Abstract
IN 1959, Li et al1 reported a case of pernicious anemia due to the presence of an in vivo intrinsic factor inhibitor, diagnosed in childhood, with a twenty-five-year follow-up. Since then, "defective absorption of vitamin B12 due to intrinsic factor inhibitor in gastric secretion" has been part of the etiologic classification of the megaloblastic anemias due to vitamin B12 deficiency. In the intervening years, it was demonstrated that blood group substances may block intrinsic factor action and it was speculated that secretors of blood group substance into their gastric juice may, to a variable extent, block the action of . . .