No abstract

The independent risk factors for death in patients admitted for asthma exacerbation have not been thoroughly investigated. This study aimed to investigate these independent risk factors and the relationship between mortality and the prescription patterns of anti-asthmatic medications in patients admitted for asthma exacerbation. Using a nested case-control design, we identified 267 cases (death after asthma admission) and 1035 controls (survival after asthma admission) from the Taiwan National Health Insurance Research Database (NHIRD) from 2001 to 2010. Conditional logistic regressions were used to estimate the odds ratios (ORs) with 95% confidence intervals (CIs). We identified the independent risk factors for death as the comorbidities of pneumonia (aOR 3.82, 95% CI 2.41-6.05), genitourinary disease (aOR 1.75, 95% CI 1.17-2.62), septicemia (aOR 4.26, 95% CI 2.61-6.94), diabetes mellitus (aOR 2.10, 95% CI 1.30-3.38), arrhythmia (aOR 2.00, 95% CI 1.14-3.50), and a history of asthmatic hospitalization (aOR 4.48, 95% CI 2.77-7.25). Moreover, the use of short-acting β 2 -agonist (SABA) and the dosage of oral corticosteroids (OCSs) >70 mg prednisolone during previous hospitalization (all p < 0.05) and the dosage of OCSs ≥110 mg prednisolone/month (aOR 2.21, 95% CI 1.08-4.50) during outpatient treatment independently increased the risk of death. The inhaled corticosteroids (ICSs) ≥4 canisters/ year (aOR 0.39, 95% CI 0.19-0.78) independently reduced the risk of death. Specific comorbidities, asthma severity, and prescription patterns of SABA, OCSs, and ICSs were independently associated with mortality in patients admitted for asthma exacerbation. These results can be utilized to help physicians identify asthmatic patients who are at a higher mortality risk and to refine the management of the condition.npj Primary Care Respiratory Medicine (2020) 30:7 ; https://doi.

No abstract

In smokers with chronic obstructive pulmonary disease, more severe lung inflammation is associated with menthol cigarette smoking compared to non-menthol cigarette smoking. However, the mechanisms remain unclear. Menthol is an activator of transient receptor potential melastatin-8 (TRPM8), which is also sensitive to reactive oxygen species (ROS). Our recent in vitro study demonstrated that the extracts of menthol cigarette smoke (M-CS) can induce greater ROS-sensitive, TRPM8-mediated, mitogen-activated protein kinase (MAPK)-dependent inflammatory responses in lung epithelial cells than the extracts of non-menthol cigarette smoke (Non-M-CS) can. In this study, we tested the hypothesis that M-CS can induce more severe lung inflammation than Non-M-CS can via the additional action of menthol in M-CS on epithelial and lung TRPM8 in mice. Compared with Non-M-CS exposure, subchronic M-CS exposure for 7 days up-regulated the epithelial and lung expression of TRPM8, induced more vigorous activation of epithelial and lung MAPKs, and caused more severe lung inflammation. The MAPK activation was evidenced by the increased expression of phosphor-extracellular signal-regulated and phosphor-c-Jun N-terminal kinases. The lung inflammation was evidenced by pathohistological findings and increases in several inflammatory indices. Moreover, treatment with a TRPM8 antagonist (N-(3-aminopropyl)-2-{[(3-methylphenyl)methyl]oxy}-N-(2-thienylmethyl)benzamide; AMTB) greatly suppressed the MAPK activation and lung inflammation induced by Non-M-CS and M-CS, and the residual responses to these two types of CS did not differ. Conversely, the levels of biomarkers of acute CS exposure (20 min), including carboxyhemoglobin and cotinine (a nicotine metabolite) in blood plasma, and superoxide and hydrogen peroxide (two major types of ROS) in bronchoalveolar lavage fluid, did not show significant differences in the mice with Non-M-CS and M-CS exposure. We concluded that M-CS could induce greater TRPM8-mediated activation of MAPKs and lung inflammation than Non-M-CS could in mice with subchronic exposure. The augmented inflammatory effects of M-CS are unlikely due to a larger total amount of CS inhaled, but may be caused by an additional stimulation of epithelial and lung TRPM8 by menthol in M-CS. A common stimulant (presumably ROS) generated by both CS types may also stimulate TRPM8, activate MAPKs, and induce lung inflammation because treatment with AMTB could reduce these responses to Non-M-CS.

Several databases of epidemiologic studies in patients with idiopathic pulmonary fibrosis (IPF) have been analyzed in the Western community. However, few studies have been reported in Asia. The objective of this study was to investigate the epidemiology of IPF in Taiwan. We collected and analyzed patients with IPF from the Taiwan National Health Insurance Research Database from 2001 to 2011. We estimated the annual incidence and cumulative prevalence of IPF and mean survival time of patients and determined the causes of death. The annual incidence rates of IPF remained stable after 2005, ranging from 0.7 to 1.3 cases per 100,000 people per year, whereas the cumulative prevalence rates increased steadily from 3.1 to 6.4 cases per 100,000 people per year during 2006–2011 based on a narrow case definition. Men older than 75 years had higher incidence compared with other age groups. The mean survival after diagnosis was 6.9 years. Old age, male sex, and respiratory hospitalization were associated with shorter survival time after diagnosis. Both the incidence and prevalence rates of IPF were lower in Taiwanese patients than Western ones. Moreover, the survival time was higher in the Asian population compared with the Western population. These results may suggest the heterogeneity of the IPF definition in different study populations and geographic locations.

No abstract

Life-long smoking cessation is a critical public health objective, but it is difficult for numerous people. This study aimed to identify the independent predictors of 1-year abstinence in smokers motivated to quit and participating in an intervention program. This 6-year retrospective observational cohort study was conducted in smokers who participated in an intervention program. The exhaled carbon monoxide (CO) was sequentially measured on day 1, 8, 15, and 22 of the intervention program. The primary outcome measure was smoking status at 1 year of follow-up. A total of 162 participants were enrolled and divided into a successful quit group (n = 52) and unsuccessful quit group (n = 110). Using a multivariate logistic regression analysis, we reported that the intention to quit (adjusted odds ratio [AOR] = 1.475, 95% confidence interval [CI] = 1.169–1.862, P-value = 0.001), varenicline use (AOR = 3.199, 95% CI = 1.290–7.934, P -value = 0.012) and the exhaled CO level on day 8 (AOR = 0.937, 95% CI = 0.885–0.992, P-value = 0.025) independently predicted 1-year smoking cessation. Moreover, the level of exhaled CO < 4.5 parts per million on day 8 significantly predict successful 1-year smoking cessation (area under curve 0.761, sensitivity 88.2%, and specificity 57.8%, P-value < 0.001). These independent predictors including intention to quit, varenicline use, and exhaled CO level on day 8, may help primary care physicians rearrange resources and refine the strategies for intervention programs to achieve a higher rate of long-term smoking cessation.

No abstract