Info about Vitamins

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Vitamin C Deficiency

Although anemia is commonly observed among patients with the vitamin C deficiency disease scurvy, the direct role of vitamin C or ascorbic acid in hemopoiesis is not well documented. Usual hematological findings in this case are normocytic, normochromic anemia with reticulocytosis, which can be corrected, with an accompanying rise in hemoglobin concentration, by vitamin C supplementation.


Vitamin C deficiency may be involved indirectly in the development of anemia through its relation to folic acid and Fe metabolism. It is well established that vitamin C increases the bioavailability of Fe in foods and facilitates intestinal Fe absorption, particularly nonheme Fe. Vitamin C also enhances the utilization of heme Fe and facilitates ferritin synthesis. It has been documented that vitamin C augments the translation of ferritin mRNA by maintaining the Fe-responsive element-binding protein in its active form. In addition, in-vitro experiments have shown that vitamin C prevents degradation and enhances the stability of ferritin. A proposed, but indirect, role of vitamin C in erythropoiesis is that vitamin C facilitates the turnover of Fe in the body. Vitamin C is also required for the maintenance of folic acid reductase, which converts folic acid to its active tetrahydrofolate form. Failure to synthesize tetrahydrofolate leads to megaloblastic anemia. Occasional megaloblastic cells have been observed among scurvy patients.