COBALT is a component of the vitamin B12 molecule and as such is essential to erythropoiesis. Thus far no clinical evidence of cobalt deficiency has been demonstrated in man. However, when cobalt is administered to man and animals in amounts far greater than the estimated daily requirement an absolute polycythemia, with hyperplasia of the bone marrow and reticulocytosis, results.1 , 2 More recently cobalt has been reported to elicit favorable responses when vitamin B12 fails in anemias of diverse etiologics: those associated with chronic infection,3 , 4 chronic renal disease,5 prematurity,6 pregnancy7 and sickle-cell disease.8 In the past three years a proprietary preparation . . .
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Robey et al. (1956) studied this question.
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