Treatment of nocturnal laryngopharyngeal reflux
PPI plus H2-receptor agonist is the only therapy that works
Laryngopharyngeal-reflux disease (LPRD) is a backflow of the gastrointestinal tract's acidic stomach contents up into the esophagus and the throat. In the throat, the pharynx and larynx are much more sensitive to stomach acid and digestive enzymes, so that small amounts of reflux can result in damage. Symptoms are frequently chronic but intermittent, and are caused by direct tissue damage from the gastric-acid refluxate and vagally mediated mechanisms.
The clinical description of LPRD, however, is still very much in its infancy, and there is scientific argument among clinicians since it was identified. Much debate accompanies its every aspect, from an enumeration of its signs and symptoms to the recommendation of the most appropriate diagnostic and therapeutic strategies.
There is no clear consensus on the findings or clinical manifestations of LPRD, according to Dr. Kiminori Sato of the Kurume University School of Medicine in Japan. "There are no ideal diagnostic procedures for evaluating LPRD and the diagnostic criteria are ambiguous," he said during a symposium organized by HI-Eisai Pharmaceutical in last year's convention of the PhiliPPIne Society of Otolaryngology-Head and Neck Surgery.
The ambiguity lies chiefly at the distinction between LPRD and a closely related disease--gastroesophageal-reflux disease (GERD). "The relationship between laryngopharyngeal-reflux disease and gastroesophageal-reflux disease is controversial," said Sato. "It is said that patients with laryngopharyngeal reflux appear to have a different pathophysiologic mechanism and pattern of reflux compared with [those who have] GERD."
According to Dr. Jamie Koufman, the fundamental disparity is anatomic: the primary defect of LPRD lies at the upper esophageal sphincter, that of GERD at the lower esophageal sphincter. Also, LPRD differs from "typical" GERD in symptom presentation, pattern of reflux, and response to medical treatment. Both LPRD and GERD involve the reflux of acidic contents that become dangerous to surfaces unaccustomed to the low pH milieu. With the mechanical and physiologic events that occur whenever a person sleeps at night, variants termed nocturnal LPRD and nocturnal GERD are recognized.
"Nocturnal LPRD refers to the backflow of stomach contents into the laryngopharynx at night," said Sato, adding that acid breakthrough, swallowing, and obstructive sleep apnea are clinical events that are associated with it. Cases of nocturnal LPRD resistant to the usual treatment with proton-pump inhibitors (PPIs) have been reported, and Sato pointed out that the underlying cause is nocturnal acid breakthrough (NAB)- a phenomenon first seen in nocturnal GERD. NAB is characterized as a dip in the intragastric pH to less than four, lasting for at least an hour within 12 hours from the evening intake of PPI.
"The mechanism of this phenomenon has been unclear," Sato admitted, "and the treatment of reflux caused by NAB on PPI is still controversial." Referring to a study by Fackler et al. (Gastroenterology 2002), Sato said, "the administration of PPI and one day of H2-receptor antagonist is the only therapy that significantly decreases the percentage of time with <4 gastric pH level for the supine period, compared with PPI twice daily alone." The study noted, however, that "the combination of PPI and H2-receptor-antagonist therapy only reduces nocturnal acid breakthrough and the efficacy of the H2-receptor antagonist decreases with continuous administration."
Sato advocates the use of tetraprobe 24-hour pH monitoring in examining LPRD with NAB on PPI. "It is well known that saliva secretion decreases during sleep," said Sato. "Impaired deglutition and saliva secretion during sleep reduce pharyngeal clearance. Consequently, acid retention and bacterial proliferation occur and cause nocturnal-acid-related and aspiration-related diseases."
Also being studied is the contribution of obstructive sleep apnea to the pathogenesis of nocturnal LPRD. The upper-airway obstruction present in obstructive sleep apnea increases an individual's breathing effort, which results in negative intrathoracic and esophageal pressures. These are thought to influence, by an unknown process, the temporary relaxation of lower esophageal sphincters, thus promoting gastroesophageal reflux.
Sato stressed the need for a multidisciplinary approach to managing nocturnal LPRD and GERD. Left unchecked, laryngopharyngeal reflux may cause substantial damage to the throat mucosa and lead to laryngeal cancer, an association reported in literature. Moreover, its impact on a patient's quality of life poses a serious challenge to physicians. From the ordinary worker moderately incapacitated by frequent awakenings to the professional singer challenged by the vocal requirements of her art, the costs of untreated laryngopharyngeal reflux are tremendous.
In the last decade, medical science has progressed from acknowledging the existence nocturnal of such a syndrome to unearthing some of its secrets, but relevant clinical knowledge is still lacking. Sato said: "More investigation and follow-up will be needed."
|
