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Am Fam Physician. 2000;61(12):3564-3567

to the editor: We found the article “Evaluation and Management of Dyspepsia,”1 to be a comprehensive review of this condition. However, an apparent oversight was the lack of discussion related to alcohol and its contribution to dyspepsia. Alcohol is only listed twice in the article—first in a table of agents causing dyspepsia and second in another table as a risk factor for chronic pancreatitis.1 The use of alcohol is implicated in many other gastrointestinal complaints, including but not limited to gastroesophageal reflux disease (GERD), peptic ulcer disease, gastric adenocarcinoma, acute and chronic pancreatitis and liver disease. Therefore, we feel the issue of alcohol use is significant in any discussion of dyspepsia.

First, alcohol can reduce lower esophageal sphincter (LES) tone.2 By lowering LES tone, alcohol facilitates the onset of different disease processes, first and foremost, GERD. In turn, GERD can progress to reflux esophagitis and finally, Barrett's metaplasia of the esophagus.3 Barrett's metaplasia can eventually lead to stricture. All of these disease processes could present as “dyspepsia.” Alcohol also slows gastric emptying.4 Slower gastric emptying, or gastroparesis (also defined as dysmotility dyspepsia) will present as bloating and abdominal distension.1

A third mechanism by which alcohol affects the gastrointestinal system is stimulation of gastric secretions.5 By stimulating acid production, alcohol contributes to what the article described as structural dyspepsia. Hyperacidity not only plays a role in the exacerbation of GERD, it also damages the gastric mucosa, leading to peptic ulcer disease, and gastric adenocarcinoma.6 Last, alcohol can directly injure gastric mucosa. Chronic exposure of alcohol to the mucosa leads to chronic alcoholic gastritis.4 Alcoholic gastritis, just like gastritis induced by nonsteroidal anti-inflammatory drugs (NSAIDs) or other drugs, will present as dyspepsia.

The 30 percent prevalence of alcohol abuse in society is substantial.4 Therefore, we feel that the inclusion of an alcohol history is warranted in the evaluation of a patient for dyspepsia. Taking a directed history for the use of alcohol to include the amount and the type of alcohol consumed, administering the “CAGE” questionnaire and assessing other risk factors for alcohol abuse and any family history of alcohol abuse is imperative. Although dyspepsia can present as reflux, ulcer, dysmotility or functional types, it is obvious that alcohol is directly related to each of these pathophysiologic processes.5 Thus, we feel it plays a key role in the evaluation of dyspepsia.

in reply: We appreciate the interest in our article “Evaluation and Management of Dyspepsia”1 and acknowledge the concern regarding the minimal discussion of alcohol and its contribution to dyspepsia. However, the lack of discussion related to alcohol and its contribution to dyspepsia was not an oversight but, rather, an evidence-based decision.

At the very least, the link between alcohol and dyspepsia is controversial. Three studies24 suggest that alcohol may not be an important risk factor for dyspepsia in the community. The reference supporting alcohol as the cause of chronic alcoholic gastritis states just the opposite, “there was no change in histologic findings . . . indicating that alcohol itself was not a major causative agent . . . our data suggest that H. pylori, rather than alcohol, causes chronic gastritis in alcoholics.”5

In the review article referenced by Drs. Keck and Higgins, the authors state that alcohol lowers esophageal sphincter pressure, reduces acid clearance and alters esophageal epithelial function.6 While encouraging lifestyle modifications is recommended in patients with GERD, the authors also admit that no controlled studies have specifically evaluated the effect of such modifications.

Because recommendations of lifestyle modifications are all well founded based on the current understanding of the physiologic determinants of reflux, we believe that they provide at least theoretic benefit but are not strongly supported by the evidence in the literature. It should be recognized that data do not implicate alcohol (in moderation) in peptic ulcer disease, although intuitively it seems it cannot be helpful.

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This series is coordinated by Kenny Lin, MD, MPH, deputy editor.

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