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Clinical manifestations of laryngopharyngeal reflux.


Laryngopharyngeal reflux (LPR) is ubiquitous and associated with many head and neck symptoms and diagnoses. In some cases, the symptom is the diagnosis--for example, LPR can cause sore throat, chronic cough, globus pharyngeus, and laryngospasm. Alternately, LPR can be associated with specific histopathologic lesions--for example, vocal process granulomas. LPR can be the sole cause or an etiologic cofactor in the development of many disorders of the aerodigestive tract.


This article provides an overview of the protean manifestations of laryngopharyngeal reflux (LPR) (table (1-106)), and it includes a comprehensive list of references. We have intentionally not included all reflux-related conditions. For example, many conditions related to gastroesophageal reflux disease (GERD)--such as reflex bradycardia, noncardiac chest pain, esophageal dysmotility, and stricture--are adequately covered in the GERD literature and are not discussed in this article. We have focused primarily on the otolaryngologic manifestations of LPR.

The most common symptom of LPR is hoarseness/dysphonia (92%). (6) Koufman reported that patients with intermittent hoarseness often complained of several episodes a year of "laryngitis" that lasted for a period of days or weeks. (6) Additional symptoms experienced by most patients included chronic throat clearing (50%), chronic cough (44%), globus pharyngeus (33%), and dysphagia (27%). More than half of these patients denied having any heartburn whatsoever; among the rest, 13% had two or fewer episodes per week, and only 10% complained of more frequent heartburn.

Although many patients with LPR experience mild to moderate dysphonia as their primary symptom, some experience more serious conditions. Less common laryngeal manifestations of LPR include laryngospasm, arytenoid fixation, laryngeal stenosis, and carcinoma. (1,3,6,13-38,47-51) LPR is also associated with the development of polypoid degeneration (Reinke's edema), (1,56) vocal fold nodules (figure 1), (1,22,55) and functional voice disorders. (1,52-54)

Certain reflux-related conditions are worthy of specific mention and discussion. These conditions include granulomas, paroxysmal laryngospasm, polypoid degeneration, laryngeal stenosis, carcinoma of the larynx, and reflux and functional voice disorders.


The etiology of laryngeal granulomas is multifactorial, but LPR should always be suspected as possibly playing a role. Granulomas can occur as a result of the combination of acute mucosal ulceration of the vocal process, LPR, and chronic vocal trauma caused by throat clearing and/or a hard glottal attack. (1,7,39-47) By itself, chronic vocal trauma can lead to vocal fold ulcers and granulomas, but LPR is a cofactor in most cases. The clinician should consider each of the possible contributing etiologic factors and correct each if therapy is to be effective. In the case of granulomas, effective antireflux therapy is sufficient to allow for healing in most patients, as long as vocally abusive behaviors also are corrected. (40,41)

Paroxysmal laryngospasm

Laryngospasm is an uncommon complaint, but patients who experience this frightening symptom are usually able to describe events in vivid detail. (6,49-51) If the clinician mimics the characteristics of severe inspiratory stridor, the patient will confirm that his or her breathing during an attack does sound similar. Laryngospasm is often paroxysmal, and it usually occurs without warning. An attack wakes some patients from their sleep. In other cases, attacks occur during the day. In some cases, the attacks have a predictable pattern--for example, during exercise. Some patients are aware of a relationship between LPR and their laryngospasm attacks, while others are not. (49) In our experience, most patients with paroxysmal laryngospasm respond well to antireflux therapy; antireflux surgery (fundoplication) is sometimes necessary for patients who fail medical treatment. (7,49,50)

In a canine model, Loughlin et al showed that chemoreceptors on the epiglottis responded to acid stimulation at a pH level of 2.5 or less by triggering reflex laryngospasm. (50) The afferent limb of this reflex is supplied by the superior laryngeal nerve; nerve interruption abolished the laryngospasm reflex. (50)

LPR-induced laryngospasm can also be associated with paradoxical vocal fold movement and even with sudden infant death syndrome. (86-92) These areas clearly deserve further research.

Polypoid degeneration

Polypoid degeneration (Reinke's edema) occurs as a result of chronic laryngeal irritation over a period of many years. It is usually bilateral and occurs most often in elderly women who smoke. It is also seen in nonsmoking patients with LPR and/or hypothyroidism.

Polypoid degeneration can improve with antireflux therapy and smoking cessation, but most patients with these lesions require surgical treatment. It is interesting to note that this group of patients has been reported to have a very high incidence (41%) of prolonged (>4 wk) postoperative dysphonia. (5) This, in part, might have to do with continued (or inadequately treated) LPR after surgery.

Most patients with polypoid degeneration have abnormal findings on pH monitoring (pH-metry). (1) Consequently, LPR should be considered in the differential diagnosis. At the very least, patients who undergo vocal fold surgery for this condition should receive intense antireflux treatment prior to surgery and during the perioperative period.

Laryngeal stenosis

LPR is the primary cause of subglottic (figure 2) and posterior glottic stenosis. (1,3,6,13-32) Chronic, intermittent, or chronic-intermittent LPR can cause, or indefinitely perpetuate, laryngeal inflammation. It has been shown in a canine model that intermittent (three times per week only) applications of acid and pepsin to the subglottic region following mucosal injury results in nonhealing ulceration of the cricoid and in subglottic stenosis. (24) LPR documented by pH-metry has been found in 92% of stenosis cases. (6) In our experience, aggressive antireflux treatment coupled with gentle precision surgical intervention is highly effective in the care of these patients.

Carcinoma of the larynx

The most important risk factors for the development of laryngeal carcinoma are tobacco and alcohol use, but LPR also appears to be an important cofactor, especially in nonsmokers. (1,6,33-38) Koufman reported 31 consecutive cases of laryngeal carcinoma; LPR was documented in 84%, but only 58% overall were active smokers. (6) The exact relationship between LPR and malignant degeneration remains to be proved, but the available [blank.sub.p.H]-metry data suggest that most patients who develop laryngeal malignancy both smoke and have LPR. (33) In addition, leukoplakia and other premalignant-appearing lesions can resolve or partially regress with antireflux therapy. (6)

Tobacco and alcohol adversely influence almost all of the body's antireflux mechanisms. They delay gastric emptying, they decrease both upper and lower esophageal sphincter pressures and esophageal motility, they decrease mucosal resistance, and they increase gastric acid secretion. As a result, smokers and frequent drinkers are strongly predisposed to reflux. The use of [blank.sub.p.H]-metry, followed by antireflux treatment, is recommended for all patients who have laryngeal neoplasia, regardless of the presence or absence of other risk factors. (6,33).

Reflux and functional (nonorganic) voice disorders

The term functional voice disorder applies to a variety of vocal abuse, misuse, and overuse syndromes. These conditions are also called muscle tension dysphonias, because abnormal patterns of laryngeal biomechanics are seen on fiberoptic laryngoscopy. The most common pattern is supraglottic contraction--either anteroposterior contraction (foreshortening of the vocal folds), false vocal fold approximation/compression (plica ventricularis), or both. (52-44)

Functional voice disorders are often associated with the secondary development of histopathologic changes in the vocal folds--including hematomas, nodules, ulcers, granulomas, and Reinke's edema. Some [blank.sub.p.H]-metry data suggest that 70% of patients with these functional lesions have LPR in addition to abnormal laryngeal biomechanics. (1,52) In our experience, antireflux treatment will resolve vocal fold nodules in many patients who have LPR.

Clinical manifestations reported to be related to LPR

Type of mainfestation Reference

 Reflux laryngitis 1-12
 Subglottic and tracheal stenosis 1,3,6,13-32
 Carcinoma of the larynx 1,6,33-38
 Endotracheal intubation injury 6,28
 Contact ulcers and granulomas 1,7,39-47
 Posterior glottic stenosis 6,24
 Arytenoid fixation 47,48
 Paroxysmal laryngospasm 6,49-51
 Paradoxical vocal fold movement 52-54
 Vocal fold nodules 1,22,55
 Polypoid degeneration 1,56
 Laryngomalacia 57-61
 Recurrent respiratory papillomas 1,62
 Pachydermia laryngis 2,6,11
 Recurrent leukoplakia 6

 Globus pharyngeus 4,6,47,63-66
 Chronic sore throat 6,47,66
 Dysphagia 6,47,66
 Zenker's diverticulum 67

 Chronic cough 68-71
 Exacerbation of asthma/COPD * 68,69,72-82
 Bronchiectasis 68,69
 Aspiration pneumonia 83-85

 Sudden infant death syndrome 86-92
 Sinusitis 93-97
 Otitis media 98-101
 Obstructive sleep apnea syndrome 102,103
 Dental erosions 104-106

* Chronic obstructive pulmonary disease.


(1.) Koufman JA, Amin MR, Panetti M. Prevalence of reflux in 113 consecutive patients with laryngeal and voice disorders. Otolaryngol Head Neck Surg 2000;123:385-8.

(2.) Delahunty JE. Acid laryngitis. J Laryngol Otol 1972;86:335-42.

(3.) Bain WM, Harrington JW, Thomas LE, Schaefer SD. Head and neck manifestations of gastroesophageal reflux. Laryngoscope 1983;93:175-9.

(4.) Sataloff RT, Speigel JR, Hawkshaw M, Rosen DC. Gastroesophageal reflux laryngitis. Ear Nose Throat J 1993;72:113-4.

(5.) Koufman JA, Blalock PD. Is voice rest never indicated? J Voice 1989;3:87-91.

(6.) Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): A clinical investigation of 225 patients using ambulatory 24-hour [blank.sub.p.H] monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. Laryngoscope 1991;101(Suppl 53): 1-78.

(7.) Toohill RJ, Kuhn JC. Role of refluxed acid in pathogenesis of laryngeal disorders. Am J Med 1997;103(5A):100S-106S.

(8.) Shaker R, Milbrath M, Ren J, et al. Esophagopharyngeal distribution of refluxed gastric acid in patients with reflux laryngitis. Gastroenterology 1995;109:1575-82.

(9.) AI-Sabbagh G, Wo JM. Supraesophageal manifestations of gastroesophageal reflux disease. Semin Gastrointest Dis 1999;10:113-9.

(10.) Ulualp SO, Toohill RJ, Hoffmann R, Shaker R. Pharyngeal [blank.sub.p.H] monitoring in patients with posterior laryngitis. Otolaryngol Head Neck Surg 1999;120:672-7.

(11.) Ward PH, Berci G. Observations on the pathogenesis of chronic non-specific pharyngitis and laryngitis. Laryngoscope 1982;92:1377-82.

(12.) Wilson JA, White A, von Haacke NP, et al. Gastroesophageal reflux and posterior laryngitis. Ann Otol Rhinol Laryngol 1989;98:405-10.

(13.) Andze GO, Brandt ML, St. Vil D, et al. Diagnosis and treatment of gastroesophageal reflux in 500 children with respiratory symptoms: The value of pH monitoring. J Pediatr Surg 1991;26:295-300.

(14.) Bauman NM, Oyos TL, Murray DJ, et al, Postoperative care following single-stage laryngotracheoplasty. Ann Otol Rhinol Laryngol 1996;105:317-22.

(15.) Boyle JT. Gastroesophageal reflux disease in the pediatric patient. Gastroenterol Clin North Am 1989;18:315-37.

(16.) Contencin P, Maurage C, Ployct MJ, et al. Gastroesophageal reflux and ENT disorders in childhood. Int J Pediatr Otorhinolaryngol 1995;32(Suppl):S135-44.

(17.) Gray S, Miller R, Myer CM III, Cotton RT. Adjunctive measures for successful laryngotracheal reconstruction. Ann Otol Rhinol Laryngol 1987;96:509-13.

(18.) Halstead LA. Gastroesophageal reflux: A critical factor in pediatric subglottic stenosis. Otolaryngol Head Neck Surg 1999;120:683-8.

(19.) Halstead LA. Role of gastroesophageal reflux in pediatric upper airway disorders. Otolaryngol Head Neck Surg 1999;120:208-14.

(20.) Fligny I, Francois M, Aigrain Y, et al. [Subglottic stenosis and gastroesophageal reflux]. Ann Otolaryngol Chir Cervicofac 1989; 106: 193-6.

(21.) Jindal JR, Milbrath MM, Shaker R, et al. Gastroesophageal reflux disease as a likely cause of idiopathic subglottic stenosis. Ann Otol Rhinol Laryngol 1994; 103:186-91.

(22.) Koufman J, Sataloff RT, Toohill R. Laryngopharyngeal reflux: (Consensus conference report. J Voice 1996;l0:215-6.

(23.) Hebra A, Hoffman MA. Gastroesophageal reflux in children. Pediatr Clin North Am 1993;40:1233-51.

(24.) Little FB, Koufman JA, Kohut RI, Marshall RB. Effect of gastric acid on the pathogenesis of subglottic stenosis. Ann Otol Rhinol Laryngol 1985;94:516-9.

(25.) Malfroot A, Vandenplas Y, Vernlinden M, et al. Gastroesophageal reflux and unexplained chronic respiratory disease in infants and children. Pediatr Pulmonol 1987;3:208-13.

(26.) Orenstein SR, Orenstein DM, Whitington PF. Gastroesophageal reflux causing stridor. Chest 1983;84:301-2.

(27.) Toohill RJ, Ulualp SO, Shaker R. Evaluation of gastroesophageal reflux in patients with laryngotracheal stenosis. Ann Otol Rhinol Laryngol 1998;107:1010-14.

(28.) Little JP, Matthews BL, Glock MS, et al. Extraesophageal pediatric reflux: 24-hour double-probe pH monitoring in 222 children. Ann Otol Rhinol Laryngol Suppl 1997; 169:1-16.

(29.) Yellon RF, Goldberg H. Update on gastroesophageal reflux disease in pediatric airway disorders. Am J Med 2001; 111(Suppl 8A):78S-84S.

(30.) Burton DM, Pransky SM, Katz RM, et al. Pediatric airway manifestations of gastroesophageal reflux. Ann Otol Rhinol Laryngol 1992;101:742-9.

(31.) Maronian NC, Azadeh H, Waugh P, Hillel A. Association of laryngopharyngeal reflux disease and subglottic stenosis. Ann Otol Rhinol Laryngol 2001;110:606-12.

(32.) Walner DL, Stern Y, Gerber ME, et al. Gastroesophageal reflux in patients with subglottic stenosis. Arch Otolaryngol Head Neck Surg 1998;124:551-5.

(33.) Koufman JA, Burke AJ. The etiology and pathogenesis of laryngeal carcinoma. Otolaryngol Clin North Am 1997;30:1-19.

(34.) Morrison MD. Is chronic gastroesophageal reflux a causative factor in glottic carcinoma? Otolaryngol Head Neck Surg 1988; 99:370-3.

(35.) Ward PH, Hanson DG. Reflux as an etiological factor of carcinoma of the laryngopharynx. Laryngoscope 1988;98: 1195-9.

(36.) Adams J, Heintz P, Gross N, et al. Acid/pepsin promotion of carcinogenesis in the hamster cheek pouch. Arch Otolaryngol Head Neck Surg 2000;126:405-9.

(37.) Freije JE, Beatty TW, Campbell BH, et al. Carcinoma of the larynx in patients with gastroesophageal reflux. Am J Otolaryngol 1996;17:386-90.

(38.) Glanz H, Kleinsasser O. [Chronic laryngitis and carcinoma (author's transl)]. Arch Otorhinolaryngol 1976;212:57-75.

(39.) Cherry J, Margulies SI. Contact ulcer of the larynx. Laryngoscope 1968;78:1937-40.

(40.) Havas TE, Priestley J, Lowinger DS. A management strategy for vocal process granulomas. Laryngoscope 1999;109:301-6.

(41.) Koufman JA. Contact ulcer and granuloma of the larynx. In: Gates GA, ed. Current Therapy in Otolaryngology-Head and Neck Surgery. 5th ed. St. Louis: Mosby, 1994:456-9.

(42.) Emami AJ, Morrison M, Rammage L, Bosch D. Treatment of laryngeal contact ulcers and granulomas: A 12-year retrospective analysis. J Voice 1999;13:612-7.

(43.) Miko TL. Peptic (contact ulcer) granuloma of the larynx. J Clin Pathol 1989;42:800-4.

(44.) Hoffman HT, Overholt E, Karnell M, McCulloch TM. Vocal process granuloma. Head Neck 2001;23:1061-74.

(45.) Ylitalo R, Ramel S. Gastroesophagopharyngeal reflux in patients with contact granuloma: A prospective controlled study. Ann Otol Rhinol Laryngol 2002;111:178-83.

(46.) Haggitt RC. Histopathology of reflux-induced esophageal and supraesophageal injuries. Am J Med 2000;108(Suppl 4a):109S-111S.

(47.) Olson NR. Laryngopharyngeal manifestations of gastroesophageal reflux disease. Otolaryngol Clin North Am 1991;24:1201-13.

(48.) Benjamin B, Roche J. Vocal granuloma, including sclerosis of the arytenoid cartilage: Radiographic findings. Ann Otol Rhinot Laryngol 1993;102:756-60.

(49.) Loughlin CJ, Koufman JA. Paroxysmal laryngospasm secondary to gastroesophageal reflux, Laryngoscope 1996;106:1502-5.

(50.) Loughlin CJ, Koufman JA, Averill DB, et al. Acid-induced laryngospasm in a canine model. Laryngoscope 1996;106:1506-9.

(51.) Bortolotti M. Laryngospasm and reflex central apnoea caused by aspiration of refluxed gastric content in adults. Gut 1989;30:233-8.

(52.) Koufman JA, Blalock PD. Functional voice disorders. Otolaryngol Clin North Am 199l;24:1059-73.

(53.) Koufman JA. Medicine in the vocal arts. N C Med J 1993;54:79-85.

(54.) Ross JA, Noordzji JP, Woo P. Voice disorders in patients with suspected laryngo-pharyngeal reflux disease. J Voice 1998;12: 84-8.

(55.) Kuhn J, Toohill RJ, Ulualp SO, et al. Pharyngeal acid reflux events in patients with vocal cord nodules. Laryngoscope 1998; 108:1146-9.

(56.) Rothstein SG. Reflux and vocal disorders in singers with bulimia. J Voice 1998;12:89-90.

(57.) Belmont JR, Grundfast K. Congenital laryngeal stridor (laryngomalacia): Etiologic factors and associated disorders. Ann Otol Rhinol Laryngol 1984;93:430-7.

(58.) Matthews BL, Little JP, McGuirt WF, Jr., Koufman JA. Reflux in infants with laryngomalacia: Results of 24-hourdouble-probe pH monitoring. Otolaryngol Head Neck Surg 1999;120:860-4.

(59.) Bobin S, Attal P. Laryngotracheal manifestations of gastroesophageal reflux in children. Pediatr Pulmonol Suppi 1999;18:73-5.

(60.) Giannoni C, Sulek M, Friedman EM, Duncan NO III. Gastroesophageal reflux association with laryngomalacia: A prospective study. Int J Pediatr Otorhinolaryngol 1998;43:11-20.

(61.) Bibi H, Khvolis E, Shoseyov D, et al. The prevalence of gastroesophageal reflux in children with tracheomalacia and laryngomalacia. Chest 2001;119:409-13.

(62.) Borkowski G, Sommer P, Stark T, et al. Recurrent respiratory papillomatosis associated with gastroesophageal reflux disease in children. Eur Arch Otorhinolaryngol 1999;256:370-2.

(63.) Smit CF, van Leeuwen JA, Mathus-Vliegen LM, et al. Gastropharyngeal and gastroesophageal reflux in globus and hoarseness. Arch Otolaryngol Head Neck Surg 2000;126:827-30.

(64.) Ossakow SJ, Elta G, Colturi T, et al. Esophageal reflux and dysmotility as the basis for persistent cervical symptoms. Ann Otol Rhinol Laryngol 1987;96:387-92,

(65.) Hill J, Stuart RC, Fung HK, et al. Gastroesophageal reflux, motility disorders, and psychological profiles in the etiology of globus pharyngis. Laryngoscope 1997;107:1373-7.

(66.) Issing WJ, Gross M, Tauber S. [Manifestations of gastroesophageal reflux in the otorhinolaryngology tract]. Laryngorhinootologie 2001;80:464-9.

(67.) Feussner H, Siewert JR. Zenker's diverticulum and reflux. Hepatogastroenterology 1992;39:100-4.

(68.) Harding SM, Richter JE. The role of gastroesophageal reflux in chronic cough and asthma. Chest 1997;111:1389-402.

(69.) Sontag SJ, O'Connell S, Khandelwal S, et al. Most asthmatics have gastroesophageal reflux with or without bronchodilator therapy. Gastroenterology 1990;99:613-20.

(70.) HarperPC, Bergner A, Kaye MD. Antireflux treatment in asthma. Improvement in patients with associated gastroesophageal reflux. Ann Intern Med 1987;147:56-60.

(71.) Holinger LD, Sandcrs AD. Chronic cough in infants and children: An update. Laryngoscope 1991;101:596-605.

(72.) Mays EE, Dubois JJ, Hamilton GB. Pulmonary fibrosis associated with tracheobronchial aspiration: A study of the frequency of hiatal hernia and gastroesophageal reflux in interstitial pulmonary fibrosis of obscure etiology. Chest 1976;69:512-15.

(73.) Euler AR, Byrne WJ, Ament ME, et al. Recurrent pulmonary disease in children: A complication of gastroesophageal reflux. Pediatrics 1979;63:47-51.

(74.) Allen JL, Wohl ME. Pulmonary function in older children and young adults with gastroesophageal reflux. Clin Pediatr (Phila) 1986;25:541-6.

(75.) Dai AG, Liang YK, Liu QL. [Application of radionuclide gastroesophageal reflux imaging in patients with chronic bronchitis and asthma]. Zhonghua Jie He He Hu Xi Za Zhi 1994;17:227-9, 255.

(76.) David P, Denis P, Nouvet G, et al. [Lung function and gastroesophageal reflux during chronic bronchitis (author's transl)]. Bull Eur Physiopathol Respir 1982;18:81-6.

(77.) Ducolone A, Vandevenne A, Jouin H, et al. [Gastroesophageal reflux in asthmatic and chronic bronchitis patients]. Allerg Immunol (Paris) 1988;20:218-25.

(78.) Irwin RS, Corrao WM, Pratter MR. Chronic persistent cough in the adult: The spectrum and frequency of causes and successful outcome of specific therapy. Am Rev Respir Dis 1981;123:413-7.

(79.) Kanazawa M. [Gastroesophageal reflux and airway disease]. Nippon Geka Gakkai Zasshi 1997;98:936-41.

(80.) Kardos P. Gebhardt T. [Chronic persistent cough in general practice: Diagnosis and therapy in 329 patients over the course of 2 years]. Pneumologie 1996;50:437-41.

(81.) Keller R, Breitenbucher A. [Gastroesophageal reflux and lung diseases]. Pneumologie 1990;44(Suppl 1):153-7.

(82.) Mansfield LE. Gastroesophageal reflux and respiratory disorders: A review. Ann Allergy 1989;62:158-63.

(83.) Bestetti A, Carola F, Carnevali-Ricci P, et al. 99mTc-sulfur colloid gastroesophageal scintigraphy with late lung imaging to evaluate patients with posterior laryngitis. J Nucl Med 2000;41:1597-602.

(84.) Kinni ME, Stout MM. Aspiration pneumonitis: Predisposing conditions and prevention. J Oral Maxillofac Surg 1986;44:378-84.

(85.) Crausaz FM, Favez G. Aspiration of solid food particles into lungs of patients with gastroesophageal reflux and chronic bronchial disease. Chest 1988;93:376-8.

(86.) Wetmore RF. Effects of acid on the larynx of the maturing rabbit and their possible significance to the sudden infant death syndrome. Laryngoscope 1993;103:1242-54.

(87.) Lanier B, Richardson MA, Cummings C. Effect of hypoxia on laryngeal reflex apnea--implications for sudden infant death. Otolaryngol Head Neck Surg 1983;91:597-604.

(88.) Schan CA, Harding SM, Haile JM, et al. Gastroesophageal reflux-induced bronchoconstriction. An intraesophageal acid infusion study using state-of-the-art technology. Chest 1994;106:731-7.

(89.) Duke SG, Postma GN, MeGuirt WF, Jr., et al. Laryngospasm and diaphragmatic arrest in immature dogs after laryngeal acid exposure: A possible model for sudden infant death syndrome. Ann Otol Rhinol Laryngol 2001;l10:729-33,

(90.) Page M, Jeffery H. The role of gastro-oesophageal reflux in the aetiology of SIDS. Early Hum Dev 2000;59:127-49.

(91.) Faure C, Leluyer B, Aujard Y, et al. [Sleeping position, prevention of sudden death syndrome and gastroesophageal reflux]. Arch Pediatr 1996;3:598-601.

(92.) Gorrotxategi P, Eizaguirre I, Saenz de Ugarte A, et al. Characteristics of continuous esophageal pH-metering in infants with gastroesophageal reflux and apparent life-threatening events. Eur J Pediatr Surg 1995;5:136-8.

(93.) Ulualp SO, Toohill RJ, Hoffmann R, Shaker R. Possible relationship of gastroesophagopharyngeal acid reflux with pathogenesis of chronic sinusitis. Am J Rhinol 1999;13:197-202.

(94.) Barbero GJ. Gastroesophageal reflux and upper airway disease. Otolaryngol Clin North Am 1996;29:27-38.

(95.) Bouchard S, Lallier M, Yazbeck S, Bensoussan A. The otolaryngologic manifestations of gastroesophageal reflux: When is a pH study indicated? J Pediatr Surg 1999;34:1053-6.

(96.) DiBaise JK, Olusola BF, Huerter JV, Quigley EM. Role of GERD in chronic resistant sinusitis: A prospective, open label, pilot trial. Am J Gastroenterol 2002;97:843-50.

(97.) Bothwell MR, Parsons DS, Talbot A, et al. Outcome of reflux therapy on pediatric chronic sinusitis. Otolaryngol Head Neck Surg 1999;121:255-62.

(98.) Rozmanic V. Velepic M, Ahel V, et al. Prolonged esophageal pH monitoring in the evaluation of gastroesophageal reflux in children with chronic tubotympanal disorders. J Pediatr Gastroenterol Nutr 2002;34:278-80.

(99.) Tasker A, Dettmar PW, Panetti M, et al. Reflux of gastric juice and glue ear in children [letter]. Lancet 2002;359:493.

(100.) Poelmans J, Tack J, Feenstra L. Chronic middle ear disease and gastroesophageal reflux disease: A causal relation? Otol Neurotol 2001;22:447-50.

(101.) Velepic M, Rozmanic V, Velepic M, Bonifacic M. Gastroesophageal reflux, allergy and chronic tubotympanal disorders in children. Int J Pediatr Otorhinolaryngol 2000;55:187-90.

(102.) Suganuma N, Shigedo Y, Adachi H, et al. Association of gastroesophageal reflux disease with weight gain and apnea, and their disturbance on sleep. Psychiatry Clin Neurosci 2001;55:255-6.

(103.) Senior BA, Khan M, Schwimmer C, et al. Gastroesophageal reflux and obstructive sleep apnea. Laryngoscope 200l;111:2144-6.

(104.) Ali DA, Brown RS, Rodriguez LO, et al. Dental erosion caused by silent gastroesophageal reflux disease. J Am Dent Assoc 2002;133:734-7.

(105.) Dahshan A, Patel H, Delaney J, et al. Gastroesophageal reflux disease and dental erosion in children. J Pediatr 2002;140:474-8.

(106.) Gregory-Head BL, Curtis DA, Kim L, Cello J. Evaluation of dental erosion in patients with gastroesophageal reflux disease. J Prosthet Dent 2000;83:675-80.
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Author:Koufman, James A.
Publication:Ear, Nose and Throat Journal
Geographic Code:1USA
Date:Sep 1, 2002
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