Monday, February 29, 2016

World Rare Disease Day 2016

Rare Disease Day® takes place on the last day of February each year. The main objective of Rare Disease Day is to raise awareness amongst the general public and decision-makers about rare diseases and their impact on patients’ lives.  Learn more about the history of Rare Disease Day.
The 2016 global theme, “Patient Voice,” recognizes the crucial role that patients play in voicing their needs and in instigating change that improves their lives and the lives of their families and carers.

The National Organization for Rare Disorders (NORD) is the official Sponsor of Rare Disease Day in the United States alongside our sister organization, EURORDIS (The European Organization for Rare Disorders), which organizes the official international campaign.  Over 80 countries participated in Rare Disease Day 2015.  To learn what’s happening around the world, visit the global Rare Disease Day website at
Anyone can get involved in Rare Disease Day awareness.  On this site, U.S. participants can find, suggest and get involved in events taking place across the country.  We also have suggested activities for those who are new.

Antibiotic Therapy for Adults Hospitalized With Community-Acquired Pneumonia in 2016

Objective  To assess the associations between 3 key aspects of antibiotic therapy (optimal time to antibiotic initiation, initial antibiotic selection, and criteria for the transition from intravenous to oral therapy) and short-term mortality in adults hospitalized with community-acquired pneumonia.
Evidence Review  Bibliographic databases of MEDLINE, EMBASE, and the Cochrane Collaboration were searched for studies of adults hospitalized with radiographically confirmed community-acquired pneumonia published from January 1, 1995, until November 5, 2015.
Findings  Twenty studies (17 observational and 3 randomized trials) met eligibility criteria. Among 8 observational studies identified, the 4 largest (study populations of 2878 to 1 170 022) found that antibiotic initiation within 4 to 8 hours of hospital arrival was associated with relative reductions of 5% to 43% in mortality; the 4 smallest studies (study populations of 451 to 2076) found no associations between the timing of antibiotic initiation and mortality. One cluster randomized trial (n = 1737) demonstrated noninferiority of β-lactam monotherapy (n = 506) vs β-lactam plus macrolide combination therapy (n = 566), with an absolute adjusted difference of 2.5% (90% CI, −0.6% to 5.2%) in 90-day mortality favoring β-lactam monotherapy. A second randomized trial (n = 580) failed to demonstrate noninferiority of β-lactam monotherapy vs β-lactam plus macrolide combination therapy, with an absolute difference of 7.6% (1-sided 90% CI upper limit, 13.0%) in attainment of clinical stability on hospital day 7 favoring β-lactam plus macrolide combination therapy. Six of 8 observational studies (study populations of 1188 to 24 780) found that β-lactam plus macrolide combination therapy was associated with relative reductions of 26% to 68% in short-term mortality and all 3 observational studies (study populations of 2068 to 24 780) reported that fluoroquinolone monotherapy was associated with relative reductions of 30% to 43% in mortality compared with β-lactam monotherapy. One randomized trial (n = 302) reported significantly reduced hospital length of stay (absolute difference, 1.9 days; 95% CI, 0.6 to 3.2 days), but no differences in treatment failure when objective clinical criteria were used to decide when to transition patients from intravenous to oral therapy.

Conclusions and Relevance  In adults hospitalized with community-acquired pneumonia, antibiotic therapy consisting of β-lactam plus macrolide combination therapy or fluoroquinolone monotherapy initiated within 4 to 8 hours of hospital arrival was associated with lower adjusted short-term mortality, supported predominantly by low-quality observational studies. One randomized trial supports the use of objective clinical criteria to guide the transition from intravenous to oral antibiotic therapy.

Sunday, February 21, 2016

Link between LUNG and inflammatory bowel diseases and chronic liver diseases

Dear Respiratory Friends we are happy to present you new article on hot topic Lung and  inflammatory bowel diseases and chronic liver diseases from ERJ 2016!
This review is devoted to the distinct associations of inflammatory bowel diseases (IBD) and chronic liver disorders with chronic airway diseases, namely chronic obstructive pulmonary disease and bronchial asthma, and other chronic respiratory disorders in the adult population. While there is strong evidence for the association of chronic airway diseases with IBD, the data are much weaker for the interplay between lung and liver multimorbidities. The association of IBD, encompassing Crohn's disease and ulcerative colitis, with pulmonary disorders is underlined by their heterogeneous respiratory manifestations and impact on chronic airway diseases.
The potential relationship between the two most prevalent liver-induced pulmonary vascular entities, i.e. portopulmonary hypertension and hepatopulmonary syndrome, and also between liver disease and other chronic respiratory diseases is also approached. Abnormal lung function tests in liver diseases are described and the role of increased serum bilirubin levels on chronic respiratory problems are considered.
link to article:

Saturday, February 13, 2016

Love your Lungs and Clean Air on St.Valentines Day 2016!

Here are nine ways you can love your lungs a little more:
  • Quit smoking. Yes, it’s easier said than done, but most lung cancer victims smoke tobacco.
  • Get your loved one to stop smoking Inside. Second-hand smoke puts a non-smoker who is living with a smoker at a greater risk of developing lung cancer.
  • Check the water for arsenic. Drinking water with high levels of arsenic is a possible contributing factor to lung cancer. This odorless, tasteless metalloid is typically found in well water. It’s prevalent in Western states like California, Nevada and Arizona, but it can be found in other places across the United States as well.
  • Know your history. Genetics play a role in your susceptibility to lung cancer. If you already had lung cancer, or anyone in your family, such as siblings, parents or children have lung cancer, you are at a greater risk. 
  • Avoid supplements. Specifically avoid taking beta carotene if you smoke. Studies have shown that this supplement increases a smoker’s risk of lung cancer.
  • Avoid air pollution. This can be difficult in cities with high-traffic and dense populations. In that case, avoid the outdoors on polluted days.
  • Check for radon. Radon can be a cause of lung cancer in both smokers and non-smokers,, but studies have shown that smokers are at greater risk. This radioactive gas is found in homes all over the United States. Radon testing is the only way to truly know if your home’s radon levels are safe. Make sure to check the radon levels in any home you are looking to purchase, because even a next door neighbor’s home can have different levels than yours. The EPA has maps of radon zones for every state.
  • Avoid asbestos and diesel exhaust. People who work around or are exposed to asbestos are more likely to die of lung cancer. This is in addition to the other type of cancer asbestos causes, which hurts the lining surrounding the lungs.
  • Go for a walk. Do something physical, like yoga or ride a bike. Pumping fresh oxygen and blood through system helps to clean out your lungs

Sunday, February 7, 2016

Aspirin-Exacerbated Respiratory Disease (full text from NEJM)

Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, chronic rhinosinusitis with nasal polyposis, and pathognomonic respiratory reactions to aspirin (Samter’s triad). It has been estimated that this syndrome affects 7% of adults with asthma and 14% of those who have severe asthma. Pathologically, AERD is characterized by marked eosinophilic inflammation and ongoing mast-cell activation in the respiratory mucosa. The frequent recurrence of nasal polyps after surgery, as well as the requirement for high-dose glucocorticoids to manage the asthma, reflect the aggressive, persistent nature of the disease. The typical onset is in adulthood, with or without preexisting asthma, rhinitis, or atopy. An absence of familial clustering argues against a strong genetic basis, and the identification of variants of candidate genes in small studies has not been replicated.

All nonsteroidal antiinflammatory drugs (NSAIDs) that inhibit both cyclooxygenase (COX)-1 and COX-2 may provoke the pathognomonic reactions in AERD; these reactions are accompanied by idiosyncratic activation of respiratory tract mast cells. In contrast, patients with AERD can usually be treated with COX-2–selective drugs without having these reactions. The fact that structurally diverse NSAIDs that block COX-1 all provoke reactions reflects an enigmatic requirement for COX-1–derived prostaglandins to maintain a tenuous homeostasis. Curiously, the reactions also induce a refractory state in which NSAIDs can be used with diminished or no sequelae (desensitization); in fact, after desensitization, high-dose aspirin has therapeutic benefits. Insights into the mechanisms responsible for the pathogenesis of AERD or its treatment have been limited.
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Thursday, February 4, 2016

Pathways connecting inflammation and Lung Cancer (2016 American Journal of Respiratory and Critical Care Medicine)
Lung cancer is the leading cause of cancer mortality worldwide, and at only 18%, it has one of the lowest 5-year survival rates of all malignancies. With its highly complex mutational landscape, treatment strategies against lung cancer have proved largely ineffective. However with the recent success of immunotherapy trials in lung cancer, there is renewed enthusiasm in targeting the immune component of tumors. Macrophages make up the majority of the immune infiltrate in tumors and are a key cell type linking inflammation and cancer. Although the mechanisms through which inflammation promotes cancer are not fully understood, two connected hypotheses have emerged: an intrinsic pathway, driven by genetic alterations that lead to neoplasia and inflammation, and an extrinsic pathway, driven by inflammatory conditions that increase cancer risk. Here, we discuss the contribution of macrophages to these pathways and subsequently their roles in established tumors. We highlight studies investigating the association of macrophages with lung cancer prognosis and discuss emerging therapeutic strategies for targeting macrophages in the tumor microenvironment.

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World Cancer Day - 4 February 2016

In recognition of World Cancer Day on February 4, we are supporting the World Cancer Day 2016: ‘We Can. I Can.’ campaign. The global campaign highlights how everyone, as a collective or as individuals, can do their part to reduce the global burden of cancer. 
Next year alone, nearly 9 million people are likely to die of cancer, and left unchecked, the number of deaths will increase to 13 million per year by 2030. World Cancer Day is a chance to reflect on what you can do: make a pledge and take action. Whatever you choose to do ‘We Can. I Can.’ will make a difference to the fight against cancer. The initiative outlines nine targets to be achieved by 2025 with the overarching goal to reduce cancer deaths by 25% by 2025. The targets include strengthening health systems, measuring cancer burden and impact of cancer plans in all countries, reducing exposure to cancer risk factors, universal coverage of HPV and HBV vaccination, reduction of stigma and dispelling myths about cancer, universal access to screening and early detection for cancer, improvement in access to services across the cancer care spectrum, universal availability of pain control and distress management, and improvement in education and training of healthcare professionals.
According to the World Health Organization, lung cancer is the most common cancer worldwide, accounting for 1.8 million new cases in 2012, and is responsible for nearly one in five deaths. While most understand that smoking is the single greatest risk factor for lung cancer, regular exposure to secondhand smoke also increases the risk. In addition, environmental exposure to radon, asbestos, arsenic, beryllium, and uranium have all been linked to lung cancer. The risk of lung cancer also increases with a history of cancer in another part of the body, age, family history, radiation to the chest area, and lung diseases like COPD and tuberculosis.

Monday, February 1, 2016

Treatable traits: toward precision medicine of chronic airway diseases (ERJ paper)

Dear friends, this is new article on new approaches in asthma and COPD from todays European Respiratory Journal! 
Asthma and chronic obstructive pulmonary disease (COPD) are two prevalent chronic airway diseases that have a high personal and social impact. They likely represent a continuum of different diseases that may share biological mechanisms (i.e. endotypes), and present similar clinical, functional, imaging and/or biological features that can be observed (i.e. phenotypes) which require individualised treatment. Precision medicine is defined as “treatments targeted to the needs of individual patients on the basis of genetic, biomarker, phenotypic, or psychosocial characteristics that distinguish a given patient from other patients with similar clinical presentations”. In this Perspective, we propose a precision medicine strategy for chronic airway diseases in general, and asthma and COPD in particular.

Full text: