Purpose: Eradicate all manifestations of GERD while monitoring esophageal histology.
Methods: In abstracts to ACG in 2003 and 2005 I reported on 10 cases with regression of specialized intestinal metaplasia (SIM) of the esophagus. There are now 5 more cases, totaling 15 patients in this series. None had dysplasia. All were encouraged to adopt lifestyle changes. The mainstay of pharmacology was proton pump inhibitor (PPI) therapy titrated to eradicate noxious, autonomic effects caused by GERD. The previous 10 cases required PPI daily dose 160 mg to 360 mg; regression in these 5 cases proved more pharmacologically diverse. The daily dose of PPI varied from 30 mg to 360 mg (two cases regressed on 80 mg). One, intolerant of all PPI's, took ranitadine 600 mg daily. All demonstrated normalization of histology.
Results: Fifteen patients previously confirmed to have SIM have regressed at surveillance endoscopy. The clinical course, the endoscopy and the histology are concordant.
Conclusions: Titration of antisecretory therapy is absolutely essential to eliminate noxious signs and symptoms induced by GERD. Doctors Hatlebakk, Katz and Castell reported in 1999, “The oral bioavailability of PPI varies considerably between subjects, by a factor of at least 6 …. The considerable intersubject variation in pharmacologic response means that the clinician must be prepared to individualize the dosage regimen to obtain adequate treatment response in each patient”.
Cough, hoarseness, sore throat and a mirad of detrimental autonomic manifestations are associated with GERD. These findings are consistent with Reilly's Syndrome where vasomotor disorders, increased capillary permeability, edema and lesions of the reticuloendothelial system result from “sympathetic stimulation” with “physical agents.” Regurgitated digestive juices evoke a protective response from the Vagally innervated gastroesophageal junction. Activation of efferent nerve trunks results in aerodigestive tissue responses beyond the endangered esophagus. With successful therapy, chronic Vagal response moderates and normal physiology ensues. The alerted clinician can monitor signs of GERD such as: sternal tenderness to palpation, nasal turbinate hypertrophy, exagerated gag reflex, uvular edema and more. The clinical findings suggest cessation of reflux due to normalized function/physiology of the esophagus.
The 2003 abstract reported a 71% regression rate (5 of 7 cases). I understand the unprescendented nature of the findings. These 15 patients represent a reproducible clinical phenomenon in disease management of GERD and Barrett's Esophagus.