E. Solcia et al., DISTINCT PATTERNS OF CHRONIC GASTRITIS ASSOCIATED WITH CARCINOID AND CANCER AND THEIR ROLE IN TUMORIGENESIS, The Yale journal of biology & medicine, 65(6), 1992, pp. 793-804
A series of 60 gastric endocrine tumors comprised 44 body-fundus argyr
ophil carcinoids, of which 23 arose in a background of hypergastrinemi
a and type A chronic atrophic gastritis (A-CAG), mainly with histologi
c patterns suggestive of an autoimmune process. Only 22 percent (compa
red with 19 percent of 58 tumor-free A-CAG cases) of 36 carcinoids and
21 percent of 19 A-CAG carcinoids investigated had Helicobacter pylor
i (HP) colonization, against 50 percent of 14 CAG-associated neuroendo
crine carcinomas or mixed endocrine-exocrine tumors, 84 percent of 150
cases with early gastric cancer (p < 0.001 versus carcinoids), mostly
with B- or AB-type CAG, 76 percent of 97 tumor-free AB-CAG, and 95 pe
rcent of 151 tumor-free B-CAG cases. Secondary hypergastrinemia and lo
cal mechanisms activated by chronic autoimmune gastritis are among fac
tors involved in the pathogenesis of relatively indolent CAG-associate
d carcinoids, whereas active HP gastritis in cooperation with environm
ental carcinogens may likely cause more severe epithelial transformati
on, leading to ordinary cancer and, possibly, to neuroendocrine carcin
omas or mixed endocrine-exocrine tumors.