Abstract
Hyperhomocysteinaemia is an established risk factor for cardiovascular disease. The modification of traditional cardiovascular risk factors has resulted in better morbidity and mortality outcomes, so the treatment of hyperhomocysteinaemia is explored for a similar benefit. Vitamin B6, vitamin B12 and folate, co-factors in the metabolism of homocysteine, are used in the treatment of hyperhomocysteinaemia. Betaine, a methyl-donor in a separate homocysteine metabolism pathway, is also used to treat hyperhomocysteinaemia. These supplements have been used in various doses and combinations for different periods of time, with favourable outcomes. There is still no concensus whether hyperhomocysteinaemia should be treated with folic acid alone or in combination with vitamin B6 and vitamin B12. The dose of the supplements required to normalise fasting homocysteine remains to be determined, especially in diabetic nephropathy, haemodialysis and renal transplant patients. The benefits from lowering homocysteine levels have mainly been demonstrated in surrogate cardiovascular outcomes. The treatment of hyperhomocysteinaemia cannot be firmly advocated until there are trials that demonstrate a beneficial clinical end point. In patients who have cardiovascular disease in the absence of more established risk factors, investigation and treatment of hyperhomocysteinaemia should be considered. Current treatment approaches to hyperhomocysteinaemia are limited to natural vitamins in relatively low doses. Such treatment is sometimes ineffective, particularly in patients in situations such as renal failure. Newer treatment options such as those discussed in the patent literature may be important.