Absence of Alveolar Neutrophilia Predictive of Negative Bacterial Pneumonia

By Dr Deepu

Results of a study published in the American Journal of Respiratory and Critical Care Medicine has revealed that  Patients undergoing evaluation for ventilator-associated pneumonia who had an alveolar neutrophil percentage <50% had a negative predictive value >90% for bacterial pneumonia.
Bronchoalveolar lavage specimens from patients undergoing evaluation for ventilator-associated pneumonia at an urban academic medical center were analyzed retrospectively for associations between alveolar neutrophilia and bacterial pneumonia diagnosis. All lavage samples were processed for flow-cytometry sorting within 12 hours of collection. Pneumonia was defined as ≥104 colony-forming units/mL of a bacterial species on quantitative culture in the setting of a clinical suspicion of infection and an abnormal chest radiograph.
Of the 1156 bronchoalveolar lavage specimens screened for inclusion, 851 were included in the final analysis. Of these 851 specimens, 344 (40.4%) met the definition for bacterial pneumonia. The most common pathogens isolated were Pseudomonas aeruginosa, methicillin-resistant Staphylococcus aureus, and Klebsiella pneumoniae. The area under the curve for bronchoalveolar lavage neutrophilia was 0.751 (95% CI, 0.719-0.784). When bronchoalveolar lavage neutrophils were <50%, the negative predictive value for pneumonia was 91.5%.
 the researchers concluded The absence of alveolar neutrophilia is useful in ruling out bacterial pneumonia in mechanically ventilated patients with suspected infection. A combination of cellular and molecular analysis of the host and pathogen in [bronchoalveolar lavage] fluid shows promise for improving the diagnosis and management of pneumonia.

Original article reference
Walter J, Ren Z, Yacoub T, et al. Multidimensional assessment of the host response in mechanically ventilated patients with suspected pneumonia [published online November 6, 2018]. Am J Respir Crit Care Med. doi:10.1164/rccm.201804-0650OC

Flu shot can save heart failure patients’ lives- study suggests

By Dr Deepu

Getting an annual flu shot can save heart failure patients’ lives, according to new research in the American Heart Association’s journal Circulation.
Flu season usually begins in the fall and runs through the spring, with cases often peaking during the winter months. Annual flu vaccination is regarded as a safe, low-cost way to reduce flu-related deaths and complications and is routinely recommended for patients with histories of heart disease and stroke. However, little is known about the possible impact a simple flu shot may have on the survival of heart failure patients.

Influenza can be very serious or even fatal for patients with heart failure because heart failure patients are often older than 65, have compromised circulation and other health complications, and infection may exacerbate heart failure symptoms. Moreover, heart failure is expected to increase over the next decade as the population ages, highlighting a greater need to provide better care for these patients.
In this study, researchers analyzed data on 134,048 patients with newly diagnosed heart failure over a 12-year period. Flu vaccination rates ranged from 16% in 2003 to 52% in 2015 with a peak of 54% in 2009. Among the researchers’ findings:
Flu vaccination was associated with an 18% reduced risk of premature death, even after accounting for other factors such as medications, other health conditions, income and education
Annual flu vaccination following a heart failure diagnosis was associated with a 19% reduction in both all-cause and cardiovascular death when compared with no vaccination.
Flu vaccination frequency mattered; getting a flu shot less than once per year but more than not at all was associated with a 13% reduced risk of all-cause death and an 8% reduced risk of cardiovascular death.
Timing mattered; there was a greater reduction in cardiovascular and all-cause death when vaccination occurred earlier in the flu season during September and October vs in November and December.
Read free access original study in AHA journal website

Blood Decorin Levels May Serve as Prognostic Marker for IPF Patients After Acute Exacerbation, Study Suggests

By Dr Deepu
A new research has suggested Reduced levels of decorin proteins in the blood may be linked to a lower risk of death among patients with idiopathic pulmonary fibrosis (IPF) who have experienced acute exacerbations. “Serum decorin is a potential prognostic biomarker in patients with acute exacerbation of idiopathic pulmonary fibrosis,” published in the Journal of Thoracic Diseases has shed light on the topic. Acute worsening of respiratory function, also known as acute exacerbations, can have a significant negative impact on the clinical outcome of patients with IPF. These acute events have been reported to occur in about 8.6% of IPF cases one year after diagnosis, increasing to 23.9% three years after diagnosis. After the onset of acute exacerbations, the death rate of IPF patients is about 50%. This high mortality rate highlights the importance of recognizing risk factors that could contribute to the development of these acute events to ensure adequate prevention. Researchers have now evaluated the role of the decorin protein in the development and progression of acute exacerbations in patients with IPF and idiopathic interstitial pneumonia (IIP), which is also a fibrotic lung disease. Decorin is known to regulate inflammation and wound healing. In IPF, decorin can be found at fibrotic lesions and was shown to prevent lung fibrosis in mice. This protein was also shown to inhibit collagen production by fibroblasts, which is a key mechanism in fibrosis progression. The team evaluated the levels of decorin in blood samples collected from 21 IPF patients, 35 patients with IIP (other than IPF) who were hospitalized due to acute exacerbations, and 36 healthy volunteers. They also evaluated the protein levels in 97 patients who had stable IIP (no disease exacerbations). Researchers found that IIP patients who had acute exacerbations had reduced levels of decorin by about 23.8% (7,183.8 vs. 9,430.2 ng/mL), compared with stable IIP patients, and 35.7% (7,183.8 vs. 11,171.9 ng/mL), compared with healthy controls. The team also compared the levels of decorin in 34 IIP patients between when they were clinically stable and during an acute exacerbation period. The analysis showed that blood decorin levels were significantly lower during an acute exacerbation than in the clinically stable phase in IPF patients, with a mean reduction of about 21.4% (6,894.5 vs. 8,778.5 ng/mL). However, this difference was not found in the non-IPF patient subgroup. Further analysis failed to find any correlation between blood decorin levels and any clinical parameter after hospital admission due to acute exacerbation, including blood laboratory results, SIRS score, and APACHE II score — two commonly used prognostic measures. Overall, the survival rate 60 days after hospital admission was 53.6% in IIP patients. Comparison of mean decorin levels between survivors and non-survivors did not reveal a significant difference. However, when the team divided IPF patients into high and low blood decorin groups — using median decorin level as a reference — the survival rate was significantly higher in patients with low decorin levels than in those with high levels. Still, the team could not find any significant differences in clinical parameters except PF ratio, which is the arterial partial pressure of carbon dioxide/fraction of inspiratory oxygen ratio, a measure of respiratory function. Overall, the team found that “decorin levels were lower in IIP patients than in HVs [healthy volunteers], and decreased during AE [acute exacerbation];” that “decorin levels during AE were not correlated with any clinical characteristics except for PF ratio in IPF patients; and [that] “IPF patients with lower serum decorin levels had better prognosis than those with higher levels after the onset of AE.” Based on these results, the team believes that “[blood] decorin level is a potential prognostic biomarker after the onset of acute exacerbations in patients with IPF.” Still, additional studies are necessary to clarify the role of decorin in the underlying mechanisms of both IPF and IIP

Exercise Training May Improve Daily Life For Obese Individuals With Asthma, Study Suggests

By Dr Deepu

Obese adults with asthma have an increased number of comorbidities and reduced daily life physical activity (DLPA), which may worsen asthma symptoms. Exercise is recommended to improve asthma outcomes; however, the benefits of exercise for psychosocial comorbidities and physical activity levels in obese adults with asthma have been poorly investigated.

The objective of the study was assess the effects of exercise on DLPA, asthma symptoms and psychosocial comorbidities in obese adults with asthma. The study included  Fifty-five grade II obese adults with asthma, the study subjects were randomly assigned to either a weight-loss program+exercise program (WL+E group, n=28) or a weight loss program +sham (WL+S group, n=27). The WL+E group incorporated aerobic and resistance muscle training into the weight-loss program (nutrition and psychological therapies), while the WL+S group performed breathing and stretching exercises. DLPA, asthma symptoms, sleep quality and anxiety and  depression  symptoms were quantified before and after treatment.

The results obtained after 3 months were positive, the WL+E group presented a significant increase in daily step counts (3,068 ± 2,325 vs. 729 ± 1,118 steps/day) and the number of asthma-symptom-free days (14.5 ± 9.6 vs. 8.6 ± 11.4 d/mo) compared with the WL+S group. The proportion of participants with improvements in depression symptoms (76.4 vs. 16.6 %) and a lower risk of developing obstructive sleepapnea (56.5 vs. 16.3%) was greater in the WL+E group than in the WL+S group (P<0.05). Significant improvements in sleep efficiency (6.6 ± 5.1 vs. 1.3 ± 4.7%) and latency (-3.7 ± 5.9 vs. 0.2 ± 5.6 min) were also observed in the WL+E group.

The authors concluded that exercise training plus a weight loss program improves DLPA, sleep efficiency and depressionand asthma symptoms in obese adults with asthma.

The three-month program targeted both weight loss and exercise through aerobic and resistance training, the study authors wrote in the journal Medicine and Science in Sports and Exercise.

When contacted over the email Dr Celso R F Carvalho gave the following insights into the study "In my opinion, the more important results of our study are the fact that exercise reduced the comorbidities of the obese asthmatic patients. I am not aware of any other non-pharmacological intervention that has presented such strong impact (bariatric surgery or diet support).

This is important because, in our clinical practice, most patients complain about having problems sleeping, lack of energy (sedentarism) and lower self-esteem (maybe due to the depression symptoms).

It is also important to reinforce that the effect in our study is compared with patients having an important support (nutritional and psychological). Then, the exercise had, on average, a 3-fold effect size compared with the "control group".

At last, I consider that the association we evaluated (Figures 4A-D) also suggest (or explain) how improvement in daily steps and depression symptoms are explained."

Read the findings of the study here.

Electrocautery snaring of endobronchial tumor

By Dr Deepu
Video of bronchoscopic guided electrocautery snaring of endobronchial tumor
Video courteously: Dr Ashok Kuwal

Flu may increase heart attack risk, study suggests

By Dr Deepu

"Cardiovascular events triggered by influenza are potentially preventable by vaccination," the researchers wrote.

       The study used confirmed cases of flu, analyzing 364 heart attacks from mid-2008 through mid-2015 among Ontario residents age 35 or older who were registered with the province’s publicly funded health insurance program.
The investigators found that the heart attack rate was 20.0 admissions per week during the seven days after diagnosis of the flu, versus 3.3 per week during the 52 weeks before and 51 weeks after that seven-day window.
The  above results were based on study involving 148,307 cases of  patients who were tested for influenza. Among all of those tests, 19,729 turned up positive for the flu. And among those cases, there were 332 patients who had at least one heart attack in the year before or after their flu specimen was tested. (The study authors tallied 364 hospitalizations for acute myocardial infarction overall, meaning that some unlucky folks had two or more heart attacks during the two-year observation period.)

Twenty of those heart attacks occurred within one week of a positive flu test. That, of course, was a rate of 20 heart attacks per week.
The other 344 heart attacks happened some other time in the two-year observation period. That worked out to 3.3 heart attacks per week.
That means the risk of a heart attack was six times greater in the first week after flu testing than at other times when the flu was much less likely to be a factor.

The researchers redid their analysis by splitting up that danger week into two parts. They found that heart attack risk was 6.3 times greater during the first three days after a flu test and 5.8 times greater in days four through seven.

About one-quarter of the patients in the study were 65 years old, and the rest were older. When the researchers examined those two groups separately, the link between flu infection and heart attack risk held up only for the older group.

There was no sign of an increased heart attack risk in the rest of the first month after getting a flu test.

The data in the study came from Ontario, Canada, where residents have public health insurance and universal access to medical care. Information on influenza test results came from the Flu and Other Respiratory Viruses Research Cohort, and heart attack hospitalizations were tracked by the Discharge Abstract Database of the Canadian Institute for Health Information.

The researchers, led by Dr. Jeffrey C. Kwong of the University of Toronto, acknowledged that they couldn't do their analysis based on the date when patients were actually infected with the influenza virus, or when they first began having symptoms, because that information was not available. However, in cases where patients get a flu test, they have typically been sick for only one or two days first.

Also, not all flu cases are severe enough to prompt patients to go and get tested. That means the results of this study may not apply to people with milder illnesses, they added.

The researchers did notice that when flu test results came back positive for certain other kinds of respiratory infections instead of for influenza, there was still an increased (though smaller) short-term risk for heart attacks. That suggests that it's not the flu itself that's the problem — it's the biological impact of a respiratory infection.

For instance, an infection can create conditions that make blood clots more likely to form and cause blood vessels to constrict. Infections also cause inflammation and can reduce blood pressure. All of these are risk factors for a heart attack, Kwong and his colleagues wrote.

The study results suggest that people who want to avoid a heart attack should be sure to get a flu shot — and that doctors and public health officials should encourage them to do so.

Regular aspirin use may reduce progression of COPD, study suggests

By Dr Deepu

Regular aspirin use was associated with a more than 50% reduction in emphysema/chronic obstructive pulmonary disease (COPD) progression in an elderly cohort over a decade in a longitudinal analysis of data from a large lung study, researchers reported.
The findings were published in the journal CHEST.
The important findings of the Study are:

*Emphysema increased 0.60 percentage points over 10 years (95% CI 0.35 to 0.94) on an average.

*Aspirin users showed slower progression of percent emphysema was compared to non-aspirin users (fully adjusted model: -0.34% per 10 years, 95% CI -0.60 to -0.08; P=0.01).

*Results were similar in ever-smokers and for doses of 81 mg and 300-325 mg. A greater magnitude effect was seen among participants with airflow limitations.

*No association was found between aspirin use and change in lung function.
The association was seen in a wide range of aspirin usage, and was greatest in older study participants with significant airflow obstruction.
These findings, along with supportive results in animals, suggest that further study of aspirin and platelet activation in emphysema may be warranted.
They mentioned that platelet activation reduces pulmonary microvascular blood flow and contributes to inflammation, which has been shown to be important in the pathogenesis of COPD/emphysema.

The hypothesis of the Study was that regular use of aspirin, a platelet-inhibitor, would be associated with slower progression of emphysema-like lung on computed tomography (CT), and slower decline in lung function. Percent emphysema assessment was limited to the lower two-thirds of the lungs and baseline differences in emphysema were significant among aspirin users and non-users, with users having a greater percent emphysema.
The study used data from the Multi-Ethnic Study of Atherosclerosis (MESA) Lung Study, which assessed the percentage of emphysema-like lung below-950 Hounsfield units ("percent emphysema") on cardiac and full-lung CT. There were 4,257 participants from the MESA Lung Study. Their mean (±SD) age was 61±10 years, 54% were ever-smokers, and 22% used aspirin regularly.

Spirometry was conducted during 2004-2007 and repeated in 2010-2012 in accordance with American Thoracic Society-European Respiratory Society guidelines following the MESA Lung protocol.
The airflow obstruction was defined as pre-bronchodilator FEV₁/FVC <0.70 and restrictive ventilatory defect as FVC<lower limit of normal and FEV₁/FVC≥0.7.
Regular aspirin use included 3 or more days per week and mixed effects models adjusted for demographics, anthropometry, smoking, hypertension, ACE-inhibitor use, C-reactive protein, sphingomyelins, and scanner factors.
Results were similar after propensity score weighting and when the exposure was defined as any aspirin use at baseline, and there was no evidence for effect modification associated with age and race/ethnicity.
Results were also similar after adjustment for inhaler, NSAID, COX-2 inhibitor, ADP-receptor inhibitors, statin, and diuretic use.
This is the first study of which we are aware to show an association between aspirin use and longitudinal progression of percent emphysema.
Prior studies have found platelet-receptor related genes serotonin receptor 4 (HTR4), von Willebrand factor (VWF) and its platelet-receptor, GP1BA, to be associated with FEV₁ and COPD. Additionally, platelet factor 4  increased emphysema when added to a neutrophil elastase animal model of emphysema, and platelet activation was found to be greater in COPD compared to controls, and during exacerbation.

Leaving Bedroom Door Or Window Open May Be Linked To Better Sleep Quality, Study Suggests

By Dr Deepu

A research from Netherlands suggests “leaving a bedroom door or window open may help people sleep better.” Researchers found that “open windows and doors helped reduce carbon dioxide levels and improve ventilation and air flow, which was related to better sleep quality for the healthy young adults in the study.” The findings were published in the journal Indoor Air.
For one night of the study, 17 volunteers slept with an open window or internal door. On another night, the windows and door to the room were kept closed. In the meantime, Mishra and colleagues monitored carbon dioxide levels, temperature, background noise and humidity. The study participants were asked not to drink alcoholic beverages or caffeinated drinks, which could influence sleep. They each slept alone, and the bedroom layout with furniture arrangement was kept consistent.
For measuring sleep quality, participants wore an armband that measures skin temperature, heat flux, bed temperature and skin moisture levels. They also wore a sensor that tracked their movements at night, including indications of restlessness.
Closed environments tended to have less background noise – but they also had significantly higher carbon dioxide levels, which indicated lower ventilation levels.
Open conditions were slightly cooler than closed, although humidity levels were similar across settings, according to the report in the journal Indoor Air.
Notably, carbon dioxide levels were lower when windows or doors were open.
Overall, skin temperature and the bed temperature were higher in closed conditions than open conditions. The number of awakenings and sleep efficiency improved as carbon dioxide levels decreased.
A limitation of the study is that the motion sensor often slipped off the sleepers at night.

Mounier - Kuhn Syndrome

By Dr Deepu

Mounier-Kuhn syndrome is characterized by distinct tracheobronchial dilation that is due to atrophy of the muscular and elastic tissues in the trachea and main bronchial wall. It is more common in men and is typically diagnosed in the 3rd or 4th decades of life. The clinical presentation varies widely, from minimal disease in which lung function is preserved to severe respiratory failure and death. Involvement occurs at different levels, from the trachea down to the 4th bronchial branch.Although its cause is not fully known, tracheobronchomegaly is reportedly linked to familial susceptibility and is perhaps inherited through an autosomal recessive mechanism. Cases are often sporadic.

Mounier-Kuhn syndrome has 3 subtypes. In type 1, there is a slight symmetric dilation in the trachea and main bronchi. In type 2, the dilation and diverticula are distinct. In type 3, diverticular and saccular structures extend to the distal bronchi. The main problems associated with this disease are ineffective cough consequent to pathologic dilation in the tracheobronchial tree and the impairment of mucociliary activity. These cause difficulty in expectorating secretions and lead to recurrent LRTIs.The symptoms of Mounier-Kuhn syndrome are nonspecific. In the absence of infection, the disease can develop asymptomatically. Bronchiectasis and LRTIs are clinically prominent, and recurrent pneumonia and fibrosis can develop.

Diagnosis is often made by using CT, through which abnormally large air passages are detected. In adults, the diagnostic criteria are diameters of the trachea, >30 mm; of the right main bronchus, 20 mm; and of the left main bronchus, 18 mm.Upon pulmonary function testing, decreased bronchial flow speed, increased tidal volume, and dead spaces may be observed. Bronchoscopy can detect the pathologic processes that affect the tracheobronchial structures—specifically, dilation in the trachea and main bronchi during inspiration, and constriction and even collapse during expiration and coughing.

Connective-tissue diseases, ataxia-telangiectasia, ankylosing spondylitis, Ehlers-Danlos syndrome, Marfan syndrome, Kenny-Caffey syndrome, Brachmann-de Lange syndrome, and cutis laxa (elastolysis) are also associated with secondary tracheobronchial enlargement.All of these conditions should be considered in the differential diagnosis.

Asymptomatic patients require no specific treatment. Cessation of smoking is highly beneficial, as is minimizing exposure to industrial and occupational irritants and pollutants. In symptomatic patients, therapy is supportive but is limited to respiratory physiotherapy for clearing secretions and to antibiotic use during infectious exacerbations.Although tracheal stenting has been helpful in severe cases, surgery is rarely performed because of the diffuse nature of the disease. Lung transplantation provided no proved benefit in regard to the risk of morbidity and death.

Schwartz M, Rossoff L. Tracheobronchomegaly. Chest 1994; 106(5):1589–90. [PubMed]

Mounier-Kuhn P. Dilatation de la trachee: constatations radiographiques et bronchoscopiques. Lyon Med 1932;150:106–9.

 Damgaci L, Durmus S, Pasaoglu E. Mounier-Kuhn syndrome (tracheobronchomegaly). Tanisal ve Girisimsel Radyoloji 2002;8(1):165–6.

Dunne MG, Reiner B. CT features of tracheobronchomegaly. J Comput Assist Tomogr 1988;12(3):388–91.[PubMed]

Noori F, Abduljawad S, Suffin DM, Riar S, Pi J, Bennett-Venner A, et al. Mounier-Kuhn syndrome: a case report. Lung 2010;188(4):353–4.[PubMed]

Menon B, Aggarwal B, Iqbal A. Mounier-Kuhn syndrome: report of 8 cases of tracheobronchomegaly with associated complications. South Med J 2008;101(1):83–7. [PubMed]

Ghanei M, Peyman M, Aslani J, Zamel N. Mounier-Kuhn syndrome: a rare cause of severe bronchial dilatation with normal pulmonary function test: a case report. Respir Med 2007; 101(8):1836–9. [PubMed]

Noninvasive ventilation may be beneficial for patients with acute hypercapnic respiratory failure during COPD exacerbations, data indicate

By Dr Deepu

A review of a recent meta-analysis published in the Annals of Emergency Medicine indicates that noninvasive ventilation provides benefit in patients with acute hypercapnic respiratory failure during chronic obstructive pulmonary disease (COPD) exacerbations, reducing mortality and the need for mechanical ventilation.

Authors also added that noninvasive ventilation also may improve length of hospital stay, serum pH, and oxygen partial pressure. The meta-analysis included 17 randomized controlled trials with 1264 patients.

The review authors noted that severe COPD is characterized by hyperinflation, airway obstruction, and decreased respiratory muscle function. In this setting, exacerbation can result in hypercarbic respiratory failure. Usual care includes controlled oxygenation, bronchodilators, corticosteroids, and antibiotics. If these interventions fail, intubation is initiated.

Limitations of the meta-analysis include the variability of usual care and noninvasive ventilation duration in the studies, the potential for publication bias regarding the need for intubation, and low heterogeneity for both mortality and the need for intubation.

The meta-analysis provides strong evidence that noninvasive ventilation reduces mortality, the need for intubation, and hospital length of stay in patients with acute hypercapnic respiratory failure during an acute exacerbation of COPD. The findings support a trial of noninvasive ventilation in patients with a pH of less than 7.30 before proceeding with intubation.

Sputum eosinophil count may predict severity of COPD in smokers, research suggests

- Blood eosinophil count alone not predictive in SPIROMICS cohort
By Dr Deepu

Investigators found that “sputum eosinophil count proved to be a better biomarker of chronic obstructive pulmonary disease (COPD) severity and exacerbations than blood eosinophil count alone in a study involving a large group of smokers with a broad range of airflow obstruction severities.” The investigators found, “in the analysis...blood eosinophil count as a single biomarker was not predictive of sputum eosinophils and was not associated with disease severity or exacerbations unless combined with sputum count.” But, “increased sputum eosinophil inflammation...was found to be associated with more severe COPD, decreased lung function, worse emphysema and air trapping, and a greater likelihood of exacerbations.” The findings were published in The Lancet Respiratory Medicine

Patients enrolled in SPIROMICS had a smoking history of at least 20 pack-years and were recruited from six clinical sites and subsites in the U.S. between November 2010 and spring 2015. All had complete baseline blood cell counts, and a subset had acceptable sputum counts.

A total of 2,499 participants with available blood counts were stratified by mean blood eosinophil count: 1,262 patients with low (<200 cells per μL) and 1,237 with high (≥200 cells per μL) blood eosinophil counts.

A total of 827 patients were eligible for stratification by mean sputum eosinophil percentage including 656 with low (<1.25%) and 171 with high (≥1.25%) sputum eosinophil percentages. Analyses were also conducted involving blood eosinophil cutoffs of 300 cells/μL and sputum eosinophil cutoffs of 2%.

The high sputum eosinophil group had significantly lower median forced expiratory volume in 1 second (FEV)₁ percentage predicted than the low sputum eosinophil group, both before (65.7% [IQR 51.8-81.3] versus 75.7% [59.3-90.2], P<0·0001) and after (77.3% [63.1-88·5] versus 82.9% [67.8-95.9], P=0.001) bronchodilation.

Qualitative computed tomography (CT) density measures for emphysema and air trapping were significantly higher in the high sputum eosinophil group than in the low sputum eosinophil group and exacerbations requiring corticosteroids treatment were more common in the high versus low sputum eosinophil group (P=0.002).
The main findings of the study are:

FEV₁ percentage predicted was significantly different between low and high blood eosinophil groups, but differences were less than those observed between the sputum groups

The high blood eosinophil group had slightly increased airway wall thickness (0.02 mm difference, P=0·032), higher St George Respiratory Questionnaire symptom scores (P=0.037), and increased wheezing (P=0.018, but no evidence of an association with COPD exacerbations (P=0.35) or the other indices of COPD severity, such as emphysema measured by CT density, COPD assessment test scores, BMI, airflow Obstruction, Dyspnea, and Exercise index, or Global Initiative for Chronic Obstructive Lung Disease stage

Blood eosinophil counts showed a weak but significant association with sputum eosinophil counts (receiver operating characteristic area under the curve of 0.64, P<0.0001), but with a high false-discovery rate of 72%

With the higher blood eosinophil cutoff of 300 cells/μL, no significant differences were seen between the high and low count groups. But at the higher 2% sputum eosinophil cutoff, significant differences were seen between the low and high groups for all categories of COPD exacerbations.

The ECLIPSE study reported that 1,483 patients stratified by blood eosinophil counts did not have different numbers of COPD exacerbations in the previous year. Researchers noted that higher blood eosinophils are not associated with COPD exacerbations except when combined with increased sputum eosinophils or with other characteristics, such as a previous history of exacerbations. In the SPIROMICS cohort, higher sputum eosinophil counts alone are associated with exacerbations even in mild to moderate COPD

Survival Rates Have Improved Among Patients With Early Stage NSCLC, Research Indicates

By Dr Deepu

Finally a ray of hope for lung cancer patients, in a finding, researchers report that survival rates have improved among those with early stage disease.

The study included more than 65,000 people diagnosed with stage 1 non-small-cell lung cancer between 2000 and 2010. In that group, 62 percent had surgery, 15 percent received radiation therapy, 3 percent had both surgery and radiation and 18 percent received neither treatment.

The two-year survival rate for people treated with either surgery or radiation therapy rose from 61 percent in 2000 to 70 percent in 2009 -- corresponding to a 3.5 percent annual decrease in death from lung cancer.

Author also noted that while the proportion of patients who did not receive treatment fell from about 20 percent in 2000 to just under 16 percent in 2010, too many still do not receive treatment for "an otherwise highly curable disease."

Read the full study

E-Cigarettes May Cause Unique Harm To Innate Lung Immunity, Research Suggests

By Dr Deepu

Research indicates “e-cigarettes cause unique harm to innate lung immunity, challenging the concept that they are a healthier alternative to traditional cigarettes.” The findings were published in the American Journal of Respiratory Critical Care Medicine.

Researchers collected induced sputum samples from 15 current e-cigarette users, 14 current cigarette smokers, and 15 never-smokers. They analyzed the samples using quantitative proteomics, as well as total and individual mucin concentrations. Neutrophil extracellular trap (NET) formation was also analyzed and compared among the groups.

The researchers found that both cigarette smokers and e-cigarette users had a significant increase in oxidative stress-related proteins, such as thioredoxin (TXN), compared with nonsmokers (P ≤ 0.05 for all levels). These proteins are markers of activation of the innate defense mechanisms associated with lung disease, the researchers explain.

Compared with cigarette smokers and nonsmokers, e-cigarette users had higher levels of neutrophil granulocyte- and NET-related proteins, including matrix metalloproteinase-9 (MMP-9), a major contributor to chronic lung disease (P ≤ 0.05 for all levels). These elevations were seen despite no increase in the sputum neutrophil cell counts.

Total mucin concentrations were highest in the sputum of smokers and were similar among e-cigarette users and nonsmokers. But, mucin composition, which has been correlated to progression of lung disease in previous studies, was similar between smokers and e-cigarette users.

The elevated levels of markers known to be associated with cigarette smoke and lung disease/inflammation, such as TXN and MMP-9, in the sputum of both cigarette smokers and e-cigarette users, indicates commonality in the impacts of these products on airway physiology, such as increased oxidative stress and activation of innate defense mechanisms.
12 of the 15 e-cigarette users smoked cigarettes in the past, and 5 said they occasionally still smoked cigarettes.

Authors wrote "In conclusion, our results challenge the concept that e-cigarettes are a healthier alternative to cigarettes and reverse smoking-induced adverse health effects,".