Multiple gastric carcinoids.

Abstract

We read with interest and appreciation the “Images for Surgeons” article by Johnson and colleagues relating to the issue of multiple gastric carcinoids. There is no doubt that current interest in gastric carcinoid tumors remains elevated, reflecting the enigma of the disease, the recognition of the intriguing relationship to gastrin, and the much adumbrated upon yet putative relationship to the longterm use and ubiquitous usage of acid suppressive medication. The article that attracted our attention cited a 1999 publication by Kulke and Mayer noting that gastric carcinoids comprise less than 1% of all gastric neoplasms. Despite its most valuable contribution to the subject, it unfortunately omitted to recognize that a recent review of 13,715 carcinoid cases indicates that this figure may well be a significant underestimate of the “true” percentage of gastric carcinoids. Indeed, it appears from the latter data that the incidence of gastric carcinoids is actually rising—and perhaps precipitously. Whether this reflects increased awareness, a broader use of endoscopy, or an alteration in the pathogenesis of the lesion is unclear and open to debate. Nevertheless, the data bear serious recognition because they represent the largest collection of such information available and are as indubitably valid as material of this nature can be, given that it represents mandated information gathered under a broad-based federal agency directive (National Cancer Institute’s Surveillance, Epidemiology, and End Results [SEER]) established many decades ago. In addition to the 16,710 noncarcinoid gastric cancers registered in the SEER database between 1992 and 1999, there were 292 gastric carcinoids. So 1.77% of gastric neoplasms noted during this period were carcinoids. Interestingly, this represents a 221% increase in incidence from cases registered in the SEER database from 1973 to 1991, and a 491% increase compared with gastric carcinoid incidence rates generated from historical data collected as part of the Third National Cancer Survey (1969–1971). The incidences of gastric carcinoids among all carcinoid tumors in the registry time periods, in chronological order, are 2.41%, 5.76%, and 8.66%. It would seem prudent to consider the increasing incidence of gastric carcinoids among all carcinoids and not overlook this formerly rare and exotic lesion. A further means by which these lesions could be differentiated is to persuade the SEER program directors to include in their categorization scheme a means to differentiate between types I, II, and III gastric carcinoids. This would enable additional and useful epidemiologic data to be extracted from their immense database resource. Johnson and coworkers, in reporting their experience with this case of multiple gastric carcinoids, deserve much credit for drawing attention to this fascinating conundrum of human pathobiology. What is now required is an exploration of the genesis of the disease; ie, what is the mechanism by which elevated gastrin transforms fundic enterochromaffin-like cells from their normal cycle into autonomous proliferating cells independent of gastrin stimulation. Indeed, gastric carcinoid warrants considerable further investigation because it represents a unique human neoplasm in which the endogenous biologic agent responsible for inciting and driving the neoplastic process is identifiable, quantifiable, and open to mechanistic exploration. Despite such issues it should be stressed that the incidence of gastric carcinoids is rising, and of even more significance is the clear recognition that the disease entity is not merely a benign and fascinating oddity, but may represent a cellular icon akin to the Rosetta stone. The mechanistic exploration of this may yield the translation of the biologic basis of cell transformation.