The presence of underlying asthma should be investigated in patients diagnosed with ACE inhibitor induced cough


Yilmaz İ. , Türk M., Baran K. , Çetinkaya Z. , Tutar N. , Oymak F. S. , ...More

Clinical Respiratory Journal, vol.14, no.4, pp.382-388, 2020 (Journal Indexed in SCI Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 14 Issue: 4
  • Publication Date: 2020
  • Doi Number: 10.1111/crj.13143
  • Title of Journal : Clinical Respiratory Journal
  • Page Numbers: pp.382-388
  • Keywords: ACE-inhibitor induced cough, angiotensin converting enzyme inhibitors, asthma, bronchial hyperreactivity, cough, hypertension, ANGIOTENSIN-CONVERTING ENZYME, GENE POLYMORPHISM, ADVERSE-REACTIONS, KEY COMPONENTS, METHACHOLINE, METAANALYSIS, LISINOPRIL, ENALAPRIL, FREQUENCY, CAPTOPRIL

Abstract

© 2020 John Wiley & Sons LtdIntroduction: Why do only some of patients who are prescribed angiotensin converting enzyme inhibitors (ACE-I) develop cough? The pathogenesis of ACE-I-induced cough remains controversial and requires further studies. Objective: We aim to investigate whether asthma is a contributing cause of ACE-I-induced cough. Methods: Patients attending a cardiology clinic between March 2016 and March 2017 who were diagnosed with ACE-I induced cough were included in this study. ACE-I-induced cough was defined as cough which developed within 4 weeks after initiation of ACE-I therapy and which improved within 4 weeks after discontinuation of the ACE-I. Patients who had received ACE-I treatment for at least 6 months without side effects were included in the study as a control group. Face-to-face questionnaires, pulmonary function tests (PFT) and skin prick tests were applied to all the patients. If there was discordance between asthma history and PFT results, a methacholine bronchial provocation test (BPT) was performed. Results: A total of 43 patients with ACE-I induce cough were compared with 50 controls. Bronchial hyperreactivity (BHR), rhinitis, atopy and family history of asthma were more frequent in patients with ACE-I induced cough (P <.001). Patients with ACE-I-induced cough had significantly higher incidence of diagnosed asthma [OR = 8.28 (95%CI: 3.26-21.03) P <.001]. Conclusions: Asthma and an atopic background constitute a substantial risk factor for ACE-I induced cough. The presence of underlying asthma should be investigated in patients diagnosed with ACE inhibitor induced cough. However, the fact that most asthma patients tolerate ACE-I therapy, indicates that other cofactors are likely involved.