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The effect of corticosteroids on the gastric mucosa in patients with pernicious anemia is of particular interest in view of the possibility that atrophic gastritis, the primary pathologic lesion in pernicious anemia, may result from destruction of gastric glands by an autoimmune process (1). The first observation which suggested that corticosteroids might enhance vitamin B12 absorption in patients with pernicious anemia was made by Doig, Girdwood, Duthie, and Knox (2). Three of four patients treated with prednisolone exhibited a hematologic response with a reticulocytosis, an increase in hemoglobin and red blood cell count, and correction of the megaloblastic to normoblastic erythropoiesis. In several studies that were stimulated by this observation, it was suggested alternatively that prednisolone enhanced vitamin B12 absorption in the absence of intrinsic factor (3) and that prednisolone stimulated the gastric secretion of intrinsic factor in these patients (4, 5). Kristensen and Friis (6) proved that the latter mechanism was responsible for the increase in vitamin B12 absorption during corticosteroid therapy. They found that gastric juice collected from pernicious anemia patients with enhanced vitamin B12 absorption during therapy with prednisolone contained intrinsic factor on in vivo assay.

The effect of prednisolone on gastric mucosal histology, gastric secretion, and vitamin B 12 absorption in patients with pernicious anemia.