Mr. G., a fifty-year-old male professional, developed chronic ear problems following a viral respiratory illness last winter. He had the typical prodrome of sore throat and chills followed by intense rhinorrhea and cough. This proved to be a self-limiting illness that required no prescription medications. Subsequently, he noted fullness in both ears leading to hearing loss. A course of amoxicillin therapy failed to resolve these symptoms. A second course of antibiotics with azithromycin was likewise ineffective.
The patient was in good general health and did not smoke. Alcohol was limited to four ounces weekly. There was no history of environmental allergies, pyrosis or chronic sinusitis. He didn’t take any medications on a long-term basis. He was referred to an otolaryngologist for further evaluation of the hearing loss. He also reported long-standing problems on airplane flights with excruciating otalgia and, on one occasion rupture of the eardrum. The examination showed tympanic membrane retractions with fluid in both middle ear cavities. The Rinne test with a 512 Hz tuning fork showed better bone conduction than air conduction, suggesting a conductive hearing loss. These physical findings were confirmed via formal audiometric testing. There was no sensorineural component to the hearing loss.
The patient was significantly distressed by the hearing loss, as it interfered with his ability to function effectively at work. A therapeutic tympanocentesis was offered, which he accepted. This was performed bilaterally using local anesthetic with excellent results. He reported an immediate improvement in hearing.
Unfortunately, our patient was disappointed when symptoms of deafness gradually returned over the next three weeks. There had been no further respiratory illness and he’d been otherwise well. He returned to the specialist for further advice. Audiometric testing confirmed recurrence of fluid with a conductive hearing loss. The patient consented to have a tympanostomy tube implanted unilaterally to improve hearing. Fluid was removed bilaterally again. But the patient hoped for an explanation and long-term cure for his distressing problem.
What is your diagnosis?
A laryngoscopic exam at Mr. G.’s second visit (see case on p. 13) showed closure of the nasopharyngeal opening of the Eustachian tube, some postnasal discharge and marked erythema of the vocal cords. Again, he denied pyrosis or chest discomfort. However, dysphonia was noted. The patient admitted that there had been changes in his lifestyle. He now worked late into the evening consuming his last meal approximately one hour before retiring to sleep. Similarly, he consumed alcohol later in the day as well. He was slim with a BMI of 23 and hadn’t suffered from gastroesophageal reflux disease (GERD).
A diagnosis of extraesophageal reflux disease was made. This entity has also been called laryngopharyngeal reflux disease and silent reflux, as chest discomfort is often absent. Patients usually present with chronic laryngitis, sore throat or cough upon recumbency. Evaluation of gastric HCL production in normal subjects has shown a circadian rhythm with increased production of gastric acid nocturnally, from 8 pm to 4 am.1 There’s also reduced upper and lower esophageal sphincter tone during sleep. This can lead to acid reflux superior to the level of the esophagus. There may be damage to the vocal cords, sore throat, Eustachian tube dysfunction, increased postnasal discharge and bronchospasm, leading to shortness of breath, wheezing and cough. The latter may be neurally mediated without direct contact of refluxate with the tracheobronchial mucosa.2 This condition should be distinguished from GERD, which presents with pyrosis, regurgitation and dyspepsia.
Mr. G. was prescribed the proton pump inhibitor rabeprazole and re-evaluated 2 months later. He’d developed post-tympanostomy tube otorrhea (PTTO), which was managed by instillation of ciprofloxacin and dexamethasone drops. Normal hearing was maintained in the ear with the tympanostomy tube. There was a partial decline in hearing in the other ear but the patient was pleased with the results.
He was apprehensive, though, over the long-term use of PPIs. A recent prospective study by Rozgony et al (2010) reported a significant decline in vitamin B12 levels in seniors on PPIs.3 Gray et al (2010) reported a small increase in vertebral, forearm and wrist fractures and a marginal decline in hip bone mineral density in postmenopausal women using PPIs.4 Two retrospective cohort studies reported an increase in C. difficile infection.5,6 Laheij et al (2004) have reported an increase in community-acquired pneumonia in PPI users.7 Animal studies have shown an association between achlorhydria and bacterial overgrowth, with micronutrient malabsorption due to competition between bacteria and the intestine, as well as hypergastrinemia leading to gastric mucosa hyperplasia and potentially, gastric cancer.8 There’s an age-related increase in the incidence of achlorhydria and gastric cancer in humans as well. PPIs reduce basal and meal time elevations of gastric acid.
The H2-receptor antagonist ranitidine blocks histamine activation of oxyntic (parietal) cells, which occurs in response to meals. Whereas PPIs inactivate the final common pathway for HCL secretion, ranitidine only blocks histamine-stimulated acid secretion, there being at least two other effectors for gastric acid secretion: acetylcholine and gastrin. In spite of rabeprazole’s brief plasma half-life of one hour, its effect upon acid suppression is measurable 24 hours later due to prolonged inactivation of the H/K ATPase system (CPS, 2010).
The patient declined to continue rabeprazole and chose to control symptoms with ranitidine. Finally, he discontinued all medications using lifestyle modifications instead: he did not eat 4 hours prior to sleeping, eliminated caffeine, and slept with his upper body propped upon 3 pillows. This approach proved a success, and at the last meeting with his family doctor, he reported good hearing, with no dysphonia and no nocturnal cough.
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