Skip directly to search Skip directly to A to Z list Skip directly to navigation Skip directly to page options Skip directly to site content


Hot Topics of the Day|PHGKB
Search PHGKB:

Archive

Hot Topics of the Day are picked by experts to capture the latest information and publications on public health genomics and precision health for various diseases and health topics. Sources include published scientific literature, reviews, blogs and popular press articles.

Search Archive:
60 hot topic(s) found with the query "Chronic obstructive pulmonary disease"

Genetics of chronic respiratory disease.
Ian Sayers et al. Nat Rev Genet 2024 3 (Posted: Mar 07, 2024 8AM)

From the abstract: "Chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD), asthma and interstitial lung diseases are frequently occurring disorders with a polygenic basis that account for a large global burden of morbidity and mortality. Recent large-scale genetic epidemiology studies have identified associations between genetic variation and individual respiratory diseases and linked specific genetic variants to quantitative traits related to lung function. "

Deep learning model improves COPD risk prediction and gene discovery.
et al. Nat Genet 2023 4 (Posted: Apr 28, 2023 8AM)

Liability scores for chronic obstructive pulmonary disease obtained from our deep learning model improve genetic association discovery and risk prediction. We trained our model using full spirograms and noisy medical record labels obtained from self-reporting and hospital diagnostic codes, and demonstrated that the machine-learning-based phenotyping approach can be generalized to diseases that lack expert-defined annotations.

Inference of chronic obstructive pulmonary disease with deep learning on raw spirograms identifies new genetic loci and improves risk models.
Justin Cosentino et al. Nat Genet 2023 4 (Posted: Apr 20, 2023 9AM)

Here we train a deep convolutional neural network on noisy self-reported and International Classification of Diseases labels to predict COPD case–control status from high-dimensional raw spirograms and use the model’s predictions as a liability score. The machine-learning-based (ML-based) liability score accurately discriminates COPD cases and controls and predicts COPD-related hospitalization without any domain-specific knowledge.

Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk.
Nick Shrine et al. Nature genetics 2023 3 (3) 410-422 (Posted: Mar 15, 2023 6PM)

Lung-function impairment underlies chronic obstructive pulmonary disease (COPD) and predicts mortality. In the largest multi-ancestry genome-wide association meta-analysis of lung function to date, comprising 580,869 participants, we identified 1,020 independent association signals implicating 559 genes supported by =2 criteria from a systematic variant-to-gene mapping framework. These genes were enriched in 29 pathways. Individual variants showed heterogeneity across ancestries, age and smoking groups, and collectively as a genetic risk score showed strong association with COPD across ancestry groups.

Identifying acute exacerbations of chronic obstructive pulmonary disease using patient-reported symptoms and cough feature analysis
S Claxton et al, NPJ Digital Medicine, July 2, 2021 (Posted: Jul 03, 2021 7AM)

Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are commonly encountered in the primary care setting, though the accurate and timely diagnosis is problematic. Using technology like that employed in speech recognition technology, we developed a smartphone-based algorithm for rapid and accurate diagnosis of AECOPD.

Disease-associated gut microbiome and metabolome changes in patients with chronic obstructive pulmonary disease
KL Bowerman et al, Nature Medicine, November 18, 2020 (Posted: Nov 18, 2020 10AM)

Chronic obstructive pulmonary disease (COPD) is a progressing disease, with lung but not gut microbiota implicated in its etiology. Here the authors compare the stool from patients with COPD and healthy controls to find specific gut bacteria and metabolites associated with active disease, thereby hinting at a potential role for the gut microbiome in COPD.

Diagnosing Chronic Obstructive Airway Disease: a diagnostic accuracy study of a smartphone delivered algorithm combining patient-reported symptoms and cough analysis for use in acute care consultations.
P Porter et al, MEDRXIV, September 25, 2020 (Posted: Sep 26, 2020 10AM)

The aim of this study was to develop a rapid, smartphone-based algorithm for the detection of COPD, in the presence or absence of acute respiratory infection, and then evaluate diagnostic accuracy on an independent validation set.

Risk Factors for Hospitalization, Mechanical Ventilation, or Death Among 10 131 US Veterans With SARS-CoV-2 Infection
GN Ioannou et al, JAMA Network Open, September 23, 2020 (Posted: Sep 23, 2020 1PM)

In this national cohort of VA patients, most SARS-CoV-2 deaths were associated with older age, male sex, and comorbidity burden. Many factors previously reported to be associated with mortality in smaller studies were not confirmed, such as obesity, Black race, Hispanic ethnicity, chronic obstructive pulmonary disease, hypertension, and smoking.

The therapeutic potential of exosomes
J Madhusoodanan, Nature Outlook, May 13, 2020 (Posted: May 18, 2020 9AM)

Extracellular vesicles released in response to cigarette smoke might trigger chronic obstructive pulmonary disease, but engineered versions could be a treatment.

Screening for chronic obstructive pulmonary disease with artificial intelligence
JE Bibault et al, Lancet Digital Health, April 21, 2020 (Posted: Apr 22, 2020 8AM)

Risk factors for severe corona virus disease 2019 (COVID-19) patients : a systematic review and meta analysis
L Xu et al, MEDRXIV, April 1, 2020 (Posted: Apr 02, 2020 10AM)

In this review and meta-analysis, we found that elderly male patients with a high body mass index, high breathing rate and a combination of underlying diseases (such as hypertension, diabetes, cardiovascular disease, and chronic obstructive pulmonary disease) were more likely to become critically ill.

Clinical Epidemiology of COPD: Insights From 10 Years of the COPDGene Study.
Maselli Diego J et al. Chest 2019 May (Posted: Jul 01, 2019 1PM)

COPDGene study is a noninterventional, multicenter, longitudinal analysis of > 10,000 subjects, including smokers with a ¡Ý 10 pack-year history with and without COPD and healthy never smokers. The goal was to characterize disease-related phenotypes and explore associations with susceptibility genes. The subjects were extensively phenotyped with the use of comprehensive symptom and comorbidity questionnaires, spirometry, CT scans of the chest, and genetic and biomarker profiling. The paper highlights the influence of age, sex, and race on the natural history of COPD.

New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries
N Shrine et al, Nature Genetics, February 25, 2019 (Posted: Feb 25, 2019 11AM)

Genetic landscape of chronic obstructive pulmonary disease identifies heterogeneous cell-type and phenotype associations
Nature Genetics, February 25, 2019 (Posted: Feb 25, 2019 11AM)

Advances in managing COPD related to α 1 -antitrypsin deficiency: An under-recognized genetic disorder.
Craig Timothy J et al. Allergy 2018 Nov (11) 2110-2121 (Posted: Nov 21, 2018 0PM)

Genetic risk factors for the development of pulmonary disease identified by genome-wide association.
Hall Robert et al. Respirology (Carlton, Vic.) 2018 Nov (Posted: Nov 21, 2018 0PM)

Chronic Obstructive Pulmonary Disease and Lung Cancer: Underlying Pathophysiology and New Therapeutic Modalities.
Eapen Mathew Suji et al. Drugs 2018 Nov (16) 1717-1740 (Posted: Nov 21, 2018 0PM)

Precision medicine in COPD exacerbations.
Agusti Alvar et al. The Lancet. Respiratory medicine 2018 Jul (Posted: Jul 25, 2018 8AM)

Living With COPD
Brand (Posted: Apr 30, 2018 1PM)

Current Approaches for Phenotyping as a Target for Precision Medicine in COPD Management.
Lopez-Campos Jose Luis et al. COPD 2018 Mar 1-10 (Posted: Mar 21, 2018 4PM)

Microbiome in chronic obstructive pulmonary disease.
Monsó Eduard et al. Annals of translational medicine 2017 Jun (12) 251 (Posted: Jan 16, 2018 0PM)

What do polymorphisms tell us about the mechanisms of COPD?
Li Yan et al. Clinical science (London, England : 1979) 2017 Dec (24) 2847-2863 (Posted: Jan 16, 2018 0PM)

New study offers insights on genetic indicators of COPD risk
NHLBI, Jan 16, 2018 Brand (Posted: Jan 16, 2018 0PM)

National COPD Awareness Month
Brand (Posted: Nov 27, 2017 1PM)

Personalized medicine and chronic obstructive pulmonary disease.
Wouters E F M et al. Current opinion in pulmonary medicine 2017 May (3) 241-246 (Posted: Oct 25, 2017 3PM)

Chronic Obstructive Pulmonary Disease Phenotypes: Implications for Care.
Mirza Shireen et al. Mayo Clinic proceedings 2017 Jul (7) 1104-1112 (Posted: Oct 25, 2017 3PM)

Role of the Lung Microbiome in the Pathogenesis of Chronic Obstructive Pulmonary Disease.
Wang Lei et al. Chinese medical journal 2017 Sep (17) 2107-2111 (Posted: Oct 25, 2017 3PM)

Using omics approaches to understand pulmonary diseases.
Kan Mengyuan et al. Respiratory research 2017 Aug (1) 149 (Posted: Oct 25, 2017 3PM)

COPD National Action Plan
NHLBI, 2017 Brand (Posted: Jul 17, 2017 8PM)

Personalized Medicine in Respiratory Disease: Role of Proteomics.
Priyadharshini V S et al. Advances in protein chemistry and structural biology 2016 115-46 (Posted: Feb 06, 2017 1PM)

Recent advances in understanding and treating COPD related to α1-antitrypsin deficiency.
Henao Maria Paula et al. Expert review of respiratory medicine 2016 Dec (12) 1281-1294 (Posted: Feb 06, 2017 1PM)

Genetic loci associated with chronic obstructive pulmonary disease overlap with loci for lung function and pulmonary fibrosis
BD Hobbs, February 6, 2017 (Posted: Feb 06, 2017 1PM)

Genome-wide association analyses for lung function and chronic obstructive pulmonary disease identify new loci and potential druggable targets
LV Wain et al, Nature Genetics, February 6, 2017 (Posted: Feb 06, 2017 1PM)

Novel insights into the genetics of smoking behaviour, lung function, and chronic obstructive pulmonary disease (UK BiLEVE): a genetic association study in UK Biobank.
Wain Louise V et al. The Lancet. Respiratory medicine 2015 Oct (10) 769-81 (Posted: Nov 16, 2015 2PM)

Epigenetic mechanisms in chronic obstructive pulmonary disease.
Zong D-D et al. European review for medical and pharmacological sciences 2015 (5) 844-56 (Posted: Nov 16, 2015 2PM)

Candidate genes for COPD: current evidence and research.
Kim Woo Jin et al. International journal of chronic obstructive pulmonary disease 2015 2249-55 (Posted: Nov 16, 2015 2PM)

Novel insights into the genetics of smoking behaviour, lung function, and chronic obstructive pulmonary disease (UK BiLEVE): a genetic association study in UK Biobank
LV Wain et al, Lancet Respiratory Medicine, September 28, 2015 (Posted: Sep 28, 2015 7AM)

Too many sidelined by COPD
JAMA, news from the CDC, May 12, 2015 (Posted: May 14, 2015 11AM)

Familial transmission of chronic obstructive pulmonary disease in adoptees: a Swedish nationwide family study.
Zöller Bengt et al. BMJ Open 2015 (4) e007310 (Posted: Apr 25, 2015 11AM)

Asthma-COPD Overlap. Clinical Relevance of Genomic Signatures of Type 2 Inflammation in Chronic Obstructive Pulmonary Disease.
Christenson Stephanie A et al. Am. J. Respir. Crit. Care Med. 2015 Apr 1. (7) 758-66 (Posted: Apr 22, 2015 1PM)

An official american thoracic society/european respiratory society statement: research questions in chronic obstructive pulmonary disease.
Celli Bartolome R et al. Am. J. Respir. Crit. Care Med. 2015 Apr 1. (7) e4-e27 (Posted: Apr 04, 2015 6PM)

Genetic susceptibility for chronic bronchitis in chronic obstructive pulmonary disease.
Lee Jin Hwa et al. Respir. Res. 2014 (1) 113 (Posted: Mar 27, 2015 5PM)

Genetic control of gene expression at novel and established chronic obstructive pulmonary disease loci.
Castaldi Peter J et al. Hum. Mol. Genet. 2015 Feb 15. (4) 1200-10 (Posted: Mar 27, 2015 5PM)

The COPD Knowledge Base: enabling data analysis and computational simulation in translational COPD research.
Cano Isaac et al. J Transl Med 2014 Nov 28. S6 (Posted: Mar 27, 2015 5PM)

Vitamin D binding protein genotype variants and risk of chronic obstructive pulmonary disease: a meta-analysis.
Horita Nobuyuki et al. Respirology 2015 Feb (2) 219-25 (Posted: Mar 27, 2015 5PM)

Genome Wide Association Study Identifies Novel Loci Associated with Airway Responsiveness in COPD.
Hansel Nadia N et al. Am. J. Respir. Cell Mol. Biol. 2014 Dec 16. (Posted: Mar 27, 2015 5PM)

Integrative analysis of DNA methylation and gene expression data identifies EPAS1 as a key regulator of COPD.
Yoo Seungyeul et al. PLoS Genet. 2015 Jan (1) e1004898 (Posted: Mar 27, 2015 5PM)

Identifying a gene expression signature of frequent COPD exacerbations in peripheral blood using network methods.
Morrow Jarrett D et al. BMC Med Genomics 2015 Jan 13. (1) 1 (Posted: Mar 27, 2015 5PM)

Targeted screening programmes in COPD: how to identify individuals with a1-antitrypsin deficiency.
Chorostowska-Wynimko Joanna et al. Eur Respir Rev 2015 Mar (135) 40-45 (Posted: Mar 27, 2015 5PM)

Diagnosing a1-antitrypsin deficiency: how to improve the current algorithm.
McElvaney Noel G et al. Eur Respir Rev 2015 Mar (135) 52-57 (Posted: Mar 27, 2015 5PM)

Vitamin D-binding protein gene polymorphisms and chronic obstructive pulmonary disease susceptibility: A meta-analysis.
Xie Xinming et al. Biomed Rep 2015 Mar (2) 183-188 (Posted: Mar 27, 2015 5PM)

CDC Information: The Burden of COPD
Brand (Posted: Feb 25, 2015 0PM)

Understanding the rise in medical costs for people with COPD
Brand (Posted: Feb 25, 2015 0PM)

Chronic Obstructive Pulmonary Disease (COPD)
Brand (Posted: Feb 25, 2015 0PM)

Smoking and Your Heart
From NHLBI health topic site Brand (Posted: Jan 01, 2014 0AM)

How Does Smoking Affect the Heart and Blood Vessels? Cigarette smoking causes about 1 in every 5 deaths in the United States each year. It's the main preventable cause of death and illness in the United States. Smoking harms nearly every organ in the body, including the heart, blood vessels, lungs, eyes, mouth, reproductive organs, bones, bladder, and digestive organs. This article focuses on how smoking affects the heart and blood vessels. Other Health Topics articles, such as COPD (chronic obstructive pulmonary disease), Bronchitis, and Cough, discuss how smoking affects the lungs. Overview Smoking and Your Heart and Blood Vessels The chemicals in tobacco smoke harm your blood cells. They also can damage the function of your heart and the structure and function of your blood vessels. This damage increases your risk of atherosclerosis. Atherosclerosis is a disease in which a waxy substance called plaque builds up in the arteries. Over time, plaque hardens and narrows your arteries. This limits the flow of oxygen-rich blood to your organs and other parts of your body. Coronary heart disease (CHD) occurs if plaque builds up in the coronary (heart) arteries. Over time, CHD can lead to chest pain, heart attack, heart failure, arrhythmias, or even death. Smoking is a major risk factor for heart disease. When combined with other risk factors?such as unhealthy blood cholesterol levels, high blood pressure, and overweight or obesity?smoking further raises the risk of heart disease. Smoking also is a major risk factor for peripheral artery disease (P.A.D.). P.A.D. is a condition in which plaque builds up in the arteries that carry blood to the head, organs, and limbs. People who have P.A.D. are at increased risk for heart disease, heart attack, and stroke. Smoking and Atherosclerosis The image shows how smoking can affect arteries in the heart and legs. Figure A shows the location of coronary heart disease and peripheral artery disease. Figure B shows a detailed view of a leg artery with atherosclerosis?plaque buildup that's partially blocking blood flow. Figure C shows a detailed view of a coronary (heart) artery with atherosclerosis. The image shows how smoking can affect arteries in the heart and legs. Figure A shows the location of coronary heart disease and peripheral artery disease. Figure B shows a detailed view of a leg artery with atherosclerosis?plaque buildup that's partially blocking blood flow. Figure C shows a detailed view of a coronary (heart) artery with atherosclerosis. Any amount of smoking, even light smoking or occasional smoking, damages the heart and blood vessels. For some people, such as women who use birth control pills and people who have diabetes, smoking poses an even greater risk to the heart and blood vessels. Secondhand smoke also can harm the heart and blood vessels. Secondhand smoke is the smoke that comes from the burning end of a cigarette, cigar, or pipe. Secondhand smoke also refers to smoke that's breathed out by a person who is smoking. Secondhand smoke contains many of the same harmful chemicals that people inhale when they smoke. Secondhand smoke can damage the hearts and blood vessels of people who don't smoke in the same way that active smoking harms people who do smoke. Secondhand smoke greatly increases adults' risk of heart attack and death. Secondhand smoke also raises children and teens' risk of future CHD because it: ?Lowers HDL cholesterol (sometimes called "good" cholesterol) ?Raises blood pressure ?Damages heart tissues The risks of secondhand smoke are especially high for premature babies who have respiratory distress syndrome (RDS) and children who have conditions such as asthma. Researchers know less about how cigar and pipe smoke affects the heart and blood vessels than they do about cigarette smoke. However, the smoke from cigars and pipes contains the same harmful chemicals as the smoke from cigarettes. Also, studies have shown that people who smoke cigars are at increased risk for heart disease. Benefits of Quitting Smoking and Avoiding Secondhand Smoke One of the best ways to reduce your risk of heart disease is to avoid tobacco smoke. Don't ever start smoking. If you already smoke, quit. No matter how much or how long you've smoked, quitting will benefit you. Also, try to avoid secondhand smoke. Don't go to places where smoking is allowed. Ask friends and family members who smoke not to do it in the house and car. Quitting smoking will reduce your risk of developing and dying from heart disease. Over time, quitting also will lower your risk of atherosclerosis and blood clots. If you smoke and already have heart disease, quitting smoking will reduce your risk of sudden cardiac death, a second heart attack, and death from other chronic diseases. Researchers have studied communities that have banned smoking at worksites and in public places. The number of heart attacks in these communities dropped quite a bit. Researchers think these results are due to a decrease in active smoking and reduced exposure to secondhand smoke. Outlook Smoking or exposure to secondhand smoke damages the heart and blood vessels in many ways. Smoking also is a major risk factor for developing heart disease or dying from it. Quitting smoking and avoiding secondhand smoke can help reverse heart and blood vessel damage and reduce heart disease risk. Quitting smoking is possible, but it can be hard. Millions of people have quit smoking successfully and remained nonsmokers. A variety of strategies, programs, and medicines are available to help you quit smoking. Not smoking is an important part of a heart-healthy lifestyle. A heart-healthy lifestyle also includes heart-healthy eating, aiming for a healthy weight, managing stress, and physical activity.

COPD
From NHLBI health topic site Brand (Posted: Jan 01, 2014 0AM)

What Is Also known as chronic obstructive pulmonary disease; chronic bronchitis; or emphysema. COPD, or chronic obstructive pulmonary disease, is a progressive disease that makes it hard to breathe. Progressive means the disease gets worse over time. COPD can cause coughing that produces large amounts of a slimy substance called mucus, wheezing, shortness of breath, chest tightness, and other symptoms. Cigarette smoking is the leading cause of COPD. Most people who have COPD smoke or used to smoke. However, up to 25 percent of people with COPD never smoked. Long-term exposure to other lung irritants?such as air pollution, chemical fumes, or dusts?also may contribute to COPD. A rare genetic condition called alpha-1 antitrypsin (AAT) deficiency can also cause the disease. Overview To understand COPD, it helps to understand how the lungs work. The air that you breathe goes down your windpipe into tubes in your lungs called bronchial tubes or airways. Within the lungs, your bronchial tubes branch many times into thousands of smaller, thinner tubes called bronchioles. These tubes end in bunches of tiny round air sacs called alveoli. Small blood vessels called capillaries run along the walls of the air sacs. When air reaches the air sacs, oxygen passes through the air sac walls into the blood in the capillaries. At the same time, a waste product, called carbon dioxide (CO2) gas, moves from the capillaries into the air sacs. This process, called gas exchange, brings in oxygen for the body to use for vital functions and removes the CO2. The airways and air sacs are elastic or stretchy. When you breathe in, each air sac fills up with air, like a small balloon. When you breathe out, the air sacs deflate and the air goes out. In COPD, less air flows in and out of the airways because of one or more of the following: ?The airways and air sacs lose their elastic quality. ?The walls between many of the air sacs are destroyed. ?The walls of the airways become thick and inflamed. ?The airways make more mucus than usual and can become clogged. Normal Lungs and Lungs With COPD Figure A shows the location of the lungs and airways in the body. The inset image shows a detailed cross-section of the bronchioles and alveoli. Figure B shows lungs damaged by COPD. The inset image shows a detailed cross-section of the damaged bronchioles and alveolar walls. Figure A shows the location of the lungs and airways in the body. The inset image shows a detailed cross-section of the bronchioles and alveoli. Figure B shows lungs damaged by COPD. The inset image shows a detailed cross-section of the damaged bronchioles and alveolar walls. In the United States, the term COPD includes two main conditions?emphysema and chronic bronchitis. In emphysema, the walls between many of the air sacs are damaged. As a result, the air sacs lose their shape and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and larger air sacs instead of many tiny ones. If this happens, the amount of gas exchange in the lungs is reduced. In chronic bronchitis, the lining of the airways stays constantly irritated and inflamed, and this causes the lining to swell. Lots of thick mucus forms in the airways, making it hard to breathe. Most people who have COPD have both emphysema and chronic bronchitis, but the severity of each condition varies from person to person. Thus, the general term COPD is more accurate. Outlook COPD is a major cause of disability, and it is the fourth leading cause of death in the United States. Currently, 16 million people are diagnosed with COPD. Many more people may have the disease and not even know it. COPD develops slowly. Symptoms often worsen over time and can limit your ability to do routine activities. Severe COPD may prevent you from doing even basic activities like walking, cooking, or taking care of yourself. Most of the time, COPD is diagnosed in middle-aged or older adults. The disease is not contagious, meaning it cannot be passed from person to person. COPD has no cure yet, and doctors do not know how to reverse the damage to the lungs. However, treatments and lifestyle changes can help you feel better, stay more active, and slow the progress of the disease.

Cough
From NHLBI health topic site Brand (Posted: Jan 01, 2014 0AM)

A cough is your body?s natural reflex to help clear your airways of irritants and prevent infection. Overview Common irritants include smoke, mucus, or allergens such as pollen, mold, or dust. Some medical conditions or medicines irritate the nerve endings in your airways and cause coughing. A cough may be acute, subacute, or chronic depending on how long it lasts. Acute coughs last less than three weeks and usually are caused by the common cold or other infections such as sinusitis or pneumonia. Subacute coughs last three to eight weeks and remain after the initial cold or respiratory infection is over. Chronic coughs last more than eight weeks and can be caused by gastroesophageal reflux disease (GERD), postnasal drip from sinus infections or allergies, or chronic lung conditions such as asthma, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, and interstitial lung diseases. Your doctor will consider your medical history, physical exam, and test results when diagnosing and treating cough. Quitting smoking and avoiding smoke, other irritants, or certain medicines may help relieve your cough. Medicines to control coughing are usually used only for coughs that cause extreme discomfort or interfere with sleep. Talk to your doctor about how to treat your child?s cough.

Pneumonia
From NHLBI health topic site Brand (Posted: Jan 01, 2014 0AM)

Pneumonia is a bacterial, viral, or fungal infection of one or both sides of the lungs that causes the air sacs, or alveoli, of the lungs to fill up with fluid or pus. Symptoms can be mild or severe and may include a cough with phlegm (a slimy substance), fever, chills, and trouble breathing. Many factors affect how serious pneumonia is, such as the type of germ causing the lung infection, your age, and your overall health. Pneumonia tends to be more serious for children under the age of five, adults over the age of 65, people with certain conditions such as heart failure, diabetes, or COPD (chronic obstructive pulmonary disease), or people who have weak immune systems due to HIV/AIDS, chemotherapy (a treatment for cancer), or organ or blood and marrow stem cell transplant procedures. To diagnose pneumonia, your doctor will review your medical history, perform a physical exam, and order diagnostic tests. This information can help your doctor determine what type of pneumonia you have. If your doctor suspects you got your infection while in a hospital, you may be diagnosed with hospital-acquired pneumonia. If you have been on a ventilator to help you breathe, you may have ventilator-associated pneumonia. The most common form of pneumonia is community-acquired pneumonia, which is when you get an infection outside of a hospital. Treatment depends on whether bacteria, viruses, or fungi are causing your pneumonia. If bacteria are causing your pneumonia, you usually are treated at home with oral antibiotics. Most people respond quickly to treatment. If your symptoms worsen you should see a doctor right away. If you have severe symptoms or underlying health problems, you may need to be treated in a hospital. It may take several weeks to recover from pneumonia. Explore this Health Topic to learn more about pneumonia, our role in research and clinical trials to improve health, and where to find more information.

Pulmonary Rehabilitation
From NHLBI health topic site Brand (Posted: Jan 01, 2014 0AM)

What Is Pulmonary Rehabilitation? Pulmonary (PULL-mun-ary) rehabilitation, also called pulmonary rehab or PR, is a broad program that helps improve the well-being of people who have chronic (ongoing) breathing problems. For example, PR may benefit people who have COPD (chronic obstructive pulmonary disease), sarcoidosis (sar-koy-DOE-sis), idiopathic pulmonary fibrosis, or cystic fibrosis. PR also can benefit people who need lung surgery, both before and after the surgery. PR doesn't replace medical therapy. Instead, it's used with medical therapy and may include: ?Exercise training ?Nutritional counseling ?Education on your lung disease or condition and how to manage it ?Energy-conserving techniques ?Breathing strategies ?Psychological counseling and/or group support PR involves a long-term commitment from the patient and a team of health care providers. The PR team may include doctors, nurses, and specialists. Examples of specialists include respiratory therapists, physical and occupational therapists, dietitians or nutritionists, and psychologists or social workers. PR often is an outpatient program based in a hospital or clinic. Some patients also can receive PR in their homes. When you start PR, your rehab team will create a plan that's tailored to your abilities and needs. You'll likely attend your PR program weekly. Your team also will expect you to follow your plan, including exercises and lifestyle changes, at home. PR has many benefits. It can improve your ability to function and your quality of life. The program also may help relieve your breathing problems. Even if you have advanced lung disease, you can still benefit from PR.

Respiratory Failure
From NHLBI health topic site Brand (Posted: Jan 01, 2014 0AM)

What Is Respiratory (RES-pih-rah-tor-e) failure is a condition in which not enough oxygen passes from your lungs into your blood. Your body's organs, such as your heart and brain, need oxygen-rich blood to work well. Respiratory failure also can occur if your lungs can't properly remove carbon dioxide (a waste gas) from your blood. Too much carbon dioxide in your blood can harm your body's organs. Both of these problems?a low oxygen level and a high carbon dioxide level in the blood?can occur at the same time. Diseases and conditions that affect your breathing can cause respiratory failure. Examples include COPD (chronic obstructive pulmonary disease) and spinal cord injuries. COPD prevents enough air from flowing in and out of the airways. Spinal cord injuries can damage the nerves that control breathing. Overview To understand respiratory failure, it helps to understand how the lungs work. When you breathe, air passes through your nose and mouth into your windpipe. The air then travels to your lungs' air sacs. These sacs are called alveoli (al-VEE-uhl-eye). Small blood vessels called capillaries run through the walls of the air sacs. When air reaches the air sacs, the oxygen in the air passes through the air sac walls into the blood in the capillaries. At the same time, carbon dioxide moves from the capillaries into the air sacs. This process is called gas exchange. In respiratory failure, gas exchange is impaired. Respiratory failure can be acute (short term) or chronic (ongoing). Acute respiratory failure can develop quickly and may require emergency treatment. Chronic respiratory failure develops more slowly and lasts longer. Signs and symptoms of respiratory failure may include shortness of breath, rapid breathing, and air hunger (feeling like you can't breathe in enough air). In severe cases, signs and symptoms may include a bluish color on your skin, lips, and fingernails; confusion; and sleepiness. One of the main goals of treating respiratory failure is to get oxygen to your lungs and other organs and remove carbon dioxide from your body. Another goal is to treat the underlying cause of the condition. Acute respiratory failure usually is treated in an intensive care unit. Chronic respiratory failure can be treated at home or at a long-term care center. Outlook The outlook for respiratory failure depends on the severity of its underlying cause, how quickly treatment begins, and your overall health. People who have severe lung diseases may need long-term or ongoing breathing support, such as oxygen therapy or the help of a ventilator (VEN-til-a-tor). A ventilator is a machine that supports breathing. It blows air?or air with increased amounts of oxygen?into your airways and then your lungs. Other Names ?When respiratory failure causes a low level of oxygen in the blood, it's called hypoxemic (HI-pok-SE-mik) respiratory failure. ?When respiratory failure causes a high level of carbon dioxide in the blood, it's called hypercapnic (HI-per-KAP-nik) respiratory failure.


Disclaimer: Articles listed in Hot Topics of the Day are selected by Public Health Genomics Branch to provide current awareness of the scientific literature and news. Inclusion in the update does not necessarily represent the views of the Centers for Disease Control and Prevention nor does it imply endorsement of the article's methods or findings. CDC and DHHS assume no responsibility for the factual accuracy of the items presented. The selection, omission, or content of items does not imply any endorsement or other position taken by CDC or DHHS. Opinion, findings and conclusions expressed by the original authors of items included in the Clips, or persons quoted therein, are strictly their own and are in no way meant to represent the opinion or views of CDC or DHHS. References to publications, news sources, and non-CDC Websites are provided solely for informational purposes and do not imply endorsement by CDC or DHHS.
TOP