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In three different groups of patients presenting severe folate deficiency (purely nutritional folate deficiency, chronic alcoholism or various intestinal diseases), vitamin B12 absorption has been tested by Schilling test in order to investigate the possible effect of folate deficiency on B12 absorption. Following this study, it appears that folate deficiency in itself, even severe, cannot induce vitamin B12 malabsorption, since in the first group, consisting of malnourished old people, the Schilling test was always normal even in those who presented a lowered B12 serum level; in the group of patients with intestinal disease, the Schilling test was abnormal as expected in some patients; 3 alcoholics out of 12 presented a malabsorption of B12 on the Schilling test; the follow-up of 2 of them exhibited complete correction after normal diet and alcohol suppression. Consequently, folate deficiency does not seem responsible for a secondary B12 malabsorption unless another etiological factor is present, such as alcohol or ileopathy.

Absorption of cobalamin free or bound to chicken serum was assessed in nine patients with pancreatic insufficiency. Simultaneously the in vitro effect of duodenal juice collected from six patients and seven controls was tested on labelled cobalamin complexed to chicken serum or to R salivary binder. Malabsorption of free cobalamin was observed in one of nine patients and in four of nine patients when cobalamin was administered bound to chicken serum. The in vitro effect of duodenal juice on cobalamin complexed to chicken serum or to R salivary binder was studied: the percentage of free cobalamin released was significantly decreased in pancreatic insufficiency compared with controls whatever the binder used; the degradation of R salivary binder was different in pancreatic insufficiency and in controls. Despite the in vitro abnormalities observed in pancreatic insufficiency, these did not correlate with the in vivo absorption of cobalamin which was often normal in our patients.

The effects of ranitidine, a new potent histamine H2-receptor antagonist, on gastric intrinsic factor (IF) secretion and protein-bound cobalamin absorption were evaluated in 6 patients with duodenal ulcer, before, during and after discontinuation of ranitidine therapy. Oral ranitidine (150 mg twice a day) resulted in a non significant decrease of IF concentration and IF output but was responsible for malabsorption of protein-bound cobalamin. This malabsorption was reversible upon discontinuation of ranitidine. These results indicate that occurrence of cobalamin deficiency cannot be excluded during long-term ranitidine treatment and emphasize the need for careful follow-up in these patients.