IN-VITRO STUDIES OF GASTRIC-JUICE IN PATIENTS WITH FOOD-COBALAMIN MALABSORPTION

Food-cobalamin absorption depends on the initial release of cobalamin from its binders in food. Therefore, the characterization of patients' gastric juices and their behavior in this process was undertaken. Pen tagastrin-stimulated gastric juice specimens from three patients with severe food-cobalamin malabsorption, six patients with mild malabsorpt ion, and five patients with normal absorption were tested for pH, peps in, intrinsic factor content, and an in vitro method that quantitates transfer of cobalamin from egg yolk to gastric R binder. Transfer of c obalamin correlated best with in vivo egg yolk-cobalamin absorption te st results in the 14 patients (r = 0.731, P < 0.005). Transfer also co rrelated inversely with gastric juice pH (r = -0.619, P < 0.02). Basal gastric juice specimens, with their higher pH, from the same subjects failed to promote cobalamin transfer until their pH was lowered to 1. 0-1.3. Pepsin levels did not correlate with in vitro transfer or with absorption in vivo; nevertheless, raising the low pepsin concentration of one stimulated gastric juice improved transfer, while inhibiting p epsin activity with pepstatin A inhibited transfer. Mixing experiments with selected stimulated gastric juices demonstrated that poor in vit ro transfer, which in a few cases seemed unrelated to pH or pepsin lev els, was not due to any inhibitory activity of such gastric juices. Th ese studies confirm that gastric acid and pepsin play a central role i n releasing food-bound cobalamin and transferring it to R binder, but suggest that other, still unidentified gastric defects occasionally co ntribute to impaired transfer; the latter defects are not inhibitory i n nature but seem to involve the absence of a permissive activity. The finding that the ability of a gastric juice to promote the transfer o f cobalamin in vitro was the best overall indicator of a patient's abi lity to absorb food cobalamin in vivo suggests that gastric juice defe cts are responsible for most cases of food-cobalamin malabsorption. Th e phenomenon may also provide a practical in vitro estimate of a patie nt's ability to absorb food cobalamin.