Abstract
ACCORDING to the present concept of the pathogenesis of pernicious anemia, the primary change consists in a loss, abiotrophic in nature, of the ability to elaborate sufficient gastric intrinsic factor for normal hematopoiesis. The loss of this function, judged by the clinical course of the disease,1 occurs in a progressive manner, interrupted by a remarkable tendency to remissions. The latter are of decreasing effectiveness, however, and the final outcome in the case without treatment is fatal. For reasons which are not understood, the disease almost exclusively affects persons who have achlorhydria, and in many cases it has been shown that the gastric anacidity is present for years before the development of anemia. Lack of antianemia principle in the body resulting from faulty gastric secretion is followed by a train of inflammatory and atrophic changes in the stomach, small intestine and other parts of the alimentary tract, notably the tongue.

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