© 2005 Oxford University Press
CORRESPONDENCE |
RESPONSE: Re: The Role of Overdiagnosis and Reclassification in the Marked Increase of Esophageal Adenocarcinoma Incidence
Affiliation of author: Department of Gastroenterology and Hepatology, Charite Campus Virchow, Universitaetsklinikum Berlin, Mittelallee 11, 13344 Berlin, Germany (HP); Dartmouth College, VA Outcomes Group, White River Junction, VT (HGW)
Correspondence to: H. Gilbert Welch, MD, MPH, Dartmouth College, VA Outcomes Group (111B), VAMC215 North Main Street, White River Junction, VT 05009 (e-mail: h.gilbert.welch{at}dartmouth.edu).
We thank Dr. Forman for his interest in our study and appreciate his comments. Dr. Forman suggests that there are two reasons why changes in the classification of stomach cancers near the gastroesophageal junction may have led us to overstate the observed increase in esophageal adenocarcinoma.
First, he argues that because adenocarcinoma of the cardia and the esophagus cannot be reliably distinguished microscopically, the two sites should be combined when making comparisons over time. Although the distinction between adenocarcinoma of the cardia and the esophagus can be difficult, the presence of Barrett's epithelium may help to make the distinction, as will the macroscopic description by the gastroenterologist or the surgeon. Furthermore, if misclassification were common, then the distinctions between the two cancers in epidemiologic and etiologic studies would not be made. The incidence ratios of men to women and whites to blacks (1) are different for esophageal adenocarcinoma and adenocarcinoma of the cardia. Gastroesophageal reflux disease (2) and obesity (3) are strong risk factors for esophageal adenocarcinoma but are weak risk factors for cardia adenocarcinoma. Although the absence of Helicobacter pylori infection appears to be associated with an increased risk for esophageal adenocarcinoma, it is not associated with cardia adenocarcinoma (4). Thus, we find it hard to accept the idea that the two cancers cannot be reasonably well distinguished and must, therefore, be combined.
Second, Dr. Forman suggests that the falling incidence of unspecified gastric cancers may have contributed to a spurious rise in cancers of the gastroesophageal junction. However, the decrease in unspecified gastric cancer may also relate to the falling incidence of gastric cancer in general. This decrease in gastric cancer incidence began more than 50 years ago and preceded the rise in adenocarcinoma of the cardia and of the esophagus by many years, arguing less for a problem of reporting and classification, but perhaps for the presence of a common etiologic factor. This factor may be associated with an increased risk of gastric cancer and a decreased risk of esophageal adenocarcinoma, but its presence may have declined over the past decades. H. pylori infection may present such a factor.
Of course, some portion of the rise in esophageal adenocarcinoma incidence may be due to changes in classification. However, based on our work, we think that this portion is small.
REFERENCES
(1) El-Serag HB, Mason AC, Petersen N, Key CR. Epidemiological differences between adenocarcinoma of the oesophagus and adenocarcinoma of the cardia in the USA. Gut 2002;50:368–72.
(2) Lagergren J, Bergstrom R, Lindgren A, Nyren O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999;340:825–31.
(3) Lagergren J, Bergstrom R, Nyren O. Association between body mass and adenocarcinoma of the esophagus and gastric cardia. Ann Intern Med 1999;130:883–90.
(4) Ye W, Held M, Lagergren J, Engstrand L, Blot WJ, McLaughlin JK, Nyren O. Helicobacter pylori infection and gastric atrophy: Risk of adenocarcinoma and squamous-cell carcinoma of the esophagus and adenocarcinoma of the gastric cardia. J Natl Cancer Inst 2004;96(5):388–96.
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J Natl Cancer Inst 2005 97: 1013-1014.
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