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Reflux Anyone?: First Part


A 32-year-old male came for consult six months ago because of a 3 month history of chronic intermittent cough and hoarseness. He claimed that his voice fatigues near the end of the day. He is a call center agent. He really had no other complaints other than that; specifically, no heartburn, ear pain, difficulty of swallowing, or foreign body sensation. Chest xray was unremarkable. On laryngoscopy, he had normal vocal cord mobility and no suspicious mucosal lesions. There was however extensive erythema of the posterior glottis and inner arytenoid space. My impression then was Laryngopharyngeal reflux disease (LPRD) and I started him on omeprazole 20 mg 2x a day, advised him on dietary modification and reflux precautions. He responded very well to that and on follow up recently, after 3 months, he had complete resolution of symptoms. I maintained him on ranitidine 150 mg 2x a day and reiterated my previous advices.

One of the more common cases I see in my practice is LPRD. Patients come in because of hoarseness, foreign body sensation in the throat, cough that is not relieved by cough preparations and antibiotics, and sometimes, throat pain. They are either a teacher, call center agent, bar singer or a ‘coffee’ addict. In most of them, the LPRD treatment regimen worked and so I think awareness to this disease should be increased, thus this post.

Reflux literally means backflow. It is derived from the Latin words re, meaning back, and fluere, meaning to flow. Everyone experiences physiologic reflux to some degree after eating. Gastroesophageal reflux is defined as backflow of stomach contents into the esophagus. This may be physiologic and actually occurs in normal persons up to 50 times a day. Gastroesophageal reflux disease is GER that is excessive and this results in tissue damage, i.e. esophagitis and or clinical symptoms, i.e. heartburn. Then there is laryngopharyngeal reflux, which is backflow of the stomach contents into the laryngopharynx (throat area) and this consists mainly of acid and activated pepsin. There are prolonged periods of acid exposure in GERD, but not LPR. It is really a short exposure, but has high damage potential. Patients with GERD have dysmotility and prolonged esophageal acid clearance and this is typically not true in LPR patients. Again, the primary defect in GERD is lower esophageal dysfunction while the primary defect in LPR is upper esophageal sphincter dysfunction. Saying all that, it is important to point out that some will have both LPR and GERD.

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