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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 18  |  Issue : 2  |  Page : 168-175

Study of asthma–chronic obstructive pulmonary disease overlap syndrome among an Egyptian sample of chronic obstructive pulmonary disease and asthmatic patients


1 Department of Chest, Al-Azhar University, Al-Zahraa University Hospital, Egypt
2 Department of Clinical Pathology, Al-Azhar University, Al-Zahraa University Hospital, Egypt

Date of Submission17-Feb-2020
Date of Decision02-Apr-2020
Date of Acceptance14-May-2020
Date of Web Publication24-Jul-2020

Correspondence Address:
MD Heba H Eltrawy
Department of Chest, Al-Azhar University, Al-Zahraa University Hospital, 11517 Al-Abaseya, Cairo 11517
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AZMJ.AZMJ_29_20

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  Abstract 


Background Asthma–chronic obstructive pulmonary diseases overlap syndrome (ACOS) carries a higher risk than either condition alone, with more symptoms, more exacerbations, higher cost, and increased mortality, so the diagnosis and accurate treatment of patients with ACOS is very important in the clinical setting.
Aim To study the prevalence of ACOS among patients with asthma and those with COPD and to detect the predictive factors of ACOS.
Patients and methods We conducted an observational cross-sectional study involving 100 patients with bronchial asthma and 100 patients with COPD. We recorded demographic data, spirometric data, chest radiograph finding, peripheral blood eosinophil and neutrophils, and response to inhaled corticosteroids.
Results Among the 200 studied patients, 16% of patients with asthma and 20% of patients with COPD fulfilled the ACOS criteria. Male sex and prebronchodilator forced expiratory volume in first second/forced vital capacity% are predictors of ACOS development in asthmatic patients and that blood eosinophil are predictors of ACOS development in patients with COPD using odds ratio.
Conclusion ACOS should be considered as an independent subgroup distinguished by demographic data, symptoms, spirometric indices, and granulocytic pattern.

Keywords: asthma–chronic obstructive pulmonary diseases overlap syndrome, bronchial asthma, chronic obstructive pulmonary diseases


How to cite this article:
Eltrawy HH, Elshennawy S. Study of asthma–chronic obstructive pulmonary disease overlap syndrome among an Egyptian sample of chronic obstructive pulmonary disease and asthmatic patients. Al-Azhar Assiut Med J 2020;18:168-75

How to cite this URL:
Eltrawy HH, Elshennawy S. Study of asthma–chronic obstructive pulmonary disease overlap syndrome among an Egyptian sample of chronic obstructive pulmonary disease and asthmatic patients. Al-Azhar Assiut Med J [serial online] 2020 [cited 2020 Oct 25];18:168-75. Available from: http://www.azmj.eg.net/text.asp?2020/18/2/168/290605




  Introduction Top


Chronic obstructive pulmonary diseases (COPD) and asthma are mixed conditions, and each of them has various causes. The differentiation between bronchial asthma and COPD is not particulary distinctive and a crucial percentage of patients with COPD have sharing symptoms of both disorders [1]. Asthma–COPD overlap might have many fundamental reasons. It can develop in current cigarette smoker, past smokers, or nonsmokers, especially in elderly. The main background of asthma–chronic obstructive pulmonary diseases overlap syndrome (ACOS) include obstinate airflow obstruction in symptomatic patients 40 years and older, a well-documented history of asthma during juvenile or early maturity, and a substantial exposure history to smoking or biomass smoke [2].

Discrepancy among classic asthma (e.g. juvenile-onset allergic asthma) and classic COPD (e.g. emphysema in heavy smokers) is easy. However, it might be problematic to discriminate asthma from obstructive airway disease in adults having concomitant symptoms. These persons are pronounced as asthma–COPD overlap patients. Asthma–COPD overlap is recently acknowledged as a vital medical problem [3],[4].

Asthma–COPD overlap is recognized in clinical practice by sharing characterstics with both Asthma and COPD. Research studies have shown that people with asthma–COPD overlap might have airway neutrophil, eosinophilia, or a heterogeneous form of airway irritation and may have systemic inflammation. People with asthma–COPD overlap often develop bad disease consequences, including great want for health care facilities; more recurrent and severe respiratory exacerbations and hospitalizations; more wheezing, dyspnea, cough, and sputum production; and worse quality of life than patients with obstructive airway disease or bronchial asthma only, as well as poorer pulmonary function demonstrated by spirometer than those with unaccompanied obstructive airway disease despite lesser average contact to tobacco smoke [5].


  Patients and methods Top


Type, time, and place of the study

This cross-sectional research was done at pulmonology department, Al-Zahraa University Hospital, Al-Azhar University, during the period from August 2017 to February 2019.

Ethical approval

This study was done after approval by the ethical review agency of Al-Azhar University. All data were kept secret and coded to ensure privacy of the participants. Each participant signed an informed printed agreement before being recruited into the study.

Selection of study participants

  1. A total of 100 known patients with COPD, who attended the pulmonology outpatient clinic for steady follow-up. They were diagnosed according to the GOLD 2016 criteria [6] [postbronchodilator (BD) forced expiratory volume in first second (FEV1)/forced vital capacity (FVC) ratio <0.7].
  2. A total of 100 known asthmatic patients, who attended the pulmonology outpatient clinic for regular follow-up. They were diagnosed according to GINA 2019.


Exclusion criteria

Patients with chest diseases other than COPD or asthma and patients treated by cytotoxic or immunosuppressive drugs other than corticosteroids were excluded from the study.

All patients were subjected to full medical history and general examination, including age, sex, smoking habits, and BMI.

Spirometer data were reported by Medisoft-Hyperair compact. Spirometer data was done before and after inhaling a short-acting B2-agonist. FEV1%, FVC%, FEV1/FVC ratio, and forced expiratory flow rate 25–75% (FEF25–75%) were measured. Spirometric indices calculation was done using best out of three technically satisfactory performances according to the recommendations of GOLD, 2016 [6].

Radiograph chest film, complete blood film, and differential leukocytic count were performed. Differential leukocytic count was done to detect peripheral blood eosinophil and neutrophils, performed on SYSMEX XP 300.

Routine analysis of blood is performed on blood films stained with Romanowsky stains such as Giemsa stain; these stains allow for the detection of white blood cell, (neutrophils normal%=50–70% and eosinophil normal%=2–6%) to confirm instrument result.

All were done to detect the prevalence of ACOS among patients with asthma and patients with COPD and to detect the predictive factors of ACOS, which was diagnosed by the criteria for diagnosis of ACOS according to European Respiratory Journal 2016 [7].

Statistical analysis

Recorded data were analyzed using the statistical package for social sciences, version 20.0 (SPSS Inc., Chicago, Illinois, USA). Quantitative data were expressed as mean±SD. Qualitative data were expressed as frequency and percentage.

The following tests were done:
  1. Independent samples t-test of significance was used when comparing between two means.
  2. A one-way analysis of variance when comparing between more than two means.
  3. Post-hoc test: least significant difference was used for multiple comparisons between different variables.
  4. χ2 test of significance was used to compare proportions between qualitative parameters.
  5. Binary logistic regression was used to predict the outcome of categorical variable based on one or more predictor variables.
  6. The confidence interval was set to 95%, and the margin of error accepted was set to 5%. So, the P value was considered significant as follows:
    1. P value.
    2. P value less than or equal to 0.05 was considered significant.
    3. P value less than or equal to 0.001 was considered as highly significant.
    4. P value more than 0.05 was considered insignificant.



  Results Top


There were highly statistically significant differences between COPD and asthma groups regarding age, sex, BMI, positive smoking history, symptoms and signs of atopy, response to inhaled corticosteroids (ICS), physician diagnosis of asthma and hyperinflation, VC%, FVC%, FEV1/FVC. FEF25–75%, pre-BD FEV1/FVC%, post-BD FEV1/FVC%, post-BD FEV1%, post-BD FEV1/FVC%, reversibility, blood eosinophil% and status, and blood neutrophils% and status (P<0.01) ([Table 1] and [Table 2]).
Table 1 Criteria for diagnosis of asthma–chronic obstructive pulmonary disease overlap syndrome [7]

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Table 2 Comparison of all studied variables between patients with bronchial asthma and patients with chronic obstructive pulmonary diseases

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Our study reported among 200 studied patients that 17 (16%) patients with asthma patients and 19 (20%) of patients with COPD had ACOS criteria, and the patients were classified into three groups: bronchial asthma, COPD, and ACOS ([Table 3]).
Table 3 Comparison of all studied variables among patients with bronchial asthma, chronic obstructive pulmonary diseases, and asthma–chronic obstructive pulmonary diseases overlap syndrome

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There were highly statistically significant increases in asthma than COPD group (P1) regarding female sex, BMI, VC%, FVC%, pre-BD FEV1/FVC%, post-BD FEV1%, post-BD FEV1/FVC% more than 70%, number of patients responding to ICS, symptoms and signs of atopy, physician diagnosis of asthma, reversibility, blood eosinophil%, eosinophilic patient number, normal neutrophil status, and neutropenia patient number ([Table 3]).

There was a highly statistically significant decrease in asthma than COPD group (P1) regarding male sex, positive smoking history, blood neutrophils%, and neutrophilic patient number ([Table 3]).

There were highly statistically significant increases in ACOS than asthma group (P2) regarding age (46.9±11.9 vs. 34.5±12.4 years), male sex (75.0% in ACOS vs. 33.7% in asthma), positive smoking history (77.8% in ACOS vs. 27.7% in asthma), smoking pack/year (29.7±8.5 in ACOS vs. 21.6±7.1 in asthma) and hyperinflation (61.1% in ACOS vs. 0.0% in asthma), and post-BD FEV1/FVC% less than 70% (100.0% of ACOS vs. 3.6% of asthma group), blood eosinophil%, and blood neutrophils% ([Table 3]).

However, there were highly statistically significant decreases in ACOS than asthma group (P2) regarding response to ICS, VC% (55.1±14.5 vs. 75.0±13.5, FVC% (52.3±14.0 vs. 71.9±14.6), pre-BD FEV1% (42.5±11.6 vs. 51.3±12.9), pre-BD FEV1/FVC% (42.5±11.6 vs. 70.8±7.0), FEF25–75% (36.8±18.2 vs. 52.8±13.7), post-BD FEV1/FVC% (61.0±7.1 vs. 85.1±7.4), post-BD FEV1% (59.5±12.0 vs. 70.1±11.9), and number of patients responding to ICS (P<0.01) ([Table 3]).

There were highly statistically significant increases in ACOS than COPD group (P3) regarding BMI, smoking pack/year, VC%, FVC%, pre-BD FEV1/FVC%, post-BD FEV1%, number of patients responding to ICS, symptoms and signs of atopy, physician diagnosis of asthma, reversibility, blood eosinophil%, and blood neutrophils%.

There is a statistically significant increase in ACOS than COPD group (P3) regarding pre-BD FEV1/%, post-BD FEV1/FVC% less than 70%, and number of eosinophilic patients. There was a highly statistically significant decrease in ACOS than COPD group (P3) regarding age ([Table 3]).

It was shown by odds ratio that BMI, male sex, smokers, symptoms and signs of atopy, VC%, FVC%, pre-BD FEV1%, pre-BD FEV1/FVC%, post-BD FEV1/FVC%, post-BD FEV1%, blood eosinophils%, blood eosinophil status, blood neutrophils%, and blood neutrophil status all were univariate predictors of ACOS development in asthmatic patients ([Table 4]).
Table 4 Univariate logistic regression analysis using backward (Wald) method for predictors of asthma–chronic obstructive pulmonary diseases overlap syndrome in asthma group

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It was shown by an odds ratio that male sex and pre-BD FEV1/FVC% all were multivariate predictors of ACOS development in asthmatic patients ([Table 5]).
Table 5 Multivariate logistic regression analysis using backward (Wald) method for predictors of asthma–chronic obstructive pulmonary diseases overlap syndrome in asthma group

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Age, BMI, smoking pack year, nonresponse to ICS, pre-BD FEV1/FVC, post-BD FEV1, blood eosinophil%, and blood eosinophil status all were univariate predictors of ACOS development in patients with COPD by an odds ratio ([Table 6]).
Table 6 Univariate logistic regression analysis for predictors of asthma–chronic obstructive pulmonary diseases overlap syndrome in chronic obstructive pulmonary diseases group

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Blood eosinophil% is one of multivariate predictive factors of ACOS development in patients with COPD by an odds ratio ([Table 7]; [Figure 1],[Figure 2],[Figure 3],[Figure 4],[Figure 5]).
Table 7 Multivariant logistic regression analysis using backward (Wald) method for predictors of asthma–chronic obstructive pulmonary diseases overlap syndrome in chronic obstructive pulmonary diseases group

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Figure 1 ACOS percentage according to sex. ACOS, asthma–chronic obstructive pulmonary diseases overlap syndrome.

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Figure 2 BMI distribution among the three groups.

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Figure 3 ACOS percentage according to smoking history. ACOS, asthma–chronic obstructive pulmonary diseases overlap syndrome.

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Figure 4 ACOS percentage according to post-BD FEV1/FVC. ACOS, asthma–chronic obstructive pulmonary diseases overlap syndrome; BD, bronchodilator; FEV1, forced expiratory volume in first second; FVC, forced vital capacity.

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Figure 5 Blood eosinophil percentage among the three groups.

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  Discussion Top


Several present ACOS explanations are complex, and many of the diagnostic criteria are tough to use in practice [8].

The aim of the study was to assess the prevalence of ACOS among patients with bronchial asthma and those with obstructive airway disease and to detect the predictive factors of ACOS that may assist clinicians in identification of patients with ACOS and most notably allow scientists to design therapeutic and clinical trainings to identify epidemiology, pathophysiology, and managing strategies

This observational cross-sectional study was conducted on 100 patients with bronchial asthma and 100 patients with COPD at pulmonology department, Al-Zahraa University Hospital. Among 200 studied patients, 17 (16%) patients of asthmatic patients and 19 (20%) of patients with COPD had ACOS.

A post-hoc analysis of data shows that male sex, smoking history, and post-BD FEV1/FVC% all are multivariate predictors of ACOS development in asthmatic patients.

A post-hoc analysis of data shows that blood eosinophil and blood eosinophil status all are multivariate predictors of ACOS development in patients with COPD by odds ratio.

ACOS contains the subclass of patients with airways disease having characteristics of both bronchial asthma and COPD. Although descriptions of ACOS fluctuate, it is generally supposed to cover fixed airflow limitation in a patient with either a history of bronchial asthma or great BD reversibility. In our study, ACOS affected about 20% of patients with COPD and 16% of the patients who were formerly diagnosed as having asthma. This result is in concordance with many research studies in which the incidence of ACOS was ∼20% of patients with obstructive airway disease [2],[9].

The clinical features detected in this work were also like those of preceding studies, including old age, male sex, and smoking history, and little standard FEV1 [10].

Our study proved that if a patient showed FEV1\FVC less than 0.7 and a smoking history of more than 10 PYs, the case is more appropriate diagnosis as typical COPD than ACOS but if the case was associated with sharing symptoms with asthma as blood eosinophilia we should suspect ACOS also we defined a fixed airway obstruction as aconstant post –BD FEV1\FVC less than 0.7 in general, post-BD FEV1\FVC is frequently used as an indicator for a fixed airway obstruction [8].

In comparison with their deferential diagnosis with asthma or COPD alone, patients with ACOS have suggestively poorer breathing symptoms, lesser quality of life, and enlarged risk of exacerbations and hospitalizations. Either this condition appears after gradual shifts in airway remodeling and inflammation in a patient with COPD, or as the consequence of harmful exposure in an individual with asthma, or even as a de novo illness, with its private pathology still under determination. Nonetheless, using treatments developed for asthma or COPD that target eosinophilic, neutrophilic, or paucigranulocytic airway inflammation might be a supportive approach to these groups of patients until further clinical experiments can be done [11].

Patients with ACOS have the shared danger factors of smoking and atopy, are generally younger age than patients with obstructive airway disease, and develop acute exacerbations with greater rates of occurrence and more severity than COPD alone. Pharmacotherapeutic prospects need an cohesive approach, first to recognize the related clinical phenotype(s), then to define the best accessible treatment. An international agreement on the description of ACOS is needed to plan prospective, randomized clinical studies to assess precise drug involvements on vital outcomes such as pulmonary function, severe exacerbations, quality of life, and death rate [12].

Limitation of study

There is a necessity to conduct great quality therapeutic experiments to decide the greatest optimal managing plans for these patients. There is also a crucial necessity of easy, low-cost biomarkers to precisely recognize patients with ACOS and to lead therapeutic selections.


  Conclusion Top


Our results advise that ACOS should be defined as an isolated subgroup distinguished by demographic data, symptoms, spirometric indices, and granulocytic pattern.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Reddel HK: Treatment of overlapping asthma-chronic obstructive pulmonary disease: can guidelines contribute in an evidence-free zone? J Allergy Clin Immunol Pract 2015; 136:546–552.  Back to cited text no. 1
    
2.
Bateman ED, Reddel HK, van Zyl-Smit RN, Agusti A. The asthma-COPD overlap syndrome: towards a revised taxonomy of chronic airways diseases? Lancet Respir Med 2015; 3:719–728.  Back to cited text no. 2
    
3.
Global Initiative for Asthma (GINA). Diagnosis and initial treatment of asthma, COPD and asthma-COPD overlap: A joint project of GINA and GOLD updated April 2017. https://ginasthma.org/wp-content/uploads/2019/11/GINA-GOLD-2017-overlap-pocket-guide-wms-2017-ACO.pdf. [Accessed on November 18, 2019].  Back to cited text no. 3
    
4.
Gibson PG, Simpson JS. The overlap syndrome of asthma and COPD: what are its features and how important is it? Thorax 2009; 64:728–735.  Back to cited text no. 4
    
5.
Postma DS, Weiss ST, van den Berge M. Revisiting the Dutch hypothesis. J Allergy Clin Immunol 2015; 136:521–529.  Back to cited text no. 5
    
6.
Global initiative for chronic Obstructive Lung Disease Global Strategy for the Diagnosis Management and Prevention of COPD, Definition and diagnosis of COPD (2016), Chapter 2, page 30. https://www.goldcopd.org/guidelines-global-strategy-for-diagnosis-management, updated 2019.  Back to cited text no. 6
    
7.
Sin DD, Miravitlles M, Mannino DM, Soriano JB, Price D, Celli BR et al. What is asthma−COPD overlap syndrome? Towards a consensus definition from a round table discussion. Eur Respir J 2016; 48:664–673. DOI: 10.1183/13993003.00436-2016.  Back to cited text no. 7
    
8.
Park S-Y, Jung H, Kim J-H, Seo B, Choi S, Oh B, Kwon H-S et al. Longitudinal analysis to better characterize Asthma‐COPD overlap syndrome: Findings from an adult asthma cohort in Korea (COREA). Clin Exp Allergy 2019; 49:603–614.  Back to cited text no. 8
    
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Gibson PG, McDonald VM. Asthma‐COPD overlap, 2015: now wearesix. Thorax 2015; 70:683–691.21.  Back to cited text no. 9
    
10.
Lee HY, Kang JY, Yoon HK, Kwon SS, Kim YK. Clinical characteristics of asthma combined with COPD feature. Yonsei Med J 2014; 55:980–986.  Back to cited text no. 10
    
11.
Leung JM, Sin DD. Asthma-COPD overlap syndrome: pathogenesis, clinical features, and therapeutic targets. BMJ 2017; 358:j3772.  Back to cited text no. 11
    
12.
Sin DD. Asthma-COPD overlap syndrome: what we know and what we don’t. Tuberc Respir Dis (Seoul) 2017; 80:11–20.  Back to cited text no. 12
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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