Gk. Crompton et al., Comparison of Pulmicort (R) pMDI plus Nebuhaler (R) and Pulmicort (R) Turbuhaler (R) in asthmatic patients with dysphonia, RESP MED, 94(5), 2000, pp. 448-453
Background. Dysphonia is a known local adverse effect of inhaled corticoste
roids. This symptom was investigated by laryngoscopy and assessment in a vo
ice laboratory. The effects of changing the treatment of patients with dysp
honia, reported whilst using the pMDI, to pMDI plus Nebuhaler(R) or Tubuhal
er(R) was also assessed.
Methods. Seventy-two patients reporting dysphonia and taking inhaled steroi
ds from a pMDI entered a 12-week, open, parallel group study. Fifty-one com
pleted the study per protocol; 26 in the Nebuhaler group [21 female, mean a
ge 57 years (22-77)] and 25 in the Turbuhaler(R) group [18 female, mean age
58 years (11-81)]. A dysphonia diary card was completed weekly. Voice labo
ratory assessments and laryngoscopy were performed on entry and at 12 weeks
.
Results. There were no differences in voice laboratory data, laryngoscopic
evidence of disordered glottic closure and diary data between the two group
s at 12 weeks. At study entry laryngoscopic appearances were normal in almo
st half the patients. Vocal cord bowing was rarely seen. Glottic closure ch
anged in nine patients during the study period, but there was no correlatio
n with voice symptoms. The trend of symptomatic improvement of voice status
in the Turbuhaler(R) group did not correlate with voice laboratory assessm
ents and laryngoscopic evidence of disordered glottic closure.
After 4 weeks, 40% of patients using Turbuhaler(R) and 8% in the Nebuhaler(
R) group scored their voice status as better (P < 0.02) but there was no si
gnificant difference between the two groups at 12 weeks (Turbuhaler(R) 52%,
Nebuhaler(R) 23%, P = 0.08).
Conclusion. This study does not support the view that dysphonia in asthmati
cs inhaling corticosteroids is usually caused by myopathic bowing of the vo
cal cord muscles.