Background: Air pollution contributes to an estimated six million deaths per year. Epidemiological and experimental studies show an association between air pollutant exposure and respiratory allergy. Objective:We aimed to write a narrative review of the epidemiology of air pollution-related respiratory-related allergic disorders (including asthma and allergic rhinitis) and the effects of air pollutants -with an emphasis on the particulate matter -on respiratory allergy-related health.Methods: PubMed Medline was searched, and representative epidemiologic and controlled-exposure studies were selected by using terms for air pollutants, particulate matter, and respiratory allergy including asthma and allergic rhinitis.Results: Epidemiological studies showed methodologic heterogeneity, including variability in study populations, geographical regions, types and sources of pollutants, methods for exposure estimation, approaches to controlling for confounding, and case definitions. This heterogeneity affected measures of association between studies. There is strong evidence to support an association between exposure to particulate matter and asthmatic exacerbations. Although data are inconclusive, several studies suggest exposure to particulate matter contributes to the development of asthma, allergic sensitization, and allergic rhinitis. Experimental studies, such as controlled-exposure studies, support a causal association between particulate matter and adverse health effects.Conclusions: Particulate matter exposure can exacerbate pre-existing asthma and may contribute to developing asthma, allergic rhinitis, and aeroallergen sensitization. Short-term and long-term strategies are needed to reduce disease severity and prevent new-onset disease development. Additional research is needed to identify effective avoidance strategies and therapeutic approaches.
Background Ventilator-associated pneumonia (VAP) is a common nocosomial infection in intensive care unit (ICU). Local microbiological surveillance of pathogens and resistance patterns for early-onset VAP (EOVAP) and late-onset VAP (LOVAP) will help to choose appropriate empiric antibiotics. Objective To compare the multi-drug resistant (MDR) pathogens, treatment outcomes, and factors associated with hospital mortality of VAP. Method A cross-sectional study between 1 January 2015 and 31 December 2017 at Srinagarind hospital, Khon Kaen University was conducted. The demographic data, causative pathogens, hospital length of stay (LOS), ICU LOS, mechanical ventilator (MV) days, and hospital mortality were retrospectively reviewed. Results One hundred and ninety patients were enrolled; 42 patients (22%) were EOVAP and 148 patients (78%) were LOVAP. Acinetobacter baumannii was the most common pathogen in both groups (50% EOVAP vs 52.7% LOVAP). MDR pathogens were significant greater in LOVAP (81.8%) than EOVAP (61.9%) (p = 0.007). The EOVAP had a significantly better ICU LOS [median (interquartile range, IQR) 20.0 (11.0, 30.0) vs. 26.5 (17.0, 43.0) days], hospital LOS [median (IQR) 26.5 (15.0, 44.0) vs. 35.5 (24.0, 56.0) days] shorter MV days [median (IQR) 14.0 (10.0, 29.0) vs. 23.0 (14.0, 35.5) days] and lower hospital mortality (16.7% vs 35.1%) than LOVAP (p < 0.05). The factor associated with hospital mortality was having simplified acute physiology (SAP) II score ≥ 40 with an adjusted odds ratio (aOR) of 2.22 [95% confidence interval (CI), 1.08–4.54, p = 0.02]. Conclusion LOVAP had significantly higher MDR pathogens, MV days, ICU LOS, hospital LOS and hospital mortality than EOVAP. A broad-spectrum antibiotic to cover MDR pathogens should be considered in LOVAP. The factor associated with hospital mortality of VAP was a SAPII score ≥ 40.
BackgroundOn high-resolution computed tomography (HRCT), pulmonary artery (PA) dimensions may hint at the presence of pulmonary hypertension. We aimed to determine how accurately various measures of the PA, as viewed on HRCT, predict right heart catheterisation (RHC)-confirmed pulmonary hypertension.MethodsWe retrospectively reviewed patients who had HRCT and RHC between 2010 and 2018. Analyses considered respiratory cycle, pulmonary hypertension diagnostic criteria, time between HRCT and RHC, and subgroup analysis in interstitial lung disease (ILD) and chronic obstructive pulmonary disease (COPD).ResultsOf 620 patients, 375 had pulmonary hypertension. For pulmonary hypertension (defined as mean PA pressure (mPAP) ≥25 mmHg) and from HRCT performed within 60 days of RHC, main PA diameter (MPAD) ≥29 mm had a sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of 88%, 42%, 0.70 and 0.70, respectively, while ratio of the diameter of the PA to the diameter of the ascending aorta (PA:Ao) ≥1.0 showed 53%, 85%, 0.84 and 0.54, respectively. In general, results were similar when the interval between HRCT and RHC varied from 7 to 60 days and when measured on expiratory images. In ILD, the sensitivity of MPAD was higher; in COPD, the specificity of PA:Ao was higher. There was moderately positive correlation between mPAP and inspiratory MPAD, PA:Ao, right PA diameter (RPAD), left PA diameter (LPAD) and (RPAD+LPAD)/2 (r=0.48, 0.51, 0.34, 0.34 and 0.36, respectively), whereas there was weak negative correlation between mPAP and PA angle (r= −0.24).ConclusionsFindings on HRCT may assist in the diagnosis of RHC-confirmed pulmonary hypertension. MPAD ≥29 mm had high sensitivity and PA:Ao ≥1.0 had high specificity. Compared with the entire cohort, MPAD had greater sensitivity in ILD and PA:Ao had higher specificity in COPD.
There are limited data nationwide on the burden of systemic sclerosis (SSc)-related mortality. We aimed to determine recent trends in SSc and SSc-related pulmonary arterial hypertension (PAH) mortality overall and across population subgroups.Using death certificate data from the National Center for Health Statistics, we computed the age-adjusted mortality rates of SSc and SSc-SSc−PAH, a lethal prevailing complication, across demographic groups, geographic regions and comorbid cardiorespiratory conditions, and used Joinpoint regression analysis to calculate the average annual percentage change (APC) in mortality.From 2003 to 2016, 25 175 death records contained a code for SSc. Decedents were predominantly female (81%) and white (73%), with an average age of 66±14 years. The age-adjusted mortality rate decreased by 3% per year from 6.6 in 2003 to 4.3 per 1 000 000 population in 2016. Also, a decreasing trend was found when SSc was stratified by age, sex, race and geographic region. The prevalence of PAH was 23%. The odds of PAH were highest in female and black decedents, and in decedents with concomitant pulmonary embolism, cardiomyopathy and interstitial lung disease (ILD). SSc−PAH mortality remained stable from 2003 to 2008 then decreased by 3% per year from 2008 to 2016. In decedents with SSc−PAH, among all concomitant comorbidities, the mortality rate associated with ILD had the highest increase (average APC 6%, 95% CI 2%−10%).The mortality rate from SSc decreased from 2003 to 2016. Decreases in mortality rates were similar across demographic groups and geographic regions. SSc−PAH-related mortality remained stable. The death rate for SSc−ILD and concomitant PAH increased during this period.
Background: Ventilator-associated pneumonia (VAP) is a common nocosomial infection in intensive care unit (ICU). Local microbiological surveillance of pathogens and resistance patterns for early-onset VAP (EOVAP) and late-onset VAP (LOVAP) will help to choose appropriate empiric antibiotics. Objective: To compare the multi-drug resistant (MDR) pathogens, treatment outcomes, and factors associated with hospital mortality of VAP. Method: A cross-sectional study between 1 January 2015 and 31 December 2017 at Srinagarind hospital, Khon Kaen University was conducted. The demographic data, causative pathogens, hospital length of stay (LOS), ICU LOS, mechanical ventilator (MV) days, and hospital mortality were retrospectively reviewed. Results: One hundred and ninety patients were enrolled; 42 patients (22%) were EOVAP and 148 patients (78%) were LOVAP. Acinetobacter baumannii was the most common pathogen in both groups (50 % EOVAP vs 52.7% LOVAP). MDR pathogens were significant greater in LOVAP (81.8 %) than EOVAP (61.9%) (p = 0.007). The EOVAP had a significantly better ICU LOS (median (interquartile range, IQR) 20.0 (11.0, 30.0) vs. 26.5 (17.0, 43.0) days), hospital LOS (median (IQR) 26.5 (15.0, 44.0) vs. 35.5 (24.0, 56.0) days) shorter MV days (median (IQR) 14.0 (10.0, 29.0) vs. 23.0 (14.0, 35.5) days) and lower hospital mortality (16.7% VS 35.1%) than LOVAP (p < 0.05). The factor associated with hospital mortality was having simplified acute physiology (SAP) II score ≥ 40 with an adjusted odds ratio (aOR) of 2.22 (95% confidence interval (CI), 1.08-4.54, p = 0.02). Conclusion: LOVAP had significantly higher MDR pathogens, MV days, ICU LOS, hospital LOS and hospital mortality than EOVAP. A broad-spectrum antibiotic to cover MDR pathogens should be considered in LOVAP. The factor associated with hospital mortality of VAP was a SAPII score ≥ 40.
Background: N-terminal pro-brain natriuretic peptide (NT-proBNP) and cardiopulmonary exercise testing (CPET) are useful for severity assessment in patients with pulmonary hypertension (PH). Correlations between these tests in pre-capillary PH patients is less well studied. Methods: We studied 23 patients with pre-capillary PH: 8 with idiopathic pulmonary arterial hypertension (IPAH), 6 with systemic sclerosis-associated PAH (SSc-PAH), and 9 with chronic thromboembolic pulmonary hypertension (CTEPH). Clinical evaluation, NT-proBNP levels, six-minute walking test (6MWT), spirometry, and CPET were evaluated on the same day. Correlation between NT-proBNP levels and CPET parameters were investigated. Results: In all patients, NT-proBNP levels were significantly correlated with peak oxygen uptake (VO2) ( r = −0.47), peak oxygen pulse ( r = −0.43), peak cardiac output (CO) ( r = −0.57), peak end-tidal partial pressure of carbon dioxide (PETCO2) ( r = −0.74), ventilatory equivalent to carbon dioxide (VE/VCO2) at anaerobic threshold (AT) ( r = 0.73), and VE/VCO2 slope ( r = 0.64). Significant correlations between NT-proBNP levels and peak PETCO2 and VE/VCO2 were found in IPAH and CTEPH subgroups, and a significant correlation between NT-proBNP levels and VO2 at AT was found in the CTEPH subgroup. No significant correlation was found in the SSc-PAH subgroup. Conclusion: NT-proBNP levels were significantly correlated with CPET parameters in patients with IPAH and CTEPH subgroups, but not in SSc-PAH subgroup. A further study with larger population is required to confirm these preliminary findings.
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