Loss of secondary esophageal peristalsis is not a contributory pathogenetic factor in posterior laryngitis

Citation
So. Ulualp et al., Loss of secondary esophageal peristalsis is not a contributory pathogenetic factor in posterior laryngitis, ANN OTOL RH, 110(2), 2001, pp. 152-157
Citations number
23
Categorie Soggetti
Otolaryngology,"da verificare
Journal title
ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY
ISSN journal
00034894 → ACNP
Volume
110
Issue
2
Year of publication
2001
Pages
152 - 157
Database
ISI
SICI code
0003-4894(200102)110:2<152:LOSEPI>2.0.ZU;2-#
Abstract
Secondary esophageal peristalsis helps prevent the entry of gastric acid in to the pharynx by clearing the refluxed gastric contents back into the stom ach. Because the loss of this mechanism may contribute to the pathogenesis of reflux-induced laryngeal disorders, our aim was to study the frequency o f stimulation and parameters of secondary esophageal peristalsis in patient s with posterior laryngitis (PL). We studied 14 patients (45 +/- 5 years) w ith PL documented by videolaryngoscopy and 11 healthy controls (46 +/- 6 ye ars). The upper esophageal sphincter (UES) pressure was monitored by a slee ve assembly incorporating an injection port 5 cm distal to the sleeve. The esophageal body and lower esophageal sphincter (LES) pressures were measure d by an LES sleeve assembly. Primary esophageal peristalsis was induced by 5-mL water swallows. Secondary esophageal peristalsis was induced by abrupt injection of volumes of air. incrementally increased by 5 mt, into the eso phagus. Secondary esophageal peristalsis could not be elicited by injection of any volume (up to 60 mL) in 3 PL patients and 2 controls. These 5 subje cts had normal primary peristalsis. The threshold volume of air required to stimulate secondary esophageal peristalsis in PL patients (median, 15 mL) was similar to that of controls (median, 10 mL). The parameters of the seco ndary esophageal peristaltic pressure wave were similar in both groups, and in both groups, they were similar to those of primary peristalsis. The UES response to the injection of the threshold volume that induced secondary e sophageal peristalsis in PL patients was contraction in 58% of the trials, partial relaxation in 3%, and no response in 39%. The findings were similar to those in the controls. The LES response to injection of the threshold v olume was complete relaxation in both the PL patients and the controls. We conclude that the integrity of secondary esophageal peristalsis is preserve d in PL patients.