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As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of vitamin B 6, folic acid (vitamin B 9), and vitamin B 12 can lead to high homocysteine levels. [2] Other possible causes of hyperhomocysteinemia include genetics, excessive methionine intake, and other diseases.
Folate and vitamin B 12 deficiency anemia usually presents with high RDW and high MCV. Mixed-deficiency (iron + B 12 or folate) anemia usually presents with high RDW and variable MCV. Recent hemorrhages typically present with high RDW and normal MCV. A false high RDW reading can occur if EDTA anticoagulated blood is used instead of citrated blood.
It thus is also a biomarker for intracellular levels of folate. The FIGLU test is used to identify vitamin B₁₂ deficiency, folate deficiency, and liver failure or liver disease. [1] [2] It is elevated with folate trapping, where it is accompanied by decreased methylmalonic acid, increased folate and a decrease in homocysteine. [3]
Folate deficiency is diagnosed by analyzing a complete blood count (CBC) and plasma vitamin B 12 and folate levels. A serum folate of 3 μg/L or lower indicates deficiency. [98] Serum folate level reflects folate status, but erythrocyte folate level better reflects tissue stores after intake. An erythrocyte folate level of 140 μg/L or lower ...
This functionality is lost in vitamin B 12 deficiency, resulting in an increased homocysteine level and the trapping of folate as 5-methyl-tetrahydrofolate, from which THF (the active form of folate) cannot be recovered. THF plays an important role in DNA synthesis, so reduced availability of THF results in ineffective production of cells with ...
Common levels in Western populations are 10 to 12 μmol/L, and levels of 20 μmol/L are found in populations with low B-vitamin intakes or in the elderly (e.g., Rotterdam, Framingham). [ 17 ] [ 18 ] It is decreased with methyl folate trapping, where it is accompanied by decreased methylmalonic acid, increased folate, and a decrease in ...
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Methylenetetrahydrofolate reductase deficiency is the most common genetic cause of elevated serum levels of homocysteine (hyperhomocysteinemia). It is caused by genetic defects in MTHFR, which is an important enzyme in the methyl cycle. [1] Common variants of MTHFR deficiency are asymptomatic and have only minor effects on disease risk. [2]