Development of the cestode parasite Taenia taeniaeformis in the liver of rats results in gross hyperplastic changes in the stomach and small intestine. In this study we investigated the mechanism by which these lesions are induced. Acutely infected rats were joined surgically to syngeneic noninfected partners in parabiosis. When hyperplastic gastropathy developed in those rats with heavy hepatic infections with cestodes, it also occurred in the uninfected partners of the parabiotic pairs. Gastric changes were usually more severe in the uninfected partner. Duodenal mastocytosis developed in both partners, even when parasite burdens were light in the infected rats. intact chronically infected rats with hyperplastic gastropathy developed markedly elevated serum levels of the hormone, gastrin (approximately 30-fold greater than normal). When rats were antrectomized 24-48 h after infection, gastric hyperplasia still developed, but hypergastrinemia was prevented or was of only moderate degree. There was no correlation between serum gastrin levels and the degree of gastrointestinal change in the intact rats, but hypergastrinemia never developed in infected animals which did not show hyperplasia in the stomach or intestine. When infected rats were bled serially over the first 100 days of infection, hypergastrinemia developed abruptly between 50 and 60 days after infection. These results suggest that the alterations in serum gastrin levels were secondary to the development of hyperplastic changes in the gastrointestinal tract of infected rats. The primary stimuli for both the hyperplasia and the hypergastrinemia remain unknown.