The presence of underlying asthma should be investigated in patients diagnosed with ACE inhibitor induced cough
Clinical Respiratory Journal, cilt.14, sa.4, ss.382-388, 2020 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 14 Sayı: 4
- Basım Tarihi: 2020
- Doi Numarası: 10.1111/crj.13143
- Dergi Adı: Clinical Respiratory Journal
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, EMBASE, MEDLINE
- Sayfa Sayıları: ss.382-388
- Anahtar Kelimeler: ACE-inhibitor induced cough, angiotensin converting enzyme inhibitors, asthma, bronchial hyperreactivity, cough, hypertension
- Erciyes Üniversitesi Adresli: Evet
Özet
© 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.