV and its co-infections, malignancies and other complications; reduce the epidemic’s impact on the most vulnerable populations; and characterize HIV reservoirs, with the goal of developing drugs or other approaches to eliminate or control HIV infection.
All of this work will be on display at AIDS 2012. In addition to presenting cutting-edge research throughout the conference, NIH leaders will be featured in several high-level sessions, including an opening day satellite, New Frontiers in NIH AIDS Research, (Sunday, 22 July 11:15 am; Session Room 6), which will outline NIH AIDS research findings and achievements to date and priorities moving forward. Panelists for this interactive satellite will include NIH Director Dr. Francis Collins, NIAID Director Dr. Anthony S. Fauci, NIDA Director Dr. Nora Volkow, and other research leaders from across the NIH. The program for New Frontiers in NIH AIDS Research is available here .
On Monday, July 23, NIAID Director Dr. Anthony S. Fauci will give an opening plenary entitled, Ending the HIV Epidemic: From Scientific Advances to Public Health Implementation (8:30 am; session room 1). NIH Director Dr. Francis Collins will moderate a panel entitled, The Science of HIV: What Lies Ahead (Monday, 23 July 1:00 pm; session room 5). Dr. Collins will also speak at and moderate a session on The Future of Genomics in HIV Medicine (Wednesday, 25 July, 11:00 am; session room 1).
Other NIH satellites include No “Getting to Zero AIDS” Without Scale-Up of Stigma Reduction on Sunday 22 July at 1:30 p.m. in Session Room 8 and HIV and Aging: A Global Perspective on Research, Care and Prevention on Monday 23 July at 6:30 p.m. in Session Room 6.
The NIH exhibit (Booth #72 in the U.S. Pavilion) at AIDS 2012 will include dozens of “Meet the Expert” sessions featuring researchers from the National Institute on Drug Abuse, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Cancer Institute, National Institute of Mental Health, Fogarty International Center and many of the other 27 NIH Institutes and Centers that are conduct and support AIDS research. A full schedule of NIH “Meet the Expert” sessions, fact sheets, and other conference materials are available at http://aids2012.oar.nih.gov.
AIDS 2012 provides a unique opportunity to examine how far we have come in our response to this global pandemic, and how far we have yet to go. NIH-supported researchers on the NIH campus and at more than 3,000 universities, medical schools and other research institutions around the world will continue working on the many research challenges associated with HIV, until the day when we all live in a world without AIDS.
Interview with U. Schneider, CEO of Freenius in todays Wall St. J.
http://www.bing.com/search?q=WSJ+schneider+fresinus&src=IE-SearchBox&Form=IE8SRC&adlt=strict
Something applicable to AEMD -
WSJ - The US Govt reined in dialysis payments, a big chunk of your services business, beginning last year. How is Fresinus coping?
Mr. Schneider - We have been finding ways to provide the same quality with lesser costs. Maybe a few years down the road...you take a more holistic view of the patient: Don't just treat the one disease that you'rebeing paid for, but rather, pay attention to how that blends in with what some of the other doctors are doing. That has medical advantages. You're creating savings.
Loss of protein SPDEF allows prostate cancer cells to gain foothold at possible sites of metastasis
Presence of SPDEF may mark prostate cancers unable to metastasize and so not requiring treatment; manipulation of SPDEF may make cancer cells unable to metastasize
Prostate cancer doesn't kill in the prostate — it's the disease's metastasis to other tissues that can be fatal. A University of Colorado Cancer Center study published this week in the Journal of Biological Chemistry shows that prostate cancer cells containing the protein SPDEF continue to grow at the same pace as their SPDEF- cousins, but that these SPDEF+ cells are unable to survive at possible sites of metastasis.
"It's as if these cancer cells with SPDEF can't chew into distant tissue and so are unable to make new homes," says Hari Koul, PhD, investigator at the CU Cancer Center and director of urology research at the University of Colorado School of Medicine, the study's senior author.
Koul and his group discovered the homesteading power of cancer cells that have lost SPDEF by introducing a gene into cells that makes them glow in the presence of a dye, and then introducing them into the bloodstream of animal models. Cells without SPDEF traveled through the blood and successfully attached to tissue, surviving and so fluorescing many weeks later when dye was introduced. However, cells with SPDEF flowed through the blood but were unable to successfully establish new colonies and so soon died out.
In fact, the protein SPDEF doesn't act directly to allow cells to attach at possible metastasis sites, but is a transcription factor that controls the production (or lack thereof) of two other proteins MMP9 and MMP13. These two downstream proteins work to break down tissue, like a dissolving agent – they are the cleaning crew that clears space for new and different growth, and in the case of prostate cancer metastasis they chip the tissue footholds that cancer cells need to create micrometastases.
"Given that MMP9 and perhaps MMP13 are also involved in metastasis of several other cancers including lung, ovarian, breast and colon to name a few, our findings could potentially have far-reaching consequences outside prostate cancer," adds Koul
The group's continuing work points in two directions.
"First, we hope that the presence of SPDEF could help doctors recognize prostate cancers that don't require treatment." If future studies confirm the group's initial findings, the presence of SPDEF could predict prostate cancers that are unable to metastasize and so unable to kill. These cancers could be left to run their course without the use of treatments that sometimes carry difficult side effects.
"And second," Koul says, "we hope to regulate expression of this protein to remove prostate cancers' ability to metastasize."
Koul points to small molecules, gene therapy or nanodelivery as possible mechanisms for introducing SPDEF into cells that lack the protein.
"With this discovery we have opened a hopeful door into a future in which prostate and potentially other cancers are unable to metastasize," Koul says.
The multifaceted exosome: Biogenesis, role in normal and aberrant cellular function, and frontiers for pharmacological and biomarker opportunities
http://www.sciencedirect.com/science/article/pii/S0006295211009531
The Roles of Tumor-Derived Exosomes in Cancer Pathogenesis
http://www.hindawi.com/journals/cdi/2011/842849/
The protumorigenic potential of tumor-derived exosomes in cancer patients is supported by the observations that in patients with breast or ovarian cancer, the level of circulating exosomes and exosomes with tumor markers is much higher than nonmalignant individuals and increases with tumor progression [29, 105], and that exosomes isolated from the sera of patients with oral or ovarian cancer can impair T lymphocytes function and induce their apoptosis [54, 106]. Therefore, it has been proposed that removing immunosuppressive tumor-derived exosomes from the blood circulation of a cancer patient would improve antitumor immune response and delay the progression and spread of malignancy. A novel hollow-fiber cartridge (Hemopurifier) system which is able to selectively deplete circulating virus using a lectin-based resin with high affinity for glycosylated viral surface proteins was developed by the San Diego biotechnology company Aethlon Medical [107]. Effective removal of HIV particles has been demonstrated [108–110] and this system has become an attractive device for depletion of exosomes, which have a size similar to viral particles and are also highly glycosylated on their membrane proteins. The selective removal of exosomes can be enhanced by attaching antibodies against exosome surface proteins onto the resin of the cartridge. However, there are still technical barriers in how to carefully distinguish tumor-derived from nontumor-derived exosomes and concerns such as the physiological outcome of removing all exosome-like vesicles in the blood.
Potential New Treatment For Metastatic Colon Cancer (From Medical news Today)
12 Jul 2012
How does a tumor cell set up a signaling pathway in order to metastasize? Scientists at Technische Universitat Munchen's (TUM) Klinikum rechts der Isar and Helmholtz Zentrum Munchen have made a significant discovery in this area by studying colon cancer. They have learned that the tumor cells release certain proteins known as chemokines. In the case of metastatic colon cancer cells, the chemokine concerned is CCL2. The CCL2 chemokine docks on to the cells of the inner blood vessel walls (endothelial cells) and activates the corresponding receptor (CCR2 receptor). This connection makes the endothelial cells permeable - creating a clear path for the tumor cells.
Professor Mathias Heikenwälder of TUM's Institute of Virology explains that the tumor cells use a clever trick to migrate: "The tumor cells outwit the endothelial cells by emitting a signal used by healthy cells." To date, research has mainly focused on macrophage cells attracted by the chemokines of the tumors. "By understanding the role of chemokine receptors in relation to endothelial cells we have potentially uncovered a brand new approach to cancer treatment," says Heikenwälder.
"Measuring the number of chemokines could allow us to draw clear conclusions on the likely spread of a primary tumor to other organs and predict the risk of metastasis in patients," continues Heikenwälder. "Furthermore, the option of blocking the chemokine receptor CCR2 at the endothelial cells gives healthcare professionals a new way of preventing metastases both before and following an operation."
For their research, the scientists used colon cancer tissue and colon cancer cell lines from mice and humans. The next steps will involve studying the findings in greater detail and examining how the new concept can be transferred to other types of cancer.
--------------------------------------------------------------------------------
References:
Original publication:
Monika Wolf et al., 2012. Endothelial CCR2 signaling induced by colon carcinoma cells enables extravasation via the JAK2-Stat5 and p38MAPK pathway, Cancer Cell, 07/2012.
Technische Universitaet Muenchen
--------------------------------------------------------------------------------
Citations:
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MLA
Technische Universitaet Muenchen. "Potential New Treatment For Metastatic Colon Cancer." Medical News Today. MediLexicon, Intl., 12 Jul. 2012. Web.
14 Jul. 2012. <http://www.medicalnewstoday.com/releases/247689.php> APA
Technische Universitaet Muenchen. (2012, July 12). "Potential New Treatment For Metastatic Colon Cancer." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/247689.php.
Please note: If no author information is provided, the source is cited instead.
Paul Duffin
Research Scientist at Aethlon Medical, Inc
http://www.linkedin.com/profile/view?id=49794418&pid=13491300&authType=name&authToken=wkMN&trk=pbmap
Research Scientist at Aethlon Medical
http://www.linkedin.com/profile/view?id=13491300&pid=49426355&authType=name&authToken=jfbQ&trk=pbmap
Research Scientist at Aethlon Medical, Inc
http://www.linkedin.com/in/roylefkowitz
Reduction in Hepatic Inflammation Is Associated With Less Fibrosis Progression and Fewer Clinical Outcomes in Advanced Hepatitis C (Actually this is a link from Nature - just could not access it in Nature. Again, this article just shows how effective the HP can be in reducing long term complications of Hep C and that too more quickly, and effeciently, then anything available in the market currently by decreasing the viral load significantly in a few days.)
Chihiro Morishima, Mitchell L Shiffman, Jules L Dienstag, Karen L Lindsay, Gyongyi Szabo, Gregory T Everson, Anna S Lok, Adrian M Di Bisceglie, Marc G Ghany, Deepa Naishadham, Timothy R Morgan, Elizabeth C Wright and for the HALT-C Trial Group15
Abstract
CONCLUSIONS:
Reduced hepatic inflammation (measured 1.5 and 3.5 years after randomization) was associated with profound virological suppression during lead-in treatment with full-dose peginterferon/ribavirin and with decreased fibrosis progression and clinical outcomes, independent of randomized treatment.
OBJECTIVES:
During the Hepatitis C Antiviral Long-term Treatment against Cirrhosis Trial, 3.5 years of maintenance peginterferon-alfa-2a therapy did not affect liver fibrosis progression or clinical outcomes among 1,050 previous interferon nonresponders with advanced fibrosis or cirrhosis. We investigated whether reduced hepatic inflammation was associated with clinical benefit in 834 patients with a baseline and follow-up biopsy 1.5 years after randomization to peginterferon or observation.
The American Journal of Gastroenterology , (12 June 2012) | doi:10.1038/ajg.2012.137
yielddude - Thank you. eom
FoMD discovery increases understanding of how bacteria spread
http://www.med.ualberta.ca/Home/NewsEvents/News/article.cfm?ID=2427
Nanosphere Receives FDA Authorization to Market its Gram-Positive Blood Culture Test
http://www.nanosphere.us/news/nanosphere-receives-fda-authorization-market-its-gram-positive-blood-culture-test
April 2012, InTech launches New Scientific Peer-reviewed Journal Exosomics
http://www.intechopen.com/news/article/intech-launches-new-scientific-peer-reviewed-journal-exosomics
Emerging Role of Neuronal Exosomes in the Central Nervous System
http://www.frontiersin.org/Membrane_Physiology_and_Biophysics/10.3389/fphys.2012.00145/abstract
Bronchoalveolar lavage fluid exosomes contribute to cytokine and leukotriene production in allergic asthma.
http://www.ncbi.nlm.nih.gov/pubmed/22620679
Diagnostic Applications of Exosomes
http://selectbiosciences.com/conferences/index.aspx?conf=DAE2012
Plasma exosomes can deliver exogenous short interfering RNA to monocytes and lymphocytes
http://nar.oxfordjournals.org/content/early/2012/05/22/nar.gks463
Pregnancy-linked miRNA Cluster in Exosomes May Spark Adenomas
http://epigenie.com/pregnancy-linked-mirna-cluster-in-exosomes-may-spark-adenomas/
Aethlon Medical Announces Notice of Allowance of U.S. Patent Application Covering a Medical Device to Remove Microvesicular Particles, Including Exosomes
http://aethlonmedical.investorroom.com/2012-06-19-Aethlon-Medical-Announces-Notice-of-Allowance-of-U.S.-Patent-Application-Covering-a-Medical-Device-to-Remove-Microvesicular-Particles-Including-Exosomes
Circulating tumour cells in non-metastatic breast cancer: a prospective study
The identification of circulating tumour cells correlate with poor prognosis in metastatic breast cancer, but there are few data describing the importance of circulating tumour cells in patients with non-metastatic disease. Our aim was to establish if circulating tumour cells predicted worse outcome in patients with non-metastatic breast cancer.
Interpretation
The presence of one or more circulating tumour cells predicted early recurrence and decreased overall survival in chemonaive patients with non-metastatic breast cancer. These results suggest that assessment of circulating tumour cells might provide important prognostic information in these patients.
Prof Anthony Lucci MD a , Carolyn S Hall PhD a, Ashutosh K Lodhi MD a, Anirban Bhattacharyya MD a, Amber E Anderson BS a, Lianchun Xiao MS c, Isabelle Bedrosian MD a, Prof Henry M Kuerer MD a, Prof Savitri Krishnamurthy MD b
Funding
Society of Surgical Oncology, Morgan Welch Inflammatory Breast Cancer Program, The University of Texas MD Anderson Cancer Center, and the State of Texas Rare and Aggressive Breast Cancer Research Program.
Scientists Receive Grant to Pioneer Personalized Medicine Approach to Melanoma
http://www.scripps.edu/newsandviews/e_20111219/schork.html
A quarter of L.A. homeless have hepatitis C; half don't know it
http://www.latimes.com/news/science/sciencenow/la-sci-sn-homeless-hepatitis-c-20120612,0,3158331.story
Addressing Viral Hepatitis at the Department of Veterans Affairs
Posted: 30 May 2012 09:53 AM PDT
By Janet M. Durfee, RN, MSN, APRN, Deputy Chief Consultant, Clinical Public Health, Office of Public Health, U.S. Department of Veterans Affairs
The U.S. Department of Veterans Affairs (VA) recognizes viral hepatitis as a highly prevalent chronic disease among Veterans in VA care. VA continues to be proactive in addressing viral hepatitis, and is actively taking part in the implementation of the Action Plan for the Prevention, Care and Treatment of Viral Hepatitis, which is led by the U.S. Department of Health and Human Services (HHS).
Chronic viral hepatitis is a major public health problem in the United States because of the millions of persons who are chronically infected and because of the potential for untreated viral hepatitis to progress to cirrhosis, liver cancer, and other life-threatening conditions. Hepatitis C virus (HCV) and hepatitis B virus (HBV) are the major causes of chronic viral hepatitis in the U.S.
In the late 1990s, VA characterized HCV as a significant health problem requiring early detection and has taken a number of steps to address the issue. In 1998, the VA’s Under Secretary for Health issued an Information Letter outlining standards for provider evaluation and testing for HCV in the Veterans Health Administration (VHA). Subsequently, VA conducted a nationwide surveillance activity, testing over 26,000 Veterans for HCV in March 1999. The testing revealed a prevalence rate of 6.6% with a wide variation by geography and era of military service. In 2000, the VA’s Under Secretary for Health designated additional funding to be distributed across VHA for outreach, testing, counseling, and treating Veterans with hepatitis C.
By 2002, a VHA National Viral Hepatitis Program had been established, and HCV screening and testing guidelines were published. All Veterans were to be screened for risk factors for HCV and tested if they had a previous or ongoing risk, or if they simply asked to be tested. Testing was also offered to those who served during the Vietnam-era and to those with a history of alcohol abuse or dependence due to the high prevalence of HCV in these populations.
VHA’s external peer review program data show that rates of testing at-risk patients are very high. In fiscal year 2005, based on a sample of 16,000 Veterans receiving care at VA medical facilities, 98% had been screened for HCV risk factors and 93% of the approximately 8,000 veterans with risk factors had been tested for HCV.
Since 2002, VHA’s National Viral Hepatitis Program has used a comprehensive population health-based approach to HCV care for Veterans, emphasizing access to high-quality clinical care and testing, counseling, patient and provider education, and quality improvement efforts. Clinical reminders in the electronic medical record have been found to be an effective way to trigger clinicians to screen Veterans for HCV risk and offer testing when appropriate. Clinical reminders were made widely available and have been successfully used to improve screening efforts.
The VA’s National Hepatitis C Program accomplishments have included extensive screening of at-risk Veterans, early and broad access to anti-viral therapy such as HCV protease inhibitors, and improvements in the management of other co-existing conditions such as depression, alcohol misuse and other substance use disorders.
VHA is the single largest HCV care provider in the U.S., with a seroprevalence rate three times that of the general U.S. population; currently there are over 170,000 Veterans in VHA care with confirmed chronic HCV. The gradual progression of HCV in affected Veterans over a period of decades has led to increasing numbers of patients with cirrhosis, end-stage liver disease, and liver cancer. Of note, over the last ten years, the number of HCV-infected Veterans in care diagnosed with cirrhosis has tripled to over 25,000, while over the same time period the cumulative number of HCV-infected Veterans diagnosed with liver cancer has increased by ten-fold.
It has also been recognized that Veterans are at higher risk for exposure to HBV than the general U.S. population. Current VHA recommendations for HBV screening are that at risk Veterans should be offered testing for HBV, and linked to care if found to be positive. Better understanding of the prevalence of HBV in the Veteran population, the number of Veterans who have been tested, and missed opportunities for testing, will help guide appropriate HBV screening/testing recommendations in the future.
VHA is committed to identifying Veterans at risk for viral hepatitis and linking those who are found to be positive to high quality care within our healthcare system. VHA will continue to work side by side with colleagues from HHS and other federal and non-federal partners to coordinate and implement a number of strategies to promote awareness around viral hepatitis and to ensure high quality of care to those who are living with these chronic diseases.
Ms. Durfee is the Department of Veterans Affairs representative on the cross-agency work group coordinating implementation of the Action Plan for the Prevention Care and Treatment of Viral Hepatitis.