Multiple gastric carcinoids.

Abstract

We read with great interest in the “Images for Surgeons” section of the Journal the report of a case of “Multiple Gastric Carcinoids” by Johnson and colleagues, followed by the comments by Modlin and coauthors as a letter to the editor. We recently reported a case of multiple gastric carcinoids in a woman with systemic lupus erythematosus. Our case and the review of the literature gave us a new insight into this unusual condition and prompted us to contribute a few comments to the case reported in your journal. Johnson and colleagues described an interesting case of a 62-year-old woman with multiple type I gastric carcinoid tumors. Type I gastric carcinoid is associated with atrophic (autoimmune) gastritis and chronically elevated gastrin production that stimulates enterochromaffin-like cells cells to sequenced gastrointestinal endocrine proliferation, including hyperplasia, dysplasia, and development of carcinoid. Hypergastrinemia alone is probably only effective in causing the development of gastric carcinoid when this state is present for a very long period of time. This explains the peak incidence between 60 and 80 years of age. Other cofactors are probably necessary for earlier degeneration. Although gastric carcinoids are rarely seen at young age, the physician should be alert for such tumors when a young patient is diagnosed with an associated autoimmune disorder other than autoimmune atrophic gastritis. The latter was stressed in our recently published case report and literature review. Its exact etiologic role remains unknown. Autoimmune disorders could possibly contribute to development of gastric carcinoids indirectly by their relation to atrophic autoimmune gastritis; a direct effect of those autoimmune disorders on induction or promotion of neoplastic growth is less likely. In their reported case, Johnson and colleagues chose close followup of the patient rather than surgical resection because of the poor clinical condition of their patient and the absence of symptoms. Although the natural behavior of type I tumors is indeed usually indolent, one should not be too reluctant to perform therapeutic interventions. Simple endoscopic or surgical resection of the lesion(s), with or without antrectomy, has been recommended in the majority of cases, as stated in treatment guidelines of recent reviews. Antrectomy is probably able to prevent development of new gastric carcinoids and to discontinue progression of existing hyperplastic and dysplastic lesions by eradicating the stimulating effect of gastrin. Generally, total gastrectomy is reserved only for invasive disease and recurrence after antrectomy. Our reported case of a 23-year-old woman illustrates that in some patients the new development of multiple carcinoids may be very rapid, so radical surgery is unavoidable. In this case, initially, a solitary carcinoid tumor was diagnosed. In a time span of only 5 months, a large number of carcinoid lesions developed over the entire corpus of the stomach. Additionally, the patient’s compliance for endoscopic surveillance was very poor; she refused gastroscopic examination repeatedly. So additional indications for total gastrectomy in the absence of invasive disease should include expected poor compliance of the patient that would interfere with regular followup gastroscopy and patients with large numbers and rapid progression of multifocal lesions, making sufficient local tumor control with endoscopic interventions and conservative surgery practically impossible. In conclusion, to answer the query in the title of a recent paper by Modlin and coauthors, it seems that gastric carcinoids are probably small tumors that often cause larger problems.