Pathogenesis of Pernicious Anemia

Nieweg (1953) suggests that deficiency of ribonucleic acid synthesis affects especially the long axons of nerve cells in the spinal cord. Another possible mechanism, both for the spinal cord damage and for the abnormal destruction of red blood cells, is considered below. 

Possible Interplay between Toxic and Nutritional Factors in Megaloblastic Anemia 

Several facts, some clinical or biochemical, others derived from experiments with animals or marrow culture, are difficult to reconcile with the simple nutritional concepts. Some manifestations of megaloblastic anemia are not readily explicable on a nutritional basis. 

Hemolysis. In some patients, at least, there is excessive destruction of circulating erythrocytes. The survival of the patient s own eells may be followed after the hemoglobin in them has been labeled by administering N -labeled glycine (London and West, 1950 James and Abbott, 1953). In Addisonian pernicious anemia in relapse some red cells have a normal survival time and some are destroyed rapidly and at random. Using the Ashby technique of differential agglutination, Hamilton et al. (1952) demonstrated that even fresh normal erythrocytes transfused into patients with pernicious anemia in relapse may be destroyed with abnormal rapidity in a random fashion. The survival rate of tian used cells was normal in patients who received vitamin Bu 9 to 12 days before transfusion. 

Thus destruction of red cells in pernicious anemia is not due solely to an inherent abnormality in the red cells there must also be an extra-corpuscular mechanism. The existence of a hemolytic agent in the blood of patients with pernicious anemia is discussed by Paschkis and Taylor (1934), Dock (1938), and Bloomfield (1944). 

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Tochowioz (110) agreed mth Font and Thivolle that some of the trouble in pernicious anemia lies in faulty protein metabolism. He found not only impaired absorption of amino acids from the gastro-intestinal tract, in pernicious anemia, but lessened retention of the amino acids by the tissues and their increased elimination in the urine. From the results of blood studies of normal people as well as those suffering from posthemorrhagic and pernicious anemias, he concluded that although tryptophane may play some role in Biermer s anemia, histidine is of no importance in either the pathogenesis or the treatment of the disease. 

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