Asthma-COPD Overlap Syndrome (ACOS): Current Understanding and Future Perspectives

Abstract

This chapter resumes our current understanding of asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS), pretending to offer a comprehensive approach for the practicing physician, and provides some future perspectives on this entity. Although different studies recognize the presence of ACOS, the detection, diagnosis, and treatment of these patients in clinical practice are not always simple and are subject to different interpretations. These patients are of special interest, because they are usually excluded from clinical trials with new medications, and also represent a clinically very important and quite prevalent population, with particular characteristics: more respiratory symptoms, frequent exacerbations, and worse health-related quality of life. They are also characterized by an increase in comorbidity and a greater consumption of health care resources compared to patients with only asthma or COPD alone. There are currently no universally accepted, validated criteria for the diagnosis of ACOS. The differences between clinical guidelines are discussed here (GINA 2014, GEMA 2015, and GOLD 2014). However, to obtain clear and validated criteria, we think that further research about the underlying mechanisms is needed. Several potential pathways that might lead to the adult presentation of ACOS are revised. The therapeutic recommendations of the Spanish consensus guideline for patients with overlap phenotype COPD-asthma are provided, and other possible future therapies are discussed in this chapter.

Osteoporosis in Patients with Asthma–Chronic Obstructive Pulmonary Disease Overlap Syndrome

“…Therefore, it is important to control systemic inflammation and disease activity to prevent osteoporosis. Thus, an appropriate use of ICS may reduce acute exacerbations and control inflammation, thereby leading to a reduction in systemic steroid use and a reduction in disease severity in ACOS patients 20 .…”

Comparative RNA-Seq Transcriptome Analysis on Pulmonary Inflammation in a Mouse Model of Asthma–COPD Overlap Syndrome

“…The release of T H 1 cytokine (IFN-γ) was reduced in ACO patients, and the production of T H 2 cytokines (IL-4) and IgE increased, indicating that ACO patients converted to a T H 2 immune response advantage ( Kalinina et al, 2016 ). The presence of both sputum eosinophils and sputum neutrophils is increased in ACO ( Iwamoto et al, 2014 ); especially, eosinophils play an important role in this ( Bobolea and Llano, 2016 ). In terms of pathology, ACO patients have significantly increased bronchial wall thickening and increased airway remodeling compared with asthma and COPD patients ( Backman et al, 1997 ; Fujimoto et al, 2012 ).…”

“…In terms of pathology, ACO patients have significantly increased bronchial wall thickening and increased airway remodeling compared with asthma and COPD patients ( Backman et al, 1997 ; Fujimoto et al, 2012 ). Several potential ways that can lead to ACO were that patients’ early-onset asthma exposure to cigarette smoke leads to the formation of fixed airflow limitation and the development of COPD ( Bobolea and Llano, 2016 ), or that patients with COPD showing signs of late-onset asthma in later years ( Bobolea and Llano, 2016 ). In this study, according to the clinical manifestations and possible causes of ACO, on the basis of the methods of asthma and COPD airway inflammation mouse models established, an ACO mouse model was established by using OVA, LPS, and smoke costimulation.…”

Is ACOS an independent nosology? Clinical signs and diagnosis of ACOS

“…В соответствии с рекомендациями GINA и GOLD для диагностики ACOS разработаны следующие критерии [9] [18]. Анализ результатов 19 исследований ACOS свидетельствует о наличии этого синдрома у 29 % больных ХОБЛ [19].…”

“…У некоторых больных БА необратимая обструкция дыхательных путей (ДП) развивается из-за ремоделирования бронхов, в результате такие лица напоминают пациентов с ХОБЛ; также обратимая обструкция ДП может формироваться при ХОБЛ, а больные начинают напоминать пациентов с БА [8]. Установлено, что БА и ХОБЛ являются гетерогенными патологическими состояниями, при этом у лиц с ХОБЛ может наблюдаться эозинофилия мокроты, а у больных БА -эозинофильно-нейтрофильная цитограмма мокроты; ACOS характеризуется наличием признаков воспаления как в случае ХОБЛ (главным образом Тh1), так и БА (Тh2) [9]. При этом подчеркивается, что ACOS нельзя рассматривать как одно заболевание и один фенотип, т. к. в него включены различные фенотипы -больные ХОБЛ с эозинофильным воспалением и курящие лица с БА, у кото-рых преобладает нейтрофильное воспаление и формируется необратимая обструкция бронхов (ОБ) [10].…”