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Antacid Drug Use and Risk of Esophageal and Gastric Adenocarcinomas in Los Angeles County

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Antacid Drug Use and Risk of Esophageal and Gastric Adenocarcinomas in Los Angeles County 526 Antacid Drug Use and Risk of Esophageal and Gastric Adenocarcinomas in Los Angeles County Lei Duan,1 Anna H. Wu,2 Jane Sullivan-Halley,1 and Leslie Bernstein1,2 1City of Hope National Medical Center, Duarte, California and 2Department of Preventive Medicine, Keck School of Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, California Abstract Objectives: Concern has been expressed that antacid among persons with no UGI disorder than among drugs increase the risk of esophageal and gastric those with an UGI disorder (homogeneity of trends adenocarcinomas. P = 0.07). Regular use of nonprescription acid Methods: This population-based case-control study neutralizing agents was not associated with risk of recruited patients with incident esophageal adeno- adenocarcinomas of the gastric cardia or distal carcinoma (n = 220), gastric cardiac adenocarcinoma stomach. Regular use of prescription acid suppressive (n = 277), or distal gastric adenocarcinoma (n = 441) drugs was not associated with risk for any of these diagnosed between 1992 and 1997, and 1,356 control cancers. participants in Los Angeles County. Unconditional Conclusion: We found risk of esophageal adenocarci- polychotomous multivariable logistic regression anal- noma was greater among long-term nonprescription yses were done to evaluate the association between acid neutralizing drugs in participants without physi- antacid drug use and these cancers. cian-diagnosed UGI conditions than among those with Results: Among participants who took nonprescription these conditions; this may represent self medication for acid neutralizing agents for >3 years, the odds ratio for undiagnosed precursor conditions or it may be that esophageal adenocarcinoma was 6.32 compared with nonprescription acid neutralizing drugs, taken without P never users (95% confidence interval, 3.14-12.69; trend limitation on amount used when symptoms are most < 0.01). Analyses stratified by history of physician intense, may permit alkaline bile reflux into the lower diagnosed upper gastrointestinal (UGI) disorders esophagus, thereby increasing esophageal adenocarci- revealed a greater increase in esophageal adenocarci- noma risk. (Cancer Epidemiol Biomarkers Prev noma risk associated with nonprescription antacid use 2009;18(2):526–33) Introduction Histamine2-receptor antagonists and proton pump are significantly more effective than H2-receptor antag- inhibitors (PPI) were introduced to the market, in the onists in reducing gastric acid secretion. These drugs late 1970s and 1980s, correspondingly, and became do not permanently change the acid milieu; although widely used in the treatment of acid-peptic disorders they raise gastric pH and provide rapid relief of such as peptic ulcer disease, gastresophageal reflux symptoms; evidence of this impermanence is that disease (GERD), and acute stress ulcers. H2-receptor erosive esophagitis recurs in most patients within 6 antagonists are competitive inhibitors of histamine months after discontinuing the drug therapy (3). binding at the parietal cell H2 receptor. Gastric acid Therefore, chronic maintenance therapy is generally secretion is suppressed if the parietal cell H2 receptor is required. Although today, some doses of these drugs not bound with histamine in the stomach (1). PPIs are available without prescription, initially all required suppress gastric acid secretion by irreversibly blocking prescription. the hydrogen/potassium adenosine triphosphatase en- Some concerns have been expressed that long term zyme system of the gastric parietal cell (2). Because gastric acid suppression, particularly by H2-receptor PPIs target the terminal-step in acid production, they antagonists, may be associated with increased risk of esophageal and gastric adenocarcinomas (4). Some epidemiologic studies, both prospective studies and retrospective studies, have attempted to evaluate associ- Received 8/18/08; revised 10/3/08; accepted 11/4/08; published OnlineFirst 02/03/2009. ations of H2-receptor antagonists and PPIs with esoph- Grant support: 3RT-0122 and 10RT-0251 from the California Tobacco Related ageal and gastric adenocarcinoma risk (5-15), but the Research Program, grant CA59636 from the National Cancer Institute, and NIEHS results have not been consistent. Although some inves- Grant 5P30 ES07048. Incident cancer cases for this study were collected by the University of Southern California Cancer Surveillance Program, which is supported tigators have reported positive associations between under subcontract by the California Department of Health. The Cancer Surveillance antacid drug use and increased risk of gastric cancer Program is also part of the National Cancer Institute’s Division of Cancer Prevention and Control Surveillance, Epidemiology, and End Results Program, under contract (8, 11, 14) or esophageal cancer (12, 15), others find no number N01CN25403. effect (5, 7, 9, 13). Only one study stratified participants Requests for reprints: Leslie Bernstein, Division of Cancer Etiology, Department of according to whether or not they had severe GERD (7). Population Sciences, City of Hope National Medical Center, 1500 East Duarte Road, Duarte, CA 91010. Phone: 626-471-7315; Fax: 626-471-7308. E-mail: [email protected] It is important to consider the effect of GERD when Copyright D 2009 American Association for Cancer Research. examining the association between antacid use and risk doi:10.1158/1055-9965.EPI-08-0764 of esophageal and gastric adenocarcinomas because Cancer Epidemiol Biomarkers Prev 2009;18(2). February 2009 Downloaded from cebp.aacrjournals.org on September 26, 2021. © 2009 American Association for Cancer Research. Cancer Epidemiology, Biomarkers & Prevention 527 GERD itself is a strong independent risk factor for interview queried general background information adenocarcinomas of the esophagus and gastric cardia such as ethnicity, marital status, birthplace, highest (5, 7, 9, 16). level of education, smoking history, lifetime use of all We have explored the association between use of types of alcoholic beverages, usual diet, weight at ages antaciddrugsandriskofesophagealandgastric 20 and 40 y and on the reference date, and height. In adenocarcinomas using data from a large population- addition, we asked detailed questions regarding per- based case-control study conducted among residents of sonal and family history of various nonmalignant Los Angeles County. To understand any observed diseases. association better and to assess confounding of results We explicitly asked about 26 over-the-counter (OTC) by indication for use of the drug, we have investigated and 19 prescription brand name antacid and related the relationship separately in groups with a history of drugs in the questionnaire. For each of the listed upper gastrointestinal (UGI) disorders and those without medications, we first asked the participants whether such a history. they had ever used the drug before their reference date. If the answer was ‘‘no’’, the participant was classified as a nonuser. If the answer was ‘‘yes’’, the participant was Materials and Methods asked if he or she had ever taken the drug two or more times a week for one month or longer. If the answer was Study Population. The details of the study popula- no, the participant was classified as an ‘‘irregular user’’. tion and study design have been described elsewhere Otherwise, the participant was defined as a ‘‘regular (16-21). Basically, incident cancer cases for this study user’’ and was asked further about ages at first and last were identified by the University of Southern Califor- use, duration of use, usual frequency and dosage of use, nia Cancer Surveillance Program. This cancer registry and the primary reason for each use. We also asked the covers the ethnically diverse Los Angeles County participants if they had used any medications that were population of >9.5 million people. Case patients who not on our list and recorded the drug name and details of were newly diagnosed with first incident esophageal use if the participant had used the medication ‘‘regular- adenocarcinoma (GCA; International Classification of ly’’. All of the antacid medications in the study were Disease for Oncology code C15.0-C15.9), gastric cardiac categorized as requiring a prescription or as nonpre- adenocarcinoma (GCA; International Classification of scription (OTC). At the time the study was conducted, Disease for Oncology code C16.0), or distal gastric nonprescription (OTC) antacid drugs were limited to adenocarcinoma (DGA; International Classification of acid neutralizing agents (e.g., Tums, Pepto-Bismol, and Disease for Oncology codes C16.1-C16.6 and C16.8- Maalox); the majority of prescription antacids at that time C16.9) between 1992 and 1997 were identified and were H2-receptor antagonists. Only a very small number contacted for participation. Control participants were of participants reported use of the PPI, which also matched individually to each case patient on sex, race, required a prescription. age (F5 y), and neighborhood of residence. To increase To assess medical history, we provided a list of the statistical power, we sought two control partic- diseases, including heart disease, gastrointestinal tract ipants for each case patient whenever possible. Of the disorders, and diabetes, and asked if the participant 938 case patients interviewed, 523 had one control had any of those conditions diagnosed by a physician participants, 381 had 2 or more control participants, before the
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