Etiology of cobalamin deficiency. Seven patients (Tables 1 and 3) had serum antibodies to intrinsic factor, establishing the diagnosis of pernicious anemia. In 4, there was a history of gastric or ileal surgery. Fourteen patients, 7 in each group, were felt to have severe chronic atrophic gastritis (which could cause either intrinsic factor deficiency or food-cobalamin malabsorption)27,28 using a combination of serum pepsinogen and gastrin concentrations29-31 (see footnote to Table 1). Three had poor dietary animal protein intake and 3 were taking agents reported to cause food cobalamin malabsorption. Hematologic and neurologic responses. Hematologic and neurologic responses to cyanocobalamin are shown in Tables 1 and 3 and are summarized in Table 5. They are similar to those observed in a larger study that used only parenteral cobalamin.34 In approximately one half of the patients in each group, a major decrease in MCV occurred. The mean decrease after 4 months of treatment was highly significant in each group (P , .005). Substantial increments in hematocrit attributable to cobalamin therapy were seen in a minority of both groups, most strikingly in patients no. 2 and 3 on oral cyanocobalamin. Four patients on each treatment experienced dramatic improvement of neurologic complaints. Improvement in mental status, gait, or vibration sense was documented in 2 and 3 patients, respectively, after oral and parenteral therapy.