Anemia Pernicious

Senga Whittingham, Centre for Molecular Biology and Medicine, Monash University, Clayton, Victoria, Australia

Pernicious anemia is an anemia which occurs in the terminal stages of the chronic destructive autoimmune disease, autoimmune gastritis. The anemia results from the death of parietal cells in the body of the stomach due to an immunologic reaction and in the absence of gastric parietal cells, a blood-sustaining vitamin B12 is no longer transported to its site of absorption.

Thomas Addison is acknowledged as the physician who, in 1849, described the clinical features of the anemia. The term 'pernicious' emphasized the inevitable progress and fatal outcome of the anemia and this description given by Biermer in 1972 has endured despite the knowledge that it is appropriate only to the terminal phase of the disease. The disease is, in fact, autoimmune gastritis for which histologic evidence was documented by Fenwick in 1870. However the importance of the link between the anemia and gastritis was not recognized until many years later.

Treatment played a major role in the eventual understanding of the development of pernicious anemia. The earliest studies were directed towards halting the progress of the anemia, and the prevention of death from the disease. Meals of crude extracts of hog stomach or cooked liver produced a reticulocyte response, indicating that new erythrocytes were made in response to ingestion of such meals. The reason for this became clear when Castle, in the 1950s, showed that the response was dependent on the pres ence in food of an extrinsic factor which reacted with intrinsic factor secreted into gastric juice. However, despite intensive treatment, relapses occurred and, in some instances, the anemia became refractory to treatment. The refractory state appeared to be due to the development of an inhibitory factor in the serum because serum mixed with gastric juice inhibited the effectiveness of the gastric juice. Rabbits injected with gastric juice produced antibodies which showed the same inhibitory effect. The essential factor, extrinsic factor, in food was shown to be vitamin B12 and the inhibitory factor in gastric juice (and serum) was autoantibody which reacted with the receptor for vitamin B12 on intrinsic factor. Binding of vitamin B12 to intrinsic factor was inhibited and the inhibition of this normal physiologic process prevented the transportation of vitamin B12 to its site of absorption. Blood cells deprived of their essential building block, vitamin B12, failed to mature and the outcome was the development of a pernicious and progressively fatal anemia.

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