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Factors associated with chronic obstructive pulmonary disease exacerbation, based on big data analysis.

ABSTRACT: Preventing exacerbation in chronic obstructive pulmonary disease (COPD) patients is crucial, but requires identification of the exacerbating factors. To date, no integrated analysis of patient-derived and external factors has been reported. To identify factors associated with COPD exacerbation, we collected data, including smoking status, lung function, and COPD assessment test scores, from 594 COPD patients in the Korean COPD subgroup study (KOCOSS), and merged these data with patients' Korean Health Insurance Review and Assessment Service data for 2007-2012. We also collected primary weather variables, including levels of particulate matter <10 microns in diameter, daily minimum ambient temperature, as well as respiratory virus activities, and the logs of web queries on COPD-related issues. We then assessed the associations between these patient-derived and external factors and COPD exacerbations. Univariate analysis showed that patient factors, air pollution, various types of viruses, temperature, and the number of COPD-related web queries were associated with COPD exacerbation. Multivariate analysis revealed that the number of exacerbations in the preceding year, female sex, COPD grade, and influenza virus detection rate, and lowest temperature showed significant association with exacerbation. Our findings may help COPD patients predict when exacerbations are likely, and provide intervention as early as possible.

SUBMITTER: Lee J

PROVIDER: S-EPMC6491439 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Factors associated with chronic obstructive pulmonary disease exacerbation, based on big data analysis.

Lee Jongmin J Jung Hyun Myung HM Kim Sook Kyung SK Yoo Kwang Ha KH Jung Ki-Suck KS Lee Sang Haak SH Rhee Chin Kook CK

Scientific reports 20190430 1

Preventing exacerbation in chronic obstructive pulmonary disease (COPD) patients is crucial, but requires identification of the exacerbating factors. To date, no integrated analysis of patient-derived and external factors has been reported. To identify factors associated with COPD exacerbation, we collected data, including smoking status, lung function, and COPD assessment test scores, from 594 COPD patients in the Korean COPD subgroup study (KOCOSS), and merged these data with patients' Korean ...[more]

PMID: 31040338

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Project description:BackgroundChronic obstructive pulmonary disease (COPD) exacerbations are heterogenous and profoundly impact the disease trajectory. Bioactive lipid lysophosphatidic acid (LPA) has been implicated in airway inflammation but the significance of LPA in COPD exacerbation is not known. The aim of the study was to investigate the utility of serum LPA species (LPA16:0, 18:0, 18:1, 18:2, 20:4) as biomarkers of COPD exacerbation.Patients and methodsLPA species were measured in the baseline placebo sera of a COPD randomized controlled trial. Tertile levels of each LPA were used to assign patients into biomarker high, medium, and low subgroups. Exacerbation rate and risk were compared among the LPA subgroups.ResultsThe levels of LPA species were intercorrelated (rho 0.29-0.91). Patients with low and medium levels of LPA (LPA16:0, 20:4) had significantly higher exacerbation rate compared to the respective LPA-high patients [estimated rate per patient per year (95% CI)]: LPA16:0-low = 1.2 (0.8-1.9) (p = 0.019), LPA16:0-medium = 1.3 (0.8-2.0) (p = 0.013), LPA16:0-high = 0.5 (0.2-0.9); LPA20:4-low = 1.4 (0.9-2.1) (p = 0.0033), LPA20:4-medium = 1.2 (0.8-1.8) (p = 0.0089), LPA20:4-high = 0.4 (0.2-0.8). These patients also had earlier time to first exacerbation (hazard ratio (95% CI): LPA16:0-low = 2.6 (1.1-6.0) (p = 0.028), LPA16:0-medium = 2.7 (1.2-6.3) (p = 0.020); LPA20.4-low = 2.8 (1.2-6.6) (p = 0.017), LPA20:4-medium = 2.7 (1.2-6.4) (p = 0.021). Accordingly, these patients had a significant increased exacerbation risk compared to the respective LPA-high subgroups [odd ratio (95% CI)]: LPA16:0-low = 3.1 (1.1-8.8) (p = 0.030), LPA16:0-medium = 3.0 (1.1-8.3) (p = 0.031); LPA20:4-low = 3.8 (1.3-10.9) (p = 0.012), LPA20:4-medium = 3.3 (1.2-9.5) (p = 0.025). For the other LPA species (LPA18:0, 18:1, 18:2), the results were mixed; patients with low and medium levels of LPA18:0 and 18:2 had increased exacerbation rate, but only LPA18:0-low patients had significant increase in exacerbation risk and earlier time to first exacerbation compared to the LPA18:0-high subgroup.ConclusionsThe study provided evidence of association between systemic LPA levels and exacerbation in COPD. Patients with low and medium levels of specific LPA species (LPA16:0, 20:4) had increased exacerbation rate, risk, and earlier time to first exacerbation. These non-invasive biomarkers may aid in identifying high risk patients with dysregulated LPA pathway to inform risk management and drug development.

Project description:BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) can experience 'exacerbations' of their conditions. An exacerbation is an event defined in terms of subjective descriptors or symptoms, namely dyspnoea, cough and sputum that worsen sufficiently to warrant a change in medical management. There is a need for reliable markers that reflect the pathological mechanisms that underlie exacerbation severity and that can be used as a surrogate to assess treatment effects in clinical studies. Little is known as to how existing study variables and suggested markers change in both the stable and exacerbation phases of COPD. In an attempt to find the best surrogates for exacerbations, we have reviewed the literature to identify which of these markers change in a consistent manner with the severity of the exacerbation event. METHODS: We have searched standard databases between 1966 to July 2004 using major keywords and terms. Studies that provided demographics, spirometry, potential markers, and clear eligibility criteria were included in this study. Central tendencies and dispersions for all the variables and markers reported and collected by us were first tabulated according to sample size and ATS/ERS 2004 Exacerbation Severity Levels I to III criteria. Due to the possible similarity of patients in Levels II and III, the data was also redefined into categories of exacerbations, namely out-patient (Level I) and in-patient (Levels II & III combined). For both approaches, we performed a fixed effect meta-analysis on each of the reported variables. RESULTS: We included a total of 268 studies reported between 1979 to July 2004. These studies investigated 142,407 patients with COPD. Arterial carbon dioxide tension and breathing rate were statistically different between all levels of exacerbation severity and between in out- and in-patient settings. Most other measures showed weak relationships with either level or setting, or they had insufficient data to permit meta-analysis. CONCLUSION: Arterial carbon dioxide and breathing rate varied in a consistent manner with exacerbation severity and patient setting. Many other measures showed weak correlations that should be further explored in future longitudinal studies or assessed using suggested mathematical modelling techniques.

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Factors associated with chronic obstructive pulmonary disease exacerbation, based on big data analysis.

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Factors associated with chronic obstructive pulmonary disease exacerbation, based on big data analysis.

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