Thursday, August 19, 2010, 11:00
A groundsman at the University of Bath who had a liver transplant seven years ago will be preparing the site for the British Transplant Games.
Mike Pooley, from Bathwick, was given a new lease of life after his transplant on New Year's Eve in 2003.
Now the 49-year-old is one of the groundsmen who will be preparing the university site for the transplant athletes taking part in the games.
Mr Pooley was first admitted to hospital with pains that were initially put down to gall stones.
But doctors discovered something else was wrong and he spent five weeks in the Royal United Hospital having tests.
The results showed that Mr Pooley had been accidently given hepatitis C in a blood transfusion when he was 14, and as a result his liver was now failing.
Mr Pooley said: "In those days they didn't screen the blood as carefully, and I was given blood with hepatitis C.
"My liver was not able to cope anymore and so I needed a transplant."
After the diagnosis he was sent to the Queen Elizabeth Hospital in Birmingham for assessment, before being put on the transplant list.
Mr Pooley then had to spend the next month waiting for the call, along with his wife Susan.
He said: "It was quite a worrying time, for both me and my family.
"I was told that I had to keep my phone on me at all times in case a suitable liver became available.
"Every time my phone rang my heart was in my mouth as I thought it was the call.
"I had to have a bag packed, as I had to be ready to leave with an hour's notice.
"I tried to keep things as normal as possible but it was hard, as you never know when you will get the call and have to go to hospital.
"It was really hard for Susan as there was nothing she could do to help."
After the operation Mr Pooley faced a long road to recovery.
He spent weeks in bed, with just walking to the toilet being a huge effort, and it took nine months before he was fit enough to go back to work. Now Mr Pooley is fighting fit, and feels like he has been given a second chance.
He said: "I feel brilliant now, and am back to full health.
"It feels like I have been given a second chance of life, and I can now live it to the full.
"Having my transplant on New Year's Eve meant that I started the new year with new hope.
"Organ donation really is the gift of life.
"It is important that people sign up to the organ donor register, as there are so many people who are waiting for transplants.
"Others may not be as lucky as I was."
The British Transplant Games take place during the next four days at various locations throughout the city.
For more information, see our games schedule.
Source
August 19, 2010
Taiwan, Canada develop new method for hepatitis C detection
2010/08/19 17:05:03
Taipei, Aug. 19 (CNA) Researchers from Taiwan and Canada have developed a new microscopy technology that allows for low-cost, portable imaging of the hepatitis C virus, making it more convenient to conduct screenings, a Taiwanese researcher said Thursday.
Under the sponsorship of Taiwan's National Science Council, the Industrial Technology Research Institute and National Research Council (NRC) Canada, an international research team recently combined technologies developed in Canada and Taiwan to create a screening device that can be carried in one hand.
Led by Kao Fu-jen, a professor at National Yang-Ming University, and Albert Stolow and John Pezacki from NRC Canada, the team jointly developed the high-sensitivity imaging system by re-engineering a DVD reading and writing head so that it can detect optical signals including fluorescence and tiny vibrations from a technique called coherent anti-Stokes Raman scattering.
The device creates images from cell samples that allow researchers to determine whether the hepatitis C virus is present. The development is expected to help sharply increase the efficiency of the diagnosis of chronic hepatitis C, Kao said in a press release.
The size of the device allows for point-of-care testing, which is diagnostic testing at or near the site of patient care.
According to Kao, the hepatitis C virus is spread through contact with infected blood, and about 170 million worldwide are infected with it. Currently, there is no vaccine against the virus.
How the hepatitis C virus harms the livers of long-term carriers is still unknown, but the risk of people with hepatitis C contracting liver cancer is 10 times higher than for ordinary people, the press release said.
The goal of the collaboration project between Taiwan and Canada is to develop real-time, unobtrusive and efficient biomedical detection methods and instruments for widespread application for hepatitis C and other infectious diseases, it said.
(By Y.L. Kao)
Source
Community-based Screening for Hepatocellular Carcinoma in Elderly Residents in a Hepatitis B and C Endemic Area
Yen-Chieh Huang MD 1,2,†, Chih-Fang Huang MD 1,3,†, Kuo-Chin Chang MD 4,5, Shu-Fen Hung RN 4, Jing-Houng Wang MD 4,5, Chao-Hung Hung MD 4,5, Chien-Hung Chen MD, PhD 4,5, Po-Lin Tseng MD 4,5, Kwong-Ming Kee MD 4,5, Yi-Hao Yen MD 4,5, Pei-Shan Tsai RN, MPH 6, Chin-Chen Tsai MD 6, Sheng-Nan Lu MD, MPH, PhD 4,5,*
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06476.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Author Information
1 Departments of Family Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan;
2 Departments of Family Medicine, Antai Tian-Sheng Memorial Hospital, Tongkang, Pingtung, Taiwan;
3 Graduate Institute of Natural Healing Science, College of Science and Technology, Nanhua University, Chiayi, Taiwan;
4 Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan;
5 School of Medicine, Chang Gung University College of Medicine, Taoyuan, Taiwan; and
6 Health Center of Zihguan Township, Kaohsiung, Taiwan.
*Correspondence: Sheng-Nan Lu MD, MPH, PhD,
*Correspondence: Sheng-Nan Lu M.D., M.P.H, Ph.D., Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, 123 Ta Pei Road, Niao Sung 833, Kaohsiung, Taiwan. Tel: +886-7-731-7123 ext. 8301 Fax: +886-7-732-2402 E-mail: juten@ms17.hinet.netc
†* Yen-Chieh Huang, MD and Chih-Fang Huang, MD contributed equally to this study and manuscript
Publication History
Accepted manuscript online: 17 AUG 2010 12:20PM EST
Received date: 08-Jan 2010 Accepted date: 01-Aug-2010
Keywords:
alpha-fetoprotein (AFP);platelet count;community screening;hepatitis C virus (HCV);hepatocellular carcinoma (HCC)
ABSTRACT
Background and Aim: To elucidate a reasonable model and efficacy of hepatocellular carcinoma (HCC) screening on an elderly population.
METHODS: A two-staged HCC screening was conducted in an HCV-endemic area. Firstly, participants underwent blood tests for hepatitis B surface antigen (HBsAg), anti-Hepatitis C (HCV) antibody, serum fetoprotein (AFP), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and platelet count, and subjects who were abnormal for any of the 6 markers were enrolled for 2nd stage ultrasonography. Suspected cases were referred for confirmation. HCC cases were followed for 4 years. All subjects were linked to national mortality and cancer register databases to identify newly developed HCC 30 months after screening.
RESULTS: 461 men and 541 women were screened for HCC, with 15.1% of them testing positive for HBsAg and 44.3% positive for anti-HCV. Among them, 619 (61.8%) met the criteria of ultrasonographic screening; 527 (85.1%) responded, and 16 confirmed HCC (M/F = 8/8, 68.8 ± 8.0 years) cases were detected. All tumor diameters were less than 5cm and 6 of them were less than 2cm. AFP and thrombocytopenia were two independent predictive factors of HCC. Overall survival rates of detected cases were 93.8% and 56.3% in years 1, and 4, respectively. The only good prognostic predictor was “underwent curative treatment”. Besides, another 7 developed HCC and 5 of them were with either thrombocytopenia or AFP elevation.
CONCLUSIONS: Under economical consideration, AFP and platelet count should be feasible screening markers of risk identification. Early detection and prompt treatment resulted in good prognosis of an aged population.
Source
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06476.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Author Information
1 Departments of Family Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan;
2 Departments of Family Medicine, Antai Tian-Sheng Memorial Hospital, Tongkang, Pingtung, Taiwan;
3 Graduate Institute of Natural Healing Science, College of Science and Technology, Nanhua University, Chiayi, Taiwan;
4 Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan;
5 School of Medicine, Chang Gung University College of Medicine, Taoyuan, Taiwan; and
6 Health Center of Zihguan Township, Kaohsiung, Taiwan.
*Correspondence: Sheng-Nan Lu MD, MPH, PhD,
*Correspondence: Sheng-Nan Lu M.D., M.P.H, Ph.D., Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, 123 Ta Pei Road, Niao Sung 833, Kaohsiung, Taiwan. Tel: +886-7-731-7123 ext. 8301 Fax: +886-7-732-2402 E-mail: juten@ms17.hinet.netc
†* Yen-Chieh Huang, MD and Chih-Fang Huang, MD contributed equally to this study and manuscript
Publication History
Accepted manuscript online: 17 AUG 2010 12:20PM EST
Received date: 08-Jan 2010 Accepted date: 01-Aug-2010
Keywords:
alpha-fetoprotein (AFP);platelet count;community screening;hepatitis C virus (HCV);hepatocellular carcinoma (HCC)
ABSTRACT
Background and Aim: To elucidate a reasonable model and efficacy of hepatocellular carcinoma (HCC) screening on an elderly population.
METHODS: A two-staged HCC screening was conducted in an HCV-endemic area. Firstly, participants underwent blood tests for hepatitis B surface antigen (HBsAg), anti-Hepatitis C (HCV) antibody, serum fetoprotein (AFP), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and platelet count, and subjects who were abnormal for any of the 6 markers were enrolled for 2nd stage ultrasonography. Suspected cases were referred for confirmation. HCC cases were followed for 4 years. All subjects were linked to national mortality and cancer register databases to identify newly developed HCC 30 months after screening.
RESULTS: 461 men and 541 women were screened for HCC, with 15.1% of them testing positive for HBsAg and 44.3% positive for anti-HCV. Among them, 619 (61.8%) met the criteria of ultrasonographic screening; 527 (85.1%) responded, and 16 confirmed HCC (M/F = 8/8, 68.8 ± 8.0 years) cases were detected. All tumor diameters were less than 5cm and 6 of them were less than 2cm. AFP and thrombocytopenia were two independent predictive factors of HCC. Overall survival rates of detected cases were 93.8% and 56.3% in years 1, and 4, respectively. The only good prognostic predictor was “underwent curative treatment”. Besides, another 7 developed HCC and 5 of them were with either thrombocytopenia or AFP elevation.
CONCLUSIONS: Under economical consideration, AFP and platelet count should be feasible screening markers of risk identification. Early detection and prompt treatment resulted in good prognosis of an aged population.
Source
Hepatitis Delta: Seek and Ye Shall Find
The Journal of Infectious Diseases 2010;202:822–824
© 2010 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2010/20206-0002$15.00
DOI: 10.1086/655809
EDITORIAL COMMENTARY
Scott D. Holmberg and John W. Ward
Division of Viral Hepatitis, National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia
Received 10 June 2010; accepted 10 June 2010; electronically published 11 August 2010.
(See the article by Kucirka et al, on pages 845–852.)
Reprints or correspondence: Dr Scott Holmberg, Division of Viral Hepatitis, Centers for Disease Control and Prevention, MS G‐37, 1600 Clifton Rd NE, Atlanta, GA 30333 (sdh1@cdc.gov).
Hepatitis delta virus (HDV) was discovered in 1977 by Rizzetto and colleagues [1], and—as he expressed it 30 years later—HDV “would have possibly died away as another odd antigenic subtype” of hepatitis B virus (HBV) had it not been for an international collaboration among investigators from Turin, Italy, the National Institutes of Health, and Georgetown University [2]. Chimpanzee experiments demonstrated that the delta antigen, rather than being a component of HBV, was its own defective form that required HBV for its infection and replication, a “virus’s virus.” Dual HBV‐HDV infection was quickly recognized to have worldwide distribution, to be associated with more severe and rapidly progressive hepatitis, and to be especially resistant to treatment.
In the past few decades, remarkable strides in understanding the complex interplay between HBV and HDV at the molecular level have been achieved [3]. But many mysteries remain when these insights are applied to human disease, in which levels of HBV DNA and HDV RNA may fluctuate in relation to each other or not at all in individual patients [4]. Furthermore, some of the groups with HBV‐HDV coinfection, such as injection drug users, also have hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfections. Unrecognized coinfections with these viruses—ie, before the availability of reliable screening tests for HIV (1985) or HCV (1992)—may have confounded early observations of the clinical course of patients with HBV‐HDV coinfections. Indeed, one of the helpful observations of the article by Kucirka and colleagues [5] in the current issue of the Journal is the still very high infection rate found among a sample of injection drug users from 2005 to 2006 when tested for HCV (92%) or HIV (38%).
When first examined in the 1980s, it was clear that there were areas of high endemicity, especially in the Amazon Basin, Eastern Europe, and several regions of Africa and the Middle East, of intermediate endemicity in Southern Europe, and low endemicity in Northern Europe and North America. Over the next 10 years, there was a dramatic decline in HDV infection prevalence in Europe, considered to be the result of declining numbers of hepatitis B surface antigen (HBsAg)–positive injection drug users, vaccination for hepatitis B, and the effects of public health interventions related to the HIV epidemic. However, it has been noted that no additional declines in HDV have been observed in the past decade [6], perhaps because of the influx of immigrants dually infected with HBV‐HDV to the United States from highly endemic areas.
In the United States, several early studies in the late 1970s through the mid‐1980s showed antibodies to delta antigen in HBsAg‐positive blood donors (3.8%) in 1979 [7], persons with acute and chronic hepatitis B infection in Los Angeles (homosexual men, 15%; injection drug users, 22%) [8, 9], and developmentally disabled persons in Illinois state facilities (30%) [10]. Relatively high rates of HDV prevalence were seen in injection drug users in New York City (67%) [11]. Furthermore, a retrospective study of serum collected from 1972 to 1975 from drug‐using HBsAg‐positive patients at several Veterans Administration facilities at US locales showed that 42% had antibodies to delta antigen [12].
Few outbreaks of HDV in the United States (and these among injection drug users) have been detected and examined in the last 25 years. Over a 21‐month period between 1983 and 1985, Lettau and colleagues [13] investigated an outbreak of severe hepatitis among injection drug users in western Massachusetts associated with dual delta and hepatitis B viruses. Another 15 years elapsed before there was detection and investigation of a similar outbreak among injection drug users in Pierce County, Washington, by the Centers for Disease Control and Prevention (CDC) [14]. However, aside from these outbreaks, in recent years only about 6–10 cases of “confirmed” infections with HDV have been reported to the CDC from various states each year. Thus, it is quite difficult to know what is happening with HDV without specific reports such as the one by Kucirka and colleagues [5].
So, where is HDV headed in this country? On the one hand, there has been a gratifying decrease in prevalence of HDV in Asia and Europe, attributed to the expanding rate of hepatitis B vaccination activities over the last 20 years. We should expect a similar decline in HDV in the United States as we progressively remove its “host virus.” Or should we?
Previous outbreaks have shown a high prevalence of HDV coinfection among HBV‐infected injection drug users—54% in Massachusetts and 34.5% in Washington state—whereas HBV‐infected non‐drug users in those outbreaks had much lower HDV coinfection rates (9% in both states) [13, 14]. Indeed, a study of female prostitutes showed that, among those who used intravenous drugs, HBV and HDV coinfection rates were 21%, whereas the HBV‐infected women who were not injection drug users had an HDV coinfection rate of 6% [15]. Similarly, early analyses demonstrated high hepatitis D infection rates among hemophilic men (19%) [16] but not in gay men (0%) [17].
One unifying explanation for these numbers is that HDV, like other bloodborne pathogens, may be more efficiently transmitted parenterally than by sexual contact. If this is the case, perhaps we should not expect the same drop‐off in HDV coinfection rates as seen between 1980 and 2000 in places as diverse as Italy, Japan, Taiwan, and Turkey [6], where proportionately more HBV infection is acquired perinatally, sexually, or horizontally (in households), and proportionately less as the result of injection drug use. This hypothesis would also fit the current observation, albeit from a small sample, that fully 50% of HBV‐infected injection drug users in Baltimore in 2005–2006 had concurrent HDV infection.
Trends in HDV‐HBV coinfection and morbidity are contingent on successes in hepatitis B vaccination and screening. Approximately 15% of persons reported with acute hepatitis B infection in the United States are injection drug users [18]. In 1991, the United States adopted a vaccine‐based strategy to eliminate HBV transmission, with subsequent gains in immunization coverage particularly among children and adolescents [19]. Despite a long‐standing recommendation for hepatitis B vaccination, hepatitis B vaccine coverage among injection drug users remains low. As a result, 20%–70% of injection drug users have evidence of past or current HBV infection, with many lacking serologic evidence of hepatitis B vaccination and thus greater susceptibility to HBV [20]. When barriers to vaccination such as vaccine costs are removed, drug treatment centers successfully integrate hepatitis B vaccination as a routine service and greatly increase the numbers of injection drug users vaccinated [21]. To increase vaccination of injection drug users, the CDC recommends hepatitis B vaccination for all adults in correctional institutions and drug abuse prevention and treatment clinics; the CDC and other federal resources are available to defray the cost of vaccine purchase for these settings [19, 21]. In addition to vaccination, all injection drug users should be screened for HBV [19]. An estimated 3%–11% of injection drug users have chronic HBV infection, and many remain undiagnosed, reflecting inadequate HBV screening services in settings such as drug treatment programs [22]. Management of persons with chronic hepatitis B infection should include interventions to reduce behavioral risks of HBV transmission and referral for medical care. The data from Kucirka et al [5] highlight the importance of HDV testing as a component of clinical management for persons with chronic HBV infection. Unfortunately, few data are available to monitor whether injection drug users are receiving recommended hepatitis B prevention and care services.
Indeed, the study by Kucirka and colleagues [5] is not only useful as a marker of where we are in the US hepatitis D epidemic, but of where we are not. Very few studies such as this can or will be done, simply because there are too few cohorts of injection drug users currently being followed in the United States. The HIV/AIDS epidemic stimulated federal agencies such as the National Institute on Drug Abuse and (then) the CDC to establish studies of HIV and, eventually, of hepatitis virus infections among large populations of injection drug user in several cities. At present, the Baltimore study (ALIVE [AIDS Link to Intravenous Experience]) as reported here is the longest running US cohort study; in fact, its predecessor, “Man ALIVE,” predated the AIDS epidemic but is now one of few such studies left. This stymies our understanding not only of HDV and the “carrier” HBV epidemics in the United States but also of the continuing HCV and, to a lesser extent, HIV epidemics. Thus, we should expect our understanding of the evolution of the HDV epidemic—as well as HBV, HCV, and HIV epidemics—in this country, especially in one of the transmission risk groups most affected, to remain spotty and infrequent. It is a truism to write that “more research is needed,” but there is probably no more fitting comment on the implications of the research of the companion paper in this issue of the Journal.
References
•1.Rizzetto M, Canese MG, Gerin JL, et al. Immunofluorescence detection of new antigen‐antibody system (delta/anti‐delta) associated to hepatitis B virus in liver and serum of HBsAg carriers. Gut 1977;18(12):997–1003.
•2.Rizzetto M. Hepatitis D: thirty years after [review]. J Hepatol 2009;50:1043–1050.
•3.Taylor JM. Hepatitis delta virus. Virology 2006;344:71–76.
•4.Wedemeyer H. Re‐emerging interest in hepatitis delta: new insights into the dynamic interplay between HBV and HDV. J Hepatol 2010;52(5):627–629.
•5.Kucirka LM, Farzadegan H, Field JJ, et al. Prevalence, correlates, and viral dynamics of hepatitis delta among injection drug users. J Infect Dis 2010;202(6):845–852 (in this issue).
•6.Rizzetto M. Hepatitis D: the comeback? Liver Int 2009;29:140–142.
•7.Nath N, Mushawar IK, Fang CT, Berberian H, Dodd RY. Antibodies to delta antigen in asymptomatic hepatitis B surface antigen‐reactive blood donors in the United States and their association with other markers of hepatitis B virus. Am J Epidemiol 1985;122:218–225.
•8.De Cock KM, Niland JC, Lu HP, et al. Experience with human immunodeficiency virus infection in patients with hepatitis B virus and hepatitis delta virus infections in Los Angeles, 1977–1985. Am J Epidemiol 1988;127:1250–1260.
•9.Govindarajan S, Kanel GC, Peters RL. Prevalence of delta‐antibody among chronic hepatitis B virus infected patients in the Los Angeles area: its correlation with liver biopsy diagnosis. Gastroenterology 1983;85:160–162.
•10.Hershow RC, Chomel BB, Graham DR, et al. Hepatitis D virus infection in Illinois state facilities or the developmentally disabled: epidemiology and clinical manifestations. Ann Intern Med 1989;110:779–785.
•11.Novick DM, Farci P, Croxson TS, et al. Hepatitis D virus and human immunodeficiency virus antibodies in parenteral drug abusers who are hepatitis B surface antigen positive. J Infect Dis 1988;158:795–803.
•12.Ponzetto A, Seeff LB, Buskell‐Bales Z, et al. Hepatitis B markers in United States drug addicts with special emphasis on the delta hepatitis virus. Hepatology 1984;4:1111–1115.
•13.Lettau LA, McCarthy JG, Smith MH, et al. Outbreak of severe hepatitis due to delta and hepatitis B viruses in parenteral drug abusers and their contacts. N Engl J Med 1987;317:1256–1262.
•14.Bialek SR, Bower WA, Mottram K, et al. Risk factors for hepatitis B in an outbreak of hepatitis B and D among injection drug users. J Urban Health 2005;82:468–478.
•15.Rosenblum L, Darrow W, Witte J, et al. Sexual practices in the transmission of hepatitis B virus and prevalence of hepatitis delta virus infection in female prostitutes in the United States. JAMA 1992;267:2477–2481.
•16.Troisi CL, Hollinger FB, Hoots WK, et al. A multicenter study of viral hepatitis in a United States hemophilic population. Blood 1993;81:412–418.
•17.Weisfuse IB, Hadler SC, Fields HA, et al. Delta hepatitis in homosexual men in the United States. Hepatology 1989;9:872–874.
•18.Daniels D, Grytdal S, Wasley A. Surveillance for acute hepatitis—United States, 2007. MMWR 2009;58(Suppl 3):1–27.
•19.Centers for Disease Control and Prevention. A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States: recommendations of the Advisory Committee on Immunization Practices (ACIP). Part II: immunization of adults. MMWR Morb Mortal Wkly Rep 2006;55:1–33.
•20.Centers for Disease Control and Prevention. Recommendations for identification and public health management of persons with chronic hepatitis B virus infection. MMWR Morb Mortal Wkly Rep 2008;57:1–20.
•21.Kresina TF, Hoffman K, Lubran R, Clark HW. Integrating hepatitis services into substance abuse treatment programs: new initiatives from SAMHSA. Public Health Rep 2007;122(Suppl 2):96–98.
•22.Substance Abuse and Mental Health Services Administration, Center for Substance Abuse Treatment. Screening for infectious diseases among substance abusers (Treatment Improvement Protocol [TIP] Series 6; DHHS publication [SMA] 95–3060). Rockville, Maryland: NIH, 1993. http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=hssamhsatip&part=A25461. Accessed 19 April 2010.
Potential conflicts of interest: none reported.
Source
© 2010 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2010/20206-0002$15.00
DOI: 10.1086/655809
EDITORIAL COMMENTARY
Scott D. Holmberg and John W. Ward
Division of Viral Hepatitis, National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia
Received 10 June 2010; accepted 10 June 2010; electronically published 11 August 2010.
(See the article by Kucirka et al, on pages 845–852.)
Reprints or correspondence: Dr Scott Holmberg, Division of Viral Hepatitis, Centers for Disease Control and Prevention, MS G‐37, 1600 Clifton Rd NE, Atlanta, GA 30333 (sdh1@cdc.gov).
Hepatitis delta virus (HDV) was discovered in 1977 by Rizzetto and colleagues [1], and—as he expressed it 30 years later—HDV “would have possibly died away as another odd antigenic subtype” of hepatitis B virus (HBV) had it not been for an international collaboration among investigators from Turin, Italy, the National Institutes of Health, and Georgetown University [2]. Chimpanzee experiments demonstrated that the delta antigen, rather than being a component of HBV, was its own defective form that required HBV for its infection and replication, a “virus’s virus.” Dual HBV‐HDV infection was quickly recognized to have worldwide distribution, to be associated with more severe and rapidly progressive hepatitis, and to be especially resistant to treatment.
In the past few decades, remarkable strides in understanding the complex interplay between HBV and HDV at the molecular level have been achieved [3]. But many mysteries remain when these insights are applied to human disease, in which levels of HBV DNA and HDV RNA may fluctuate in relation to each other or not at all in individual patients [4]. Furthermore, some of the groups with HBV‐HDV coinfection, such as injection drug users, also have hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfections. Unrecognized coinfections with these viruses—ie, before the availability of reliable screening tests for HIV (1985) or HCV (1992)—may have confounded early observations of the clinical course of patients with HBV‐HDV coinfections. Indeed, one of the helpful observations of the article by Kucirka and colleagues [5] in the current issue of the Journal is the still very high infection rate found among a sample of injection drug users from 2005 to 2006 when tested for HCV (92%) or HIV (38%).
When first examined in the 1980s, it was clear that there were areas of high endemicity, especially in the Amazon Basin, Eastern Europe, and several regions of Africa and the Middle East, of intermediate endemicity in Southern Europe, and low endemicity in Northern Europe and North America. Over the next 10 years, there was a dramatic decline in HDV infection prevalence in Europe, considered to be the result of declining numbers of hepatitis B surface antigen (HBsAg)–positive injection drug users, vaccination for hepatitis B, and the effects of public health interventions related to the HIV epidemic. However, it has been noted that no additional declines in HDV have been observed in the past decade [6], perhaps because of the influx of immigrants dually infected with HBV‐HDV to the United States from highly endemic areas.
In the United States, several early studies in the late 1970s through the mid‐1980s showed antibodies to delta antigen in HBsAg‐positive blood donors (3.8%) in 1979 [7], persons with acute and chronic hepatitis B infection in Los Angeles (homosexual men, 15%; injection drug users, 22%) [8, 9], and developmentally disabled persons in Illinois state facilities (30%) [10]. Relatively high rates of HDV prevalence were seen in injection drug users in New York City (67%) [11]. Furthermore, a retrospective study of serum collected from 1972 to 1975 from drug‐using HBsAg‐positive patients at several Veterans Administration facilities at US locales showed that 42% had antibodies to delta antigen [12].
Few outbreaks of HDV in the United States (and these among injection drug users) have been detected and examined in the last 25 years. Over a 21‐month period between 1983 and 1985, Lettau and colleagues [13] investigated an outbreak of severe hepatitis among injection drug users in western Massachusetts associated with dual delta and hepatitis B viruses. Another 15 years elapsed before there was detection and investigation of a similar outbreak among injection drug users in Pierce County, Washington, by the Centers for Disease Control and Prevention (CDC) [14]. However, aside from these outbreaks, in recent years only about 6–10 cases of “confirmed” infections with HDV have been reported to the CDC from various states each year. Thus, it is quite difficult to know what is happening with HDV without specific reports such as the one by Kucirka and colleagues [5].
So, where is HDV headed in this country? On the one hand, there has been a gratifying decrease in prevalence of HDV in Asia and Europe, attributed to the expanding rate of hepatitis B vaccination activities over the last 20 years. We should expect a similar decline in HDV in the United States as we progressively remove its “host virus.” Or should we?
Previous outbreaks have shown a high prevalence of HDV coinfection among HBV‐infected injection drug users—54% in Massachusetts and 34.5% in Washington state—whereas HBV‐infected non‐drug users in those outbreaks had much lower HDV coinfection rates (9% in both states) [13, 14]. Indeed, a study of female prostitutes showed that, among those who used intravenous drugs, HBV and HDV coinfection rates were 21%, whereas the HBV‐infected women who were not injection drug users had an HDV coinfection rate of 6% [15]. Similarly, early analyses demonstrated high hepatitis D infection rates among hemophilic men (19%) [16] but not in gay men (0%) [17].
One unifying explanation for these numbers is that HDV, like other bloodborne pathogens, may be more efficiently transmitted parenterally than by sexual contact. If this is the case, perhaps we should not expect the same drop‐off in HDV coinfection rates as seen between 1980 and 2000 in places as diverse as Italy, Japan, Taiwan, and Turkey [6], where proportionately more HBV infection is acquired perinatally, sexually, or horizontally (in households), and proportionately less as the result of injection drug use. This hypothesis would also fit the current observation, albeit from a small sample, that fully 50% of HBV‐infected injection drug users in Baltimore in 2005–2006 had concurrent HDV infection.
Trends in HDV‐HBV coinfection and morbidity are contingent on successes in hepatitis B vaccination and screening. Approximately 15% of persons reported with acute hepatitis B infection in the United States are injection drug users [18]. In 1991, the United States adopted a vaccine‐based strategy to eliminate HBV transmission, with subsequent gains in immunization coverage particularly among children and adolescents [19]. Despite a long‐standing recommendation for hepatitis B vaccination, hepatitis B vaccine coverage among injection drug users remains low. As a result, 20%–70% of injection drug users have evidence of past or current HBV infection, with many lacking serologic evidence of hepatitis B vaccination and thus greater susceptibility to HBV [20]. When barriers to vaccination such as vaccine costs are removed, drug treatment centers successfully integrate hepatitis B vaccination as a routine service and greatly increase the numbers of injection drug users vaccinated [21]. To increase vaccination of injection drug users, the CDC recommends hepatitis B vaccination for all adults in correctional institutions and drug abuse prevention and treatment clinics; the CDC and other federal resources are available to defray the cost of vaccine purchase for these settings [19, 21]. In addition to vaccination, all injection drug users should be screened for HBV [19]. An estimated 3%–11% of injection drug users have chronic HBV infection, and many remain undiagnosed, reflecting inadequate HBV screening services in settings such as drug treatment programs [22]. Management of persons with chronic hepatitis B infection should include interventions to reduce behavioral risks of HBV transmission and referral for medical care. The data from Kucirka et al [5] highlight the importance of HDV testing as a component of clinical management for persons with chronic HBV infection. Unfortunately, few data are available to monitor whether injection drug users are receiving recommended hepatitis B prevention and care services.
Indeed, the study by Kucirka and colleagues [5] is not only useful as a marker of where we are in the US hepatitis D epidemic, but of where we are not. Very few studies such as this can or will be done, simply because there are too few cohorts of injection drug users currently being followed in the United States. The HIV/AIDS epidemic stimulated federal agencies such as the National Institute on Drug Abuse and (then) the CDC to establish studies of HIV and, eventually, of hepatitis virus infections among large populations of injection drug user in several cities. At present, the Baltimore study (ALIVE [AIDS Link to Intravenous Experience]) as reported here is the longest running US cohort study; in fact, its predecessor, “Man ALIVE,” predated the AIDS epidemic but is now one of few such studies left. This stymies our understanding not only of HDV and the “carrier” HBV epidemics in the United States but also of the continuing HCV and, to a lesser extent, HIV epidemics. Thus, we should expect our understanding of the evolution of the HDV epidemic—as well as HBV, HCV, and HIV epidemics—in this country, especially in one of the transmission risk groups most affected, to remain spotty and infrequent. It is a truism to write that “more research is needed,” but there is probably no more fitting comment on the implications of the research of the companion paper in this issue of the Journal.
References
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•2.Rizzetto M. Hepatitis D: thirty years after [review]. J Hepatol 2009;50:1043–1050.
•3.Taylor JM. Hepatitis delta virus. Virology 2006;344:71–76.
•4.Wedemeyer H. Re‐emerging interest in hepatitis delta: new insights into the dynamic interplay between HBV and HDV. J Hepatol 2010;52(5):627–629.
•5.Kucirka LM, Farzadegan H, Field JJ, et al. Prevalence, correlates, and viral dynamics of hepatitis delta among injection drug users. J Infect Dis 2010;202(6):845–852 (in this issue).
•6.Rizzetto M. Hepatitis D: the comeback? Liver Int 2009;29:140–142.
•7.Nath N, Mushawar IK, Fang CT, Berberian H, Dodd RY. Antibodies to delta antigen in asymptomatic hepatitis B surface antigen‐reactive blood donors in the United States and their association with other markers of hepatitis B virus. Am J Epidemiol 1985;122:218–225.
•8.De Cock KM, Niland JC, Lu HP, et al. Experience with human immunodeficiency virus infection in patients with hepatitis B virus and hepatitis delta virus infections in Los Angeles, 1977–1985. Am J Epidemiol 1988;127:1250–1260.
•9.Govindarajan S, Kanel GC, Peters RL. Prevalence of delta‐antibody among chronic hepatitis B virus infected patients in the Los Angeles area: its correlation with liver biopsy diagnosis. Gastroenterology 1983;85:160–162.
•10.Hershow RC, Chomel BB, Graham DR, et al. Hepatitis D virus infection in Illinois state facilities or the developmentally disabled: epidemiology and clinical manifestations. Ann Intern Med 1989;110:779–785.
•11.Novick DM, Farci P, Croxson TS, et al. Hepatitis D virus and human immunodeficiency virus antibodies in parenteral drug abusers who are hepatitis B surface antigen positive. J Infect Dis 1988;158:795–803.
•12.Ponzetto A, Seeff LB, Buskell‐Bales Z, et al. Hepatitis B markers in United States drug addicts with special emphasis on the delta hepatitis virus. Hepatology 1984;4:1111–1115.
•13.Lettau LA, McCarthy JG, Smith MH, et al. Outbreak of severe hepatitis due to delta and hepatitis B viruses in parenteral drug abusers and their contacts. N Engl J Med 1987;317:1256–1262.
•14.Bialek SR, Bower WA, Mottram K, et al. Risk factors for hepatitis B in an outbreak of hepatitis B and D among injection drug users. J Urban Health 2005;82:468–478.
•15.Rosenblum L, Darrow W, Witte J, et al. Sexual practices in the transmission of hepatitis B virus and prevalence of hepatitis delta virus infection in female prostitutes in the United States. JAMA 1992;267:2477–2481.
•16.Troisi CL, Hollinger FB, Hoots WK, et al. A multicenter study of viral hepatitis in a United States hemophilic population. Blood 1993;81:412–418.
•17.Weisfuse IB, Hadler SC, Fields HA, et al. Delta hepatitis in homosexual men in the United States. Hepatology 1989;9:872–874.
•18.Daniels D, Grytdal S, Wasley A. Surveillance for acute hepatitis—United States, 2007. MMWR 2009;58(Suppl 3):1–27.
•19.Centers for Disease Control and Prevention. A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States: recommendations of the Advisory Committee on Immunization Practices (ACIP). Part II: immunization of adults. MMWR Morb Mortal Wkly Rep 2006;55:1–33.
•20.Centers for Disease Control and Prevention. Recommendations for identification and public health management of persons with chronic hepatitis B virus infection. MMWR Morb Mortal Wkly Rep 2008;57:1–20.
•21.Kresina TF, Hoffman K, Lubran R, Clark HW. Integrating hepatitis services into substance abuse treatment programs: new initiatives from SAMHSA. Public Health Rep 2007;122(Suppl 2):96–98.
•22.Substance Abuse and Mental Health Services Administration, Center for Substance Abuse Treatment. Screening for infectious diseases among substance abusers (Treatment Improvement Protocol [TIP] Series 6; DHHS publication [SMA] 95–3060). Rockville, Maryland: NIH, 1993. http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=hssamhsatip&part=A25461. Accessed 19 April 2010.
Potential conflicts of interest: none reported.
Source
The efficacy of peginterferon-α-2a plus ribavirin for patients aged 60 years and older with chronic hepatitis C in Korea
Dong Hyun Sinn 2, Su Rin Shin 3, Jae Sook Kil 1, Jeong Kim 1, Geum-Youn Gwak 1, Moon Seok Choi 1, Joon Hyeok Lee 1, Kwang Cheol Koh 1, Byung Chul Yoo 1, Seung Woon Paik 1,*
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06478.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Author Information
1 Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea
2 Department of Medicine, Armed Forces Capital Hospital, Seongnam, South Korea
3 Department of Medicine, Kangnam Sacred Heart Hospital, Hallym University, Seoul, South Korea
*Correspondence: Seung Woon Paik,
*Correspondence: Seung Woon Paik Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, Seoul, 135-710, South Korea Tel: +82-2-3410-3409 Fax: +82-2-3410-6983 E-mail: sw.paik@samsung.com
Publication History
Accepted manuscript online: 17 AUG 2010 12:20PM EST
Received date: 16-Apr-2010 Accepted date: 27-Jul-2010
Keywords:
hepatitis C virus;elderly patients;peginterferon;ribavirin;APRI
Abstract
Background and Aim: We evaluated the safety and efficacy of combination therapy with pegylated interferon and ribavirin for treating chronic hepatitis C (CHC) patients aged 60 years and older.
Methods: Three hundred fourteen CHC patients, who were treated with combination therapy, were classified into three groups according to age: younger than 50 years of age (n = 137); 50 to 59 years old (n = 109); and 60 years of age or older (n = 68). The sustained virological response (SVR) rates and discontinuation rates were compared between the three groups.
Results: Discontinuation of therapy due to adverse event was more frequent in the older patient groups: 1%, 5%, and 10% for the <50, 50-59, and ≥60-year-old patients groups, respectively (p = 0.018). However, the older patients group showed a SVR rate that was comparable to the SVR rates of the other age groups; 80%, 73% and 75% for the <50, 50-59, and ≥60-year-old patients groups, respectively (p = 0.420). Multivariate analysis showed the AST to platelet ratio index (APRI) was an independent predictor of a SVR. A SVR was achieved in 95% (19 out of 20) of the elderly patients with an APRI < 0.80.
Conclusion: Although physicians must pay more attention for adverse events in the older patients, combination therapy can be considered for older patients, especially for the patients with a low APRI.
Source
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06478.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Author Information
1 Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea
2 Department of Medicine, Armed Forces Capital Hospital, Seongnam, South Korea
3 Department of Medicine, Kangnam Sacred Heart Hospital, Hallym University, Seoul, South Korea
*Correspondence: Seung Woon Paik,
*Correspondence: Seung Woon Paik Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, Seoul, 135-710, South Korea Tel: +82-2-3410-3409 Fax: +82-2-3410-6983 E-mail: sw.paik@samsung.com
Publication History
Accepted manuscript online: 17 AUG 2010 12:20PM EST
Received date: 16-Apr-2010 Accepted date: 27-Jul-2010
Keywords:
hepatitis C virus;elderly patients;peginterferon;ribavirin;APRI
Abstract
Background and Aim: We evaluated the safety and efficacy of combination therapy with pegylated interferon and ribavirin for treating chronic hepatitis C (CHC) patients aged 60 years and older.
Methods: Three hundred fourteen CHC patients, who were treated with combination therapy, were classified into three groups according to age: younger than 50 years of age (n = 137); 50 to 59 years old (n = 109); and 60 years of age or older (n = 68). The sustained virological response (SVR) rates and discontinuation rates were compared between the three groups.
Results: Discontinuation of therapy due to adverse event was more frequent in the older patient groups: 1%, 5%, and 10% for the <50, 50-59, and ≥60-year-old patients groups, respectively (p = 0.018). However, the older patients group showed a SVR rate that was comparable to the SVR rates of the other age groups; 80%, 73% and 75% for the <50, 50-59, and ≥60-year-old patients groups, respectively (p = 0.420). Multivariate analysis showed the AST to platelet ratio index (APRI) was an independent predictor of a SVR. A SVR was achieved in 95% (19 out of 20) of the elderly patients with an APRI < 0.80.
Conclusion: Although physicians must pay more attention for adverse events in the older patients, combination therapy can be considered for older patients, especially for the patients with a low APRI.
Source
Treatment of Hepatitis C Virus Infection in Patients with End-Stage Renal Disease
Chen-Hua Liu 1,2,3, Jia-Horng Kao 1,2,3,*
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06488.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Author Information
1 Department of Internal Medicine,
2 Hepatitis Research Center, and
3 Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
*Correspondence: Jia-Horng Kao,
*Correspondence: Prof. Jia-Horng Kao Director and Distinguished Professor, Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine 1 Chang-Te St., Taipei 10002, Taiwan Tel.: 886-2-23123456 ext 67307 Fax: 886-2-23825962 E-mail: kaojh@ntu.edu.tw
Publication History
Accepted manuscript online: 17 AUG 2010 12:21PM EST
Received date: 1-Aug-2010 Accepted date: 8-Aug-2010
Keywords:
hepatitis C virus;end-stage renal disease;dialysis;interferon;ribavirin
Abstract
Hepatitis C virus (HCV) infection is a major health problem in patients with end-stage renal disease (ESRD). The incidence of acute HCV infection during maintenance dialysis is much higher than that in the general population because of the risk of nosocomial transmission. Following acute HCV infection, most develop chronic HCV infection; a significant proportion develops chronic hepatitis, cirrhosis, and even hepatocellular carcinoma (HCC). Overall, chronic hepatitis C patients on hemodialysis bear an increased risk of liver-related morbidity and mortality, either during dialysis or after renal transplantation. Interferon (IFN) therapy is modestly effective for the treatment of HCV infection in ESRD patients. Conventional or pegylated IFN monotherapy has been used to treat acute hepatitis C in ESRD patients with excellent safety and efficacy. Regarding chronic hepatitis C, about one third of the patients can achieve sustained virologic response (SVR) after conventional or pegylated IFN monotherapy. The combination of low-dose ribavirin and conventional of pegylated IFN has further improved the SVR rate in treatment-naïve or retreated ESRD patients in clinical trials. Similar to treatment of patients with normal renal function, baseline and on-treatment HCV virokinetics are useful to guide optimized therapy in ESRD patients. Of particular note, IFN-based therapy is not recommended at the post-renal transplantation stage because of the low SVR rate and risk of acute graft rejection. In conclusion, ESRD patients with HCV infection should be encouraged to receive antiviral therapy and those who achieve SVR usually have long-term durable virologic, biochemical, and histologic responses.
Source
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06488.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Author Information
1 Department of Internal Medicine,
2 Hepatitis Research Center, and
3 Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
*Correspondence: Jia-Horng Kao,
*Correspondence: Prof. Jia-Horng Kao Director and Distinguished Professor, Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine 1 Chang-Te St., Taipei 10002, Taiwan Tel.: 886-2-23123456 ext 67307 Fax: 886-2-23825962 E-mail: kaojh@ntu.edu.tw
Publication History
Accepted manuscript online: 17 AUG 2010 12:21PM EST
Received date: 1-Aug-2010 Accepted date: 8-Aug-2010
Keywords:
hepatitis C virus;end-stage renal disease;dialysis;interferon;ribavirin
Abstract
Hepatitis C virus (HCV) infection is a major health problem in patients with end-stage renal disease (ESRD). The incidence of acute HCV infection during maintenance dialysis is much higher than that in the general population because of the risk of nosocomial transmission. Following acute HCV infection, most develop chronic HCV infection; a significant proportion develops chronic hepatitis, cirrhosis, and even hepatocellular carcinoma (HCC). Overall, chronic hepatitis C patients on hemodialysis bear an increased risk of liver-related morbidity and mortality, either during dialysis or after renal transplantation. Interferon (IFN) therapy is modestly effective for the treatment of HCV infection in ESRD patients. Conventional or pegylated IFN monotherapy has been used to treat acute hepatitis C in ESRD patients with excellent safety and efficacy. Regarding chronic hepatitis C, about one third of the patients can achieve sustained virologic response (SVR) after conventional or pegylated IFN monotherapy. The combination of low-dose ribavirin and conventional of pegylated IFN has further improved the SVR rate in treatment-naïve or retreated ESRD patients in clinical trials. Similar to treatment of patients with normal renal function, baseline and on-treatment HCV virokinetics are useful to guide optimized therapy in ESRD patients. Of particular note, IFN-based therapy is not recommended at the post-renal transplantation stage because of the low SVR rate and risk of acute graft rejection. In conclusion, ESRD patients with HCV infection should be encouraged to receive antiviral therapy and those who achieve SVR usually have long-term durable virologic, biochemical, and histologic responses.
Source
The healthy range for serum ALT and the clinical significance of “unhealthy” normal ALT levels in the Korean population
Hyun Seok Kang 1, Soon Ho Um 1, Yeon Seok Seo 1,*, Hyonggin An 2, Kwang Gyun Lee 1, Jong Jin Hyun1, Eun Sun Kim 1, Sung Chul Park 1, Bora Keum 1, Ji Hoon Kim 1, Hyung Joon Yim 1, Yoon Tae Jeen1, Hong Sik Lee 1, Hoon Jai Chun 1, Chang Duck Kim 1, Ho Sang Ryu 1
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06481.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation
Author Information
1 Departments of Internal Medicine and
2 Biostatistics, Korea University College of Medicine, Seoul, Korea
* Correspondence: Yeon Seok Seo,
* Correspondence: Yeon Seok Seo, MD, PhD Division of Gastroenterology and Hepatology, Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, Anam-dong 5-ga, Seongbuk-gu, Seoul 136-705, Korea Tel: 82-2-920-6608, Fax: 82-2-953-1943, E-mail: drseo@korea.ac.kr
Publication History
Accepted manuscript online: 17 AUG 2010 12:20PM EST
Accepted date: 02 August 2010
Keywords:
aminotransferase;metabolic syndrome;insulin resistance;nonalcoholic fatty liver disease
ABSTRACT
Background and Aims: It remains unclear whether the currently used normal range for serum alanine aminotransferase (ALT) levels really reflects a healthy liver. This study was performed to evaluate the healthy range of serum ALT in the Korean adult population and to determine the clinical significance of unhealthy levels.
Methods: We reviewed the medical records, including questionnaires and the results of laboratory and radiologic tests conducted at the Health Promotion Center in Korea University Anam Hospital between March 2005 and February 2007. The records written in questionnaire form included the baseline data, including physical status, social behaviors, medication history, and past and present disease histories.
Results: The mean age of the 7403 enrolled subjects was 48 years, and 49.9% of them were men. A healthy cohort was selected after excluding subjects who showed any abnormalities of the factors that were significantly associated with serum ALT level on multivariate regression analysis. The upper limit of the healthy range of serum ALT level (i.e., 95th percentile) in the healthy population was 31 IU/L for the men and 23 IU/L for the women. The prevalence of metabolic syndrome and insulin resistance were significantly higher in subjects with an “unhealthy” normal ALT level than in subjects with a healthy ALT level.
Conclusion: In our study, the upper limit of the healthy range of serum ALT level was 31 IU/L for the men and 23 IU/L for the women. An unhealthy normal ALT level was associated with higher prevalence of metabolic syndrome and insulin resistance.
Source
Journal of Gastroenterology and Hepatology
Accepted Article (Accepted, unedited articles published online for future issues)
DOI: 10.1111/j.1440-1746.2010.06481.x
Journal compilation © 2010 Journal of Gastroenterology and Hepatology Foundation
Author Information
1 Departments of Internal Medicine and
2 Biostatistics, Korea University College of Medicine, Seoul, Korea
* Correspondence: Yeon Seok Seo,
* Correspondence: Yeon Seok Seo, MD, PhD Division of Gastroenterology and Hepatology, Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, Anam-dong 5-ga, Seongbuk-gu, Seoul 136-705, Korea Tel: 82-2-920-6608, Fax: 82-2-953-1943, E-mail: drseo@korea.ac.kr
Publication History
Accepted manuscript online: 17 AUG 2010 12:20PM EST
Accepted date: 02 August 2010
Keywords:
aminotransferase;metabolic syndrome;insulin resistance;nonalcoholic fatty liver disease
ABSTRACT
Background and Aims: It remains unclear whether the currently used normal range for serum alanine aminotransferase (ALT) levels really reflects a healthy liver. This study was performed to evaluate the healthy range of serum ALT in the Korean adult population and to determine the clinical significance of unhealthy levels.
Methods: We reviewed the medical records, including questionnaires and the results of laboratory and radiologic tests conducted at the Health Promotion Center in Korea University Anam Hospital between March 2005 and February 2007. The records written in questionnaire form included the baseline data, including physical status, social behaviors, medication history, and past and present disease histories.
Results: The mean age of the 7403 enrolled subjects was 48 years, and 49.9% of them were men. A healthy cohort was selected after excluding subjects who showed any abnormalities of the factors that were significantly associated with serum ALT level on multivariate regression analysis. The upper limit of the healthy range of serum ALT level (i.e., 95th percentile) in the healthy population was 31 IU/L for the men and 23 IU/L for the women. The prevalence of metabolic syndrome and insulin resistance were significantly higher in subjects with an “unhealthy” normal ALT level than in subjects with a healthy ALT level.
Conclusion: In our study, the upper limit of the healthy range of serum ALT level was 31 IU/L for the men and 23 IU/L for the women. An unhealthy normal ALT level was associated with higher prevalence of metabolic syndrome and insulin resistance.
Source
August 18, 2010
Radiology: 31P MR spectroscopy depicts extent of nonalcoholic fatty liver disease
Author: Manjula Puthenedam
Wednesday, August 18 2010
Proton-decoupled phosphorus 31 (31P) MR spectroscopy shows promise in grading of nonalcoholic fatty liver disease and may be useful in detecting treatment response in patients with nonalcoholic steatohepatitis (NASH), according to a study published in this month’s Radiology.
The study was conducted by Ksenia Sevastianova, MD, from the department of medicine, division of diabetes and colleagues from University of Helsinki and Minerva Medical Research Institute, Helsinki, Finland.
Sevastianova and colleagues found that 31P MR spectroscopy showed promise in differentiating stages of nonalcoholic fatty liver disease by detecting an increase in signal of nicotinamide adenine dinucleotide phosphate (NADPH), a marker of inflammation and fibrogenesis in the liver.
A 3.0-T clinical imager was used by the researchers to obtain proton-decoupled 31P MR spectra in the liver of 12 control subjects, 13 patients with biopsy-proved simple steatosis due to nonalcoholic fatty liver, nine patients with NASH, and nine patients with cirrhosis.
Liver fat was determined with hydrogen1 MR spectroscopy and the content was found to be higher in patients with nonalcoholic fatty liver disease and NASH than in patients with cirrhosis or in control subjects, noted Sevastianova and colleagues.
The 31 P spectra from the patients were analyzed for phosphormonoester, phosphodiester , phosphoethanolamine , phosphocholine, glycerophosphocholine, glycerophosphoryl ethanolamine, uridine diphosphoglucose, NADPH, inorganic phosphate, phosphoenolpyruvate, and alpha-, beta- and gamma-nucleotide triphosphate levels.
Proton-decoupled 31P MR spectroscopy revealed an elevated level of NADPH in patients with NASH and those with cirrhosis and can be used as an in vivo marker metabolite with which to detect NASH, according to Sevastianova and colleagues.
NADPH may have value as an additional tool with which to define and grade liver injury, and it should be tested in further studies that include patients with liver disease not caused by nonalcoholic fatty liver disease, added Sevastianova and colleagues.
The researchers concluded that 31P MR spectroscopy could help to select patients for invasive liver biopsy and possibly replace biopsy in some patients.
Last Updated ( Wednesday, August 18 2010 )
Source
Wednesday, August 18 2010
Proton-decoupled phosphorus 31 (31P) MR spectroscopy shows promise in grading of nonalcoholic fatty liver disease and may be useful in detecting treatment response in patients with nonalcoholic steatohepatitis (NASH), according to a study published in this month’s Radiology.
The study was conducted by Ksenia Sevastianova, MD, from the department of medicine, division of diabetes and colleagues from University of Helsinki and Minerva Medical Research Institute, Helsinki, Finland.
Sevastianova and colleagues found that 31P MR spectroscopy showed promise in differentiating stages of nonalcoholic fatty liver disease by detecting an increase in signal of nicotinamide adenine dinucleotide phosphate (NADPH), a marker of inflammation and fibrogenesis in the liver.
A 3.0-T clinical imager was used by the researchers to obtain proton-decoupled 31P MR spectra in the liver of 12 control subjects, 13 patients with biopsy-proved simple steatosis due to nonalcoholic fatty liver, nine patients with NASH, and nine patients with cirrhosis.
Liver fat was determined with hydrogen1 MR spectroscopy and the content was found to be higher in patients with nonalcoholic fatty liver disease and NASH than in patients with cirrhosis or in control subjects, noted Sevastianova and colleagues.
The 31 P spectra from the patients were analyzed for phosphormonoester, phosphodiester , phosphoethanolamine , phosphocholine, glycerophosphocholine, glycerophosphoryl ethanolamine, uridine diphosphoglucose, NADPH, inorganic phosphate, phosphoenolpyruvate, and alpha-, beta- and gamma-nucleotide triphosphate levels.
Proton-decoupled 31P MR spectroscopy revealed an elevated level of NADPH in patients with NASH and those with cirrhosis and can be used as an in vivo marker metabolite with which to detect NASH, according to Sevastianova and colleagues.
NADPH may have value as an additional tool with which to define and grade liver injury, and it should be tested in further studies that include patients with liver disease not caused by nonalcoholic fatty liver disease, added Sevastianova and colleagues.
The researchers concluded that 31P MR spectroscopy could help to select patients for invasive liver biopsy and possibly replace biopsy in some patients.
Last Updated ( Wednesday, August 18 2010 )
Source
Fast Cancer Growth In Poorer Countries -- Much Can Be Done, With Inexpensive Medications And Equipment
August 18, 2010
Eminent cancer and public health experts are urging governments and agencies to focus seriously on cancer care and prevention in poorer nations, according to a study published in the Lancet. A great deal could be done using generic, off-patent medications, educating people, and training physicians and community workers, conclude the authors.
Cancer is a significant cause of premature death in most parts of the world. Unfortunately, it is a neglected health problem in poorer nations, says Dr. Julio Frenk.
"To correct this situation we must address the staggering 5/80 cancer disequilibrium (referring to the fact that LMIC account for almost 80 percent of the burden of disease due to cancer, yet receive only 5 percent of global resources devoted to deal with this emerging challenge)," says Frenk.
The following initiatives could help address the disparities which currently exist worldwide, without having to use high-priced on-patent medications or other equipment:
For text:
http://www.medicalnewstoday.com/articles/198068.php
For study:
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)61152-X/fulltext
Source
Also See: Tackling cancer among poor doesn't have to cost dear
Eminent cancer and public health experts are urging governments and agencies to focus seriously on cancer care and prevention in poorer nations, according to a study published in the Lancet. A great deal could be done using generic, off-patent medications, educating people, and training physicians and community workers, conclude the authors.
- In 1970 lower- and middle-income countries (LMICs) accounted for 15 percent of global cancer cases.
- In 2008 the figure rose to 56 percent; experts estimate that by 2030 the percentage will reach 70 percent.
- With nearly two-thirds of global annual cancer cases occurring in LMICs, it is today a leading cause of death.
- The case fatality from cancer - estimated incidence to mortality ratio -- is 75 percent in low-income countries, compared to 46 percent in developed nations.
Cancer is a significant cause of premature death in most parts of the world. Unfortunately, it is a neglected health problem in poorer nations, says Dr. Julio Frenk.
"To correct this situation we must address the staggering 5/80 cancer disequilibrium (referring to the fact that LMIC account for almost 80 percent of the burden of disease due to cancer, yet receive only 5 percent of global resources devoted to deal with this emerging challenge)," says Frenk.
The following initiatives could help address the disparities which currently exist worldwide, without having to use high-priced on-patent medications or other equipment:
- Anti-tobacco campaigns; smoking is a huge risk factor for cancer but it is still rising in many LMICs, while it is dropping in developed nations.
- Education about early detection and screening.
- HPV (human papillomavirus) vaccination programs to prevent cervical cancer.
- Hepatitis B virus vaccination programs to prevent liver cancer.
For text:
http://www.medicalnewstoday.com/articles/198068.php
For study:
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)61152-X/fulltext
Source
Also See: Tackling cancer among poor doesn't have to cost dear
Late Conversion to Sirolimus in Liver Transplant Recipients is a Safe Clinical Strategy: Presented at ICTS
By Claire Sowerbutt
VANCOUVER -- August 18, 2010 -- Converting patients who have undergone liver transplantation to calcineurin inhibitor (CNI)-free immunosuppression with sirolimus at 5 years or more post transplant is a safe clinical strategy, as it does not increase the risk for acute rejection (ACR) or steroid resistant rejection, researchers said here at the 23rd International Congress of the Transplant Society (ICTS).
While sirolimus-based CNI-free immunosuppression is useful in managing long-term complications in liver transplant recipients, information regarding this strategy is limited.
"Concerns of potential complications and risk for late ACR in a patient with otherwise stable immunosuppression cause many clinicians to avoid late conversion, since late ACR can negatively impact survival in liver transplant," reported Greg McKenna, MD, Transplant Services Department, Baylor Regional Transplant Institute, Dallas, Texas, and colleagues. "By avoiding later conversions, these co-morbidities and complications can progress, even to the patient's detriment."
Dr. McKenna and colleagues presented findings from what is the largest experience of conversion to sirolimus-based CNI-free immunosuppression.
The single centre, retrospective analysis utilised a prospectively identified database of 2,218 orthotopic liver transplant (OLT) recipients of Baylor Transplant Institute seen from January 1985 to December 2005.
The sirolimus cohort included all patients converted to sirolimus at >=5 years (late conversion. The control group (n = 1636) consisted of all surviving patients at >=5 years post transplant who had never received sirolimus either as de novo immunosuppression or as conversion therapy. The rates of ACR and patient survival were compared between the 2 groups.
The total number of patients converted to sirolimus was 476/2218 (21.5%), with 140 (29.4%) of 476 undergoing late conversion. The leading cause of conversion was nephrotoxicity (91.6%), followed by malignancy (2.1%), neurotoxicity (1.4%), and hepatitis C virus progression (1.4%).
The median time to late conversion was 8.8 years, the median duration 4.2 years, and the number of patients currently on sirolimus is 53.3%.
Patient death occurred in 13.6% of the 140 patients who underwent late sirolimus conversion, and was the leading reason for treatment cessation. The second leading reason was pending surgical procedures (8.6%).
Compared with the control group, fewer patients who underwent late sirolimus conversion experienced ACR (2.1% vs 3.5 %, respectively) -- the difference was not significant. The 3 episodes of ACR in the late conversion cohort occurred on days 115, 175, and 986 post conversion. Steroid resistant rejection did not occur at all in the sirolimus cohort, whereas there was a 0.5% incidence in the control group.
With respect to complications, there were no incidences of hepatic artery thrombosis, cytomegalovirus, and Epstein Barr virus or bilary complications in the late conversion group. However, a 2.9% incidence of hernia (4/140), and a 0.7% (1/140) incidence of Herpes simplex virus was reported.
"There was no significant difference in patient survival between the sirolimus cohort and the control group," the authors reported. "This is in itself significant, since 90% of the patients in the sirolimus cohort were converted for renal dysfunction and would be expected to have worse patient survival."
"Late conversion to sirolimus should not be deterred by concerns of complications or risks of rejection, even in patients on long-term stable immunosuppression, and should be done if the clinical situation warrants it," they concluded.
[Presentation title: The Safety of Late Conversion to Sirolimus in Liver Transplantation. Abstract MO12.05]
Source
VANCOUVER -- August 18, 2010 -- Converting patients who have undergone liver transplantation to calcineurin inhibitor (CNI)-free immunosuppression with sirolimus at 5 years or more post transplant is a safe clinical strategy, as it does not increase the risk for acute rejection (ACR) or steroid resistant rejection, researchers said here at the 23rd International Congress of the Transplant Society (ICTS).
While sirolimus-based CNI-free immunosuppression is useful in managing long-term complications in liver transplant recipients, information regarding this strategy is limited.
"Concerns of potential complications and risk for late ACR in a patient with otherwise stable immunosuppression cause many clinicians to avoid late conversion, since late ACR can negatively impact survival in liver transplant," reported Greg McKenna, MD, Transplant Services Department, Baylor Regional Transplant Institute, Dallas, Texas, and colleagues. "By avoiding later conversions, these co-morbidities and complications can progress, even to the patient's detriment."
Dr. McKenna and colleagues presented findings from what is the largest experience of conversion to sirolimus-based CNI-free immunosuppression.
The single centre, retrospective analysis utilised a prospectively identified database of 2,218 orthotopic liver transplant (OLT) recipients of Baylor Transplant Institute seen from January 1985 to December 2005.
The sirolimus cohort included all patients converted to sirolimus at >=5 years (late conversion. The control group (n = 1636) consisted of all surviving patients at >=5 years post transplant who had never received sirolimus either as de novo immunosuppression or as conversion therapy. The rates of ACR and patient survival were compared between the 2 groups.
The total number of patients converted to sirolimus was 476/2218 (21.5%), with 140 (29.4%) of 476 undergoing late conversion. The leading cause of conversion was nephrotoxicity (91.6%), followed by malignancy (2.1%), neurotoxicity (1.4%), and hepatitis C virus progression (1.4%).
The median time to late conversion was 8.8 years, the median duration 4.2 years, and the number of patients currently on sirolimus is 53.3%.
Patient death occurred in 13.6% of the 140 patients who underwent late sirolimus conversion, and was the leading reason for treatment cessation. The second leading reason was pending surgical procedures (8.6%).
Compared with the control group, fewer patients who underwent late sirolimus conversion experienced ACR (2.1% vs 3.5 %, respectively) -- the difference was not significant. The 3 episodes of ACR in the late conversion cohort occurred on days 115, 175, and 986 post conversion. Steroid resistant rejection did not occur at all in the sirolimus cohort, whereas there was a 0.5% incidence in the control group.
With respect to complications, there were no incidences of hepatic artery thrombosis, cytomegalovirus, and Epstein Barr virus or bilary complications in the late conversion group. However, a 2.9% incidence of hernia (4/140), and a 0.7% (1/140) incidence of Herpes simplex virus was reported.
"There was no significant difference in patient survival between the sirolimus cohort and the control group," the authors reported. "This is in itself significant, since 90% of the patients in the sirolimus cohort were converted for renal dysfunction and would be expected to have worse patient survival."
"Late conversion to sirolimus should not be deterred by concerns of complications or risks of rejection, even in patients on long-term stable immunosuppression, and should be done if the clinical situation warrants it," they concluded.
[Presentation title: The Safety of Late Conversion to Sirolimus in Liver Transplantation. Abstract MO12.05]
Source
Evidence of intense ongoing endemic transmission of hepatitis C virus in Egypt
F. DeWolfe Miller a,1 and Laith J. Abu-Raddad b,c,d
a Department of Tropical Medicine, Medical Microbiology and Pharmacology, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813;
b Infectious Disease Epidemiology Group, Weill Cornell Medical College–Qatar, Cornell University, Qatar Foundation–Education City, Doha, Qatar;
c Department of Public Health, Weill Cornell Medical College, Cornell University, New York, NY 10065; and
d Vaccine and Infectious Disease Institute, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
Communicated by Kirk R. Smith, University of California, Berkeley, CA, June 22, 2010 (received for review December 24, 2009)
Abstract
Egypt has the highest prevalence of antibodies to hepatitis C virus (HCV) in the world, estimated nationally at 14.7%. An estimated 9.8% are chronically infected. Numerous HCV prevalence studies in Egypt have published various estimates from different Egyptian communities, suggesting that Egypt, relative to the other nations of the world, might be experiencing intense ongoing HCV transmission. More importantly, a new national study provided an opportunity to apply established epidemiologic models to estimate incidence. Validated mathematical models for estimating incidence from age-specific prevalence were used. All previous prevalence studies of HCV in Egypt were reviewed and used to estimate incidence provided that there was sufficient age-specific data required by the models. All reports of anti-HCV antibody prevalence were much higher than any single other national estimate. Age was the strongest and most consistently associated factor to HCV prevalence and HCV RNA positivity. It was not possible to establish a prior reference point for HCV prevalence or incidence to compare with the 2009 incidence estimates. The modeled incidence from the national study and collectively from the modeled incidence from the previous community studies was 6.9/1,000 [95% confidence interval (CI), 5.5–7.4] per person per year and 6.6/1,000 (95% CI, 5.1–7.0) per person per year, respectively. Projected to the age structure of the Egyptian population, more than 500,000 new HCV infections per year were estimated. Iatrogenic transmission is the most likely, underlining exposure to the ongoing transmission. The study demonstrates the urgency to reduce HCV transmission in Egypt.
Footnotes
1 To whom correspondence should be addressed. E-mail: dewolfe@hawaii.edu. Author contributions: F.D.M. designed research; F.D.M. and L.J.A-R. performed research; F.D.M. contributed new reagents/analytic tools; F.D.M. and L.J.A-R. analyzed data; and F.D.M. and L.J.A-R. wrote the paper.
The authors declare no conflict of interest.
Freely available online through the PNAS open access option.
Source
a Department of Tropical Medicine, Medical Microbiology and Pharmacology, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813;
b Infectious Disease Epidemiology Group, Weill Cornell Medical College–Qatar, Cornell University, Qatar Foundation–Education City, Doha, Qatar;
c Department of Public Health, Weill Cornell Medical College, Cornell University, New York, NY 10065; and
d Vaccine and Infectious Disease Institute, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
Communicated by Kirk R. Smith, University of California, Berkeley, CA, June 22, 2010 (received for review December 24, 2009)
Abstract
Egypt has the highest prevalence of antibodies to hepatitis C virus (HCV) in the world, estimated nationally at 14.7%. An estimated 9.8% are chronically infected. Numerous HCV prevalence studies in Egypt have published various estimates from different Egyptian communities, suggesting that Egypt, relative to the other nations of the world, might be experiencing intense ongoing HCV transmission. More importantly, a new national study provided an opportunity to apply established epidemiologic models to estimate incidence. Validated mathematical models for estimating incidence from age-specific prevalence were used. All previous prevalence studies of HCV in Egypt were reviewed and used to estimate incidence provided that there was sufficient age-specific data required by the models. All reports of anti-HCV antibody prevalence were much higher than any single other national estimate. Age was the strongest and most consistently associated factor to HCV prevalence and HCV RNA positivity. It was not possible to establish a prior reference point for HCV prevalence or incidence to compare with the 2009 incidence estimates. The modeled incidence from the national study and collectively from the modeled incidence from the previous community studies was 6.9/1,000 [95% confidence interval (CI), 5.5–7.4] per person per year and 6.6/1,000 (95% CI, 5.1–7.0) per person per year, respectively. Projected to the age structure of the Egyptian population, more than 500,000 new HCV infections per year were estimated. Iatrogenic transmission is the most likely, underlining exposure to the ongoing transmission. The study demonstrates the urgency to reduce HCV transmission in Egypt.
Footnotes
1 To whom correspondence should be addressed. E-mail: dewolfe@hawaii.edu. Author contributions: F.D.M. designed research; F.D.M. and L.J.A-R. performed research; F.D.M. contributed new reagents/analytic tools; F.D.M. and L.J.A-R. analyzed data; and F.D.M. and L.J.A-R. wrote the paper.
The authors declare no conflict of interest.
Freely available online through the PNAS open access option.
Source
Campaign for Hepatitis Tests in Pharmacies as Deaths Rise
Abstract
Testing in retail pharmacies is more likely to identify hepatitis than comparable screening in doctors’ offices, suggest the results of a pilot study in the UK. In response, health officials are urging the National Health Service to fund the outreach permanently. “We desperately need new approaches to testing that will find the undiagnosed patients,” said Charles Gore, CEO of the Hepatitis C Trust. “This pilot study shows pharmacy testing could be just what is needed.” Of the 236 tests run at pharmacies, 35 people were positive for hepatitis C and four were positive for hepatitis B. The testing took place in five areas at 19 pharmacies throughout the UK. Officials in the Isle of Wight added screening for HIV and syphilis to the pilot. “Pharmacies see a different cohort of people to [those who visit general practitioners] and therefore we can access and diagnose people who otherwise would not have been tested,” said Gary Warner, of the Isle of Wight’s Regent Pharmacy. “This scheme has woken a lot of people up to the problem of viral hepatitis, and we are now working with local drug and addiction services in a more integrated way than before,” Warner said.
Source
http://www.guardian.co.uk/
Date of Publication
08/18/2010
Author
Sarah Boseley
Source
Testing in retail pharmacies is more likely to identify hepatitis than comparable screening in doctors’ offices, suggest the results of a pilot study in the UK. In response, health officials are urging the National Health Service to fund the outreach permanently. “We desperately need new approaches to testing that will find the undiagnosed patients,” said Charles Gore, CEO of the Hepatitis C Trust. “This pilot study shows pharmacy testing could be just what is needed.” Of the 236 tests run at pharmacies, 35 people were positive for hepatitis C and four were positive for hepatitis B. The testing took place in five areas at 19 pharmacies throughout the UK. Officials in the Isle of Wight added screening for HIV and syphilis to the pilot. “Pharmacies see a different cohort of people to [those who visit general practitioners] and therefore we can access and diagnose people who otherwise would not have been tested,” said Gary Warner, of the Isle of Wight’s Regent Pharmacy. “This scheme has woken a lot of people up to the problem of viral hepatitis, and we are now working with local drug and addiction services in a more integrated way than before,” Warner said.
Source
http://www.guardian.co.uk/
Date of Publication
08/18/2010
Author
Sarah Boseley
Source
Time to Restart the Battle Against HIV/AIDS
There’s a decided lack of energy on AIDS coming from the gay and lesbian community today
By Tom Sheridan
Posted: August 18, 2010
Tom Sheridan is president of the Sheridan Group, which serves public interest advocacy efforts and designs socially responsible public policy initiatives. His client portfolio includes Bono's ONE Campaign, One Voice Against Cancer, Catholic Charities USA, and the America Forward coalition, and several AIDS-related charities and causes.
Today marks two major events in this country's history. Twenty years ago, the Ryan White CARE Act became law. And one year ago, Sen. Edward Kennedy passed away, having seen the bill he championed save hundreds of thousands of lives.
In 1990, as I huddled with the senator and his staff to write the nation's first response to the HIV/AIDS epidemic, we were interrupted and told that Ryan White—the brave 19-year-old who challenged our presumptions and prejudices—was losing his battle with AIDS. Kennedy picked up the phone and asked Ryan's mother, Jeanne White, if it would be appropriate to name the bill for her dying son. I've always admired the grace and courage that enabled Mrs. White to see beyond her grief. Her support helped us pass a disaster assistance bill in response to an urgent national crisis.
We now have fewer deaths, more available drugs and treatments, more systems able to respond. But the initial response, repair, and recovery process has come to an end. Today's new HIV/AIDS challenges require the same kind of innovation and boldness that we, as a nation, demonstrated two decades ago. So, on this milestone anniversary, I'm compelled to offer this challenge: Let's honor Senator Kennedy and Ryan White by writing and passing the Ryan White CARE Act 2.0.
Ryan White was written when virtually no drug or pharmaceutical interventions were available, but drug access has nevertheless become the bill's primary focus. It was written for an epidemic that raged within the gay community, but HIV/AIDS is now a leading cause of death for African Americans, those with substance abuse issues, and for men who have sex with men but don't identify as gay. The bill couldn't mention education—in 1990, that was a political hot button. But half of today's new infections are among those under age 25 who clearly aren't getting enough HIV/AIDS education. And Ryan White never mentions preventive medicine, but huge strides have been made in that area. A new microbicide gel reduces a women's risk of infection by almost 40 percent. In five or 10 years, we'll probably have the equivalent of a "morning after pill" for HIV.
Clearly, it's time for an updated battle plan that is just as innovative as its predecessor. We need a bill that nationalizes the purchase of AIDS drugs similar to the Veterans Administration's approach, which could save 74 percent over open-market prices. With those savings, we could give greater numbers of Americans with HIV access to life-saving treatments. We need to merge care and prevention strategies so that the current wave of scientific discoveries has an express lane into the new at-risk communities. And we need to remove silos in the federal government that prevent agencies from coordinating care. The Centers for Disease Control, for example, could work much more closely with the Health Resources and Service Administration to develop innovative ideas for leveraging resources.
President Barack Obama's new plan essentially maintains the status quo, but doesn't bring forward any new ideas or offer much money. Twenty years ago, led by Senator Kennedy, our thinking was bolder and demanded more. Why not now?
Is part of the reason that we're just not holding the president's feet to the fire? There's a decided lack of energy on AIDS coming from the gay and lesbian community today, raising uncomfortable questions about who cares (and doesn't) about the new face of this disease. Why have no other groups stepped forward to address the new risks to their communities?
In 20 years things go stale, stakeholders become complacent; for-profit interests embed; innovation stops; creativity becomes lethargic. Edward Kennedy and Ryan White would demand that we honor the 20th anniversary of this bill and, indeed, their memory by committing ourselves to the Ryan White CARE Act 2.0. Let's get to it!
Source
By Tom Sheridan
Posted: August 18, 2010
Tom Sheridan is president of the Sheridan Group, which serves public interest advocacy efforts and designs socially responsible public policy initiatives. His client portfolio includes Bono's ONE Campaign, One Voice Against Cancer, Catholic Charities USA, and the America Forward coalition, and several AIDS-related charities and causes.
Today marks two major events in this country's history. Twenty years ago, the Ryan White CARE Act became law. And one year ago, Sen. Edward Kennedy passed away, having seen the bill he championed save hundreds of thousands of lives.
In 1990, as I huddled with the senator and his staff to write the nation's first response to the HIV/AIDS epidemic, we were interrupted and told that Ryan White—the brave 19-year-old who challenged our presumptions and prejudices—was losing his battle with AIDS. Kennedy picked up the phone and asked Ryan's mother, Jeanne White, if it would be appropriate to name the bill for her dying son. I've always admired the grace and courage that enabled Mrs. White to see beyond her grief. Her support helped us pass a disaster assistance bill in response to an urgent national crisis.
We now have fewer deaths, more available drugs and treatments, more systems able to respond. But the initial response, repair, and recovery process has come to an end. Today's new HIV/AIDS challenges require the same kind of innovation and boldness that we, as a nation, demonstrated two decades ago. So, on this milestone anniversary, I'm compelled to offer this challenge: Let's honor Senator Kennedy and Ryan White by writing and passing the Ryan White CARE Act 2.0.
Ryan White was written when virtually no drug or pharmaceutical interventions were available, but drug access has nevertheless become the bill's primary focus. It was written for an epidemic that raged within the gay community, but HIV/AIDS is now a leading cause of death for African Americans, those with substance abuse issues, and for men who have sex with men but don't identify as gay. The bill couldn't mention education—in 1990, that was a political hot button. But half of today's new infections are among those under age 25 who clearly aren't getting enough HIV/AIDS education. And Ryan White never mentions preventive medicine, but huge strides have been made in that area. A new microbicide gel reduces a women's risk of infection by almost 40 percent. In five or 10 years, we'll probably have the equivalent of a "morning after pill" for HIV.
Clearly, it's time for an updated battle plan that is just as innovative as its predecessor. We need a bill that nationalizes the purchase of AIDS drugs similar to the Veterans Administration's approach, which could save 74 percent over open-market prices. With those savings, we could give greater numbers of Americans with HIV access to life-saving treatments. We need to merge care and prevention strategies so that the current wave of scientific discoveries has an express lane into the new at-risk communities. And we need to remove silos in the federal government that prevent agencies from coordinating care. The Centers for Disease Control, for example, could work much more closely with the Health Resources and Service Administration to develop innovative ideas for leveraging resources.
President Barack Obama's new plan essentially maintains the status quo, but doesn't bring forward any new ideas or offer much money. Twenty years ago, led by Senator Kennedy, our thinking was bolder and demanded more. Why not now?
Is part of the reason that we're just not holding the president's feet to the fire? There's a decided lack of energy on AIDS coming from the gay and lesbian community today, raising uncomfortable questions about who cares (and doesn't) about the new face of this disease. Why have no other groups stepped forward to address the new risks to their communities?
In 20 years things go stale, stakeholders become complacent; for-profit interests embed; innovation stops; creativity becomes lethargic. Edward Kennedy and Ryan White would demand that we honor the 20th anniversary of this bill and, indeed, their memory by committing ourselves to the Ryan White CARE Act 2.0. Let's get to it!
Source
Newly Recognized Factor in Mother-to-Child Transmission of Hepatitis C
August 18, 2010
In general, the children of women infected with Hepatitis C have a low risk of being born with the virus. In addition to what was previously known about this type of Hepatitis C transmission, new research finds a genetic link that can aid - or prevent - this from occurring.
by Nicole Cutler, L.Ac.
Many women with a chronic viral infection are weary of procreating, because of the chance they may pass their illness on during pregnancy or birth. For those infected with Hepatitis C, this fear is especially pronounced.
There are a handful of reasonable causes supporting a fear of carrying a baby and giving birth with Hepatitis C. They include:
· Hepatitis C is rampant in our society - affecting approximately four million Americans.
· Hepatitis C often leads to chronic liver disease.
· There is currently no guaranteed cure for Hepatitis C.
· Nearly half of those with Hepatitis C are unsure as to how they originally became infected.
Known as vertical transmission, the risk of infants acquiring Hepatitis C from their mother during pregnancy or childbirth is surprisingly low. There have been quite a few studies examining what the likelihood is of vertical transmission and what increases or decreases the risk of infecting a newborn with Hepatitis C.
Although the statistics determining the rate of vertical transmission is not uniform among these studies, experts believe the most accurate estimate of vertical transmission from mothers with Hepatitis C is five percent. Based upon a comprehensive review of trials investigating Hepatitis C vertical transmission, the following appear to represent the two largest risks for bearing a child with Hepatitis C:
1. The mother is co-infected with Hepatitis C and HIV.
2. The mother has a high Hepatitis C viral load during birth.
In addition, physicians typically relay the following information to pregnant women with Hepatitis C:
· The presence of Hepatitis C infection does not appear to result in a higher risk pregnancy or a higher incidence of poor obstetric outcome.
· Testing for the presence of Hepatitis C in infants born to infected mothers should not begin until at least one year following delivery. The natural history of Hepatitis C infected infants is poorly understood at this time.
· Prophylactic caesarian section is not recommended in Hepatitis C infected mothers. The role of cesarean delivery in mothers co-infected with Hepatitis C and HIV remains controversial.
· Breastfeeding presents a negligible risk of Hepatitis C transmission. Given the well-documented benefits of breastfeeding, it is highly recommended.
It has been a while since there were any additional factors recognized to affect the likelihood of vertical transmission. However, researchers from Italy have recently identified a genetic component that reliably foretells this possibility.
As published in the July 2009 edition of the journal Virology, a mismatch between genes carried by a mother and her infant appear to confer protection against Hepatitis C transmission. Elena Bevilacqua and colleagues from Italy investigated the role of several genes known to play a role in Hepatitis C infection. These researchers found that a specific gene, HLA-DRB1, could predict whether or not the infant acquires Hepatitis C infection from its mother. Based on this research:
1. When a mother and child have the same genetic variant of HLA-DRB1, there is no guarantee that vertical transmission will occur; it just increases the likelihood.
2. When a mother and child have different variations of HLA-DRB1, there appears to be guaranteed protection from vertical transmission.
Unfortunately, a mother cannot control the similarity or dissimilarity of her infant's genetic construction. However, whenever a trial reveals a definitive link for Hepatitis C transmission, we gain some ground in understanding this virus. Undoubtedly, the more information gathered on how Hepatitis C is transmitted, infects people, replicates and dies, the closer we are - as a whole - to putting an end to this source of chronic liver disease.
References:
http://en.wikipedia.org/wiki/HLA-DR, HLA-DR, Retrieved September 17, 2009, Wikimedia Foundation Inc., 2009.
http://www.hcvadvocate.org/hcsp/articles/HERRINE.html, Mother-to-Child Transmission of HCV, Steven K. Herrine, MD, Retrieved September 15, 2009, Hepatitis C Support Project, 2009.
http://www.hivandhepatitis.com/hep_c/news/2009/090109_a.html, Genetic Factors Influence Risk of Mother-to-child Hepatitis C Virus Transmission, Retrieved September 15, 2009, hivandhepatitis.com, 2009.
http://www.ncbi.nlm.nih.gov/pubmed/15239255, Diagnostic and prognostic value of virologic tests in vertical transmission of hepatitis C virus infection: results of a large prospective study in pregnant women, Saez, A, et al, Retrieved September 16, 2009, Hepato-Gastroenterology, July-August 2004.
http://www.ncbi.nlm.nih.gov/pubmed/19481774, Genetic factors in mother-to-child transmission of HCV infection, Bevilacqua E, et al, Retrieved September 16, 2009, Virology, July 2009.
Source
In general, the children of women infected with Hepatitis C have a low risk of being born with the virus. In addition to what was previously known about this type of Hepatitis C transmission, new research finds a genetic link that can aid - or prevent - this from occurring.
by Nicole Cutler, L.Ac.
Many women with a chronic viral infection are weary of procreating, because of the chance they may pass their illness on during pregnancy or birth. For those infected with Hepatitis C, this fear is especially pronounced.
There are a handful of reasonable causes supporting a fear of carrying a baby and giving birth with Hepatitis C. They include:
· Hepatitis C is rampant in our society - affecting approximately four million Americans.
· Hepatitis C often leads to chronic liver disease.
· There is currently no guaranteed cure for Hepatitis C.
· Nearly half of those with Hepatitis C are unsure as to how they originally became infected.
Known as vertical transmission, the risk of infants acquiring Hepatitis C from their mother during pregnancy or childbirth is surprisingly low. There have been quite a few studies examining what the likelihood is of vertical transmission and what increases or decreases the risk of infecting a newborn with Hepatitis C.
Although the statistics determining the rate of vertical transmission is not uniform among these studies, experts believe the most accurate estimate of vertical transmission from mothers with Hepatitis C is five percent. Based upon a comprehensive review of trials investigating Hepatitis C vertical transmission, the following appear to represent the two largest risks for bearing a child with Hepatitis C:
1. The mother is co-infected with Hepatitis C and HIV.
2. The mother has a high Hepatitis C viral load during birth.
In addition, physicians typically relay the following information to pregnant women with Hepatitis C:
· The presence of Hepatitis C infection does not appear to result in a higher risk pregnancy or a higher incidence of poor obstetric outcome.
· Testing for the presence of Hepatitis C in infants born to infected mothers should not begin until at least one year following delivery. The natural history of Hepatitis C infected infants is poorly understood at this time.
· Prophylactic caesarian section is not recommended in Hepatitis C infected mothers. The role of cesarean delivery in mothers co-infected with Hepatitis C and HIV remains controversial.
· Breastfeeding presents a negligible risk of Hepatitis C transmission. Given the well-documented benefits of breastfeeding, it is highly recommended.
It has been a while since there were any additional factors recognized to affect the likelihood of vertical transmission. However, researchers from Italy have recently identified a genetic component that reliably foretells this possibility.
As published in the July 2009 edition of the journal Virology, a mismatch between genes carried by a mother and her infant appear to confer protection against Hepatitis C transmission. Elena Bevilacqua and colleagues from Italy investigated the role of several genes known to play a role in Hepatitis C infection. These researchers found that a specific gene, HLA-DRB1, could predict whether or not the infant acquires Hepatitis C infection from its mother. Based on this research:
1. When a mother and child have the same genetic variant of HLA-DRB1, there is no guarantee that vertical transmission will occur; it just increases the likelihood.
2. When a mother and child have different variations of HLA-DRB1, there appears to be guaranteed protection from vertical transmission.
Unfortunately, a mother cannot control the similarity or dissimilarity of her infant's genetic construction. However, whenever a trial reveals a definitive link for Hepatitis C transmission, we gain some ground in understanding this virus. Undoubtedly, the more information gathered on how Hepatitis C is transmitted, infects people, replicates and dies, the closer we are - as a whole - to putting an end to this source of chronic liver disease.
References:
http://en.wikipedia.org/wiki/HLA-DR, HLA-DR, Retrieved September 17, 2009, Wikimedia Foundation Inc., 2009.
http://www.hcvadvocate.org/hcsp/articles/HERRINE.html, Mother-to-Child Transmission of HCV, Steven K. Herrine, MD, Retrieved September 15, 2009, Hepatitis C Support Project, 2009.
http://www.hivandhepatitis.com/hep_c/news/2009/090109_a.html, Genetic Factors Influence Risk of Mother-to-child Hepatitis C Virus Transmission, Retrieved September 15, 2009, hivandhepatitis.com, 2009.
http://www.ncbi.nlm.nih.gov/pubmed/15239255, Diagnostic and prognostic value of virologic tests in vertical transmission of hepatitis C virus infection: results of a large prospective study in pregnant women, Saez, A, et al, Retrieved September 16, 2009, Hepato-Gastroenterology, July-August 2004.
http://www.ncbi.nlm.nih.gov/pubmed/19481774, Genetic factors in mother-to-child transmission of HCV infection, Bevilacqua E, et al, Retrieved September 16, 2009, Virology, July 2009.
Source
Viral entry and escape from antibody-mediated neutralization influence hepatitis C virus reinfection in liver transplantation
Published August 16, 2010
The Rockefeller University Press, doi: 10.1084/jem.20090766
© 2010 Fafi-Kremer et al.
Article
Samira Fafi-Kremer 1,2,3, Isabel Fofana 1,2, Eric Soulier 1,2, Patric Carolla 1,2, Philip Meuleman 6, Geert Leroux-Roels 6, Arvind H. Patel 7, François-Loïc Cosset 8, Patrick Pessaux 2,4, Michel Doffoël 1,2,5, Philippe Wolf 1,2,4, Françoise Stoll-Keller 1,2,3, and Thomas F. Baumert 1,2,3,5
+ Author Affiliations
1 Institut National de la Santé et de la Recherche Médicale, Unité 748, F-67000 Strasbourg, France
2 Université de Strasbourg, F-67000 Strasbourg, France
3 Laboratoire de Virologie,
4 Pôle des Pathologies Digestives, Hépatiques et Transplantation, and
5 Pôle Hépato-digestif, Hôpitaux Universitaires de Strasbourg, F-67000 Strasbourg, France
6 Center for Vaccinology, Ghent University and Hospital, 9000 Ghent, Belgium
7 Medical Research Council Centre for Virus Research, University of Glasgow, Glasgow G11 5JR, Scotland, UK
8Institut National de la Santé et de la Recherche Médicale, Unité 758, Institut Fédératif de Recherche 128, Ecole Normale Supérieure, Université Claude Bernard Lyon 1, Université de Lyon, F-69007 Lyon, France
CORRESPONDENCE Thomas F. Baumert: Thomas.Baumert@unistra.fr OR Françoise Stoll-Keller: francoise.stoll@unistra.fr
Abstract
End-stage liver disease caused by chronic hepatitis C virus (HCV) infection is a leading cause for liver transplantation (LT). Due to viral evasion from host immune responses and the absence of preventive antiviral strategies, reinfection of the graft is universal. The mechanisms by which the virus evades host immunity to reinfect the liver graft are unknown. In a longitudinal analysis of six HCV-infected patients undergoing LT, we demonstrate that HCV variants reinfecting the liver graft were characterized by efficient entry and poor neutralization by antibodies present in pretransplant serum compared with variants not detected after transplantation. Monoclonal antibodies directed against HCV envelope glycoproteins or a cellular entry factor efficiently cross-neutralized infection of human hepatocytes by patient-derived viral isolates that were resistant to autologous host-neutralizing responses. These findings provide significant insights into the molecular mechanisms of viral evasion during HCV reinfection and suggest that viral entry is a viable target for prevention of HCV reinfection of the liver graft.
Footnotes
Abbreviations used:
ANOV Aanalysis of variance
HCV hepatitis C virus
HCVpp HCV pseudoparticle
LT liver transplantationu
PA-SCID urokinase-type plasminogen activator/severe combined immunodeficient
Submitted: 7 April 2009
Accepted: 8 July 2010
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
Source
The Rockefeller University Press, doi: 10.1084/jem.20090766
© 2010 Fafi-Kremer et al.
Article
Samira Fafi-Kremer 1,2,3, Isabel Fofana 1,2, Eric Soulier 1,2, Patric Carolla 1,2, Philip Meuleman 6, Geert Leroux-Roels 6, Arvind H. Patel 7, François-Loïc Cosset 8, Patrick Pessaux 2,4, Michel Doffoël 1,2,5, Philippe Wolf 1,2,4, Françoise Stoll-Keller 1,2,3, and Thomas F. Baumert 1,2,3,5
+ Author Affiliations
1 Institut National de la Santé et de la Recherche Médicale, Unité 748, F-67000 Strasbourg, France
2 Université de Strasbourg, F-67000 Strasbourg, France
3 Laboratoire de Virologie,
4 Pôle des Pathologies Digestives, Hépatiques et Transplantation, and
5 Pôle Hépato-digestif, Hôpitaux Universitaires de Strasbourg, F-67000 Strasbourg, France
6 Center for Vaccinology, Ghent University and Hospital, 9000 Ghent, Belgium
7 Medical Research Council Centre for Virus Research, University of Glasgow, Glasgow G11 5JR, Scotland, UK
8Institut National de la Santé et de la Recherche Médicale, Unité 758, Institut Fédératif de Recherche 128, Ecole Normale Supérieure, Université Claude Bernard Lyon 1, Université de Lyon, F-69007 Lyon, France
CORRESPONDENCE Thomas F. Baumert: Thomas.Baumert@unistra.fr OR Françoise Stoll-Keller: francoise.stoll@unistra.fr
Abstract
End-stage liver disease caused by chronic hepatitis C virus (HCV) infection is a leading cause for liver transplantation (LT). Due to viral evasion from host immune responses and the absence of preventive antiviral strategies, reinfection of the graft is universal. The mechanisms by which the virus evades host immunity to reinfect the liver graft are unknown. In a longitudinal analysis of six HCV-infected patients undergoing LT, we demonstrate that HCV variants reinfecting the liver graft were characterized by efficient entry and poor neutralization by antibodies present in pretransplant serum compared with variants not detected after transplantation. Monoclonal antibodies directed against HCV envelope glycoproteins or a cellular entry factor efficiently cross-neutralized infection of human hepatocytes by patient-derived viral isolates that were resistant to autologous host-neutralizing responses. These findings provide significant insights into the molecular mechanisms of viral evasion during HCV reinfection and suggest that viral entry is a viable target for prevention of HCV reinfection of the liver graft.
Footnotes
Abbreviations used:
ANOV Aanalysis of variance
HCV hepatitis C virus
HCVpp HCV pseudoparticle
LT liver transplantationu
PA-SCID urokinase-type plasminogen activator/severe combined immunodeficient
Submitted: 7 April 2009
Accepted: 8 July 2010
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
Source
HIV/AIDS: The Best of Times and the Worst of Times
David Mixner
Author/Activist
Posted: August 18, 2010 10:20 AM
Over the past three decades, HIV/AIDS has had a way of taunting us with progress and then reminding us of its immense devastation. Even in the early years, we had a parade of promising therapies that gave us hope, only to find out they did not contain the answer. Not until the advent of AZT, although far from perfect, were we allowed real hope for the future. Unfortunately until the development of antiretrovirals, those small steps forward were too late for so many of our brothers and sisters.
In the last few months, the media has been filled with encouraging, and even exciting, news about the progress in treating this horrendous epidemic. At the very same time, we have been dealt some real setbacks in the care and treatment of people with HIV/AIDS. The lesson is the same as it always has been to the HIV/AIDS community: embrace and celebrate the progress while not letting up the pressure until there is a cure.
The good news is indeed reason to celebrate. Real progress is being made in fighting this disease. From the International AIDS Conference in Vienna comes word that promising new gels have been developed that could dramatically lower the infection rate among at risk women. The progress toward ending mother to child transmission has been just short of a miracle. In addition, the Wall Street Journal published a story indicating that scientists have discovered three powerful antibodies which can neutralize 91% of HIV strains.
The bad news is that the economic situation is wrecking havoc with HIV/AIDS budgets, international funds to fight HIV, research and treatment and care. Many states are freezing the ability of people with HIV/AIDS to receive antiretrovirals and treatment. AIDS Drug Assistance Program (ADAP) funds have either been cut way back or frozen making it impossible for new clients to have access to them. Unless this situation is totally corrected, it could mean a death sentence for some people with HIV/AIDS.
This brings us to the need to keep up the pressure, seek new funds and most importantly hold people in government accountable for their actions. Given the uncertainty with the economy and ADAP, it makes Medicare funds for treating HIV/AIDS even more critical in assisting people with the disease.
Medicare provides a vital source of health coverage for around 100,000 people with the disease. In 2006, Medicare became the single largest source of federal financing for HIV care. The number of people with HIV receiving Medicare benefits has grown over time, reflecting growth in the size of the of the HIV positive population in the U.S. but also an increased lifespan for people with HIV due to antiretroviral medicines and other treatment advances.
When you get to accountability, we face an enormous problem with Medicare with the passage of the new health care law. Thrilled as I was with this major step forward, there is one part that is extremely disturbing to me. Especially since my journey over the years has taught me the urgent need to hold our public officials accountable for their actions in this battle for a cure.
Quite simply, with the creation of an entity called the Independent Payment Advisory Board (IPAB), we could lose our ability to put pressure for change. This new board is simply not accountable to anyone.
While the IPAB is tasked with cutting Medicare spending, it is exempt from any judicial or administrative review of its decisions and is barred from probing the government's spending patterns on specific health care providers, such as hospitals where large chunks of federal health care dollars are spent.
Shackled by such restraints and yet dangerously unaccountable to Congress, the people or the courts, this board could turn its attention to successful programs in Medicare to carry out its cost cutting mission.
The mere existence of an unchecked, powerful agency making life-determining decisions should be worrisome to all Medicare beneficiaries. Draconian decisions by IPAB to limit access to medicines to treat HIV will be free from judicial review, the need for advance public notice, or even appeals from patients.
The fact of the matter is that the IPAB, like any other agency of government, can make bad and disastrous decisions which could dramatically impact our ability to treat, fight and win the battle against HIV/AIDS. And if they do, we have absolutely no recourse to change them.....none....nada.
Yes, we can assume that the appointees would be 'enlightened people." However anyone in government knows the bizarre process of selecting appointments. We cannot count on the basic good nature of human beings and can only count on our ability to hold them accountable in a democratic and open process.
Personally, I can't think of a worse scenario than for our research leaders to be on the cusp of a cure, only to be denied the necessary resources because a government panel has blown research and development into the stone ages.
We must not be shortsighted in our zeal to bring down health care costs by thwarting future research and reversing already achieved progress. Stated simply, if we go this route, we would only blunt the more laudable and courageous goal of saving lives and one day eliminating this horrific disease once and for all.
Source
Author/Activist
Posted: August 18, 2010 10:20 AM
Over the past three decades, HIV/AIDS has had a way of taunting us with progress and then reminding us of its immense devastation. Even in the early years, we had a parade of promising therapies that gave us hope, only to find out they did not contain the answer. Not until the advent of AZT, although far from perfect, were we allowed real hope for the future. Unfortunately until the development of antiretrovirals, those small steps forward were too late for so many of our brothers and sisters.
In the last few months, the media has been filled with encouraging, and even exciting, news about the progress in treating this horrendous epidemic. At the very same time, we have been dealt some real setbacks in the care and treatment of people with HIV/AIDS. The lesson is the same as it always has been to the HIV/AIDS community: embrace and celebrate the progress while not letting up the pressure until there is a cure.
The good news is indeed reason to celebrate. Real progress is being made in fighting this disease. From the International AIDS Conference in Vienna comes word that promising new gels have been developed that could dramatically lower the infection rate among at risk women. The progress toward ending mother to child transmission has been just short of a miracle. In addition, the Wall Street Journal published a story indicating that scientists have discovered three powerful antibodies which can neutralize 91% of HIV strains.
The bad news is that the economic situation is wrecking havoc with HIV/AIDS budgets, international funds to fight HIV, research and treatment and care. Many states are freezing the ability of people with HIV/AIDS to receive antiretrovirals and treatment. AIDS Drug Assistance Program (ADAP) funds have either been cut way back or frozen making it impossible for new clients to have access to them. Unless this situation is totally corrected, it could mean a death sentence for some people with HIV/AIDS.
This brings us to the need to keep up the pressure, seek new funds and most importantly hold people in government accountable for their actions. Given the uncertainty with the economy and ADAP, it makes Medicare funds for treating HIV/AIDS even more critical in assisting people with the disease.
Medicare provides a vital source of health coverage for around 100,000 people with the disease. In 2006, Medicare became the single largest source of federal financing for HIV care. The number of people with HIV receiving Medicare benefits has grown over time, reflecting growth in the size of the of the HIV positive population in the U.S. but also an increased lifespan for people with HIV due to antiretroviral medicines and other treatment advances.
When you get to accountability, we face an enormous problem with Medicare with the passage of the new health care law. Thrilled as I was with this major step forward, there is one part that is extremely disturbing to me. Especially since my journey over the years has taught me the urgent need to hold our public officials accountable for their actions in this battle for a cure.
Quite simply, with the creation of an entity called the Independent Payment Advisory Board (IPAB), we could lose our ability to put pressure for change. This new board is simply not accountable to anyone.
While the IPAB is tasked with cutting Medicare spending, it is exempt from any judicial or administrative review of its decisions and is barred from probing the government's spending patterns on specific health care providers, such as hospitals where large chunks of federal health care dollars are spent.
Shackled by such restraints and yet dangerously unaccountable to Congress, the people or the courts, this board could turn its attention to successful programs in Medicare to carry out its cost cutting mission.
The mere existence of an unchecked, powerful agency making life-determining decisions should be worrisome to all Medicare beneficiaries. Draconian decisions by IPAB to limit access to medicines to treat HIV will be free from judicial review, the need for advance public notice, or even appeals from patients.
The fact of the matter is that the IPAB, like any other agency of government, can make bad and disastrous decisions which could dramatically impact our ability to treat, fight and win the battle against HIV/AIDS. And if they do, we have absolutely no recourse to change them.....none....nada.
Yes, we can assume that the appointees would be 'enlightened people." However anyone in government knows the bizarre process of selecting appointments. We cannot count on the basic good nature of human beings and can only count on our ability to hold them accountable in a democratic and open process.
Personally, I can't think of a worse scenario than for our research leaders to be on the cusp of a cure, only to be denied the necessary resources because a government panel has blown research and development into the stone ages.
We must not be shortsighted in our zeal to bring down health care costs by thwarting future research and reversing already achieved progress. Stated simply, if we go this route, we would only blunt the more laudable and courageous goal of saving lives and one day eliminating this horrific disease once and for all.
Source
HBV Damage Disappears With Long-Term Therapy
By Crystal Phend, Senior Staff Writer, MedPage Today
Published: August 18, 2010
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Long-term treatment with entecavir (Baraclude) at least partially reverses cirrhosis and fibrosis in most chronic hepatitis B patients, according to extended follow-up of a clinical trial.
In nucleoside-naive patients, liver biopsies taken at least six years after starting on three or more years of entecavir treatment revealed histologic improvement in 96% of patients.
Fibrosis score improved by at least one point in 88% of patients as well, found Ting-Tsung Chang, MD, of National Cheng Kung University Hospital in Tainan, Taiwan, and colleagues.
All 10 patients with advanced disease at baseline saw improvements in fibrosis and cirrhosis long term, the researchers reported in the September issue of Hepatology.
These results add to evidence challenging the idea that fibrosis is an irreversible and relentlessly progressive process, they noted.
The researchers analyzed outcomes from 69 patients who provided a long-term biopsy sample after having received entecavir for a total of at least three years as part of one of two identical phase III randomized trials, followed by rollover into an open-label study in which all patients got 1.0 mg entecavir daily.
The randomized phase of the trials showed entecavir superior to lamivudine (Epivir) for both patients with chronic e antigen-negative hepatitis B and those with e antigen-positive infections. All patients were nucleoside-naive before the trial.
Among the 57 patients who met criteria for the long-term efficacy analysis, the median time on entecavir was approximately six years (range three to seven).
The rate of histologic improvement compared with baseline rose to 96% at the long-term assessment, compared with 73% after just 48 weeks of therapy.
The same was true for the proportion with at least a one-point improvement in Ishak fibrosis score, rising from 32% at 48 weeks to 88% at the long-term assessment.
For those with necroinflammation by the Knodell classification at baseline, 75% dropped down to no or minimal necroinflammation long term. Among those with fibrosis at baseline, 72% had no or minimal fibrosis long term.
Only one of the 57 patients showed an increase in Ishak fibrosis score (1 at baseline versus 2 at long-term biopsy) despite undetectable HBV DNA, normal liver enzymes, and an improvement in necroinflammatory score long term.
Virologic suppression -- HBV DNA under 300 copies/mL -- was maintained for all patients at the time of long-term biopsy, while 86% had normalized alanine transaminase (ALT).
As expected from the sustained virologic response, there was no evidence of virologic rebound or development of antiviral drug resistance, the researchers noted.
Although 55% of patients lost e antigen and 33% had seroconversion during long-term treatment, those who didn't also showed improved liver histology and reversal of fibrosis, which Chang's group pointed to as evidence that "these outcomes are more closely associated with HBV DNA suppression than with immunologic response to therapy."
Moreover, the results confirm the value of long-term treatment for chronic hepatitis B, they concluded.
"The safety profile, potent suppression of HBV replication, and low potential for antiviral drug resistance in nucleoside-naive patients make long-term treatment of chronic hepatitis B with entecavir monotherapy possible," they wrote in the paper.
The study was sponsored by the Bristol-Myers Squibb Pharmaceutical Research Institute.
Chang reported having research funding from Gilead Sciences, Bristol-Myers Squibb, GlaxoSmithKline, Schering-Plough, and Pfizer, as well as receiving speech honoraria from Bristol-Myers Squibb and Schering-Plough.
Several co-authors reported being employees of Bristol-Myers Squibb.
Primary source: Hepatology
Source reference:
Chang T-T, et al "Long-term entecavir therapy results in reversal of fibrosis/cirrhosis and continued histologic improvement in chronic hepatitis B patients" Hepatology 2010; DOI: 10.1002/hep.23785.
Source
Published: August 18, 2010
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Long-term treatment with entecavir (Baraclude) at least partially reverses cirrhosis and fibrosis in most chronic hepatitis B patients, according to extended follow-up of a clinical trial.
In nucleoside-naive patients, liver biopsies taken at least six years after starting on three or more years of entecavir treatment revealed histologic improvement in 96% of patients.
Fibrosis score improved by at least one point in 88% of patients as well, found Ting-Tsung Chang, MD, of National Cheng Kung University Hospital in Tainan, Taiwan, and colleagues.
All 10 patients with advanced disease at baseline saw improvements in fibrosis and cirrhosis long term, the researchers reported in the September issue of Hepatology.
These results add to evidence challenging the idea that fibrosis is an irreversible and relentlessly progressive process, they noted.
The researchers analyzed outcomes from 69 patients who provided a long-term biopsy sample after having received entecavir for a total of at least three years as part of one of two identical phase III randomized trials, followed by rollover into an open-label study in which all patients got 1.0 mg entecavir daily.
The randomized phase of the trials showed entecavir superior to lamivudine (Epivir) for both patients with chronic e antigen-negative hepatitis B and those with e antigen-positive infections. All patients were nucleoside-naive before the trial.
Among the 57 patients who met criteria for the long-term efficacy analysis, the median time on entecavir was approximately six years (range three to seven).
The rate of histologic improvement compared with baseline rose to 96% at the long-term assessment, compared with 73% after just 48 weeks of therapy.
The same was true for the proportion with at least a one-point improvement in Ishak fibrosis score, rising from 32% at 48 weeks to 88% at the long-term assessment.
For those with necroinflammation by the Knodell classification at baseline, 75% dropped down to no or minimal necroinflammation long term. Among those with fibrosis at baseline, 72% had no or minimal fibrosis long term.
Only one of the 57 patients showed an increase in Ishak fibrosis score (1 at baseline versus 2 at long-term biopsy) despite undetectable HBV DNA, normal liver enzymes, and an improvement in necroinflammatory score long term.
Virologic suppression -- HBV DNA under 300 copies/mL -- was maintained for all patients at the time of long-term biopsy, while 86% had normalized alanine transaminase (ALT).
As expected from the sustained virologic response, there was no evidence of virologic rebound or development of antiviral drug resistance, the researchers noted.
Although 55% of patients lost e antigen and 33% had seroconversion during long-term treatment, those who didn't also showed improved liver histology and reversal of fibrosis, which Chang's group pointed to as evidence that "these outcomes are more closely associated with HBV DNA suppression than with immunologic response to therapy."
Moreover, the results confirm the value of long-term treatment for chronic hepatitis B, they concluded.
"The safety profile, potent suppression of HBV replication, and low potential for antiviral drug resistance in nucleoside-naive patients make long-term treatment of chronic hepatitis B with entecavir monotherapy possible," they wrote in the paper.
The study was sponsored by the Bristol-Myers Squibb Pharmaceutical Research Institute.
Chang reported having research funding from Gilead Sciences, Bristol-Myers Squibb, GlaxoSmithKline, Schering-Plough, and Pfizer, as well as receiving speech honoraria from Bristol-Myers Squibb and Schering-Plough.
Several co-authors reported being employees of Bristol-Myers Squibb.
Primary source: Hepatology
Source reference:
Chang T-T, et al "Long-term entecavir therapy results in reversal of fibrosis/cirrhosis and continued histologic improvement in chronic hepatitis B patients" Hepatology 2010; DOI: 10.1002/hep.23785.
Source
Potential HIV drug keeps virus out of cells
Public release date: 18-Aug-2010
Contact: Phil Sahm
phil.sahm@hsc.utah.edu
801-581-2517
University of Utah Health Sciences
University of Utah biochemist hopes to begin human clinical trials in two to three years
SALT LAKE CITY—Following up a pioneering 2007 proof-of-concept study, a University of Utah biochemist and colleagues have developed a promising new anti-HIV drug candidate, PIE12-trimer, that prevents HIV from attacking human cells.
Michael S. Kay, M.D., Ph.D., associate professor of biochemistry in the University of Utah School of Medicine and senior author of the study published Wednesday, Aug. 18, 2010, online by the Journal of Virology, is raising funds to begin animal safety studies, followed by human clinical trials in two to three years. Kay believes PIE12-trimer is ideally suited for use as a vaginal microbicide (topically applied drug) to prevent HIV infection. His research group is particularly focused on preventing the spread of HIV in Africa, which has an estimated two-thirds of the world's 33 million HIV patients according to the World Health Organization.
"We believe that PIE12-trimer could provide a major new weapon in the arsenal against HIV/AIDS. Because of its ability to block the virus from infecting new cells, PIE12-trimer has the potential to work as a microbicide to prevent people from contracting HIV and as a treatment for HIV infected people. HIV can develop resistance rapidly to existing drugs, so there is a constant need to develop new drugs in hopes of staying ahead of the virus." Kay said.
PIE12-trimer was designed with a unique "resistance capacitor" that provides it with a strong defense against the emergence of drug-resistant viruses.
Peptide drugs have great therapeutic potential, but are often hampered by their rapid degradation in the body. D-peptides are mirror-image versions of natural peptides that cannot be broken down, potentially leading to higher potency and longevity in the body. Despite these potential advantages, no D-peptides have yet been developed.
PIE12-trimer consists of three D-peptides (PIE12) linked together that block a "pocket" on the surface of HIV critical for HIV's gaining entry into the cell. "Clinical trials will determine if PIE12-trimer is as effective in humans as it is in the lab," Kay said.
Across the world, HIV occurs in many different strains and has the ability to mutate to resist drugs aimed at stopping it. Due to the high conservation of the pocket region across strains, PIE12-trimer worked against all major HIV strains worldwide, from Southeast Asia and South America to the United States and Africa.
To help advance toward human clinical trials, Kay and co-authors Brett D. Welch, Ph.D., and Debra M. Eckert, Ph.D., research assistant professor of biochemistry, formed a company, Kayak Biosciences, which is owned by the University of Utah Research Foundation. If PIE12-trimer proves to be an effective and safe drug against HIV, the same D-Peptide drug design principles can be applied against other viruses, according to Kay. Approval of the first D-peptide drug would also greatly stimulate development of other D-peptide drugs.
###
The study's first authors are Welch, and U of U graduate student J. Nicholas Francis. Also contributing were U graduate students Joseph Redman and Matthew Weinstock, as well as Eckert. Images of how PIE12 binds to the HIV pocket were obtained using X-ray crystallography, a technology that provides high-resolution analysis of atomic structures, and were provided by Frank Whitby, Ph.D., research assistant professor of biochemistry, and Christopher P. Hill, Ph.D., professor and co-chair of the Department of Biochemistry. The study includes colleagues from Thomas Jefferson University in Philadelphia and Monogram Biosciences, South San Francisco, Calif.
This research was funded by the National Institutes of Health and the University of Utah Research Foundation.
Source
Contact: Phil Sahm
phil.sahm@hsc.utah.edu
801-581-2517
University of Utah Health Sciences
University of Utah biochemist hopes to begin human clinical trials in two to three years
SALT LAKE CITY—Following up a pioneering 2007 proof-of-concept study, a University of Utah biochemist and colleagues have developed a promising new anti-HIV drug candidate, PIE12-trimer, that prevents HIV from attacking human cells.
Michael S. Kay, M.D., Ph.D., associate professor of biochemistry in the University of Utah School of Medicine and senior author of the study published Wednesday, Aug. 18, 2010, online by the Journal of Virology, is raising funds to begin animal safety studies, followed by human clinical trials in two to three years. Kay believes PIE12-trimer is ideally suited for use as a vaginal microbicide (topically applied drug) to prevent HIV infection. His research group is particularly focused on preventing the spread of HIV in Africa, which has an estimated two-thirds of the world's 33 million HIV patients according to the World Health Organization.
"We believe that PIE12-trimer could provide a major new weapon in the arsenal against HIV/AIDS. Because of its ability to block the virus from infecting new cells, PIE12-trimer has the potential to work as a microbicide to prevent people from contracting HIV and as a treatment for HIV infected people. HIV can develop resistance rapidly to existing drugs, so there is a constant need to develop new drugs in hopes of staying ahead of the virus." Kay said.
PIE12-trimer was designed with a unique "resistance capacitor" that provides it with a strong defense against the emergence of drug-resistant viruses.
Peptide drugs have great therapeutic potential, but are often hampered by their rapid degradation in the body. D-peptides are mirror-image versions of natural peptides that cannot be broken down, potentially leading to higher potency and longevity in the body. Despite these potential advantages, no D-peptides have yet been developed.
PIE12-trimer consists of three D-peptides (PIE12) linked together that block a "pocket" on the surface of HIV critical for HIV's gaining entry into the cell. "Clinical trials will determine if PIE12-trimer is as effective in humans as it is in the lab," Kay said.
Across the world, HIV occurs in many different strains and has the ability to mutate to resist drugs aimed at stopping it. Due to the high conservation of the pocket region across strains, PIE12-trimer worked against all major HIV strains worldwide, from Southeast Asia and South America to the United States and Africa.
To help advance toward human clinical trials, Kay and co-authors Brett D. Welch, Ph.D., and Debra M. Eckert, Ph.D., research assistant professor of biochemistry, formed a company, Kayak Biosciences, which is owned by the University of Utah Research Foundation. If PIE12-trimer proves to be an effective and safe drug against HIV, the same D-Peptide drug design principles can be applied against other viruses, according to Kay. Approval of the first D-peptide drug would also greatly stimulate development of other D-peptide drugs.
###
The study's first authors are Welch, and U of U graduate student J. Nicholas Francis. Also contributing were U graduate students Joseph Redman and Matthew Weinstock, as well as Eckert. Images of how PIE12 binds to the HIV pocket were obtained using X-ray crystallography, a technology that provides high-resolution analysis of atomic structures, and were provided by Frank Whitby, Ph.D., research assistant professor of biochemistry, and Christopher P. Hill, Ph.D., professor and co-chair of the Department of Biochemistry. The study includes colleagues from Thomas Jefferson University in Philadelphia and Monogram Biosciences, South San Francisco, Calif.
This research was funded by the National Institutes of Health and the University of Utah Research Foundation.
Source
Healthcare Quality in HCV Is Suboptimum, Based on Medicare Criteria
Laurie Barclay, MD
August 18, 2010 — Healthcare quality in chronic hepatitis C virus (HCV) infection is suboptimum based on Medicare criteria, according to the results of a retrospective cohort study reported in the August 17 issue of the Annals of Internal Medicine.
"Medicare has proposed quality-of-care indicators for chronic [HCV] infection," write Fasiha Kanwal, MD, MSHS, from the John Cochran Veterans Affairs Medical Center and Saint Louis University School of Medicine, Missouri, and colleagues. "The extent to which these standards are met in practice is largely unknown."
Using a nationwide US health insurance company research database, the investigators aimed to assess the quality of healthcare received by patients with HCV, as well as factors linked to receipt of quality care. Between 2003 and 2006, 10,385 patients with HCV were enrolled in the database. Those patients eligible for at least 1 of 7 explicit quality indicators included in Medicare's 2009 Physician Quality Reporting Initiative were included in the analysis.
All recommended care was received by only 18.5% of patients (95% confidence interval [CI], 18% - 19%). The proportions of patients who met quality indicators varied considerably, from 21.5% for vaccination to 79% for the HCV genotype testing indicator.
Factors associated with lower quality of care were older age and presence of comorbid conditions, whereas elevated liver enzyme levels, cirrhosis, and HIV infection predicted higher quality of care. The best care was received by patients who saw both generalists and specialists. Compared with collaborative care (ie, from both specialist and primary care physician), the odds ratio of receiving care for which a patient was eligible was 0.79 (95% CI, 0.66 - 0.95) when specialists alone were involved in the patient's care, and 0.44 (95% CI, 0.40 - 0.48) when the primary care physician alone was involved in the patient's healthcare.
Limitations of this study include observational retrospective design, use of a convenience sample, lack of data on patient ethnicity, and the possibility that the indicators or the reporting of the indicators of HCV care are suboptimal, rather than the care itself. In addition, some of the findings may reflect differential ascertainment and coding.
"Healthcare quality, based on Medicare criteria, is suboptimum for HCV," the study authors write. "Care that included both specialists and generalists is associated with the best quality. Our results support the development of specialist and primary care collaboration to improve the quality of HCV care."
The Saint Louis University Liver Center supported this study. Some of the study authors report various financial relationships with Veterans Affairs Health Services, Saint Louis University Liver Center, Merck/Schering-Plough, Valeant, Gilead Sciences, Three Rivers Pharma, Vertex, Human Genome Sciences, and/or Up-To-Date.
Ann Intern Med. 2010;153:231-239.
Source
Also See: Quality of Care in Patients With Chronic Hepatitis C Virus Infection
August 18, 2010 — Healthcare quality in chronic hepatitis C virus (HCV) infection is suboptimum based on Medicare criteria, according to the results of a retrospective cohort study reported in the August 17 issue of the Annals of Internal Medicine.
"Medicare has proposed quality-of-care indicators for chronic [HCV] infection," write Fasiha Kanwal, MD, MSHS, from the John Cochran Veterans Affairs Medical Center and Saint Louis University School of Medicine, Missouri, and colleagues. "The extent to which these standards are met in practice is largely unknown."
Using a nationwide US health insurance company research database, the investigators aimed to assess the quality of healthcare received by patients with HCV, as well as factors linked to receipt of quality care. Between 2003 and 2006, 10,385 patients with HCV were enrolled in the database. Those patients eligible for at least 1 of 7 explicit quality indicators included in Medicare's 2009 Physician Quality Reporting Initiative were included in the analysis.
All recommended care was received by only 18.5% of patients (95% confidence interval [CI], 18% - 19%). The proportions of patients who met quality indicators varied considerably, from 21.5% for vaccination to 79% for the HCV genotype testing indicator.
Factors associated with lower quality of care were older age and presence of comorbid conditions, whereas elevated liver enzyme levels, cirrhosis, and HIV infection predicted higher quality of care. The best care was received by patients who saw both generalists and specialists. Compared with collaborative care (ie, from both specialist and primary care physician), the odds ratio of receiving care for which a patient was eligible was 0.79 (95% CI, 0.66 - 0.95) when specialists alone were involved in the patient's care, and 0.44 (95% CI, 0.40 - 0.48) when the primary care physician alone was involved in the patient's healthcare.
Limitations of this study include observational retrospective design, use of a convenience sample, lack of data on patient ethnicity, and the possibility that the indicators or the reporting of the indicators of HCV care are suboptimal, rather than the care itself. In addition, some of the findings may reflect differential ascertainment and coding.
"Healthcare quality, based on Medicare criteria, is suboptimum for HCV," the study authors write. "Care that included both specialists and generalists is associated with the best quality. Our results support the development of specialist and primary care collaboration to improve the quality of HCV care."
The Saint Louis University Liver Center supported this study. Some of the study authors report various financial relationships with Veterans Affairs Health Services, Saint Louis University Liver Center, Merck/Schering-Plough, Valeant, Gilead Sciences, Three Rivers Pharma, Vertex, Human Genome Sciences, and/or Up-To-Date.
Ann Intern Med. 2010;153:231-239.
Source
Also See: Quality of Care in Patients With Chronic Hepatitis C Virus Infection
Live donors not an option for some waiting for liver transplants
Ginger Delgado KDVR Denver
10:11 PM MDT, August 17, 2010
GOLDEN, Colo. - There are currently 524 people in Colorado waiting for a deceased liver donor. With the average wait time about three to five years, many of them will die waiting. Some have the option of a live donor liver transplant but won't take the risk.
One of those women is Pamela Meadows, 57, of Golden. Three years ago, she was diagnosed with Stage 4 liver disease. Only 15% of her liver is still functioning. She's been on the waiting list in Colorado for three years for a deceased liver donor, but for her, a live liver donor is simply not an option.
Meadows reached out to us here at Fox 31, shortly after we aired a story about Chad and Ryan Arnold, two brothers who underwent a live donor liver transplant in which Ryan died shortly after the procedure. Meadows told us, "My heart goes out to Chad more than ever now because not only does he have the physical recovery to face but he has the emotional struggle now."
While the Arnold's story touched her heart, Meadows says a live liver transplant is not for her, "I think it would be an extremely difficult thing for me. It's just not an option. Do I want to die anytime soon? No. Do any of us? But I'm OK with whatever the plan is."
A bloated stomach and swollen feet were just a few of her symptoms when doctors told her she had Hepatitis C. Today, Meadows is weak but better and still waiting patiently for a deceased liver donor. She told FOX31, "It has been a huge hurdle for me to think about the fact that someone has to die in order for me to live. And while I know they're not technically dying for me to live, it still feels that way." Despite the emotional struggle though, and her very serious condition, Meadows is still in good spirits. She says, "I have yet to get depressed about it. I have yet to feel like woe is me."
She is now focusing on her family and living for the present with no fears about whether she gets a new liver or not. She says, "If I could possibly live a number of years more in the kind of condition I'm in now, I would be happy with that. I'm at peace with it. I really am."
For more information on how you can become an organ donor, visit wwww.donatelifecolorado.org.
Copyright © 2010, KDVR-TV
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Donor dies after live liver transplant at CU Hospital
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Study Says, Many People Unknowingly Carry One of the Hepatitis Viruses
Submitted by Barinder Khatra on Wed, 08/18/2010 - 14:36
NHS has been told to provide free-of-cost tests for hepatitis B and C in pharmacies. Hepatitis B and C cause severe damage to liver and can lead to liver cancer.
The study shows that one out of every six people is the carrier of either hepatitis C or hepatitis B virus. Both the viruses can be transmitted by infected blood.
When a pilot study was done in 19 pharmacies in five regions in the United Kingdom, it was found that more than expected people had the viruses.
The pharmacies conducted 236 tests, out of which 35 people (15%) had hepatitis C and 4 people (2%) were suffering from hepatitis B. The GP screening rate was 4% for hepatitis C and 2% for hepatitis B, respectively.
The Royal Pharmaceutical Society and the Hepatitis C Trust want that more screenings should be done on a national scale. It is worth mentioning that lot of people carry the disease for a long time without showing any symptoms.
Charles Gore, the Chief Executive of the Hepatitis C Trust says that death rates from hepatitis are increasing significantly. He also said that it is very unfortunate that the number is increasing in those people who would have otherwise survived, if they were treated properly at the right time.
Gore also mentioned that, “we desperately need new approaches to testing that will find the undiagnosed patients. This pilot study shows pharmacy testing could be just what is needed”.
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NHS has been told to provide free-of-cost tests for hepatitis B and C in pharmacies. Hepatitis B and C cause severe damage to liver and can lead to liver cancer.
The study shows that one out of every six people is the carrier of either hepatitis C or hepatitis B virus. Both the viruses can be transmitted by infected blood.
When a pilot study was done in 19 pharmacies in five regions in the United Kingdom, it was found that more than expected people had the viruses.
The pharmacies conducted 236 tests, out of which 35 people (15%) had hepatitis C and 4 people (2%) were suffering from hepatitis B. The GP screening rate was 4% for hepatitis C and 2% for hepatitis B, respectively.
The Royal Pharmaceutical Society and the Hepatitis C Trust want that more screenings should be done on a national scale. It is worth mentioning that lot of people carry the disease for a long time without showing any symptoms.
Charles Gore, the Chief Executive of the Hepatitis C Trust says that death rates from hepatitis are increasing significantly. He also said that it is very unfortunate that the number is increasing in those people who would have otherwise survived, if they were treated properly at the right time.
Gore also mentioned that, “we desperately need new approaches to testing that will find the undiagnosed patients. This pilot study shows pharmacy testing could be just what is needed”.
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Also See:
Aethlon Medical Announces Expansion of Hepatitis C Virus (HCV) Treatment Programs
AETHLON MEDICAL HEMOPURIFIER Aethlon Hemopurifier.
(PRNewsFoto/Aethlon Medical, Inc.) SAN DIEGO, CA UNITED STATES
SAN DIEGO, Aug. 18 /PRNewswire-FirstCall/ -- Aethlon Medical, Inc. (OTC Bulletin Board: AEMD), the pioneer in developing therapeutic filtration devices to address infectious disease and cancer, today announced that it has entered into an agreement with GVK Biosciences (GVK BIO) to expand the opportunity for Aethlon to commercialize its Hemopurifier® treatment technology at three to five new clinical centers in India. The therapeutic focus at each center will be the implementation of the Hemopurifier® as an adjunct therapy to accelerate the benefit of HCV standard of care (SOC) drug regimens. Therapeutic filtration at the outset of SOC improves early virus reduction kinetics to levels associated with patients most likely to achieve a sustained viral response, which is the goal of HCV therapy. GVK BIO is Asia's leading Discovery Research and Development organization.
(Photo: http://photos.prnewswire.com/prnh/20090325/LA88762LOGO-b)
(Photo: http://www.newscom.com/cgi-bin/prnh/20090325/LA88762LOGO-b)
Aethlon further disclosed that the Ethics Review Board (ERB) at Medanta, The Medicity Institute (Medicity) met on August 14th, 2010 to discuss the potential approval for Aethlon to initiate HCV treatment programs at the Medicity. Aethlon has been advised that a formal response should be expected from the Medicity ERB in the coming weeks. The Medicity is a $360 million facility recently established on a 43-acre campus to be a premier center of medical tourism in India.
About GVK Biosciences
GVK Biosciences (GVK BIO) is Asia's leading Discovery Research and Development organization. GVK BIO provides a broad spectrum of services, stand-alone and integrated, across the R&D value chain. GVK BIO's diverse portfolio of more than 100 customers includes Big Pharma, Agri & Life-sciences companies, leading biotechs and academic institutions. Spread across five locations in India and headquartered in Hyderabad, GVK BIO assists clients accelerate their research. Additional information can be accessed at http://www.gvkbio.com/.
About Aethlon Medical
At Aethlon Medical, we create revolutionary devices to address infectious disease and cancer. Our devices are designed to be novel platform solutions that fill therapeutic voids or aid in disease diagnosis and monitoring.
Our Hemopurifier® is the first medical device to selectively target the removal of infectious viruses and immunosuppressive proteins from the entire circulatory system. We recently discovered that our Hemopurifier® captures tumor-secreted exosomes that suppress the immune system of those afflicted with cancer. Prior to this discovery, a therapeutic strategy to directly inhibit or reverse the immunosuppressive destruction caused by exosomes did not exist in cancer care. By eliminating this mechanism, we believe our Hemopurifier® can fill an unmet clinical need and provide the benefit of an immune-based therapy without adding drug toxicity or interaction risks to established and emerging treatment strategies.
Human studies have documented the ability of our Hemopurifier® to safely reduce viral load in both Hepatitis-C virus (HCV) and Human Immunodeficiency Virus (HIV) infected patients without the administration of antiviral drugs. However, our initial clinical and commercialization focus is to establish our Hemopurifier® as an adjunct therapy to enhance the benefit of both infectious disease and cancer treatment regimens. In this regard, we plan to commercialize our Hemopurifier® in India as we advance our clinical strategies in the United States and the European Union. In vitro studies conducted by government and non-government research institutes have also verified that our Hemopurifier® has broad-spectrum capabilities against bioterror and emerging pandemic threats. These studies have confirmed the capture of Dengue Hemorrhagic Virus, Ebola Hemorrhagic Virus, Lassa Hemorrhagic Virus, West Nile Virus, H5N1 Avian Influenza Virus, 2009 H1N1 Influenza Virus, the reconstructed Spanish Flu of 1918 Virus, and Monkeypox Virus, which serves as a model for human Smallpox infection.
As a therapeutic device, the Hemopurifier® provides us with a pipeline into four significant market opportunities:
- Cancer: A treatment candidate to improve patient responsiveness to established cancer therapies by removing immunosuppressive exosomes from circulation.
- Hepatitis-C Virus (HCV): As an adjunct therapy to accelerate viral load reduction at the outset of standard of care drug regimens.
- Human Immunodeficiency Virus (HIV): Provides a potential therapeutic option for HIV-infected individuals to manage disease progression once they become resistant to antiviral drug regimens.
- Bioterror and Pandemic Threats: Represents the most advanced broad-spectrum strategy to address untreatable bioterror and emerging pandemic threats.
In design, our Hemopurifier® is a selective filtration device containing affinity agents that tightly bind to high-mannose structures unique to the surface of exosomes produced by cancer and glycoproteins residing on the envelope of viruses. These agents are immobilized around approximately 2800 porous hollow fibers that run the interior length of our device. The resulting design provides us the novel ability to separate both exosome and viral targets away from blood cells so they can then be selectively and permanently removed from the circulatory system. In application, blood circulation is established into the Hemopurifier® via a catheter or other blood access device. Once blood flow has been established, treatment benefit is immediate as the entire circulatory system can pass through the Hemopurifier® in as little as 15 minutes.
Our wholly owned subsidiary, Exosome Sciences, Inc. (ESI) is focused on the development of exosome-targeted products and services that improve cancer diagnosis, provide post-treatment cancer surveillance, and aid in the discovery of biomarkers that allow doctors to optimize patient therapy. Additional information regarding Aethlon Medical and Exosome Sciences can be accessed online at http://www.aethlonmedical.com/.
Certain of the statements herein may be forward-looking and involve risks and uncertainties. Such forward-looking statements involve assumptions, known and unknown risks, uncertainties and other factors which may cause the actual results, performance or achievements of Aethlon Medical, Inc. to be materially different from any future results, performance, or achievements expressed or implied by the forward-looking statements. Such potential risks and uncertainties include, without limitation, the capability of the Hemopurifier® to reduce viral loads and other disease conditions or to identify or treat disease conditions such as cancer, including the ability to capture exosomes and the impact that potential ability may have on disease conditions, the Company's ability to raise capital when needed, the Company's ability to complete the development of its planned products, the ability of the Company to obtain FDA and other regulatory approvals permitting the sale of its products, the Company's ability to manufacture its products either internally or through outside companies and provide its services, the impact of government regulations, patent protection on the Company's proprietary technology, product liability exposure, uncertainty of market acceptance, competition, technological change, and other risk factors. In such instances, actual results could differ materially as a result of a variety of factors, including the risks associated with the effect of changing economic conditions and other risk factors detailed in the Company's Securities and Exchange Commission filings.
Contacts:
James A. Joyce
Chairman, CEO
858.459.7800 x301
jj@aethlonmedical.com
John P. Salvador
Director, Communications & Investor Relations
858.459.7800 x307
jps@aethlonmedical.com
Jon Cunningham
RedChip Companies, Inc.
800.733.2447 x107
jon@redchip.com
SOURCE Aethlon Medical, Inc.
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http://www.aethlonmedical.com/
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What is Hepatitis C?
This Hackney pharmacy has been pilot testing Hep C screening
Page last updated at 12:48 GMT, Wednesday, 18 August 2010 13:48 UK
More than 45,000 Londoners are believed to have Hepatitis C without knowing it.
Latest figures by the Hepatitis C Trust suggest 53,145 suffer from the disease in the capital - 7,386 have been diagnosed but a further 45,759 are estimated to be undiagnosed.
What is Hepatitis C?
Hepatitis C is an infection with the hepatitis C virus. Although there is no vaccine to protect against infection, there is effective treatment available.
Hepatitis C is a blood-borne virus that predominantly infects the cells of the liver. This can cause inflammation of and sometimes significant damage to the liver and affect its ability to perform its many, varied and essential functions.
According to the Hepatitis C Trust, although it has always been regarded as a liver disease (hepatitis means inflammation of the liver), recent research has shown that Hepatitis C affects a number of other areas of the body including the digestive system, the lymphatic system, the immune system and the brain.
Many do not realise they have it because they have no symptoms - it can take decades for symptoms to appear and by then serious damage can be caused.
Symptoms
Possible symptoms of Hepatitis C infection include:
• Fatigue
• Weight loss
• Loss of appetite
• Joint pains
• Nausea
• Flu-like symptoms (fever, headaches, sweats)
• Anxiety
• Difficulty concentrating
• Alcohol intolerance and pain in the liver area
How is it contracted?
-- Regularly sharing razors or toothbrushes (with a person who has Hepatitis C or B)
--Tattoos/piercings/acupuncture (in unregistered premises or with possibly unsterile equipment or with needles that were not new)
-- Unprotected sex - Hepatitis B (not C)
-- Sniffing/snorting cocaine (sharing pipes, notes or straws with a person with Hepatitis B or C
-- Receiving a blood transfusion/blood products /organ transplantation prior to 1991
-- Intravenous drug use - sharing needles with someone with Hepatitis B or C
Hepatitis B
Hepatitis B can be transmitted through blood and some body fluid contact and sexually transmitted. A vaccine and treatment is available which can manage but not clear the virus.
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