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Effect of low‐proof alcoholic beverages on duodenogastro‐esophageal reflux in health and GERD
Author(s) -
Seidl H.,
Gundling F.,
Schepp W.,
Schmidt T.,
Pehl C.
Publication year - 2011
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1365-2982.2010.01614.x
Subject(s) - wine , white wine , gerd , reflux , medicine , ingestion , alcoholic liver disease , meal , gastroenterology , bile reflux , food science , disease , chemistry , cirrhosis
Background Alcoholic beverages are known to increase acidic gastro‐esophageal reflux (GER) and the risk of esophagitis. Moreover, duodenogastro‐esophageal reflux (DGER), containing bile acids, was shown to harmfully alter the esophageal mucosa, alone and synergistically with HCl and pepsin. However, studies directly addressing potential effects of different low proof alcoholic beverages on DGER in health and disease are missing. Methods Bilitec readings for beer and white, rose, and red wine were obtained in vitro from pure and from mixtures with bile. One‐hour DGER monitoring and pH‐metry were performed in 12 healthy subjects and nine reflux patients with DGER after ingestion of a standardized liquid meal together with 300 mL of water, white wine, and in the volunteers, beer and rose wine. Key Results Bilitec measurement was found to be feasible in the presence of beer, white wine, and using a threshold of 0.25, rose wine. However, the presence of red wine resulted in extinction values above this threshold. The consumption of all investigated alcoholic beverages, especially of white wine, triggered increased acidic GER, both in healthy participants and patients with reflux disease. In contrast, no relevant DGER was found after intake of alcoholic beverages. Conclusions & Inferences Fiber‐optic bilirubin monitoring can be used for DGER monitoring in combination with alcoholic beverages, except with red wine. Low‐proof alcoholic beverages are a strong trigger of GER, but not of DGER, both in healthy subjects and patients with reflux disease.