An immunologic basis for acquired resistance to oral administration of hog intrinsic factor and vitamin B12 in pernicious anemia.

In pernicious anemia, vitamin B12 deficiency develops owing to the failure of gastric intrinsicfactor secretion. Patients with this disease absorb vitamin B12 from the gastrointestinal tract when it is fed together with an extract of hog pyloric mucosa. Some patients have relapsed during the course of oral therapy with this mixture (1-3). These subjects absorb vitamin B1.2 administered with normal human gastric juice but do not absorb it when it is administered with hog preparations possessing intrinsic-factor activity (3). These patients have become refractory to the hog preparations. It has been reported that sera obtained from most of these refractory patients (4), and from a minority of nonrefractory patients and normal subjects (5, 6), possess intrinsic factor-neutralizing properties. Such observations have directed attention to a possible immunologic mechanism for the refractory state. This study was undertaken to determine whether the refractory state might be due to antibodies against the hog intrinsic-factor preparation, which could be detected in vitro.