Early COPD diagnosis and treatment: A case report

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Associated Data

Abstract

Chronic obstructive pulmonary disease (COPD) refers to a group of widely diffuse diseases that cause airflow blockage characterized by persistent respiratory symptoms such as dyspnea, chronic cough, recurrent wheezing, chronic sputum production, and progressive restricted airflow associated with exacerbations. COPD is the third leading cause of death worldwide and can only be treated not cured.

Pulmonary function tests do not permit the identification of initial obstructive airways disease. Forced expiratory flow (FEF_25-75), which calculates obstruction severity at small and medium bronchial airways levels, allows an early COPD diagnosis.

We report a 72-year-old ex-smoker male not exposed to occupational risk with symptoms suggesting early COPD. Baseline pulmonary function tests were normal, except FEF_25-75. The patient did not respond to the first 6 months of treatment with long-acting muscarinic antagonist (LAMA), whereas he showed a clear clinical and FEF_25-75 response to 1-year treatment with LAMA associated with long-acting β2 agonist (LABA).

This clinical case report highlights the usefulness of FEF_25-75 evaluation in early COPD diagnosis and monitoring and confirms the efficacy of LAMA–LABA association for small airways obstruction treatment.

Abbreviations: COPD, chronic obstructive pulmonary disease; LAMA, long acting muscarinic antagonist; LABA, long acting β2-receptor agonist; FEF 25-75, forced expiratory flow 25-75%

1. Introduction

Chronic obstructive pulmonary disease (COPD) refers to a group of widely diffuse diseases, including emphysema and chronic bronchitis, that cause airflow blockage. It is characterized by persistent respiratory symptoms such as dyspnea, chronic cough, chronic production of sputum, recurrent wheezing, and restricted airflow [1]. COPD is characterized by airflow limitation that is not fully reversible. Airflow limitation is progressive and associated with abnormal inflammatory response of the lungs, particularly caused by cigarette smoking [2].

COPD is the third leading cause of death worldwide because of associated comorbidities such as smoking, environmental pollution, and occupational risk [3]. Despite accurate studies and clinical trials analyzing COPD etiology and phenotypes, currently it can only be treated not cured.

Although COPD affects the lungs, it causes systemic damages with heart involvement developing pulmonary hypertension and cor pulmonale [4].

The importance of exacerbations is closely related to COPD clinical course, and their reduction increases the outcome and improves the quality of life (QOL). Exacerbations are events requiring therapy with antibiotics, systemic steroids, or both. The severity of exacerbations is defined by the location of care such as home and emergency room or hospital. Mild exacerbations involve upper airways and are treated with adjustments in bronchodilator or inhaled corticosteroid therapy, and moderate exacerbations involve lower respiratory tracts and are treated with antibiotics and systemic corticosteroids. Based on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines [1], the COPD classification of airflow limitation severity is defined as follows: (i) mild forced expiratory volume in 1 second (FEV₁) ≥ 80% predicted; (ii) moderate 50% ≤ FEV₁ < 80% predicted; (iii) severe 30% ≤ FEV₁ 1 25–75% depends on age and height, and the results of FEF_25–75% are little effort-dependent and representative of air movement through small airways [5,6].

The aim of this clinical case is to highlight the usefulness of pulmonary function tests and particularly FEF_25–75% in early COPD diagnosis to improve therapeutic approach, reduce acute exacerbations, QOL, and disease outcome.

2. Case report

A 72-year-old ex-smoker male, 5 pack-years, was admitted with exertional dyspnea lasting 6 months and productive cough lasting 3 months suggesting early COPD. The patient was not exposed to occupational risk and was neither affected by allergy nor other relevant comorbidities. Physical chest examination showed fine rhonchi without wheezing and crackling sounds. Cyanosis was absent, and pulse oximetry was 96% in room air. No signs of cardiovascular failure were detected.

Pulmonary function tests at baseline, including FEV₁ and FEV₁/FVC ratio, were in the normal range and did not suggest an initial obstructive airways disease. Note that the FEF_25-75 values were suggestive of moderate small airways obstruction ( Table 1 ). The patient was first treated with long-acting muscarinic antagonist (LAMA – umeclidinium bromide 65 mcg/daily). However, dyspnea and cough did not ameliorate, and the patient suffered from exacerbation responsive to antibiotics. Spirometry after 6 months of LAMA therapy showed a decrease of FEF_25-75, especially of FEF₂₅ from 59% to 50%. Then, the treatment was modified using the association of LAMA with long-acting β2 agonist (LABA – vilanterol 22 mcg/daily) according to GOLD guidelines. Patient evaluation after 12 months of LAMA–LABA therapy revealed excellent response with decreased dyspnea and cough and absence of exacerbations. Spirometry showed clear regression of small airways obstructive parameters. Notably FEF₂₅ increased from 50% to 62% ( Table 1 and Fig. 1 ).

Table 1

FEF_25-75 values before and after treatment.