BACKGROUND: Squamous cell carcinoma of the laryngopharynx has been linked to laryngopharyngeal reflux disease. Helicobacter pylori corpus gastritis decreases gastric acid secretion and provides some protection against complications of gastroesophageal reflux, including adenocarcinoma of the distal esophagus. The aim of this study was to investigate whether H. pylori infection also protects against laryngopharyngeal carcinoma. METHODS: This was a case-control study comparing patients with histologically confirmed, previously untreated laryngeal or pharyngeal squamous cell carcinomas with cancer-free controls selected from a pool of hospital-based cancer-free controls identified during a similar time period. Each subject completed a self-administered questionnaire that elicited information on age, sex, ethnicity, and tobacco and alcohol consumption. The 120 case subjects were frequency matched to 120 control subjects on age (+/- 5 years), sex, tobacco use, and alcohol use; all subjects were non-Hispanic whites. H. pylori and human papillomavirus type 16 (HPV-16) seropositivity was determined by use of an enzyme-linked immunosorbent assay. RESULTS: The serologic assay was unsuccessful in one case subject and nine control subjects; therefore, 119 case subjects and 111 control subjects were included in the analysis. The proportion of subjects with anti-H. pylori immunoglobulin G was similar between the two groups (32.8% among cases vs 27.0% among controls; p = .342). Although seropositivity was more common in the patients with laryngeal cancer (39.1%) than in the patients with pharyngeal cancer (28.8%), this difference was neither significant (p = .241) nor associated with a significant risk of laryngeal cancer (adjusted odds ratio, 1.53; 95% confidence interval, 0.69-3.41). H. pylori seropositivity was more common among patients who were HPV-16 seronegative (38.2% vs 22.9%, p = .081), and this was particularly true among patients with laryngeal cancer (47.1% vs 18.2%; p = .089). CONCLUSIONS: These results do not show that H. pylori infection either protects against or promotes laryngopharyngeal carcinoma. However, segregation analyses suggested that H. pylori may play a role in laryngeal cancers not associated with HPV-16 infection, and further study in this group is warranted. Copyright 2004 Wiley Periodicals, Inc.
BACKGROUND:Squamous cell carcinoma of the laryngopharynx has been linked to laryngopharyngeal reflux disease. Helicobacter pylori corpus gastritis decreases gastric acid secretion and provides some protection against complications of gastroesophageal reflux, including adenocarcinoma of the distal esophagus. The aim of this study was to investigate whether H. pyloriinfection also protects against laryngopharyngeal carcinoma. METHODS: This was a case-control study comparing patients with histologically confirmed, previously untreated laryngeal or pharyngeal squamous cell carcinomas with cancer-free controls selected from a pool of hospital-based cancer-free controls identified during a similar time period. Each subject completed a self-administered questionnaire that elicited information on age, sex, ethnicity, and tobacco and alcohol consumption. The 120 case subjects were frequency matched to 120 control subjects on age (+/- 5 years), sex, tobacco use, and alcohol use; all subjects were non-Hispanic whites. H. pylori and human papillomavirus type 16 (HPV-16) seropositivity was determined by use of an enzyme-linked immunosorbent assay. RESULTS: The serologic assay was unsuccessful in one case subject and nine control subjects; therefore, 119 case subjects and 111 control subjects were included in the analysis. The proportion of subjects with anti-H. pylori immunoglobulin G was similar between the two groups (32.8% among cases vs 27.0% among controls; p = .342). Although seropositivity was more common in the patients with laryngeal cancer (39.1%) than in the patients with pharyngeal cancer (28.8%), this difference was neither significant (p = .241) nor associated with a significant risk of laryngeal cancer (adjusted odds ratio, 1.53; 95% confidence interval, 0.69-3.41). H. pylori seropositivity was more common among patients who were HPV-16 seronegative (38.2% vs 22.9%, p = .081), and this was particularly true among patients with laryngeal cancer (47.1% vs 18.2%; p = .089). CONCLUSIONS: These results do not show that H. pyloriinfection either protects against or promotes laryngopharyngeal carcinoma. However, segregation analyses suggested that H. pylori may play a role in laryngeal cancers not associated with HPV-16infection, and further study in this group is warranted. Copyright 2004 Wiley Periodicals, Inc.