UK researchers are playing a part in the development of nearly a fifth of the world's potential new medicines for diseases that cause breathing difficulties, figures released by the Association of the British Pharmaceutical Industry (ABPI) show.
But at the same time, the ABPI queried how many of these medicines would be made available to British patients, despite the leading role that the country's scientists are playing in their development.
Of 262 medicines in development worldwide, 49 - or 19 per cent - are to tackle diseases such as asthma, chronic bronchitis and emphysema. Many will not make it through the development process - the attrition rate for medicines is great, making it a high-risk business - but the ABPI is questioning how many of the successful medicines will in fact reach patients.
"These figures show that British scientists are in the forefront of the fight against breathing disorders, but we are increasingly worried that the advances represented by many of these innovative medicines will not benefit UK patients," said Dr Richard Barker, Director General of the ABPI.
"At the moment, the need for medicines to prove cost-effectiveness - based on overly-narrow criteria - is preventing many such medicines from reaching patients. It is a major disincentive to companies and other organisations to continue to research medicines if they are not to be utilised fully."
Figures published by the Office of Health Economics (OHE) show that breathing disorders are responsible for an increasing number of deaths in the UK - Britain's "silent killer". Chronic Obstructive Pulmonary Disease (COPD), which includes chronic bronchitis and emphysema, has been estimated to cost the NHS more than ??800 million a year and to cause 24 million lost working days a year.
Causes for COPD include smoking - the single most important factor - environmental pollution, and hazards at work, such as dust, fumes and gases.
"Given the increase in asthma and COPD, and deaths associated with these diseases, the development of new medicines is essential to save lives," said Dr Barker. "This has been recognised by the pharmaceutical industry and other researchers, who have made the UK a world leader in this area.
"It is now down to the Government and the NHS to make sure that medicines which make it through the regulatory process are then available to patients."
Association of the British Pharmaceutical Industry
воскресенье, 31 июля 2011 г.
четверг, 28 июля 2011 г.
Early Antibiotic Treatment Associated With Improved Outcomes For Patients With Acute Exacerbations Of COPD
Among patients hospitalized for acute exacerbations of chronic obstructive pulmonary disease (COPD), those who received antibiotics in the first 2 hospital days had improved outcomes, such as a lower likelihood of mechanical ventilation and fewer readmissions, compared to patients who received antibiotics later or not at all, according to a study in the May 26 issue of JAMA.
The fourth lead?¬ing cause of death in the United States is COPD, which affects at least 12 million U.S. residents. "Acute exacerbations of COPD are responsible for more than 600,000 hos-pitalizations annually, resulting in direct costs of more than $20 billion," the authors write. "Guidelines recommend antibiotic therapy for acute exacerbations of COPD, but the evidence is based on small, heterogeneous trials, few of which include hospitalized patients."
Michael B. Rothberg, M.D., M.P.H., of Baystate Medical Center, Springfield, Mass., and colleagues examined the association between use of antibiotics and outcomes among patients (40 years of age or older) hospitalized for acute exacerbations of COPD at 413 acute care facilities throughout the United States, between January 2006 and December 2007. The primary outcomes analyzed included a composite measure of treatment failure, defined as the initiation of mechanical ventilation after the second hospital day, inpatient mortality, or readmission for acute exacerbations of COPD within 30 days of discharge; length of stay, and hospital costs.
Of 84,621 patients, 79 percent received at least 2 consecutive days of antibiotic treatment. The researchers found that compared with patients not receiving antibiotics in the first 2 days, antibiotic-treated patients were less likely to receive mechanical ventilation after the second hospital day (1.07 percent vs. 1.80 percent), had lower inpatient mortality (1.04 percent vs. 1.59 percent), a lower incidence of treatment failure (9.77 percent vs. 11.75 percent), and lower rates of readmission for acute exacerbations of COPD (7.91 percent vs. 8.79 percent). Pa?¬tients treated with and without antibiotics had similar lengths of stay, but patients treated with antibiotics had lower costs.
Patients treated with antibiotic agents had a higher rate of readmissions for the bacterial infection Clostridium difficile than those who were not treated. After further analysis, the risk of treatment failure was lower in antibiotic-treated patients. "Analysis stratified by risk of treatment failure found similar magnitudes of benefit across all subgroups," the authors write.
The researchers add that two findings, that all patient groups seemed to benefit from therapy and that harms were minimal, support the notion that all patients hospitalized with acute exacerbations of COPD should be prescribed antibiotics. "This recommendation, however, is not consistent with the fact that roughly 50 percent of COPD patients do not have a bacterial etiology for their exacerbation. Identifying these patients remains a challenge, because sputum cultures do not distinguish between active infection and colonization. New bacterial infections may cause exacerbations and are associated with increases in inflammatory markers, ... whereas colonization is not."
"... until more data are available, routine use of antibiotics for acute exacerbations of COPD may be appropriate," the authors conclude.
JAMA..2010;303[20]:2035-2042.
Source
Journal of the American Medical Association
The fourth lead?¬ing cause of death in the United States is COPD, which affects at least 12 million U.S. residents. "Acute exacerbations of COPD are responsible for more than 600,000 hos-pitalizations annually, resulting in direct costs of more than $20 billion," the authors write. "Guidelines recommend antibiotic therapy for acute exacerbations of COPD, but the evidence is based on small, heterogeneous trials, few of which include hospitalized patients."
Michael B. Rothberg, M.D., M.P.H., of Baystate Medical Center, Springfield, Mass., and colleagues examined the association between use of antibiotics and outcomes among patients (40 years of age or older) hospitalized for acute exacerbations of COPD at 413 acute care facilities throughout the United States, between January 2006 and December 2007. The primary outcomes analyzed included a composite measure of treatment failure, defined as the initiation of mechanical ventilation after the second hospital day, inpatient mortality, or readmission for acute exacerbations of COPD within 30 days of discharge; length of stay, and hospital costs.
Of 84,621 patients, 79 percent received at least 2 consecutive days of antibiotic treatment. The researchers found that compared with patients not receiving antibiotics in the first 2 days, antibiotic-treated patients were less likely to receive mechanical ventilation after the second hospital day (1.07 percent vs. 1.80 percent), had lower inpatient mortality (1.04 percent vs. 1.59 percent), a lower incidence of treatment failure (9.77 percent vs. 11.75 percent), and lower rates of readmission for acute exacerbations of COPD (7.91 percent vs. 8.79 percent). Pa?¬tients treated with and without antibiotics had similar lengths of stay, but patients treated with antibiotics had lower costs.
Patients treated with antibiotic agents had a higher rate of readmissions for the bacterial infection Clostridium difficile than those who were not treated. After further analysis, the risk of treatment failure was lower in antibiotic-treated patients. "Analysis stratified by risk of treatment failure found similar magnitudes of benefit across all subgroups," the authors write.
The researchers add that two findings, that all patient groups seemed to benefit from therapy and that harms were minimal, support the notion that all patients hospitalized with acute exacerbations of COPD should be prescribed antibiotics. "This recommendation, however, is not consistent with the fact that roughly 50 percent of COPD patients do not have a bacterial etiology for their exacerbation. Identifying these patients remains a challenge, because sputum cultures do not distinguish between active infection and colonization. New bacterial infections may cause exacerbations and are associated with increases in inflammatory markers, ... whereas colonization is not."
"... until more data are available, routine use of antibiotics for acute exacerbations of COPD may be appropriate," the authors conclude.
JAMA..2010;303[20]:2035-2042.
Source
Journal of the American Medical Association
понедельник, 25 июля 2011 г.
Rapid Lung Function Decline Raises Risk Of Death And Hospitalization
Rapid lung function decline significantly increases the risk of death and hospitalization for individuals with chronic obstructive pulmonary disease (COPD).
These findings appear in the May issue of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
David Mannino, M.D., of the University of Kentucky Medical Center, and two associates found that patients with advanced COPD and rapid lung function decline are 10 times more likely to die than individuals with normal lung function.
COPD, an important cause of hospitalization and death, results from persistent obstruction of the airways associated with either severe emphysema or chronic bronchitis. In emphysema, the tiny air sacs of the lung (alveoli) become enlarged and their walls are destroyed. In chronic bronchitis, the bronchial glands enlarge, causing chronic cough and excess mucus. Ten to 15 percent of all smokers develop COPD as a result of irritants in tobacco that causes inflammation of the alveoli.
Over the course of three years, the investigators analyzed 13,756 middle-aged adults, all of whom participated in the 1986 Atherosclerosis Risk in the Communities Study and provided baseline information on respiratory symptoms and diseases. The researchers tested the participants' lung function twice--once at the start of the study and during a follow-up three years later.
The authors classified patients with the worst lung function as "rapid decliners." Twenty-five percent of the entire study population (3,437 individuals) fell into this high-mortality category. Of the 720 subjects who died during the study, 273 (38 percent) were considered "rapid decliners."
In addition, patients in advanced stages of COPD who were also "rapid decliners" were hospitalized at rate 40 times higher than those with normal lung function at baseline who had no rapid lung decline over the three-year period.
"Mean annual loss of lung function in the overall cohort was 62 ml," said Dr. Mannino. "The mean loss of lung function (FEV1) as a percentage of the baseline value was 1.5 percent annually. Participants in the most rapidly declining quartile of FEV1 had a mean annual loss of 171 ml, which was 4.7 percent of the baseline level per year."
The authors noted that the average annual loss of 62 ml in lung function was higher than that shown in other similar studies, including the Honolulu Heart Cohort at 26 ml, the Busselton Health Study at 30 to 40 ml, the Nottingham Study at 38 ml, and the Copenhagen City Heart Study at 22 to 38 ml.
The authors acknowledged the limitations of their analysis. For example, they only measured lung function twice during the three-year investigation. "It is possible that people may have had a really good day or really bad day at either the baseline or follow-up examination, influencing our results," said Dr. Mannino.
He noted that the group in which rapid decline in FEV1 showed the greatest predictive value for death and hospitalization was also the one least like to be affected by any source of error. Although 461 "rapid decliners" were classified as having respiratory symptoms, none had either a lung abnormality or lung disease.
"The impact of rapid decline in FEV1 was stronger in adults with normal or near-normal lung function at baseline and suggests that this group of people may need more frequent screening and interventions beyond what is recommended," said Dr. Mannino.
Contact: David M. Mannino, M.D. Division of Pulmonary and Critical Care Medicine, University of Kentucky Medical Center, 800 Rose Street, MN 614, Lexington, KY 40536
Contact: Suzy Martin
American Thoracic Society
These findings appear in the May issue of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
David Mannino, M.D., of the University of Kentucky Medical Center, and two associates found that patients with advanced COPD and rapid lung function decline are 10 times more likely to die than individuals with normal lung function.
COPD, an important cause of hospitalization and death, results from persistent obstruction of the airways associated with either severe emphysema or chronic bronchitis. In emphysema, the tiny air sacs of the lung (alveoli) become enlarged and their walls are destroyed. In chronic bronchitis, the bronchial glands enlarge, causing chronic cough and excess mucus. Ten to 15 percent of all smokers develop COPD as a result of irritants in tobacco that causes inflammation of the alveoli.
Over the course of three years, the investigators analyzed 13,756 middle-aged adults, all of whom participated in the 1986 Atherosclerosis Risk in the Communities Study and provided baseline information on respiratory symptoms and diseases. The researchers tested the participants' lung function twice--once at the start of the study and during a follow-up three years later.
The authors classified patients with the worst lung function as "rapid decliners." Twenty-five percent of the entire study population (3,437 individuals) fell into this high-mortality category. Of the 720 subjects who died during the study, 273 (38 percent) were considered "rapid decliners."
In addition, patients in advanced stages of COPD who were also "rapid decliners" were hospitalized at rate 40 times higher than those with normal lung function at baseline who had no rapid lung decline over the three-year period.
"Mean annual loss of lung function in the overall cohort was 62 ml," said Dr. Mannino. "The mean loss of lung function (FEV1) as a percentage of the baseline value was 1.5 percent annually. Participants in the most rapidly declining quartile of FEV1 had a mean annual loss of 171 ml, which was 4.7 percent of the baseline level per year."
The authors noted that the average annual loss of 62 ml in lung function was higher than that shown in other similar studies, including the Honolulu Heart Cohort at 26 ml, the Busselton Health Study at 30 to 40 ml, the Nottingham Study at 38 ml, and the Copenhagen City Heart Study at 22 to 38 ml.
The authors acknowledged the limitations of their analysis. For example, they only measured lung function twice during the three-year investigation. "It is possible that people may have had a really good day or really bad day at either the baseline or follow-up examination, influencing our results," said Dr. Mannino.
He noted that the group in which rapid decline in FEV1 showed the greatest predictive value for death and hospitalization was also the one least like to be affected by any source of error. Although 461 "rapid decliners" were classified as having respiratory symptoms, none had either a lung abnormality or lung disease.
"The impact of rapid decline in FEV1 was stronger in adults with normal or near-normal lung function at baseline and suggests that this group of people may need more frequent screening and interventions beyond what is recommended," said Dr. Mannino.
Contact: David M. Mannino, M.D. Division of Pulmonary and Critical Care Medicine, University of Kentucky Medical Center, 800 Rose Street, MN 614, Lexington, KY 40536
Contact: Suzy Martin
American Thoracic Society
пятница, 22 июля 2011 г.
Bio-Matrix Scientific Group Inc. Updates Progress On The Company's New Opportunities In COPD, Tumor Banking And Cancer Treatment
Bio-Matrix Scientific Group, Inc. (OTCBB: BMSN) provided a progress report on the Company's previously announced new opportunities. The Company has been moving forward in the areas of stem cell research for treatment of Chronic Obstructive Pulmonary Disease (COPD), Tumor Banking and Cancer Treatment.
The Company is in the process of forming a relationship with a medical device manufacturer that produces encapsulation devices to be used in a study developed by Entest BioMedical (OTCBB: ENTB), on an immuno-therapeutic cancer vaccine. Entest is a publicly traded majority owned subsidiary of Bio-Matrix.
Bio-Matrix' role will be to joint venture the production of these devices which are used not only in cancer treatment but have applications in diabetes research and beyond. Bio-Matrix believes this joint venture should be consummated by the end of October 2009 and should show near term revenue in a rapidly expanding market niche.
The Company is also in the process of selecting a Contract Research Organization (CRO) to perform the animal studies which involve treating COPD with adipose derived stem cells. The Company believes selection of a CRO will be completed by the end of October, with November 2009 as the target start date.
David Koos, Chairman and CEO, stated, "We believe treatment for COPD is an under-researched area for a condition that has a major impact on our health. There are no truly effective cures for this disease. We see our approach as extremely strong in addressing this malady."
Additionally, plans are moving forward to develop a tumor bank within Bio-Matrix' facility. The Company is in discussions with several veterinary sources for animal tumor specimens. These specimens will be used by Entest BioMedical in its cancer research and will be cryogenically preserved in Bio-Matrix' facility to allow for ease of availability.
About Bio-Matrix Scientific Group
Bio-Matrix Scientific Group Inc. (OTCBB: BMSN) is a biotech research and development company headquartered in San Diego, Ca. with a 15,000 sq. ft. facility that houses two secure cryogenic stem cell banks, three research laboratories, aseptic cellular/tissue class 10,000/100 processing lab, hematology, microbiology and flow cytometry laboratories.
Source
Entest BioMedical Inc.
The Company is in the process of forming a relationship with a medical device manufacturer that produces encapsulation devices to be used in a study developed by Entest BioMedical (OTCBB: ENTB), on an immuno-therapeutic cancer vaccine. Entest is a publicly traded majority owned subsidiary of Bio-Matrix.
Bio-Matrix' role will be to joint venture the production of these devices which are used not only in cancer treatment but have applications in diabetes research and beyond. Bio-Matrix believes this joint venture should be consummated by the end of October 2009 and should show near term revenue in a rapidly expanding market niche.
The Company is also in the process of selecting a Contract Research Organization (CRO) to perform the animal studies which involve treating COPD with adipose derived stem cells. The Company believes selection of a CRO will be completed by the end of October, with November 2009 as the target start date.
David Koos, Chairman and CEO, stated, "We believe treatment for COPD is an under-researched area for a condition that has a major impact on our health. There are no truly effective cures for this disease. We see our approach as extremely strong in addressing this malady."
Additionally, plans are moving forward to develop a tumor bank within Bio-Matrix' facility. The Company is in discussions with several veterinary sources for animal tumor specimens. These specimens will be used by Entest BioMedical in its cancer research and will be cryogenically preserved in Bio-Matrix' facility to allow for ease of availability.
About Bio-Matrix Scientific Group
Bio-Matrix Scientific Group Inc. (OTCBB: BMSN) is a biotech research and development company headquartered in San Diego, Ca. with a 15,000 sq. ft. facility that houses two secure cryogenic stem cell banks, three research laboratories, aseptic cellular/tissue class 10,000/100 processing lab, hematology, microbiology and flow cytometry laboratories.
Source
Entest BioMedical Inc.
вторник, 19 июля 2011 г.
Researchers At Peoria Pulmonary Associates To Study Airway Bypass Procedure For Emphysema
Researchers at Peoria Pulmonary Associates announced the start of the EASE (Exhale Airway Stents for Emphysema) Trial, an international, multi-center clinical trial to explore an investigational procedure for advanced widespread emphysema/COPD. Conducted at Methodist Medical Center, the study focuses on a procedure called airway bypass. Airway bypass is a bronchoscopic procedure designed to reduce lung hyperinflation and shortness of breath (the clinical hallmarks of emphysema/COPD) by making new pathways for trapped air to exit the lungs.
During the airway bypass procedure, new openings are created in the airway wall connecting the damaged lung tissue to the natural airway. These pathways are supported and kept open by Exhale® Drug-Eluting Stents -- manufactured by Broncus Technologies, Inc.
"Patients with severe emphysema often live in poor physical condition, struggling with each breath," states William P Tillis, MD, Principal Investigator of the study at Peoria Pulmonary Associates. "A goal of this study is to see if, by reducing hyperinflation and improving lung function with the airway bypass procedure, these patients may breathe easier and have a better quality of life."
Emphysema, a component of COPD, is a chronic, progressive, and irreversible lung disease characterized by the destruction of lung tissue. The loss of the lungs' natural elasticity and the collapse of airways in the lung combine to make exhalation ineffective, leaving emphysema sufferers with hyperinflation because they are unable to get air out of their lungs. Breathing becomes inefficient and patients have to work very hard just to breathe -- making normal activities, like walking, eating or even bathing, difficult. There are few treatment options for most patients with emphysema and there is no cure.
Physicians commonly use bronchoscopes to examine the airways within the lungs. During the airway bypass procedure physicians will first use a Doppler probe inserted through the bronchoscope to identify a site in the airway that is away from blood vessels. A special needle is then used to make a small opening and an Exhale® Drug-Eluting Stent is placed in the passageway to keep it open. The procedure involves placing up to six drug-eluting stents. The total time of the procedure is approximately one to two hours.
This procedure is still under clinical investigation, and results from the open-label Exhale Drug-Eluting Stent feasibility study were published in the October issue of the Journal of Thoracic and Cardiovascular Surgery. Positive results in that study included a statistically significant reduction in the amount of air trapped in the lungs and an improvement in breathing for patients at six months after the airway bypass procedure.
Peoria Pulmonary Associates is currently recruiting patients for the EASE Trial. Involvement in the study will last from approximately 15 months up to 5 years (depending on whether the patient is randomized to the control or the treatment group) and include 8 to 16 physician appointments. All study-related medical procedures will be carried out at no charge to the patient and patients will be closely monitored throughout the trial. Participants will also receive at least 14 weeks of pulmonary rehabilitation therapy. If you or someone you know over the age of 35 has been diagnosed with advanced widespread emphysema and no longer smoke (or would be willing to stop smoking two months prior to the study), you may qualify to participate in this study.
EASEtrialUS
About Broncus Technologies, Inc.
Broncus Technologies, Inc. is helping people breathe easier by developing bronchoscopic interventions for the treatment of chronic lung diseases. Founded in 1997, Broncus Technologies has developed the Exhale® Drug-Eluting Stent for use in the airway bypass procedure, a minimally-invasive procedure to treat emphysema. Airway bypass creates new pathways in the lung for air to escape and may potentially improve the breathing abilities of patients with emphysema. Broncus Technologies is currently conducting the pivotal EASE Trial to evaluate the safety and efficacy of airway bypass in the treatment of advanced widespread emphysema.
Broncus Technologies, Inc.
During the airway bypass procedure, new openings are created in the airway wall connecting the damaged lung tissue to the natural airway. These pathways are supported and kept open by Exhale® Drug-Eluting Stents -- manufactured by Broncus Technologies, Inc.
"Patients with severe emphysema often live in poor physical condition, struggling with each breath," states William P Tillis, MD, Principal Investigator of the study at Peoria Pulmonary Associates. "A goal of this study is to see if, by reducing hyperinflation and improving lung function with the airway bypass procedure, these patients may breathe easier and have a better quality of life."
Emphysema, a component of COPD, is a chronic, progressive, and irreversible lung disease characterized by the destruction of lung tissue. The loss of the lungs' natural elasticity and the collapse of airways in the lung combine to make exhalation ineffective, leaving emphysema sufferers with hyperinflation because they are unable to get air out of their lungs. Breathing becomes inefficient and patients have to work very hard just to breathe -- making normal activities, like walking, eating or even bathing, difficult. There are few treatment options for most patients with emphysema and there is no cure.
Physicians commonly use bronchoscopes to examine the airways within the lungs. During the airway bypass procedure physicians will first use a Doppler probe inserted through the bronchoscope to identify a site in the airway that is away from blood vessels. A special needle is then used to make a small opening and an Exhale® Drug-Eluting Stent is placed in the passageway to keep it open. The procedure involves placing up to six drug-eluting stents. The total time of the procedure is approximately one to two hours.
This procedure is still under clinical investigation, and results from the open-label Exhale Drug-Eluting Stent feasibility study were published in the October issue of the Journal of Thoracic and Cardiovascular Surgery. Positive results in that study included a statistically significant reduction in the amount of air trapped in the lungs and an improvement in breathing for patients at six months after the airway bypass procedure.
Peoria Pulmonary Associates is currently recruiting patients for the EASE Trial. Involvement in the study will last from approximately 15 months up to 5 years (depending on whether the patient is randomized to the control or the treatment group) and include 8 to 16 physician appointments. All study-related medical procedures will be carried out at no charge to the patient and patients will be closely monitored throughout the trial. Participants will also receive at least 14 weeks of pulmonary rehabilitation therapy. If you or someone you know over the age of 35 has been diagnosed with advanced widespread emphysema and no longer smoke (or would be willing to stop smoking two months prior to the study), you may qualify to participate in this study.
EASEtrialUS
About Broncus Technologies, Inc.
Broncus Technologies, Inc. is helping people breathe easier by developing bronchoscopic interventions for the treatment of chronic lung diseases. Founded in 1997, Broncus Technologies has developed the Exhale® Drug-Eluting Stent for use in the airway bypass procedure, a minimally-invasive procedure to treat emphysema. Airway bypass creates new pathways in the lung for air to escape and may potentially improve the breathing abilities of patients with emphysema. Broncus Technologies is currently conducting the pivotal EASE Trial to evaluate the safety and efficacy of airway bypass in the treatment of advanced widespread emphysema.
Broncus Technologies, Inc.
суббота, 16 июля 2011 г.
Wider Use Of Home Oxygen Therapy Could Save Thousands Of Lives, Says RAND Study
A study expected to be published in the December issue of the medical journal Chest shows that Americans with chronic obstructive pulmonary disease (COPD) receive only about half of the recommended medical care, with care varying significantly based on individual conditions. COPD is the fourth leading cause of death in the United States.
???
In the Chest article, the authors state, "[W]e can estimate excess mortality that might result from failure to provide care specified in individual indicators. For example, only 32% of COPD patients with baseline hypoxia received home oxygen for routine management. From estimates of the numbers of hypoxic patients in the United States and the mortality reduction demonstrated from the Nocturnal Oxygen Therapy Trial, 27,000 to 54,000 annual deaths may have been reduced by appropriate oxygen use."
???
Dr. Richard A. Mularski is lead author of the study and a physician-researcher with the Center for Health Research, Kaiser Permanente. The study was conducted by RAND Health and was supported by the Robert Wood Johnson Foundation and Veterans Affairs Health Administration, which supported a fellowship for Mularski.??? rand
American Association for Homecare
625 Slaters Lane, Suite 200
Alexandria, VA 22314??? 703-535-1881
aahomecare
???
In the Chest article, the authors state, "[W]e can estimate excess mortality that might result from failure to provide care specified in individual indicators. For example, only 32% of COPD patients with baseline hypoxia received home oxygen for routine management. From estimates of the numbers of hypoxic patients in the United States and the mortality reduction demonstrated from the Nocturnal Oxygen Therapy Trial, 27,000 to 54,000 annual deaths may have been reduced by appropriate oxygen use."
???
Dr. Richard A. Mularski is lead author of the study and a physician-researcher with the Center for Health Research, Kaiser Permanente. The study was conducted by RAND Health and was supported by the Robert Wood Johnson Foundation and Veterans Affairs Health Administration, which supported a fellowship for Mularski.??? rand
American Association for Homecare
625 Slaters Lane, Suite 200
Alexandria, VA 22314??? 703-535-1881
aahomecare
среда, 13 июля 2011 г.
Chronic Lung Disease More Widespread Than First Thought And Rising, New Study
A new study by US researchers suggests that the global rate of chronic lung disease, called chronic obstructive pulmonary disease (COPD), is higher than
previous estimates have suggested and is growing steadily as the world's population gets older. The authors conclude that cost effective prevention and
treatment is the best way to stem the rising tide of this disease and its burden on health care.
Experts have welcomed the study and say it has highlighted a growing global health problem.
The study is published in the 1st September issue of The Lancet and is the work of Dr David M Mannino, Department of Preventive Medicine and
Environmental Health, University of Kentucky College of Public Health, Lexington, Kentucky, and Dr A Sonia Buist, Department of Medicine, Pulmonary and
Critical Care Medicine, Oregon Health and Science University, Portland, Oregon.
Mannino and Buist found that cigarette smoking is the biggest risk factor for COPD, followed by being exposed to pollution both in and out of doors. Other
illnesses and work related hazards are also significant risk factors.
Buist, who heads up the Pulmonary and Critical Care Medicine division of Oregon Health and Science University, said that COPD is under-diagnosed and under-
treated. It is more common than previous estimates have suggested; there is a big difference between the reality and the public health perception, she
said.
COPD is a collective term for a range of chronic lung diseases that limit airflow in the lungs. It is the fifth leading cause of death throughout the
globe.
According to the World Health Organization, the more familiar terms 'chronic bronchitis' and 'emphysema' are no longer used because they are now included in
the COPD diagnosis.
Symptoms of COPD include feeling breathless, as if one can't get enough air, excessive sputum, and a chronic cough. As the WHO explains, COPD is not "simply
a smoker's cough, but an under-diagnosed, life threatening lung disease that may progressively lead to death".
The WHO estimates that 80 million people throughout the world have moderate to severe COPD and the number who died from the disease in 2005 was near 3
million. They predict that by 2030 it will be the fourth leading cause of death in the world.
"COPD is a cumulative response of the lungs to the burden of all that's breathed in over a lifetime," said Buist. This explains why the prevalence rises as
the population ages.
Mannino and Buist studied medical information (including results from spirometry tests that measure breathing ability) on 9,425 people aged 40 and over from
12 different countries.
They found that:
The overall prevalence of COPD was 10.1 per cent.
This compares with previous estimates from another study that put the prevalence at 4.3 per cent.
Among men the prevalence of COPD was 11.8 per cent.
Among women it was 8.5 per cent.
Differences in smoking behaviour probably explains the difference in COPD rates between men and women.
The figures varied widely across different countries.
South Africa had the highest proportion of people with COPD: 22.2 per cent of men and 16.7 per cent of women.
Hanover in Germany had the lowest prevalence: 8.6 per cent of men and 3.7 per cent of women.
In the US, the overall prevalence of serious COPD is 10.1 per cent.
The risk of COPD is nearly doubled for every 10 years of age above 40.
Smoking has a similar large effect on risk.
Buist said that:
"This worldwide study showed higher levels and more advanced staging of spirometrically confirmed COPD than have typically been reported."
There is no cure for COPD and the advice of the authors is that people can reduce their COPD risk by not smoking and avoiding atmospheres that contain
pollutants and smoke, and if you have to work with pollution then wear a mask or other form of protection.
There is some room for optimism though. We now know a lot more about how to prevent and treat COPD. As the authors explained in their summary, scientific
understanding of COPD has grown in a number of areas recently. For instance we know more about how:
Other diseases affect COPD (comorbidity),
COPD affects people with different genetic backgrounds (COPD phenotypes), and
COPD affects health in ways other than lung function.
"Global burden of COPD: risk factors, prevalence, and future trends."
David M Mannino, A Sonia Buist.
The Lancet 2007; 370:765-773
Volume 370, Number 9589, 1 September 2007
DOI:10.1016/S0140-6736(07)61380-4
Click here for Abstract.
previous estimates have suggested and is growing steadily as the world's population gets older. The authors conclude that cost effective prevention and
treatment is the best way to stem the rising tide of this disease and its burden on health care.
Experts have welcomed the study and say it has highlighted a growing global health problem.
The study is published in the 1st September issue of The Lancet and is the work of Dr David M Mannino, Department of Preventive Medicine and
Environmental Health, University of Kentucky College of Public Health, Lexington, Kentucky, and Dr A Sonia Buist, Department of Medicine, Pulmonary and
Critical Care Medicine, Oregon Health and Science University, Portland, Oregon.
Mannino and Buist found that cigarette smoking is the biggest risk factor for COPD, followed by being exposed to pollution both in and out of doors. Other
illnesses and work related hazards are also significant risk factors.
Buist, who heads up the Pulmonary and Critical Care Medicine division of Oregon Health and Science University, said that COPD is under-diagnosed and under-
treated. It is more common than previous estimates have suggested; there is a big difference between the reality and the public health perception, she
said.
COPD is a collective term for a range of chronic lung diseases that limit airflow in the lungs. It is the fifth leading cause of death throughout the
globe.
According to the World Health Organization, the more familiar terms 'chronic bronchitis' and 'emphysema' are no longer used because they are now included in
the COPD diagnosis.
Symptoms of COPD include feeling breathless, as if one can't get enough air, excessive sputum, and a chronic cough. As the WHO explains, COPD is not "simply
a smoker's cough, but an under-diagnosed, life threatening lung disease that may progressively lead to death".
The WHO estimates that 80 million people throughout the world have moderate to severe COPD and the number who died from the disease in 2005 was near 3
million. They predict that by 2030 it will be the fourth leading cause of death in the world.
"COPD is a cumulative response of the lungs to the burden of all that's breathed in over a lifetime," said Buist. This explains why the prevalence rises as
the population ages.
Mannino and Buist studied medical information (including results from spirometry tests that measure breathing ability) on 9,425 people aged 40 and over from
12 different countries.
They found that:
The overall prevalence of COPD was 10.1 per cent.
This compares with previous estimates from another study that put the prevalence at 4.3 per cent.
Among men the prevalence of COPD was 11.8 per cent.
Among women it was 8.5 per cent.
Differences in smoking behaviour probably explains the difference in COPD rates between men and women.
The figures varied widely across different countries.
South Africa had the highest proportion of people with COPD: 22.2 per cent of men and 16.7 per cent of women.
Hanover in Germany had the lowest prevalence: 8.6 per cent of men and 3.7 per cent of women.
In the US, the overall prevalence of serious COPD is 10.1 per cent.
The risk of COPD is nearly doubled for every 10 years of age above 40.
Smoking has a similar large effect on risk.
Buist said that:
"This worldwide study showed higher levels and more advanced staging of spirometrically confirmed COPD than have typically been reported."
There is no cure for COPD and the advice of the authors is that people can reduce their COPD risk by not smoking and avoiding atmospheres that contain
pollutants and smoke, and if you have to work with pollution then wear a mask or other form of protection.
There is some room for optimism though. We now know a lot more about how to prevent and treat COPD. As the authors explained in their summary, scientific
understanding of COPD has grown in a number of areas recently. For instance we know more about how:
Other diseases affect COPD (comorbidity),
COPD affects people with different genetic backgrounds (COPD phenotypes), and
COPD affects health in ways other than lung function.
"Global burden of COPD: risk factors, prevalence, and future trends."
David M Mannino, A Sonia Buist.
The Lancet 2007; 370:765-773
Volume 370, Number 9589, 1 September 2007
DOI:10.1016/S0140-6736(07)61380-4
Click here for Abstract.
воскресенье, 10 июля 2011 г.
Predictive Tool May Help Determine Treatment Of COPD Patients
A new score, the ADO index, for predicting a patient's risk of dying from chronic obstructive pulmonary disease (COPD) performs better than the current test and is much more applicable in clinical practice. It could help doctors target suitable treatment options to individual patients, finds an Article to be published in this week's COPD special edition of The Lancet.
The BODE index is a widely used estimate of how likely a patient is to die from COPD based on an assessment of major risk factors for COPD such as body-mass index, airflow obstruction, shortness of breath, and exercise capacity. However, since exercise capacity is often not available in practice the BODE index is rarely used in primary care settings where most COPD patients are managed. In addition, the index fails to calculate an individual's absolute risk* accurately and is therefore not ready for doctors to use as a prognostic tool when trying to identify which treatment option to use in individual patients.
To verify if the BODE index accurately predicts those most at risk, Milo Puhan from Johns Hopkins Bloomberg School of Public Health in the USA and colleagues compared whether a patient's risk of death predicted by the BODE index matched the observed 3-year risk of all-cause mortality in two different COPD populations from Switzerland and Spain. The authors then aimed to modify the index to improve its predictive accuracy and develop a new simple score using age, shortness of breath, and airflow obstruction (ADO index), to make it more useful for doctors in primary care settings.
In total, 232 patients with longstanding and severe COPD from the Swiss Barmelweid cohort were studied, along with 342 patients from the Spanish Phenotype and Course of COPD cohort study who had their first hospital admission due to moderate-to-severe COPD. Findings showed that the original BODE index was poor at predicting 3-year risk of mortality-with a 36% relative underprediction in the Swiss cohort (median predicted risk 21.7% compared with 34.1% observed risk) and a 39% relative overprediction in the Spanish cohort (median predicted risk 16.7% compared with 12.0% observed risk). Importantly, the updated BODE and ADO indices gave more accurate predictions of 3-year mortality and matched the observed mortality in the Spanish cohort well with little difference between predicted and observed mortality.
The authors comment: "The simplified points system for the updated BODE and ADO indices??¦[is] easy to use to obtain the 3-year mortality risk in an individual patient??¦[and] allows clinicians to identify patients at moderate or high risk of mortality, for which more comprehensive treatment with respiratory rehabilitation, for example, might be appropriate to reduce their risk."
They conclude: "Both the updated BODE and ADO indices could lend support to the prognostic assessment of patients with COPD in specialised and in primary care settings. Such assessment enhances the targeting of treatments to individual patients."
In an accompanying Comment, Holger Sch??nemann from McMaster University Health Sciences Centre in Canada says the results suggest that: "Identification of baseline risks through prognostic studies might help to target therapy and can make important and long-needed contributions to, for instance, guideline development."
Link to article
Source
The Lancet
The BODE index is a widely used estimate of how likely a patient is to die from COPD based on an assessment of major risk factors for COPD such as body-mass index, airflow obstruction, shortness of breath, and exercise capacity. However, since exercise capacity is often not available in practice the BODE index is rarely used in primary care settings where most COPD patients are managed. In addition, the index fails to calculate an individual's absolute risk* accurately and is therefore not ready for doctors to use as a prognostic tool when trying to identify which treatment option to use in individual patients.
To verify if the BODE index accurately predicts those most at risk, Milo Puhan from Johns Hopkins Bloomberg School of Public Health in the USA and colleagues compared whether a patient's risk of death predicted by the BODE index matched the observed 3-year risk of all-cause mortality in two different COPD populations from Switzerland and Spain. The authors then aimed to modify the index to improve its predictive accuracy and develop a new simple score using age, shortness of breath, and airflow obstruction (ADO index), to make it more useful for doctors in primary care settings.
In total, 232 patients with longstanding and severe COPD from the Swiss Barmelweid cohort were studied, along with 342 patients from the Spanish Phenotype and Course of COPD cohort study who had their first hospital admission due to moderate-to-severe COPD. Findings showed that the original BODE index was poor at predicting 3-year risk of mortality-with a 36% relative underprediction in the Swiss cohort (median predicted risk 21.7% compared with 34.1% observed risk) and a 39% relative overprediction in the Spanish cohort (median predicted risk 16.7% compared with 12.0% observed risk). Importantly, the updated BODE and ADO indices gave more accurate predictions of 3-year mortality and matched the observed mortality in the Spanish cohort well with little difference between predicted and observed mortality.
The authors comment: "The simplified points system for the updated BODE and ADO indices??¦[is] easy to use to obtain the 3-year mortality risk in an individual patient??¦[and] allows clinicians to identify patients at moderate or high risk of mortality, for which more comprehensive treatment with respiratory rehabilitation, for example, might be appropriate to reduce their risk."
They conclude: "Both the updated BODE and ADO indices could lend support to the prognostic assessment of patients with COPD in specialised and in primary care settings. Such assessment enhances the targeting of treatments to individual patients."
In an accompanying Comment, Holger Sch??nemann from McMaster University Health Sciences Centre in Canada says the results suggest that: "Identification of baseline risks through prognostic studies might help to target therapy and can make important and long-needed contributions to, for instance, guideline development."
Link to article
Source
The Lancet
четверг, 7 июля 2011 г.
Blacks Awaiting Lung Transplants More Likely To Die Or Be Denied Than Whites
Blacks with chronic obstructive pulmonary disease (COPD) were less likely to receive a lung transplant and more likely to die or be removed from the transplant list than whites, according to Columbia University Medical Center researchers.
"These disparities are consistent with those observed among patients awaiting kidney and liver transplantation and among patients with other advanced lung diseases such as pulmonary arterial hypertension and pulmonary fibrosis," wrote lead researcher, David Lederer, M.D., M.S., of Columbia University Medical Center. "This finding was independent of age, lung function, cardiovascular risk factors, transplant center volume, type of health insurance coverage, and neighborhood poverty level."
The findings were published in the second issue for February of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
The researchers retrospectively assessed the entire cohort of 280 non-Hispanic black adults and 5,272 non-Hispanic white adults diagnosed with COPD or emphysema who were awaiting lung transplantation on the United Network for Organ Sharing (UNOS) list between January 1, 1995 and December 31, 2004. The investigators tracked the outcomes (death, transplantation, removal from the list, or still living) of the transplant-awaiting patients to the end of the study period and analyzed the results with respect to age, sex, disease severity, community poverty level and transplant center volume.
"We have shown that black patients with COPD were less likely to undergo lung transplantation after listing than white patients in the United States during the late 1990's and the early 2000's," wrote Dr. Lederer.
The researchers did find that blacks were also less likely to have private insurance and more likely to live in poorer neighborhoods and have greater cardiovascular risk factors, such as diabetes, pulmonary hypertension and lower six-minute walk distances than whites. However, even these factors did not account for the findings.
"Differences in insurance, socioeconomic status and cardiovascular risk factors explained some but not all of the higher risk of death or removal from the waiting list," said Dr. Lederer.
In the post-hoc analysis, the researchers also found that Hispanics had similar outcomes to non-Hispanic blacks.
Strikingly, only 280 black and 64 Hispanic patients with COPD were put on the lung transplant waiting list in the United States during the 10-year study period. "Based on what we know about COPD, we expected that twice as many black patients would have been put on the ling transplant waiting list. Our findings point to significant barriers to accessing lung transplantation for minorities," said Dr. Lederer.
For physicians, the implications of this research are clear. "These findings should alert primary care physicians and pulmonologists to consider referral of black patients with COPD for transplantation at the earliest signs of advanced disease."
To protect themselves from these disparities, "patients with COPD should prepare themselves for transplantation by discussing all of their treatment options with their doctor. To be eligible for lung transplantation, patients must quit smoking, use medications and oxygen as prescribed, and participate in a pulmonary rehabilitation program to increase their strength and endurance," said Dr. Lederer.
While the organ allocation system in place during the study period has been replaced with one that prioritizes patients based on the survival benefit of transplantation, Dr. Lederer cautions, the effects of poor insurance and poverty will likely still place blacks at increased risk for removal from the list or death.
"The next step will be to identify the specific barriers that patients encounter, while trying to get on the waiting list for a lung transplant. Once we figure out the root of the problem, we can begin to improve access for all patients with COPD."
American Thoracic Society (ATS)
61 Broadway
New York, NY 10006
United States
thoracic
"These disparities are consistent with those observed among patients awaiting kidney and liver transplantation and among patients with other advanced lung diseases such as pulmonary arterial hypertension and pulmonary fibrosis," wrote lead researcher, David Lederer, M.D., M.S., of Columbia University Medical Center. "This finding was independent of age, lung function, cardiovascular risk factors, transplant center volume, type of health insurance coverage, and neighborhood poverty level."
The findings were published in the second issue for February of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
The researchers retrospectively assessed the entire cohort of 280 non-Hispanic black adults and 5,272 non-Hispanic white adults diagnosed with COPD or emphysema who were awaiting lung transplantation on the United Network for Organ Sharing (UNOS) list between January 1, 1995 and December 31, 2004. The investigators tracked the outcomes (death, transplantation, removal from the list, or still living) of the transplant-awaiting patients to the end of the study period and analyzed the results with respect to age, sex, disease severity, community poverty level and transplant center volume.
"We have shown that black patients with COPD were less likely to undergo lung transplantation after listing than white patients in the United States during the late 1990's and the early 2000's," wrote Dr. Lederer.
The researchers did find that blacks were also less likely to have private insurance and more likely to live in poorer neighborhoods and have greater cardiovascular risk factors, such as diabetes, pulmonary hypertension and lower six-minute walk distances than whites. However, even these factors did not account for the findings.
"Differences in insurance, socioeconomic status and cardiovascular risk factors explained some but not all of the higher risk of death or removal from the waiting list," said Dr. Lederer.
In the post-hoc analysis, the researchers also found that Hispanics had similar outcomes to non-Hispanic blacks.
Strikingly, only 280 black and 64 Hispanic patients with COPD were put on the lung transplant waiting list in the United States during the 10-year study period. "Based on what we know about COPD, we expected that twice as many black patients would have been put on the ling transplant waiting list. Our findings point to significant barriers to accessing lung transplantation for minorities," said Dr. Lederer.
For physicians, the implications of this research are clear. "These findings should alert primary care physicians and pulmonologists to consider referral of black patients with COPD for transplantation at the earliest signs of advanced disease."
To protect themselves from these disparities, "patients with COPD should prepare themselves for transplantation by discussing all of their treatment options with their doctor. To be eligible for lung transplantation, patients must quit smoking, use medications and oxygen as prescribed, and participate in a pulmonary rehabilitation program to increase their strength and endurance," said Dr. Lederer.
While the organ allocation system in place during the study period has been replaced with one that prioritizes patients based on the survival benefit of transplantation, Dr. Lederer cautions, the effects of poor insurance and poverty will likely still place blacks at increased risk for removal from the list or death.
"The next step will be to identify the specific barriers that patients encounter, while trying to get on the waiting list for a lung transplant. Once we figure out the root of the problem, we can begin to improve access for all patients with COPD."
American Thoracic Society (ATS)
61 Broadway
New York, NY 10006
United States
thoracic
понедельник, 4 июля 2011 г.
COPD - AstraZeneca Welcomes Preliminary Results From TORCH
AstraZeneca (LSE: AZN , NYSE: AZN) has welcomed preliminary results from the TORCH (TOwards a Revolution in COPD Health) study1, suggesting combination therapies containing an inhaled corticosteroid (ICS) and long-acting beta 2 agonist (LABA) have the potential to show mortality benefits for COPD patients.
The reported 17% reduction in mortality compared to placebo shown by the combination of an ICS and LABA further demonstrates the beneficial effects of this class of medicines and the positive impact on the lives of COPD patients. AstraZeneca looks forward to a more detailed presentation of the data.
Coupled with the mortality data, the preliminary results also underline the importance of preventing exacerbations as the key driver of mortality. Reduction of exacerbations is an area where the budesonide / formoterol ICS/LABA therapy (marketed by AstraZeneca as Symbicort(R)) has strong clinical data. Of particular note, a study2 by Calverley et al. demonstrated that Symbicort reduced risk of exacerbations(i) by 30% and 29% compared to formoterol and placebo respectively, resulting in a clinically important improvement in Health Related Quality of Life (HRQL) compared to placebo.
Patients with COPD regard exacerbations as the aspect of their disease that they fear most. Severe acute exacerbations of COPD are associated independently with a poor prognosis and increased mortality. Studies have shown that between 22% - 43% of COPD patients hospitalised due to an exacerbation will be dead within one year3,4,5,6.
COPD is a major cause of death worldwide, and is currently the fourth most common cause of death after cancer, ischemic heart disease and cerebrovascular disease. Of these diseases, only COPD shows increasing rates of mortality. By 2020, COPD is anticipated to become the third most common cause of death worldwide.
References:
1) GSK Press Release 'GSK announces positive results of Seretide study in patients with chronic obstructive pulmonary disease (COPD)' 28th March 2006 (gsk/media/pressreleases.htm)
2) Calverley PM, Boonsawat Z, Zhong N, Peterson S and Olsson H. Maintenance therapy with budesonide and formoterol in chronic obstructive pulmonary disease. Eur Resp J 2003; 22; 912-919.
3) Eriksen N, et al. Ugeskr Laeger 2003;165:3499-3502
4) Groenewegen KH, et al. Chest 2003;124:459-467
5) Almagro P, et al. Chest 2002;121:1441-1448
6) Connors AF, et al. Am J Respir Crit Care Med 1996;154:959-967
(i) Definition of an exacerbation: requiring medical intervention (oral antibiotics/and/or corticosteroids or hospitalisation)
astrazeneca
The reported 17% reduction in mortality compared to placebo shown by the combination of an ICS and LABA further demonstrates the beneficial effects of this class of medicines and the positive impact on the lives of COPD patients. AstraZeneca looks forward to a more detailed presentation of the data.
Coupled with the mortality data, the preliminary results also underline the importance of preventing exacerbations as the key driver of mortality. Reduction of exacerbations is an area where the budesonide / formoterol ICS/LABA therapy (marketed by AstraZeneca as Symbicort(R)) has strong clinical data. Of particular note, a study2 by Calverley et al. demonstrated that Symbicort reduced risk of exacerbations(i) by 30% and 29% compared to formoterol and placebo respectively, resulting in a clinically important improvement in Health Related Quality of Life (HRQL) compared to placebo.
Patients with COPD regard exacerbations as the aspect of their disease that they fear most. Severe acute exacerbations of COPD are associated independently with a poor prognosis and increased mortality. Studies have shown that between 22% - 43% of COPD patients hospitalised due to an exacerbation will be dead within one year3,4,5,6.
COPD is a major cause of death worldwide, and is currently the fourth most common cause of death after cancer, ischemic heart disease and cerebrovascular disease. Of these diseases, only COPD shows increasing rates of mortality. By 2020, COPD is anticipated to become the third most common cause of death worldwide.
References:
1) GSK Press Release 'GSK announces positive results of Seretide study in patients with chronic obstructive pulmonary disease (COPD)' 28th March 2006 (gsk/media/pressreleases.htm)
2) Calverley PM, Boonsawat Z, Zhong N, Peterson S and Olsson H. Maintenance therapy with budesonide and formoterol in chronic obstructive pulmonary disease. Eur Resp J 2003; 22; 912-919.
3) Eriksen N, et al. Ugeskr Laeger 2003;165:3499-3502
4) Groenewegen KH, et al. Chest 2003;124:459-467
5) Almagro P, et al. Chest 2002;121:1441-1448
6) Connors AF, et al. Am J Respir Crit Care Med 1996;154:959-967
(i) Definition of an exacerbation: requiring medical intervention (oral antibiotics/and/or corticosteroids or hospitalisation)
astrazeneca
пятница, 1 июля 2011 г.
SERPINE2 identified as novel candidate gene for COPD, especially with smoking
Using a combination of genetic linkage, microarray gene expression and genetic association studies, a group of Brigham
and Women's Hospital/ Harvard Medical School researchers have identified a serine protease inhibitor clade E, member 2, or
SERPINE2, "as a novel candidate susceptibility gene for COPD," according to Sorachai Srisuma, who is presenting the research
at the 35th Congress of the International Union of Physiological Sciences in San Diego, March 31 - April 5, 2005.
The collaborative, multi-disciplinary team includes: Sorachai Srisuma, Dawn L. DeMeo, Brigham H. Mecham, Edwin K. Silverman,
Scott T. Weiss, Kathleen J. Haley, John J. Reilly, Steven D. Shapiro, and Thomas J. Mariani. Mariani, head of the lab where
Srisuma works, said the gene is "the most promising susceptibility candidate due to its biological relevance, its expression
correlation with disease characteristics, and the allelic association in COPD families and replication in non-familial COPD
patients."
*Paper presentation: "Expression of Serine Proteinase Inhibitor E2, a novel candidate COPD susceptibility gene, in the lung,"
12:30 p.m.-3 p.m. Tuesday April 5, Physiology 936.4/board #A490. On view 7:30 a.m. - 4 p.m.
Feature topic presentation: Srisuma also is participating in featured topic session #477, "Receptors and signaling pathways
in lung injury and repair," Sunday April 3 room 30A. It begins at 3:15 p.m. Srisuma's presentation is scheduled for 4:15 p.m.
First major study to seek SERPINE2's physiological role in lung
Srisuma said SERPINE2 "was of particular interest due to its pattern of expression and relationship to alpha-1-antitypsin,
the only gene proven to modify risk to COPD (chronic obstructive pulmonary disease). Our team of human genetic
epidemiologists, led by Dawn DeMeo and Edwin Silverman, previously identified a region on chromosome 2 they thought might
contain a gene conferring susceptibility to COPD.
"We used DNA chips, or gene expression microarrays, to identify genes within this region that were expressed in the lung,"
Srisuma noted. "Subsequently we showed that specific cells in the lungs express SERPINE2, and that its expression is altered
in individuals with certain clinical characteristics of COPD. Furthermore, specific forms of the gene, termed polymorphisms
or SNPs, were more common in people who developed COPD," he said. Taken together, "these data strongly suggest SERPINE2 is a
gene capable of modifying COPD risk, particularly in response to smoking," he added.
SERPINE2 is a major tissue and cell-associated inhibitor of thrombin and plasmin, but not elastase, Srisuma noted. But no
significant study of this protease inhibitor's expression in normal or diseased lungs had been undertaken previously. "In an
effort to begin to gain insight into the physiological role of SERPINE2 in the lung, we investigated the temporal and spatial
expression pattern of the gene in mouse and human lungs," he said.
Analysis of two independent microarray data sets describing normal mouse lung development revealed prominent SERPINE2
expression, which was maximal during formation of the airspaces, which is related to lung maturation. Immunostaining was
performed to identify the location of SERPINE2 within the lung.
SERPINE2 shows analogous pattern in diseased human, normal mouse lungs
Prominent immunolocalization of SERPINE2 was observed in a cell-associated pattern within bronchiolar airway epithelial cells
and in an extracellular matrix-associated pattern in the vascular adventitia. Immunohistochemistry in human lungs
demonstrated an analogous staining pattern. "Our studies revealed cell-specific and developmentally-regulated expression of
SERPINE2 in the lung, which supports further investigation of this gene's role in human lung diseases," Srisuma said.
Next steps. Already the group has characterized where and when SERPINE2 is expressed in the lung at various developmental
stages. "We are also investigating the specific role of SERPINE2 mutations in lung function and the risk of developing COPD
in humans and genetically modified animals," Srisuma noted. "We hope this line of investigation will show how SERPINE2
affects the risk of developing COPD and how smoking contributes to this process," he added.
In the future, Srisuma will pursue a project identifying potential biomarkers in COPD patients from New England and also in
his native Thailand. When he completes his current post-doctoral fellowship and returns home, a collaborative study will
proceed related to lung development and pathogenesis of COPD and pediatric lung diseases.
Funding. This and related research are supported by the National Institutes of Health.
Scope of the problem, hope for behavior change
About 16 million Americans suffer from COPD, a chronic inflammatory disorder characterized by a gradual loss of lung
function. Strongly associated with cigarette smoking, COPD is the only disease among the top 10 causes of death in the U.S.
with an increasing rate of newly diagnosed cases. Already the fourth leading cause of death in the U.S., some believe it
could be the leading cause of death worldwide by 2010. So far, there is no cure for COPD, and doctors can only relieve
symptoms.
Similar to diseases like cancer and heart diseases, people who smoke (or breathe second-hand smoke) have an increased risk of
developing COPD, including emphysema and chronic bronchitis. Certain individuals are more susceptible than others, in that
they have an increased risk of developing disease in response to smoking. For instance, people with a rare form of the
protein made by the gene alpha-1-antitrypsin have a high risk of developing COPD if they smoke. Individuals with the common
form of this protein have a low risk of developing emphysema, but increase their chances of getting disease if they smoke.
Srisuma said that nearly all individuals are thought to have other genes that contribute to their risk of developing COPD.
Researchers have previously identified some candidate susceptibility genes and further studies may help identify people with
increased risk of disease. "The identification of individuals with increased risk would be beneficial," he said, "if they can
modify their smoking behavior. Further research also may hasten the detection diseased individuals, which will be especially
useful if it also leads to potential therapies," Srisuma added.
The 35th IUPS Congress (iups2005) is organized by the six member
societies of the U.S. National Committee of the IUPS, the American Physiological Society, the Society for Neuroscience, the
Microcirculatory Society, the Society of General Physiologists, the Biomedical Engineering Society, and the Society for
Integrative and Comparative Biology, under the auspices of the U.S. National Academy of Sciences.
The IUPS conference, held every four years, runs concurrently this year with Experimental Biology 2005 at the San Diego
Convention Center.
The American Physiological Society (APS), which is hosting IUPS, was founded in 1887 to foster basic and applied science,
much of it relating to human health. The Bethesda, MD-based Society has more than 10,000 members and publishes nearly 4,000
articles every year in its 14 peer-reviewed journals. In May, APS received the Presidential Award for Excellence in Science,
Mathematics and Engineering Mentoring (PAESMEM).
Editor's Note: For further information or to schedule an interview with a member of the research team, please contact Mayer
Resnick at the IUPS/APS newsroom 619-525-6228 (March 31-April 6), or 301-332-4402 (cell) or 301-634-7209 (office), or Stacy
Brooks at 240-432-9697 (cell) or 301-634-7253 (office).
A searchable online program for IUPS and EB is at faseb/meetings/eb2005/call/default.htm
Contact: Mayer Resnick
mresnickthe-aps
301-332-4402 (cell)
301-634-7209 (office, outside IUPS dates)
American Physiological Society
the-aps
IUPS/APS Newsroom March 29-April 6
San Diego Convention Center
Hall E Registration Area/Flex Unit
Telephone: 619-525-6228
and Women's Hospital/ Harvard Medical School researchers have identified a serine protease inhibitor clade E, member 2, or
SERPINE2, "as a novel candidate susceptibility gene for COPD," according to Sorachai Srisuma, who is presenting the research
at the 35th Congress of the International Union of Physiological Sciences in San Diego, March 31 - April 5, 2005.
The collaborative, multi-disciplinary team includes: Sorachai Srisuma, Dawn L. DeMeo, Brigham H. Mecham, Edwin K. Silverman,
Scott T. Weiss, Kathleen J. Haley, John J. Reilly, Steven D. Shapiro, and Thomas J. Mariani. Mariani, head of the lab where
Srisuma works, said the gene is "the most promising susceptibility candidate due to its biological relevance, its expression
correlation with disease characteristics, and the allelic association in COPD families and replication in non-familial COPD
patients."
*Paper presentation: "Expression of Serine Proteinase Inhibitor E2, a novel candidate COPD susceptibility gene, in the lung,"
12:30 p.m.-3 p.m. Tuesday April 5, Physiology 936.4/board #A490. On view 7:30 a.m. - 4 p.m.
Feature topic presentation: Srisuma also is participating in featured topic session #477, "Receptors and signaling pathways
in lung injury and repair," Sunday April 3 room 30A. It begins at 3:15 p.m. Srisuma's presentation is scheduled for 4:15 p.m.
First major study to seek SERPINE2's physiological role in lung
Srisuma said SERPINE2 "was of particular interest due to its pattern of expression and relationship to alpha-1-antitypsin,
the only gene proven to modify risk to COPD (chronic obstructive pulmonary disease). Our team of human genetic
epidemiologists, led by Dawn DeMeo and Edwin Silverman, previously identified a region on chromosome 2 they thought might
contain a gene conferring susceptibility to COPD.
"We used DNA chips, or gene expression microarrays, to identify genes within this region that were expressed in the lung,"
Srisuma noted. "Subsequently we showed that specific cells in the lungs express SERPINE2, and that its expression is altered
in individuals with certain clinical characteristics of COPD. Furthermore, specific forms of the gene, termed polymorphisms
or SNPs, were more common in people who developed COPD," he said. Taken together, "these data strongly suggest SERPINE2 is a
gene capable of modifying COPD risk, particularly in response to smoking," he added.
SERPINE2 is a major tissue and cell-associated inhibitor of thrombin and plasmin, but not elastase, Srisuma noted. But no
significant study of this protease inhibitor's expression in normal or diseased lungs had been undertaken previously. "In an
effort to begin to gain insight into the physiological role of SERPINE2 in the lung, we investigated the temporal and spatial
expression pattern of the gene in mouse and human lungs," he said.
Analysis of two independent microarray data sets describing normal mouse lung development revealed prominent SERPINE2
expression, which was maximal during formation of the airspaces, which is related to lung maturation. Immunostaining was
performed to identify the location of SERPINE2 within the lung.
SERPINE2 shows analogous pattern in diseased human, normal mouse lungs
Prominent immunolocalization of SERPINE2 was observed in a cell-associated pattern within bronchiolar airway epithelial cells
and in an extracellular matrix-associated pattern in the vascular adventitia. Immunohistochemistry in human lungs
demonstrated an analogous staining pattern. "Our studies revealed cell-specific and developmentally-regulated expression of
SERPINE2 in the lung, which supports further investigation of this gene's role in human lung diseases," Srisuma said.
Next steps. Already the group has characterized where and when SERPINE2 is expressed in the lung at various developmental
stages. "We are also investigating the specific role of SERPINE2 mutations in lung function and the risk of developing COPD
in humans and genetically modified animals," Srisuma noted. "We hope this line of investigation will show how SERPINE2
affects the risk of developing COPD and how smoking contributes to this process," he added.
In the future, Srisuma will pursue a project identifying potential biomarkers in COPD patients from New England and also in
his native Thailand. When he completes his current post-doctoral fellowship and returns home, a collaborative study will
proceed related to lung development and pathogenesis of COPD and pediatric lung diseases.
Funding. This and related research are supported by the National Institutes of Health.
Scope of the problem, hope for behavior change
About 16 million Americans suffer from COPD, a chronic inflammatory disorder characterized by a gradual loss of lung
function. Strongly associated with cigarette smoking, COPD is the only disease among the top 10 causes of death in the U.S.
with an increasing rate of newly diagnosed cases. Already the fourth leading cause of death in the U.S., some believe it
could be the leading cause of death worldwide by 2010. So far, there is no cure for COPD, and doctors can only relieve
symptoms.
Similar to diseases like cancer and heart diseases, people who smoke (or breathe second-hand smoke) have an increased risk of
developing COPD, including emphysema and chronic bronchitis. Certain individuals are more susceptible than others, in that
they have an increased risk of developing disease in response to smoking. For instance, people with a rare form of the
protein made by the gene alpha-1-antitrypsin have a high risk of developing COPD if they smoke. Individuals with the common
form of this protein have a low risk of developing emphysema, but increase their chances of getting disease if they smoke.
Srisuma said that nearly all individuals are thought to have other genes that contribute to their risk of developing COPD.
Researchers have previously identified some candidate susceptibility genes and further studies may help identify people with
increased risk of disease. "The identification of individuals with increased risk would be beneficial," he said, "if they can
modify their smoking behavior. Further research also may hasten the detection diseased individuals, which will be especially
useful if it also leads to potential therapies," Srisuma added.
The 35th IUPS Congress (iups2005) is organized by the six member
societies of the U.S. National Committee of the IUPS, the American Physiological Society, the Society for Neuroscience, the
Microcirculatory Society, the Society of General Physiologists, the Biomedical Engineering Society, and the Society for
Integrative and Comparative Biology, under the auspices of the U.S. National Academy of Sciences.
The IUPS conference, held every four years, runs concurrently this year with Experimental Biology 2005 at the San Diego
Convention Center.
The American Physiological Society (APS), which is hosting IUPS, was founded in 1887 to foster basic and applied science,
much of it relating to human health. The Bethesda, MD-based Society has more than 10,000 members and publishes nearly 4,000
articles every year in its 14 peer-reviewed journals. In May, APS received the Presidential Award for Excellence in Science,
Mathematics and Engineering Mentoring (PAESMEM).
Editor's Note: For further information or to schedule an interview with a member of the research team, please contact Mayer
Resnick at the IUPS/APS newsroom 619-525-6228 (March 31-April 6), or 301-332-4402 (cell) or 301-634-7209 (office), or Stacy
Brooks at 240-432-9697 (cell) or 301-634-7253 (office).
A searchable online program for IUPS and EB is at faseb/meetings/eb2005/call/default.htm
Contact: Mayer Resnick
mresnickthe-aps
301-332-4402 (cell)
301-634-7209 (office, outside IUPS dates)
American Physiological Society
the-aps
IUPS/APS Newsroom March 29-April 6
San Diego Convention Center
Hall E Registration Area/Flex Unit
Telephone: 619-525-6228
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