Hyperhomocysteinemia The metabolism of homocysteine and the effects of elevated levels on cardiovascular, peripheral vascular and cerebrovascular disease. By: James W. Graham Hyperhomocysteinemia (in blood) and Homocysteinuria (in urine) has been known for approximately 30 years.(1,3) Hyperhomocysteinemia, which will be discussed here extensively, is elevated blood plasma level of total homocysteine (tHcy). The tHcy is considered elevated when levels are >15umol/L in blood serum. Patients with hyperhomocysteinemia commonly have tHcy levels of 250umol/L.(2) Normal levels of tHcy has been determined to range from 6.1-15.0umol/L.(6) Patients with elevated blood levels of tHcy, in several studies, has indicated in having an increased risk in cardiovascular, peripheral vascular and cerebrovascular disease.(1,2,4) Hyperhomocysteinemia has been estimated to be in 5% of the general population, and 13-47% of patients with diagnosed symptomatic atherosclerotic vascular disease, also have hyper- homocysteinemia.(1) The causative agents for hyperhomocysteinemia are deficiencies in folate (folic acid), vitamin B12, vitamin B6, a genetic disposition or even kidney problems.(1) This paper will discuss the metabolism of homocysteine and how hyperhomocysteinemia causes an increased risk in cardiovascular, peripheral vascular and cerebrovascular disease. Homocysteine (Hcy) is a sulphydryl-containing amino acid by-product that comes from the demethylation of methionine. The major source of methionine is from animal protein.(1,3) In the plasma, Hcy is available in four forms. Hcy can circulate as a free thiol, is disulphide-bound to plasma proteins such as albumin, combined with itself to form a dimer, or bound with other thiols such as a cysteine. These four forms of homocysteine will be referred to as total homocysteine (tHcy).(1) tHcy is metabolized by remethylation or trans-sulphuration.(5) | |
|
