Letters to the Editor - June 15, 2000 - American Academy of Family Physicians

Letters to the Editor

The Role of Alcohol Use in Dyspepsia

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.⁴Therefore, 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.

JEFFREY P. KECK, JR., M.D.
JAMES C. HIGGINS, D.O.
Naval Hospital Jacksonville
Family Practice Department
Jacksonville, FL 32214

REFERENCES

Bazaldua OV, Schneider FD. Evaluation and management of dyspepsia. Am Fam Physician 1999;60: 1773-84,87-8.

Weinberg DS, Kadish SL. The diagnosis and management of gastroesophageal reflux disease. Med Clin North Am 1996;80:411-29.

Eisen GM, Sandler RS, Murray S, Gottfried M. The relationship between gastroesophageal reflux disease and its complications with Barrett's esophagus. Am J Gastroenterol 1997;92:27-31.

Stein MD. Medical consequences of substance abuse. Psychiatr Clin North Am 1999;22:351-70.

Steele GH. Cost-effective management of dyspepsia and gastroesophageal reflux disease. Prim Care 1996;23:561-76.

Tarnawski A, Glick ME, Stachura J, Hollander D, Gergely H. Efficacy of sucralfate and cimetidine in protection of the human gastric mucosa against alcohol injury. Am J Med 1987;83:31-7.

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 studies^2-4suggest 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.

ORALIA V. BAZALDUA, PHARM.D., B.C.P.S.
DAVID SCHNEIDER, M.D., M.S.P.H.
GLENN W. W. GROSS, M.D.
The University of Texas Health Science Center in San Antonio
San Antonio, TX 78284

REFERENCES

Bazaldua OV, Schneider FD. Evaluation and management of dyspepsia. Am Fam Physician 1999;60: 1773-84,87-8.

Nandurkar S, Talley NJ, Xia H, Mitchell H, Hazel S, Jones M. Dyspepsia in the community is linked to smoking and aspirin use but not to Helicobacter pylori infection. Arch Intern Med 1998;158:1427-33.

Talley NJ, Zinsmeister AR, Schleck CD, Melton LJ 3rd. Smoking, alcohol, and analgesics in dyspepsia and among dyspepsia subgroups: lack of an association in a community. Gut 1994;35:619-24.

Talley NJ, McNeil D, Piper DW. Environmental factors and chronic unexplained dyspepsia. Association with acetaminophen but not other analgesics, alcohol, coffee, tea, or smoking. Dig Dis Sci 1988; 33:641-8.

Uppal R, Lateef SK, Korsten MA, Paronetto F, Lieber CS. Chronic alcoholic gastritis. Roles of alcohol and Helicobacter pylori. Arch Intern Med 1991; 151:760-4.

Weinberg DS, Kadish SL. The diagnosis and management of gastroesophageal reflux disease. Med Clin North Am 1996;80:411-29.

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Corrections

The "Clinical Quiz" in the February 1, 2000, issue (page 628) contained an error in the answer to Question 19, pertaining to the article entitled "Managing Pain in the Dying Patient." The correct answers to Q19 are B and C. Respiratory depression, which is choice D, is not a common side effect of opioids.

An item in "Tips from Other Journals," entitled "Efficacy and Safety of Therapy for Human Scabies Infestation" (January 15, 2000, page 513) contained a dosage error in the second paragraph. The correct dosage for ivermectin is 150 to 200 µg per kg in 6-mg tablets. In addition, the word "pruritus" was misspelled twice in this item.

The article "Urinary Tract Infections During Pregnancy" (February 1, 2000, page 713) contained an error in a superscript. The first paragraph on page 714, discussing bacteriuria, should have referred to 10⁵ (or 100,000) colony-forming units per mL of urine instead of 105 colony-forming units per mL.

*These corrections have been made to the online version of AFP. The links above will take you to the corrected items, which remain part of the online issues in which they were originally published.

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