Researchers characterize voice changes that occur among patients with asthma
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Dysphonia and laryngeal dysfunction during phonation were more common among patients with asthma than among a group of healthy controls, according to a study published in Clinical and Translational Allergy.
“A lot of asthmatic patients exhibit dysphonia, and it has always been suggested that dysphonia was caused by inhaled corticosteroids by inducing laryngeal mycosis or nodules on the vocal cords,” Nicolas Migueres, MD, of the division of asthma and allergy in the department of chest diseases at Strasbourg University Hospitals, told Healio.
“On the other hand, a lot of laryngeal dysfunction manifestation was described in the literature like vocal cord dysfunction,” Migueres continued.
To assess their hypothesis that dysphonia in patients with asthma occurs due to laryngeal dysfunction during phonation (LDP), the researchers compared 68 women with asthma (mean age, 46.2 years; standard deviation [SD], 13.2), all of whom had been receiving inhaled corticosteroids for at least 3 months, with 53 healthy women (mean age, 38.1 years; SD, 13.8).
The researchers assessed the patients with the Vocal Handicap Index (VHI) and GRBAS scale, which grades the hoarseness, roughness, breathiness, asthenic and strained quality of the voice. Patients with a VHI score of 18 or higher and/or a GRBAS score of 2 or higher were considered dysphonic.
Overall, more patients with asthma had dysphonia (66.2% vs. 11.3%; P < .001) and LDP (60.3% vs. 18.9%; P < .001), but there was no significant difference in organic lesions linked to LDP (OLDP) between the groups (11.8% vs. 13.2%).
These data confirm that dysphonia was due to a functional disorder and not organic disorders such as laryngeal mycosis or nodules, Migueres said.
“The main result was that laryngeal dysfunction during phonation was way more prevalent in asthmatic women than in nonasthmatic women,” he added.
Also, results of a video stroboscopic exam showed none of the patients with asthma or controls had any laryngeal candidiasis. Also, only three patients with asthma had inflammation of the laryngeal mucosa.
A pair of ENT specialists performed laryngostroboscopies on the patients but did not find any major differences in clinical features between the groups.
Researchers observed no differences in asthma characteristics among those patients with asthma who did or did not also have dysphonia, based on Global Initiative for Asthma guidelines and lung function measurements.
However, more patients with vs. without atopy had dysphonia (78.2% vs. 48.7%; P = .02), but obesity, rhinitis and age did not significantly differ between these groups.
There were no significant differences in prevalence of LDP or OLDP in relation to doses of inhaled corticosteroids among the patients with asthma, although the prevalence of dysphonia appeared to insignificantly increase with dosages.
The groups of patients with medium (500 µg to 1,000 µg per day) and high (> 1,000 µg per day) doses of inhaled corticosteroids showed higher phonation quotients.
No patients on low (< 500 µg per day) doses of inhaled corticosteroids experienced OLDP, but they did experience an insignificantly greater prevalence of LDP than those patients on medium or high doses.
Based on these findings, the researchers could not attribute the higher rates of dysphonia among patients with asthma to mucosal inflammation, laryngeal candidiasis or OLDP, nor could they find any relation between higher rates of LDP among those with asthma and doses of inhaled corticosteroids or bronchial obstruction.
However, the researchers did note that these findings changed their view of the side effects of different doses of inhaled corticosteroids among women with asthma and of the treatment of dysphonia among these patients.
“I think that we have incriminated a lot of inhaled corticosteroids in the treatment of asthmatic patients,” Migueres said, adding that this study shows how laryngeal dysfunction and dysphonia are very frequent in patients with asthma.
Speech therapy can be used to treat laryngeal dysfunction, which is the main mechanism behind dysphonia, Migueres continued.
“The main message for a clinical practitioner is that if you have an asthmatic patient who exhibits dysphonia, you have to maybe discuss speech therapy to take care of it,” he said.
Migueres cautioned that all the patients in this study were on inhaled corticosteroids, so the researchers could not say that the laryngeal dysfunction was all due to these drugs or to asthma. The researchers also did not account for the corticosteroids’ delivery systems.
Future studies should manage these limitations, Migueres said, adding that studies also should assess laryngeal dysfunction after speech therapy has been administered to see if outcomes improve.
For more information:
Nicolas Migueres, MD, can be reached at nicolas.migueres@chru-strasbourg.fr.