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Lymphocytic esophagitis (LyE) is a rare condition characterised histologically by high numbers of esophageal intraepithelial lymphocytes without significant granulocytes infiltration, in addition to intercellular edema (“spongiosis”). The clinical significance and natural history of LyE is poorly defined although dysphagia is reportedly the most common symptom. Endoscopic features range from normal appearing esophageal mucosa to features similar to those seen in eosinophilic esophagitis, including esophageal rings, linear furrows, whitish exudates, and esophageal strictures/stenosis. Symptomatic gastroesophageal reflux disease is an inconsistent association. LyE has been associated in paediatric Crohn’s disease, and recently in primary esophageal dysmotility disorder in adults. There are no studies assessing effective treatment strategies for LyE; empirical therapies have included use of proton pump inhibitor and corticosteroids. Esophageal dilatation have been used to manage esophageal strictures. LyE has been reported to run a benign course; however there has been a case of esophageal perforation associated with LyE. Here, we describe the clinical, endoscopic and histopathological features of three patients with lymphocytic esophagitis along with a review of the current literature.

In naive animals the rate of ethanol elimination is dependent on the hepatic alcohol dehydrogenase activity. Carbohydrates have been shown to modify ethanol metabolism by a mechanism that has not been determined. In this study, adult female rats, fed chow diets supplemented with fructose or glucose in their drinking water for 10 days demonstrated significantly greater ethanol elimination rates (4.85 +/- 0.28 and 4.92 +/- 1.56 microM ethanol/min/g liver, respectively) than rats receiving water (3.65 +/- 0.29). The hepatic alcohol dehydrogenase activity of the fructose (1687 +/- 101 nM ethanol/min/g liver) and the glucose (1832 +/- 15)-supplemented rats were not significantly different from that of control rats (1845 +/- 160). Dietary carbohydrate supplementation, therefore, enhanced ethanol elimination, but did not alter the activity of alcohol dehydrogenase. Thus the changes in the ethanol elimination rate following carbohydrate loading were not the consequence of an alteration in hepatic alcohol dehydrogenase.

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