Folate interaction with vitamin

Linnebank, M., Moskau, S., Semmler, A., Widman, G., Stoffel-Wagner, B., Weller, M., and Eiger, C.E., 2011. Antiepileptic drugs interact with folate and vitamin B12 serum levels. Annals of Neurology. 69 352-359. 

Carbohydrates and vitamins are low-molecular ligands that recognize specific receptors on the cell surface (Lee et al., 2014). For instance, hyaluronic acid is a polymer of disaccharides composed of o-glucuronic acid and o-A-acetylglucosamine, which interacts with cluster determinant 44 receptors overexpressed on tumors. Acid folic is a vitamin that shows high affinity to the folate receptor that is also overexpressed on tumors. They have low-molecular weight, are relatively inexpensive to synthetize and results can be more reproducible due to the limited number of inherent structural diversities of the molecules. 

Therapy, in the short term, is with intravenous unfractionated or subcutaneous low molecular weight heparin. Aspirin, given in low doses between 50 and 100 mg per day, is sufficient to diminish platelet-vessel interaction. Alternatives include 100-200 mg of sulphinpyrazone once or twice a day or dipyridamole where 100 mg four times a day can be used on its own or between 25 and 75 mg combined with aspirin three times a day. More recently thiopy-ridines, as a class, has been shown to have equivalence at 250 mg twice a day. In hyperhomocysteinaemia the risk is reduced by 5 mg of folate and 100 mg of vitamin Bg daily, with addition of oral vitamin Bi2 of less clearly defined benefit. The effect of this intervention requires re-assay at 3-monthly intervals, following standard methionine challenge, to ensure that suitable suppression has been achieved in the plasma amino acid level (Table 5). 

Homocysteine arises from dietary methioiiine. High levels of homocysteine (hyperhomocysteinemia) are a risk factor for occlusive vascular diseases including atherosclerosis and thrombosis (81—84). In a controlled study, semm folate concentrations of <9.2 nmol/L were linked with elevated levels of plasma homocysteine. Elevated homocysteine levels have been associated also with ischemic stroke (9). The mechanism by which high levels of homocysteine produce vascular damage are, as of yet, not completely understood. Interaction of homocysteine with platelets or endotheHal cells has been proposed as a possible mechanism. Clinically, homocysteine levels can be lowered by adrninistration of vitamin B, vitamin B 2j foHc acid. 

---