Heidi Rotterdam
Columbia University
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Cancer Causes & Control | 2000
Diana C. Farrow; Thomas L. Vaughan; Carol Sweeney; Marilie D. Gammon; Wong Ho Chow; Harvey A. Risch; Janet L. Stanford; Philip D. Hansten; Susan T. Mayne; Janet B. Schoenberg; Heidi Rotterdam; Habibul Ahsan; A. Brian West; Robert Dubrow; Joseph F. Fraumeni; William J. Blot
AbstractObjective: The incidence of esophageal adenocarcinoma has risen rapidly in the past two decades, for unknown reasons. The goal of this analysis was to determine whether gastroesophageal reflux disease (GERD) or the medications used to treat it are associated with an increased risk of esophageal or gastric cancer, using data from a large population-based case–control study. Methods: Cases were aged 30–79 years, newly diagnosed with esophageal adenocarcinoma (n = 293), esophageal squamous cell carcinoma (n = 221), gastric cardia adenocarcinoma (n = 261), or non-cardia gastric adenocarcinoma (n = 368) in three areas with population-based tumor registries. Controls (n = 695) were chosen by random digit dialing and from Health Care Financing Administration rosters. Data were collected using an in-person structured interview. Results: History of gastric ulcer was associated with an increased risk of non-cardia gastric adenocarcinoma (OR 2.1, 95% CI 1.4–3.2). Risk of esophageal adenocarcinoma increased with frequency of GERD symptoms; the odds ratio in those reporting daily symptoms was 5.5 (95% CI 3.2–9.3). Ever having used H2 blockers was unassociated with esophageal adenocarcinoma risk (OR 0.9, 95% CI 0.5–1.5). The odds ratio was 1.3 (95% CI 0.6–2.8) in long-term (4 or more years) users, but increased to 2.1 (95% CI 0.8–5.6) when use in the 5 years prior to the interview was disregarded. Risk was also modestly increased among users of antacids. Neither GERD symptoms nor use of H2 blockers or antacids was associated with risk of the other three tumor types. Conclusions: Individuals with long-standing GERD are at increased risk of esophageal adenocarcinoma, whether or not the symptoms are treated with H2blockers or antacids.
Clinical Gastroenterology and Hepatology | 2005
Katrina F. Trivers; Anneclaire J. De Roos; Marilie D. Gammon; Thomas L. Vaughan; Harvey A. Risch; Andrew F. Olshan; Janet B. Schoenberg; Susan T. Mayne; Robert Dubrow; Janet L. Stanford; Page E. Abrahamson; Heidi Rotterdam; A. Brian West; Joseph F. Fraumeni; Wong Ho Chow
BACKGROUND AND AIMS Risk factors for subtypes of esophageal and gastric cancer recently have been identified, but their effect on survival is unknown. METHODS Incident cases (n = 1142) from a population-based case-control study were followed-up from diagnosis (1993-1995) until 2000. Cox regression models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for esophageal and gastric cancer in relation to prediagnostic factors. RESULTS Relative to distant stage, esophageal adenocarcinoma (EA) patients with localized disease had a decreased risk for death (HR, .22; 95% CI, .15-.31), followed by those with regional spread (HR, .32; 95% CI, .23-.45). Similar patterns were seen for the other tumor types. Except for other (non-cardia) gastric adenocarcinomas (OGA), higher household income (> or =15,000 US dollars/y vs. <15,000 US dollars/y) was associated with a 33%-38% decrease in risk for death. Prediagnosis body mass index (BMI) between 25 and 29.9 kg/m 2 was associated with longer survival for EA and OGA patients (EA: HR, .67; 95% CI, .51-.88) vs. BMI <25 kg/m(2). Women with esophageal squamous cell carcinoma (ES) and OGA experienced longer survival compared with men. Age, education, cigarette smoking, alcohol intake, gastroesophageal reflux disease, and nonsteroidal anti-inflammatory drug use did not consistently predict survival. CONCLUSIONS Predictors of lengthened esophageal and gastric cancer survival included higher income (except in OGA), overweight (among EA and OGA patients), and female sex (among ES and OGA patients).
Gastrointestinal Endoscopy | 2000
Peter H. Green; Elizabeth Shane; Heidi Rotterdam; Kenneth A. Forde; Lionel Grossbard
BACKGROUND Endoscopy provides an opportunity to diagnose unsuspected celiac disease. METHODS We prospectively identified patients undergoing endoscopy for reasons other than the evaluation of diarrhea or suspected malabsorption, who had endoscopic signs in the duodenum suggestive of celiac disease and in whom villous atrophy was confirmed. Patients were assessed for nutritional deficiencies, reduced bone density, parameters of calcium metabolism, and malignancies. RESULTS Nine patients (3 women and 6 men) were identified among 1749 patients undergoing endoscopy between January 1990 and May 1998, representing a rate of unsuspected celiac disease of 1 per 194 endoscopies. The duodenal abnormalities were as follows: reduced or absent folds in 6, scalloped folds in 5, mosaic appearance in 3, and mucosal fissures in 2. Assessment revealed iron deficiency in 5, folate deficiency in 1, osteopenia in 4, osteoporosis in 1, and hypocalciuria in 4. Three had malignancies associated with celiac disease, 2 esophageal squamous carcinomas, and 1 jejunal adenocarcinoma. CONCLUSIONS Unsuspected celiac disease can be diagnosed at endoscopy by recognition of changes in the duodenum. When detected, patients have one or more manifestations of the disease. Celiac disease is more common in the United States than previously considered and endoscopy provides an opportunity to establish the diagnosis.
Journal of the National Cancer Institute | 1998
Wong Ho Chow; William J. Blot; Thomas L. Vaughan; Harvey A. Risch; Marilie D. Gammon; Janet L. Stanford; Robert Dubrow; Janet B. Schoenberg; Susan T. Mayne; Diana C. Farrow; Habibul Ahsan; A. Brian West; Heidi Rotterdam; Shelley Niwa; Joseph F. Fraumeni
Journal of the National Cancer Institute | 1997
Marilie D. Gammon; Habibul Ahsan; Janet B. Schoenberg; A. Brian West; Heidi Rotterdam; Shelley Niwa; William J. Blot; Harvey A. Risch; Robert Dubrow; Susan T. Mayne; Thomas L. Vaughan; Janet L. Stanford; Diana C. Farrow; Wong-Ho Chow; Joseph F. Fraumeni
Cancer Research | 1998
Wong Ho Chow; Martin J. Blaser; William J. Blot; Marilie D. Gammon; Thomas L. Vaughan; Harvey A. Risch; Guillermo I. Perez-Perez; Janet B. Schoenberg; Janet L. Stanford; Heidi Rotterdam; A. Brian West; Joseph F. Fraumeni
Cancer Epidemiology, Biomarkers & Prevention | 1998
Diana C. Farrow; Thomas L. Vaughan; Philip D. Hansten; Janet L. Stanford; Harvey A. Risch; Marilie D. Gammon; Wong Ho Chow; Robert Dubrow; Habibul Ahsan; Susan T. Mayne; Janet B. Schoenberg; A. Brian West; Heidi Rotterdam; Joseph F. Fraumeni; William J. Blot
Cancer Epidemiology, Biomarkers & Prevention | 2001
Susan T. Mayne; Harvey A. Risch; Robert Dubrow; Wong Ho Chow; Joseph F. Fraumeni; Marilie D. Gammon; Thomas L. Vaughan; Diana C. Farrow; Janet L. Stanford; Janet B. Schoenberg; Habibul Ahsan; Heidi Rotterdam; A. Brian West; William J. Blot
Cancer Epidemiology, Biomarkers & Prevention | 1998
Thomas L. Vaughan; Diana C. Farrow; Philip D. Hansten; Wong Ho Chow; Marilie D. Gammon; Harvey A. Risch; Janet L. Stanford; Janet B. Schoenberg; Susan T. Mayne; Heidi Rotterdam; Robert Dubrow; Habibul Ahsan; A. Brian West; William J. Blot; Joseph F. Fraumeni
Journal of the National Cancer Institute | 2006
Susan T. Mayne; Harvey A. Risch; Robert Dubrow; Wong Ho Chow; Marilie D. Gammon; Thomas L. Vaughan; Lauren Borchardt; Janet B. Schoenberg; Janet L. Stanford; A. Brian West; Heidi Rotterdam; William J. Blot; Joseph F. Fraumeni