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Validated methods to identify patients with asthma-COPD overlap in healthcare databases: a systematic review protocol.

ABSTRACT: INTRODUCTION:Asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) is characterised by patients presenting symptoms of both asthma and COPD. Many efforts have been made to validate different methods of identifying asthma-COPD overlap cases based on symptoms, spirometry and medical history in epidemiological studies using healthcare databases. There are various coding algorithm strategies that can be used and selection depends on targeted validation. The primary objectives of this systematic review are to identify validated methods (or algorithms) that identify patients with ACO from healthcare databases and summarise the reported validity measures of these methods. METHODS:MEDLINE, EMBASE databases and the Web of Science will be systematically searched by using appropriate search strategies that are able to identify studies containing validated codes and algorithms for the diagnosis of ACO in healthcare databases published, in English, before October 2018. For each selected study, we require the presence of at least one test measure (eg, sensitivity, specificity etc). We will also include studies, in which the validated algorithm is compared with an external reference standard such as questionnaires completed by patients or physicians, medical charts review, manual review or an independent second database. For all selected studies, a uniform table will be created to summarise the following vital information: name of author, publication year, country, data source, population, clinical outcome, algorithms, reference standard method of validation and characteristics of the test measure used to determine validity. PROSPERO REGISTRATION NUMBER:CRD42018087472.

SUBMITTER: Amegadzie JE

PROVIDER: S-EPMC6429878 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Validated methods to identify patients with asthma-COPD overlap in healthcare databases: a systematic review protocol.

Amegadzie Joseph Emil JE Badejo Oluwatosin O Gamble John-Michael JM Wright Mark M Farrell Jamie J Jackson Brooke B Sultana Kirin K Hashmi Maimoona M Gao Zhiwei Z

BMJ open 20190313 3

<h4>Introduction</h4>Asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) is characterised by patients presenting symptoms of both asthma and COPD. Many efforts have been made to validate different methods of identifying asthma-COPD overlap cases based on symptoms, spirometry and medical history in epidemiological studies using healthcare databases. There are various coding algorithm strategies that can be used and selection depends on targeted validation. The primary objectives of ...[more]

PMID: 30872543

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Project description:BackgroundAsthma and chronic obstructive pulmonary disease (COPD) are airway diseases with similar clinical manifestations, despite differences in pathophysiology. Asthma-COPD overlap (ACO) is a condition characterized by overlapping clinical features of both diseases. There have been few reports regarding the prevalence of ACO in COPD and severe asthma cohorts. ACO is heterogeneous; patients can be classified on the basis of phenotype differences. This study was performed to analyze the prevalence of ACO in COPD and severe asthma cohorts. In addition, this study compared baseline characteristics among ACO patients according to phenotype.MethodsPatients with COPD were prospectively enrolled into the Korean COPD subgroup study (KOCOSS) cohort. Patients with severe asthma were prospectively enrolled into the Korean Severe Asthma Registry (KoSAR). ACO was defined in accordance with the updated Spanish criteria. In the COPD cohort, ACO was defined as bronchodilator response (BDR) ≥ 15% and ≥ 400 mL from baseline or blood eosinophil count (BEC) ≥ 300 cells/μL. In the severe asthma cohort, ACO was defined as age ≥ 35 years, smoking ≥ 10 pack-years, and post-bronchodilator forced expiratory volume in 1 s/forced vital capacity < 0.7. Patients with ACO were divided into four groups according to smoking history (threshold: 20 pack-years) and BEC (threshold: 300 cells/μL).ResultsThe prevalence of ACO significantly differed between the COPD and severe asthma cohorts (19.8% [365/1,839] vs. 12.5% [104/832], respectively; P < 0.001). The percentage of patients in each group was as follows: group A (light smoker with high BEC) - 9.1%; group B (light smoker with low BEC) - 3.7%; group C (moderate to heavy smoker with high BEC) - 73.8%; and group D (moderate to heavy smoker with low BEC) - 13.4%. Moderate to heavy smoker with high BEC group was oldest, and showed weak BDR response. Age, sex, BDR, comorbidities, and medications significantly differed among the four groups.ConclusionThe prevalence of ACO differed between COPD and severe asthma cohorts. ACO patients can be classified into four phenotype groups, such that each phenotype exhibits distinct characteristics.

Project description:BackgroundIL-17 is a modulator of the inflammatory response and is implicated in lung remodeling in both asthma and chronic obstructive pulmonary disease (COPD). Well as and probably in patients with asthma-COPD overlap (ACO).MethodsIn this study, we evaluated the response of the airways and alveolar septa to anti-IL-17 treatment in an ACO model. Fifty-six male BALB/c mice were sensitized with ovalbumin (OVA group), received porcine pancreatic elastase (PPE group), or both (ACO group). Mice were then treated with either anti-IL-17 monoclonal antibody or saline. We evaluated hyperresponsiveness, bronchoalveolar lavage fluid (BALF) cell counts, and mean alveolar diameter. We quantified inflammatory, response, extracellular matrix remodeling, oxidative stress markers, and signaling pathway markers.ResultsAnti-IL-17 treatment in the ACO anti-IL-17 group reduced the maximum response of respiratory system Rrs, Ers, Raw, Gtis, this when compared to the ACO group (p<0.05). There was a reduction in the total number of inflammatory cells, neutrophils, and macrophages in the BALF in the ACO anti-IL-17 group compared to the ACO group (p<0.05). There was attenuated dendritic cells, CD4+, CD8+, FOXP3, IL-1β, IL-2, IL-6, IL-13, IL-17, IL-33 in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p<0.05). We observed a reduction of MMP-9, MMP-12, TIMP-1, TGF-β, collagen type I in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p < 0.05). We also observed a reduction of iNOS and 8-iso-PGF2α in the airways and in the alveolar septum was reduced in the ACO anti-IL-17group compared to the ACO group (p < 0.05). Regarding the signaling pathways, NF-kB, ROCK-1, and ROCK-2 in the airway and alveolar septum were attenuated in the ACO anti-IL-17 group when compared to the ACO group (p<0.05).ConclusionsOur results suggest that inhibiting IL-17 modulates cell-associated cytokine production in lung tissue, extracellular matrix remodeling, and oxidative stress in ACO through the modulation of NF-kB and FOXP3.

Project description:BackgroundMetformin is associated with improved respiratory outcomes in asthma; however, metformin in COPD and asthma-COPD overlap (ACO) remains unexplored.ObjectiveTo determine the association between metformin use and respiratory outcomes in COPD and ACO.Study design and methodsParticipants with COPD (FEV1/FVC < 0.70) in the Genetic Epidemiology of COPD study (COPDGene®) were categorized as ACO (n = 510), defined as concurrent physician-diagnosed asthma before age 40 years, or COPD alone (n = 3459). We estimated the association of baseline metformin use with (1) rate of total and severe respiratory exacerbations during follow-up, (2) cross-sectional St. George's Respiratory Questionnaire (SGRQ) score, six-minute walk distance (6MWD), and post-bronchodilator FEV1 percent predicted (FEV1pp), and (3) 5-year change in SGRQ, 6MWD, and FEV1pp. We also examined change in SGRQ, 6MWD and FEV1pp among participants who initiated metformin during follow-up (n = 108) compared to persistent metformin non-users (n = 2080). Analyses were adjusted for sociodemographic factors, medications, and comorbidities.ResultsAmong participants with ACO, metformin use was associated with lower rate of total (adjusted incidence rate ratio [aIRR] 0.3; 95% confidence interval [95%CI] 0.11, 0.77) and severe exacerbations (aIRR 0.29; 95%CI 0.10, 0.89). Among participants with COPD alone, there was no association between metformin use with total (aIRR 0.98; 95%CI 0.62, 1.5) or severe exacerbations (aIRR 1.3; 95% CI 0.68, 2.4) (p-interaction < 0.05). Metformin use was associated with lower baseline SGRQ score (adjusted mean difference [aMD] - 2.7; 95%CI - 5.3, - 0.2) overall. Metformin initiation was associated with improved SGRQ score (aMD -10.0; 95% CI - 18.7, - 1.2) among participants with ACO but not COPD alone (p-interaction < 0.05). There was no association between metformin use and 6MWD or FEV1pp in any comparison.ConclusionsMetformin use was associated with fewer respiratory exacerbations and improved quality of life among individuals with ACO but not COPD alone. Results suggest a potential role for metformin in ACO which requires further prospective study.Trial registryNCT00608764.

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Validated methods to identify patients with asthma-COPD overlap in healthcare databases: a systematic review protocol.

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Validated methods to identify patients with asthma-COPD overlap in healthcare databases: a systematic review protocol.

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