Search

Jeanne-Marie Perotin,1,2 Claire Launois,1 Maxime Dewolf,1 Antoine Dumazet,1 Sandra Dury,1 François Lebargy,1 Valérian Dormoy,2 Gaëtan Deslee1,2 1Department of Respiratory Diseases, University Hospital of Reims, Reims, France; 2INSERM UMRS 1250, University Hospital of Reims, Reims, France Abstract: Chronic cough is a common complaint and a frequent cause of medical consultation. Its management can be difficult. We present here an overview of the current guidelines for the management of chronic cough. Different steps are detailed, including the initial research of an obvious etiology and alert signs that should lead to further investigation of underlying condition. The diagnosis of the most frequent causes: asthma, non-asthmatic eosinophilic bronchitis, gastroesophageal reflux disease and upper airway cough syndrome should be considered, assessed and treated accordingly. Recent advances have been made in the comprehension of refractory chronic cough pathophysiology as well as its pharmacologic and non-pharmacologic treatment, especially speech pathology therapy. Keywords: asthma, gastroesophageal reflux, upper airway cough syndrome, chronic hypersensitivity syndrome, refractory chronic cough, speech pathology therapy

BACKGROUND: Chronic cough can be triggered by respiratory and non-respiratory tract illnesses originating mainly from the upper and lower airways, and the GI tract (ie, reflux). Recent findings suggest it can also be a prominent feature in obstructive sleep apnea (OSA), laryngeal hyperresponsiveness, and COVID-19. The classification of chronic cough is constantly updated but lacks clear definition. Epidemiological data on the prevalence of chronic cough are informative but highly variable. The underlying mechanism of chronic cough is a neurogenic inflammation of the cough reflex which becomes hypersensitive, thus the term hypersensitive cough reflex (HCR). A current challenge is to decipher how various infectious and inflammatory airway diseases and esophageal reflux, among others, modulate HCR. OBJECTIVES: The World Allergy Organization/Allergic Rhinitis and its Impact on Asthma (WAO/ARIA) Joint Committee on Chronic Cough reviewed the current literature on classification, epidemiology, presenting features, and mechanistic pathways of chronic cough in airway- and reflux-related cough phenotypes, OSA, and COVID-19. The interplay of cough reflex sensitivity with other pathogenic mechanisms inherent to airway and reflux-related inflammatory conditions was also analyzed. OUTCOMES: Currently, it is difficult to clearly ascertain true prevalence rates in epidemiological studies of chronic cough phenotypes. This is likely due to lack of standardized objective measures needed for cough classification and frequent coexistence of multi-organ cough origins. Notwithstanding, we emphasize the important role of HCR as a mechanistic trigger in airway- and reflux-related cough phenotypes. Other concomitant mechanisms can also modulate HCR, including type2/Th1/Th2 inflammation, presence or absence of deep inspiration-bronchoprotective reflex (lower airways), tissue remodeling, and likely cough plasticity, among others. ispartof: WORLD ALLERGY ORGANIZATION JOURNAL vol:14 issue:12 ispartof: location:United States status: published

Introduction Efficacy of chronic cough treatment is ambiguous. The aim of the study was to analyze chronic cough alleviation after specific treatment and the relationship between cough etiology and treatment efficacy. Material and methods A stepwise diagnostic approach was used to diagnose cough etiology in non-smoking adults with chronic cough. In all patients specific treatment was applied. Two different questionnaires – a visual analog scale and a 5-degree scale – were used to assess cough severity before and after 4-6 months of treatment. Results A significant correlation between pre-treatment and post-treatment results of both questionnaires was found (Spearman coefficient 0.43, p = 0.0003 and 0.73, p < 0.0001, respectively). Baseline questionnaire analysis revealed no differences in cough severity between patients with different cough causes or multiple cough causes. Although specific treatment resulted in a significant decrease of cough severity in the entire group, only partial improvement was noted. According to the visual analogue scale, a decrease of cough severity by at least 50% was achieved only in 54.4% of patients (37/68). Similarly, satisfactory improvement was noted in only 54.4% (37/68) of patients when using the 5-point scale. There were three sub-groups of patients, in whom no relevant decrease of cough severity was observed despite treatment: patients with 1. three coexisting cough causes, 2. non-asthmatic eosinophilic bronchitis, and 3. chronic idiopathic cough. Conclusions Cough severity does not depend on its etiology. Efficacy of chronic cough treatment in non-smoking patients is only moderate.

Background Cough hypersensitivity may be related to the pathogenesis of upper airway cough syndrome (UACS). The purpose of the study was to investigate the role of capsaicin-sensitive cough receptors on the laryngopharynx and lower airway in the cough hypersensitivity of patients with UACS. Material/Methods 59 patients with UACS, 33 patients with rhinitis/sinusitis without cough, and 39 healthy volunteers were recruited for the study. Cough threshold C5, defined as the lowest concentration of capsaicin required for the induction of ≥5 coughs upon esposure to capsaicin, were determined at baseline and after laryngopharngeal anesthesia with lidocaine in all the subjects. After induced sputum cytology, the concentrations of histamine, prostaglandin E2 (PGE2), and calcitonin-gene-related peptide (CGPR) in the induced sputum were measured by ELISA. In 15 patients with UACS, sputum cytology and measurement of the above mediators were repeated after successful therapy. Results C5 response to capsaicin was significantly lower in the UACS group than in the rhinitis/sinusitis group and healthy control groups [3.9 (0.98, 7.8) μmol/L vs. 7.8 (3.9, 93.75) μmol/L vs. 31.2 (15.6, 62.5) μmol/L, H=40.12, P=0.000]. Laryngopharngeal anesthesia with lidocaine dramatically increased C5 to capsaicin in the subjects of all 3 groups by a similar degree, but the increase in the UACS group was still the lowest, with an increased level of histamine, PGE2, and CGRP in the induced sputum. When cough resolved with the treatment of cetirizine alone or in combination with erythromycin, the levels of CGRP and histamine in the induced sputum decreased significantly in 15 patients with UACS, with no obvious change in cell differential or concentration of PGE2 in the induced sputum. Conclusions Laryngeal TRPV1 plays an important role in cough sensitivity, but sensitization of capsaicin-sensitive cough receptors in the lower airway may be more responsible for the cough hypersensitivity in patients with UACS.