Megaloblastic anemias.
Data continue to emerge that the low cobalamin levels often seen in the elderly and in various other settings represent a subtle cobalamin deficiency state. Even though such individuals do not have megaloblastic anemia and absorb free cobalamin normally, metabolic tests frequently document insufficiency of cobalamin that reverses after treatment with cobalamin. In many cases, malabsorption limited to food cobalamin seems responsible for the mild deficiency state. A major development related to folate has been the conclusive documentation that folate supplementation halves the risk of having a baby with neural-tube defect. The explanation for this phenomenon and the possible long-term side effects of regular folate supplementation remain to be determined. Another issue with public health implications is the association of mild homocysteinemia with premature cardiovascular disease and evidence that the homocysteinemia responds to vitamin supplementation. Important advances are being made with molecular biologic techniques in unraveling the structure of key transport proteins for cobalamin and folates.
Carmel
R
R
University of Southern California School of Medicine, Los Angeles, USA.
D000375:Aging / Q000378:metabolism; D000749:Anemia, Megaloblastic / Q000209:etiology* / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D005492:Folic Acid / Q000378:metabolism; D006801:Humans; D014806:Vitamin B 12 Deficiency / Q000150:complications / Q000378:metabolism
D005492:Folic Acid