Hepatitis B Vaccination Cuts Deaths From Liver Disease, Cancer: Study
Taiwan study highlights need for vaccination for all, U.S. expert says
By Steven Reinberg
HealthDay Reporter
TUESDAY, Sept. 3 (HealthDay News) -- Taiwanese researchers report a 90 percent reduction in deaths from complications of hepatitis B since the country began its infant vaccination program in 1984.
Vaccinations have also decreased the spread of hepatitis B, which can cause liver damage, liver cancer and a deadly reaction in babies called infant fulminant hepatitis, the researchers said.
"Immunization has provided 30-year protection against acute hepatitis and end-stage chronic liver diseases, including cirrhosis and liver cancer," said lead researcher Chien-Jen Chen, a vice president at the Genomics Research Center at Academia Sinica in Taipei.
The implications of the findings are global.
Chen said there are 350 million chronic carriers of hepatitis B in the world, with the highest prevalence in the Asia-Pacific region and sub-Saharan Africa. The infection can be spread from mothers to newborns.
"All newborns in high-prevalence areas should be vaccinated to reduce the liver disease burden and health care costs," he said.
The report was published in the Sept. 4 issue of the Journal of the American Medical Association.
According to the Hepatitis B Foundation, 12 million Americans have been infected with the disease -- one out of every 20 people. In addition, more than 1 million people are chronically infected and up to 100,000 new infections occur each year.
The foundation estimates that 5,000 people in the United States die each year from hepatitis B and its complications.
The new findings add even more support for the need for vaccination, a U.S. expert said.
"This is an exclamation point of what we already knew -- that infants should be vaccinated against hepatitis B," said Dr. Marc Siegel, an associate professor of medicine at the NYU Langone Medical Center in New York City. "Vaccination of infants with hepatitis B vaccine, which is highly effective, leads to a dramatic decrease in chronic infection and liver cancer, which are outcomes for up to 50 percent of those with hepatitis B."
In addition, vaccination builds herd immunity as fewer people are infected, thus reducing the spread of the disease in the population, Siegel said. "Everybody should be vaccinated against this virus -- everybody," he said. "Infants and all adults should be vaccinated."
The hepatitis B vaccine is safe, Siegel said. "The disease is scary-- the vaccine is not," he said.
For the study, Chen's team looked at the 30-year outcomes of the immunization program in Taiwan. For the first two years, the immunization program covered only newborns of mothers who carried the disease. Then it expanded to all newborns.
In July 1987, vaccinations were extended to cover preschoolers. Between 1988 and 1999, the program was extended to cover all elementary school children.
The rate of vaccinations for those born from 1984 to 2010 was about 89 percent to 97 percent, the researchers found.
For those born between 1977 and 2004, a more than 90 percent reduction occurred in deaths from chronic liver disease and liver cancer, and there were 80 percent fewer cases of liver cancer overall.
Deaths from infant fulminant hepatitis B also decreased 90 percent.
Hepatitis B is spread when blood, semen or other body fluids infected with the virus enters the body of an uninfected person, according to the U.S. Centers for Disease Control and Prevention.
The infection can be transmitted from an infected mother to her newborn. The hepatitis B virus also can be transmitted during sex with an infected person or by sharing needles, syringes or other drug-injection equipment.
Sharing razors or toothbrushes with an infected person also can transmit the disease, as can direct contact with blood or open sores of an infected person, according to the CDC.
More information
For more about hepatitis B, visit the U.S. Centers for Disease Control and Prevention.
Copyright © 2012 HealthDay. All rights reserved.
http://health.usnews.com/health-news/news/articles/2013/09/03/hepatitis-b-vaccination-cuts-deaths-from-liver-disease-cancer-study
Tuesday, September 3, 2013
ArQule to cut liver cancer drug dose on safety concerns
ArQule to cut liver cancer drug dose on safety concerns
(Reuters)
Drugmaker ArQule Inc said it would lower the dose of its experimental liver cancer drug for a second time, after a late-stage trial showed that patients on the therapy were becoming more susceptible to infection.
The company's shares fell as much as 20 percent as the setback comes after the drug, tivantinib, failed separate trials for lung and colorectal cancers.
Analysts were concerned about whether the latest cut in dose would affect the drug's efficacy.
ArQule and its Japanese partner Daiichi Sankyo Inc accepted the recommendation of an independent safety committee to reduce, from 240 mg twice daily to 120 mg, the dose to treat hepatocellular carcinoma - the most common form of liver cancer.
Last year, ArQule reduced the liver cancer drug dose to 240 mg from 360 mg during a mid-stage trial due to high incidence of anemia and neutropenia - a condition characterized by an abnormally low number of infection-fighting white blood cells.
"The key question is how effective the 120 mg dose will be in treating hepatocellular carcinoma," MLV & Co analyst George Zavoico told Reuters.
Zavoico said the company might have to stop the trial if the neutropenia incidence remains greater than expected, but added that this was unlikely to happen at the 120 mg dose.
"This is no doubt a string of bad luck, but whether or not it suggests that the drug will ultimately fail is premature," Zavoico said.
ArQule and Daiichi Sankyo stopped a late-stage trial of tivantinib to treat lung cancer last October, after determining that the drug did not improve patient survival.
Kyowa Hakko Kirin Co, which holds development rights for the drug in Japan and certain parts of Asia, halted its own lung cancer trial soon after, following a safety committee's recommendation.
About two months later, the drug failed a mid-stage trial on patients with colorectal cancer.
ArQule and Daiichi Sankyo said on Tuesday that they were unable to comment on whether the timeline for recruitment of the liver cancer trial would be delayed, as the study was in the early stages of recruitment.
ArQule shares were down 7.5 percent at $2.58 on the Nasdaq on Tuesday.
(Reporting by Esha Dey and Vrinda Manocha in Bangalore; Editing by Kirti Pandey)
http://www.reuters.com/article/2013/09/03/us-arqule-study-cancer-idUSBRE9820MT20130903
(Reuters)
Drugmaker ArQule Inc said it would lower the dose of its experimental liver cancer drug for a second time, after a late-stage trial showed that patients on the therapy were becoming more susceptible to infection.
The company's shares fell as much as 20 percent as the setback comes after the drug, tivantinib, failed separate trials for lung and colorectal cancers.
Analysts were concerned about whether the latest cut in dose would affect the drug's efficacy.
ArQule and its Japanese partner Daiichi Sankyo Inc accepted the recommendation of an independent safety committee to reduce, from 240 mg twice daily to 120 mg, the dose to treat hepatocellular carcinoma - the most common form of liver cancer.
Last year, ArQule reduced the liver cancer drug dose to 240 mg from 360 mg during a mid-stage trial due to high incidence of anemia and neutropenia - a condition characterized by an abnormally low number of infection-fighting white blood cells.
"The key question is how effective the 120 mg dose will be in treating hepatocellular carcinoma," MLV & Co analyst George Zavoico told Reuters.
Zavoico said the company might have to stop the trial if the neutropenia incidence remains greater than expected, but added that this was unlikely to happen at the 120 mg dose.
"This is no doubt a string of bad luck, but whether or not it suggests that the drug will ultimately fail is premature," Zavoico said.
ArQule and Daiichi Sankyo stopped a late-stage trial of tivantinib to treat lung cancer last October, after determining that the drug did not improve patient survival.
Kyowa Hakko Kirin Co, which holds development rights for the drug in Japan and certain parts of Asia, halted its own lung cancer trial soon after, following a safety committee's recommendation.
About two months later, the drug failed a mid-stage trial on patients with colorectal cancer.
ArQule and Daiichi Sankyo said on Tuesday that they were unable to comment on whether the timeline for recruitment of the liver cancer trial would be delayed, as the study was in the early stages of recruitment.
ArQule shares were down 7.5 percent at $2.58 on the Nasdaq on Tuesday.
(Reporting by Esha Dey and Vrinda Manocha in Bangalore; Editing by Kirti Pandey)
http://www.reuters.com/article/2013/09/03/us-arqule-study-cancer-idUSBRE9820MT20130903
Study Examines Ways to Restore Immunity to Chronic Hepatitis C Infection
Study Examines Ways to Restore Immunity to Chronic Hepatitis C Infection
Sep. 3, 2013 — The hepatitis C virus hijacks the body's immune system, leaving T cells unable to function. A new study in animal models suggests that blocking a protein that helps the virus thrive could restore immune function, allowing the body to fight infection. The work, led by teams at The Research Institute at Nationwide Children's Hospital and Emory University, was published online Aug. 26 in the Proceedings of the National Academy of Sciences.
Sep. 3, 2013 — The hepatitis C virus hijacks the body's immune system, leaving T cells unable to function. A new study in animal models suggests that blocking a protein that helps the virus thrive could restore immune function, allowing the body to fight infection. The work, led by teams at The Research Institute at Nationwide Children's Hospital and Emory University, was published online Aug. 26 in the Proceedings of the National Academy of Sciences.
Previous studies show that antibody treatments that inhibit the
protein, called programmed cell death 1 (PD-1), can shrink tumors in
humans. This new work suggests that anti-PD-1 antibodies might be
equally effective in treating hepatitis C and other persistent human
viral infections, says Christopher Walker, PhD, a senior author on the
study and director of the Center for Vaccines and Immunity at Nationwide
Children's.
PD-1 is a regulatory protein that helps keep the immune system in check. Normally, PD-1 acts as a switch to turn off immune responses when an infection is under control. Some viruses such as HCV manipulate the PD-1 off switch so that T cells lose their ability to fight the infection, a condition scientists call "T-cell exhaustion." The result is life-long persistence of HCV in the liver, which increases the risk of cirrhosis, liver cancer and other serious diseases.
The researchers treated animal models with persistent HCV infection with repeated doses of an anti-PD-1 antibody. Although the responses were mixed, one animal did show a dramatic increase in HCV-specific T cell activity in the liver and a sharp decrease in viral load. A closer examination of the data found that the animal had more HCV-specific T cells in the liver before therapy, which could mean that therapeutic success hinges on the amount of HCV-specific T cells in the liver before treatment.
"Our supposition is that these T cells remained in the liver for years at levels too low to detect before treatment, and had the capacity to expand after treatment," Dr. Walker says. "The animal that responded to therapy had a broad, strong response during the early acute phase of infection. This suggests that one predictor of response to an anti-PD-1 antibody is the quality of the T-cell response when the initial infection occurs."
Another interesting finding was the impact of the antibody on CD4+ T cells, helper cells that promote the development of killer T cells called CD8+, which target and destroy virus-infected liver cells. One hallmark of chronic HCV is the collapse of CD4+ cells.
"We have no information on whether PD-1 signaling is a primary mechanism for silencing helper cells, so recovery of the CD4+ helper cell response in this instance provides some indirect evidence that PD-1 signaling also impairs the helper cells," Dr. Walker says.
Because much of the research focus on HCV is now directed at developing antiviral therapies, it's likely that these new findings may have a greater impact on treatments for chronic hepatitis B (HBV), rather than the virus studied in this experiment, Dr. Walker says.
"Chronic hepatitis B is an even larger public health problem than HCV and direct-acting drugs control but do not eliminate the virus," he says. "Immune reconstitution is the holy grail for HBV."
Toward that end, Dr. Walker's team plans to explore the insight this new study provides into why anti- PD-1 antibody therapy sometimes succeeds and sometimes fails. Specifically, they want to know what role the quality of T-cell immunity before treatment plays in therapeutic response.
"There is wide variation in the strength of T-cell immunity when people are first infected with the virus, ranging from very strong and sustained to none," notes Dr. Walker, who also is a professor of pediatrics and molecular virology, immunology, and medical genetics at The Ohio State University.
"Those with very strong sustained responses tend to clear the virus. Anything less, and the virus persists," Dr. Walker says. "This study suggests that if your T-cell response to the initial infection is good, but not enough to clear the virus, then you may respond to PD-1 blockade years later. If your initial acute phase T cell response is limited and weak, there is less opportunity for PD-1 blockade to work."
Story Source:
The above story is based on materials provided by Nationwide Children's Hospital.
Journal Reference:
PD-1 is a regulatory protein that helps keep the immune system in check. Normally, PD-1 acts as a switch to turn off immune responses when an infection is under control. Some viruses such as HCV manipulate the PD-1 off switch so that T cells lose their ability to fight the infection, a condition scientists call "T-cell exhaustion." The result is life-long persistence of HCV in the liver, which increases the risk of cirrhosis, liver cancer and other serious diseases.
The researchers treated animal models with persistent HCV infection with repeated doses of an anti-PD-1 antibody. Although the responses were mixed, one animal did show a dramatic increase in HCV-specific T cell activity in the liver and a sharp decrease in viral load. A closer examination of the data found that the animal had more HCV-specific T cells in the liver before therapy, which could mean that therapeutic success hinges on the amount of HCV-specific T cells in the liver before treatment.
"Our supposition is that these T cells remained in the liver for years at levels too low to detect before treatment, and had the capacity to expand after treatment," Dr. Walker says. "The animal that responded to therapy had a broad, strong response during the early acute phase of infection. This suggests that one predictor of response to an anti-PD-1 antibody is the quality of the T-cell response when the initial infection occurs."
Another interesting finding was the impact of the antibody on CD4+ T cells, helper cells that promote the development of killer T cells called CD8+, which target and destroy virus-infected liver cells. One hallmark of chronic HCV is the collapse of CD4+ cells.
"We have no information on whether PD-1 signaling is a primary mechanism for silencing helper cells, so recovery of the CD4+ helper cell response in this instance provides some indirect evidence that PD-1 signaling also impairs the helper cells," Dr. Walker says.
Because much of the research focus on HCV is now directed at developing antiviral therapies, it's likely that these new findings may have a greater impact on treatments for chronic hepatitis B (HBV), rather than the virus studied in this experiment, Dr. Walker says.
"Chronic hepatitis B is an even larger public health problem than HCV and direct-acting drugs control but do not eliminate the virus," he says. "Immune reconstitution is the holy grail for HBV."
Toward that end, Dr. Walker's team plans to explore the insight this new study provides into why anti- PD-1 antibody therapy sometimes succeeds and sometimes fails. Specifically, they want to know what role the quality of T-cell immunity before treatment plays in therapeutic response.
"There is wide variation in the strength of T-cell immunity when people are first infected with the virus, ranging from very strong and sustained to none," notes Dr. Walker, who also is a professor of pediatrics and molecular virology, immunology, and medical genetics at The Ohio State University.
"Those with very strong sustained responses tend to clear the virus. Anything less, and the virus persists," Dr. Walker says. "This study suggests that if your T-cell response to the initial infection is good, but not enough to clear the virus, then you may respond to PD-1 blockade years later. If your initial acute phase T cell response is limited and weak, there is less opportunity for PD-1 blockade to work."
Story Source:
The above story is based on materials provided by Nationwide Children's Hospital.
Journal Reference:
- M. J. Fuller, B. Callendret, B. Zhu, G. J. Freeman, D. L. Hasselschwert, W. Satterfield, A. H. Sharpe, L. B. Dustin, C. M. Rice, A. Grakoui, R. Ahmed, C. M. Walker. Immunotherapy of chronic hepatitis C virus infection with antibodies against programmed cell death-1 (PD-1). Proceedings of the National Academy of Sciences, 2013; DOI: 10.1073/pnas.1312772110
A New Drug for Diabetes and Fatty Liver Disease?
A New Drug for Diabetes and Fatty Liver Disease?
Posted on September 3, 2013 by Kristine Novak, PhD, Science Editor
Obeticholic acid (OCA)—an agonist of the farnesoid X receptor (FXR)— increases insulin sensitivity and reduces markers of liver inflammation and fibrosis in patients with type 2 diabetes mellitus and nonalcoholic fatty liver disease (NAFLD), according to a study published in the September issue of Gastroenterology.
Type 2 diabetes mellitus and NAFLD are components of the metabolic syndrome—a complex disorder characterized by insulin resistance, dyslipidemia, hypertension, and visceral obesity. Although several drugs are available to improve insulin resistance in patients with diabetes, none are currently approved for NAFLD or nonalcoholic steatohepatitis.
FXR is a bile acid receptor expressed in liver, intestine, kidney, and adipose tissue. It regulates many genes involved in bile acid synthesis and transport, lipid metabolism, and glucose homeostasis. FXR also controls glucose metabolism and glycogenolysis in the liver, and peripheral insulin sensitivity in striated muscle adipose tissue. Factors that activate FXR might therefore be used to control diabetes and fatty liver disease.
OCA is a selective agonist of FXR agonist with anti-cholestatic and hepato-protective properties. In preclinical studies, OCA was found to increase insulin sensitivity, regulate glucose homeostasis, modulate lipid metabolism, and have anti-inflammatory and anti-fibrotic effects in the liver, kidney, and intestine.
Sunder Mudaliar et al. tested the effects of OCA in a Phase 2 study of 64 patients with type 2 diabetes mellitus and NAFLD. Patients were given 25 or 50 mg OCA or placebo, once daily for 6 weeks. The hyperinsulinemic-euglycemic clamp technique was used to assess insulin sensitivity. Various markers of tolerance and safety, and markers of FXR activation (increased plasma levels of FGF19 and reduced bile acid synthesis), were assessed.
Mudaliar et al. found that OCA increased hepatic and peripheral insulin sensitivity (by about 25%), whereas insulin sensitivity decreased by about 5% in subjects given placebo. OCA produced a significant decrease in levels of γ-glutamyltransferase—a marker of fatty liver disease that is a risk factor for development of diabetes in patients with NAFLD.
OCA also caused patients to lose weight (see below figure).
Serum levels of FGF19 increased, whereas levels of C4 and endogenous bile acids decreased, indicating FXR activation in patients given OCA. The authors state that this was the first phase 2 clinical trial of an FXR agonist.
In an editorial that accompanies the article, Saul Karpen says that these findings herald a new era, in which bile-acid–based strategies are used to control metabolic signaling and treat liver and other types of diseases.
However, Karpen points out that the observed increases in low-density lipoprotein, reductions in high-density lipoprotein, and lack of change in alanine aminotransferase or liver fibrosis scores in subjects receiving OCA were notable and require further analysis. Mudaliar et al. did not perform liver biopsies, so they were not able to determine the degree and effect of OCA on liver histology.
Karpen says that studies with a larger sample sizes and more analyses are needed before conclusions can be made.
More Information on Fatty Liver Disease:
Mudaliar S, Henry RR, Sanyal AJ, et al. Efficacy and safety of the farnesoid x receptor agonist obeticholic acid in patients with type 2 diabetes and nonalcoholic fatty liver disease. Gastroenterology 2013;145:574–582.e1.
Read the accompanying editorial.
Karpen SJ. Do therapeutic bile acids hit the sweet spot of glucose metabolism in NAFLD? Gastroenterology 2013;145:508–510.
http://agajournals.wordpress.com/
Posted on September 3, 2013 by Kristine Novak, PhD, Science Editor
Obeticholic acid (OCA)—an agonist of the farnesoid X receptor (FXR)— increases insulin sensitivity and reduces markers of liver inflammation and fibrosis in patients with type 2 diabetes mellitus and nonalcoholic fatty liver disease (NAFLD), according to a study published in the September issue of Gastroenterology.
Type 2 diabetes mellitus and NAFLD are components of the metabolic syndrome—a complex disorder characterized by insulin resistance, dyslipidemia, hypertension, and visceral obesity. Although several drugs are available to improve insulin resistance in patients with diabetes, none are currently approved for NAFLD or nonalcoholic steatohepatitis.
FXR is a bile acid receptor expressed in liver, intestine, kidney, and adipose tissue. It regulates many genes involved in bile acid synthesis and transport, lipid metabolism, and glucose homeostasis. FXR also controls glucose metabolism and glycogenolysis in the liver, and peripheral insulin sensitivity in striated muscle adipose tissue. Factors that activate FXR might therefore be used to control diabetes and fatty liver disease.
OCA is a selective agonist of FXR agonist with anti-cholestatic and hepato-protective properties. In preclinical studies, OCA was found to increase insulin sensitivity, regulate glucose homeostasis, modulate lipid metabolism, and have anti-inflammatory and anti-fibrotic effects in the liver, kidney, and intestine.
Sunder Mudaliar et al. tested the effects of OCA in a Phase 2 study of 64 patients with type 2 diabetes mellitus and NAFLD. Patients were given 25 or 50 mg OCA or placebo, once daily for 6 weeks. The hyperinsulinemic-euglycemic clamp technique was used to assess insulin sensitivity. Various markers of tolerance and safety, and markers of FXR activation (increased plasma levels of FGF19 and reduced bile acid synthesis), were assessed.
Mudaliar et al. found that OCA increased hepatic and peripheral insulin sensitivity (by about 25%), whereas insulin sensitivity decreased by about 5% in subjects given placebo. OCA produced a significant decrease in levels of γ-glutamyltransferase—a marker of fatty liver disease that is a risk factor for development of diabetes in patients with NAFLD.
OCA also caused patients to lose weight (see below figure).
Weight loss among patients given 25 mg or 50 mg OCA, compared with placebo.
In an editorial that accompanies the article, Saul Karpen says that these findings herald a new era, in which bile-acid–based strategies are used to control metabolic signaling and treat liver and other types of diseases.
However, Karpen points out that the observed increases in low-density lipoprotein, reductions in high-density lipoprotein, and lack of change in alanine aminotransferase or liver fibrosis scores in subjects receiving OCA were notable and require further analysis. Mudaliar et al. did not perform liver biopsies, so they were not able to determine the degree and effect of OCA on liver histology.
Karpen says that studies with a larger sample sizes and more analyses are needed before conclusions can be made.
More Information on Fatty Liver Disease:
- The American Liver Foundation
- The Mayo Clinic Website on NAFLD
- The NIDDK Website on Nonalcoholic Steatohepatitis
Mudaliar S, Henry RR, Sanyal AJ, et al. Efficacy and safety of the farnesoid x receptor agonist obeticholic acid in patients with type 2 diabetes and nonalcoholic fatty liver disease. Gastroenterology 2013;145:574–582.e1.
Read the accompanying editorial.
Karpen SJ. Do therapeutic bile acids hit the sweet spot of glucose metabolism in NAFLD? Gastroenterology 2013;145:508–510.
http://agajournals.wordpress.com/
Peru: Liver Cancer Like No Other
Sep. 2, 2013 — Liver cancer is the sixth most common cancer worldwide and the third most deadly. It mainly affects men over the age of 40, most often with cirrhosis or hepatitis B or C. But in Peru, it also uncharacteristically affects young people, even children, who do not have the identified related risk factors. An anomaly that IRD researchers and their partners recently revealed in PLoS One. The Franco-Peruvian team highlights a disturbing fact: these patients, with an average age of 25, come from the same geographical area in the Andes.
Very young patients
To make up for the lack of knowledge on liver cancer in Latin America, the researchers performed a statistical analysis of clinical cases of the disease in Peru, the country reputed to have the highest incidence on the continent. They sifted through the demographic characteristics, risk factors and causes for more than 1,500 patients from throughout the country, admitted between 1997 and 2010 at the Instituto Nacional de Enfermedades Neoplásicas (Inen ) in Lima. Their results were unexpected: 50% of the people affected do not at all match the profile of those at risk. They are young people with an average age of 25, some even children, who for the most part do not have the hepatitis B or C virus nor do they suffer from cirrhosis. In addition, a third of those affected are women, contrary to findings elsewhere in the world, where the sex ratio is much more uneven. An additional Peruvian peculiarity is that a large majority of patients had giant tumours larger than 10 cm in diameter.
A source in the Andes
Another disturbing finding: these young patients come from the Andean part of the country. The research workers defined a focal spot in the Apurimac region to the south-east, i.e. the main source of this phenomenon where the population affected has the lowest average age. Such a specific geographical area would indicate a cause related to the environment of the people affected. The initial analyses appear to eliminate any food-related source, linked to the local population's consumption of agricultural products containing mycotoxins, substances produced by fungi, known to be one of the risk factors for liver cancer. The theory of poisoning due to soil and water contamination by pollutants from human activities in the Andean region has yet to be explored. Finally, scientists are also considering the possibility of an infectious agent that is unidentified to date.
A disease that is progressing worldwide
The number of cases of liver cancer has doubled worldwide over the last two decades, due to the increase of hepatitis viruses, particularly in West Africa and South-East Asia where they are highly endemic. The disease, also known as hepatocarcinoma or hepatocellular carcinoma (HCC), now causes almost 700,000 deaths per year, according to the WHO.
This pathology responds poorly to chemotherapy treatment. Consequently, liver tumours either have to be surgically removed, or treated by chemical embolisation, i.e. by an injection directly into the tumour. Major operations such as these remain unavailable to the vast majority of patients, nearly 85% of whom live in developing countries.
Story Source:
The above story is based on materials provided by Institut de Recherche pour le Développement (IRD).
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Stéphane Bertani, Pascal Pineau, Sebastian Loli, Julien Moura, Mirko Zimic, Eric Deharo, Eloy Ruiz. An Atypical Age-Specific Pattern of Hepatocellular Carcinoma in Peru: A Threat for Andean Populations. PLoS ONE, 2013; 8 (6): e67756 DOI: 10.1371/journal.pone.0067756
Photo (Credit: © IRD / S. Bertani)
Smart syringe tells you if it's been used
2.5B injections administered in India each are deemed unsafe, study says
UPDATED 5:16 AM CDT Sep 03, 2013
(CNN) —Of the four to five billion injections given each year in India, at least 2.5 billion are unsafe, according to one study. In some cases, that means they are administered using unsterilized second-hand syringes that could be contaminated with a blood-borne disease such as hepatitis or HIV.
A simple change to the way syringes are made could dramatically reduce those figures and save thousand of lives each year, according to David Swann of Huddersfield University, in England. His design for a new kind of syringe that changes color after it has been used was nominated for an INDEX: Award.
"1.3 million people (globally) a year die from unsafe injection practices," Swann says, quoting WHO figures. "It accounts for over 30% of hepatitis A and B cases and 5% of HIV cases."
He explained that in India it is common for scavengers to hunt through landfill sites looking for old syringes that they can clean up and sell to clinics.
"When you compare a sterile syringe just out of its packaging with a syringe that's been washed, how do you determine the difference?" he said. "We conceived an intelligent ink that, if exposed to air by taking it out of the package or if the package is breached that would activate it and turn it red."
The ABC Syringe is impregnated with an ink that's sensitive to carbon dioxide and then sealed in a protective atmosphere so that it remains transparent until it is ready for use. After the seal is broken, the shell of the syringe starts to turn a dark red, alerting both doctors to the risk that the syringe may already have been used.
Swann's intention is that the introduction of the ABC syringe should be accompanied by a public information campaign so that patients would also associate a red syringe with danger and would be able to insist on sterile equipment.
"We had to be really quite clever in looking at technologies that cost next to nothing, and modified-air packaging is one of those technologies," Swann said. "It only adds 1% to the retail price, so on a two-and-a-half pence (four cents) syringe it becomes quite an interesting proposition."
According to Swann's calculations, if the ABC syringe is used for 5% of injections administered in India, after five years it will have prevented more than 700,000 infections and saved $130 million in medical costs.
Denis Maire, who works for the World Health Organization's health systems and innovation taskforce, said the ABC Syringe could help to make injections safer.
Read more: http://www.kcci.com/news/project-economy/technology/Smart-syringe-tells-you-if-it-s-been-used/-/9356860/21754050/-/mj1m5j/-/index.html#ixzz2dpPny76U
Monday, September 2, 2013
National Geographic's; Drugs Inc. "Designer Drugs"
The National Geographic Channel is offering a series of broadcasts entitled Drugs, Inc, which examines the $350 billion-a-year global drug industry from all angles. Both video excerpts (provided below) are from the "Designer Drugs" episode. The first video clip investigates synthetic drugs in the UK, the second clip takes us to Israel with a masked drug dealer talking about selling "hagigat" a designer drug similar to bath salts. The next installment of the episode will air Thursday September 5th @ 4:00PM EST.
View the complete episode guide here.
Other episodes airing on Thursday include; Windy City High
Chicago, one of the biggest open-air crack and heroin markets in America, is at saturation point. It's an addict's dream as dealers compete with high purity drugs sold in very affordable quantities. The result: record levels of overdoses and homicides as gangs fight over drug turf. Go inside the deeply entrenched and violent world of the city's drug-corner industry.
Infections Not Tied to Neutropenia in HCV/HIV Patients on PegIFN/RBV
Infections Not Tied to Neutropenia in HCV/HIV Patients on PegIFN/RBV
02 September 2013
Neutropenia caused by treatment with pegylated interferon and ribavirin (PegIFN/RBV) was not related to severe or nonsevere infections in a study of 418 HCV/HIV-coinfected people in Madrid.
Neutropenia (low white blood cell levels) is a common complication of treatment with PegIFN/RBV for hepatitis C virus infection. Because research had not addressed whether this neutropenia promotes infection in people with HCV and HIV, researchers in Madrid conducted this prospective cohort study from 2000 through 2012.
The investigators defined serious infections as those requiring hospital admission, requiring discontinuation of PegIFN/RBV, or causing death. They defined severe neutropenia as a white cell count below 500 cells/μL, while nonsevere neutropenia meant a count between 500 and 1500 cells/μL.
The study involved 418 people receiving PegIFN/RBV for 3928 person-weeks. The researchers recorded 149 infections in 123 people (29%) for an infection incidence of 3.8 per 100 person-weeks of therapy, meaning almost 4 of every 100 people got an infection every week. Almost half of infections (47%) involved the upper respiratory tract and were minor.
To identify factors associated with infection, the researchers conducted a logistic regression analysis adjusted for age, gender, CD4 count, AIDS, antiretroviral therapy, cirrhosis, neutrophil count, type of PegIFN, and granulocyte colony-stimulating factor use. None of these factors was independently associated with infection.
Twenty study participants (4.8%) had a serious infection. Serious infections were more frequent in people with severe neutropenia (8.6%) than in those with nonsevere neutropenia (4.8%) or without neutropenia (3.6%), but these differences were not statistically significant (P = 0.28). Multivariate analysis identified no factors independently associated with increased risk of serious infection.
“In this large prospective cohort of HIV/HCV-coinfected patients treated with peg-IFN plus RBV,” the researchers conclude, “serious infections were uncommon, nonfatal, and unrelated to peg-IFN-induced severe neutropenia.”
Source: Sergio Serrano-Villar, Carmen Quereda, Ana Moreno, María Jesús Pérez-Elías, José Luis Casado, Ana Royuela, Fernando Dronda, Enrique Navas, José Manuel Hermida, Santiago Moreno. Neutropenia during therapy with peginterferon and ribavirin in HIV-infected subjects with chronic hepatitis C and the risk of infections. Clinical Infectious Diseases. 2013; 57: 458-464.
Neutropenia (low white blood cell levels) is a common complication of treatment with PegIFN/RBV for hepatitis C virus infection. Because research had not addressed whether this neutropenia promotes infection in people with HCV and HIV, researchers in Madrid conducted this prospective cohort study from 2000 through 2012.
The investigators defined serious infections as those requiring hospital admission, requiring discontinuation of PegIFN/RBV, or causing death. They defined severe neutropenia as a white cell count below 500 cells/μL, while nonsevere neutropenia meant a count between 500 and 1500 cells/μL.
The study involved 418 people receiving PegIFN/RBV for 3928 person-weeks. The researchers recorded 149 infections in 123 people (29%) for an infection incidence of 3.8 per 100 person-weeks of therapy, meaning almost 4 of every 100 people got an infection every week. Almost half of infections (47%) involved the upper respiratory tract and were minor.
To identify factors associated with infection, the researchers conducted a logistic regression analysis adjusted for age, gender, CD4 count, AIDS, antiretroviral therapy, cirrhosis, neutrophil count, type of PegIFN, and granulocyte colony-stimulating factor use. None of these factors was independently associated with infection.
Twenty study participants (4.8%) had a serious infection. Serious infections were more frequent in people with severe neutropenia (8.6%) than in those with nonsevere neutropenia (4.8%) or without neutropenia (3.6%), but these differences were not statistically significant (P = 0.28). Multivariate analysis identified no factors independently associated with increased risk of serious infection.
“In this large prospective cohort of HIV/HCV-coinfected patients treated with peg-IFN plus RBV,” the researchers conclude, “serious infections were uncommon, nonfatal, and unrelated to peg-IFN-induced severe neutropenia.”
Source: Sergio Serrano-Villar, Carmen Quereda, Ana Moreno, María Jesús Pérez-Elías, José Luis Casado, Ana Royuela, Fernando Dronda, Enrique Navas, José Manuel Hermida, Santiago Moreno. Neutropenia during therapy with peginterferon and ribavirin in HIV-infected subjects with chronic hepatitis C and the risk of infections. Clinical Infectious Diseases. 2013; 57: 458-464.
For the study abstract
(Downloading the complete article requires a subscription to Clinical Infectious Diseases or an online payment; the abstract is free.)
(Downloading the complete article requires a subscription to Clinical Infectious Diseases or an online payment; the abstract is free.)
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