Vitamin deficiency Deficiencies of vitamins B6, B9 and B12 can lead to high homocysteine levels. Vitamin B12 acts as a cofactor for the enzyme methionine synthase (which forms part of the S-adenosylmethionine (SAM) biosynthesis and regeneration cycle). Vitamin B12 deficiency prevents the 5-methyltetrahydrofolate (5-MTHF) form of folate from being converted into THF due to the "methyl trap". This disrupts the folate pathway and leads to an increase in homocysteine which damages cells (for example, damage to endothelial cells can result in increased risk of thrombosis). Alcohol Chronic consumption of alcohol may also result in increased plasma levels of homocysteine. Tobacco Smokeless tobacco is implicated as risk factor for hyperhomocystemia. Smoking also causes hyperhomocystemia Genetic Homocysteine is a non-protein amino acid, synthesized from methionine and either recycled back into methionine or converted into cysteine with the aid of the B-group vitamins. * About 50% of homocysteine is converted back to methionine by remethylation via the methionine synthase major pathway. This requires active folate and vitamin B12, in order to donate a methyl group. Active folate is known as 5-methyltetrahydrofolate (5-MTHF). * Another pathway for the conversion of homocysteine back to methionine also exists, involving methylation with trimethylglycine (also called betaine or abbreviated to TMG) as a methyl donor. * The remaining homocysteine is transsulfurated to cysteine, with vitamin B6 as the co-factor. Genetic defects in 5-MTHF reductase can consequently lead to<unk> . The most common polymorphisms are known as MTHFR C677T and MTR A2756G. These polymorphisms occur in about 10% of the world's population. Elevations of homocysteine can also occur in the rare hereditary disease homocystinuria.
Hyperhomocysteinemia
Hypoprothrombinemia
Hyperprothrombinemia
Hypodysfibrinogenemia
Hypoplasminogenemia
Pseudothrombocytopenia
Dysfibrinogenemia
Hypolipoproteinemia