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J. Shobana * et al. /International Journal Of Pharmacy & Technologyrelaxing factor. In addition Hcy may directly impair the NO pathway reducing NO elaboration by endothelial cellsand increase oxidative degradation of NO 12 .HypertensionThe conditions of reduced NO production, such as in diabetes mellitus; a slight increase in Hcy might scavengeresidual endothelial NO and influence arterial regulatory tone. Recently a correlation between systolic bloodpressure and plasma Hcy has been demonstrated in a hypertensive geriatric population. However, studies whichexamine the association of hypertension and plasma Hcy levels do not seem adequate to reveal this relationclearly 13 .Multiple sclerosisMultiple sclerosis (MS) is a chronic inflammatory demylinating disease of central nervous system (CNS),with an onset typically between 20 and 40 years of age and more prevalent in women. Homocysteine may have aneurotoxin that activates N-methyl-D.aspartate receptor which leads to cell death. It may be converted intohomocysteic acid which also has a toxic effect on the neurons of cerebral cortex. So increased plasma level of totalHomocysteine (tHcy) has a neurodegenerative effect and may be a risk factor for progression of disability in MS.In one of the case control clinical trial, tHcy was compared between MS and Control group. It wasobserved that high serum tHcy is more in MS patients than healthy controls and significantly higher in the patientswith severe disability (EDSS≥3). So, serum tHcy may have a positive effect on Pathophysiology of MS 14Coagulation SystemHcy causes thrombotic tendency. Elevation of thromboxane A 2 formation (which may reflect plateletactivation), reduction of anti thrombin III activity (50% to 75% of normal) and activation of factor V, reduction offactor VII have been shown as the causes of increased coagulability in Hcy. A clot in the veins is called a venousthrombosis. Most often, venous thrombosis occurs in the legs; however, the clot can break away from the wall ofthe vein and travel to the lung, leading to a potentially fatal complication called pulmonary embolism. VenousIJPT | Dec-2010 | Vol. 2 | Issue No.4 | 551- 564Page 556
J. Shobana * et al. /International Journal Of Pharmacy & Technologyblood clots occur in approximately 1 in 1000 individuals per year. Certain studies have suggested that elevatedHomocysteine levels roughly double the risk of developing venous thrombosis 15 .Renal FailureHHcy is very frequent in renal failure, which suggests that the kidneys function is crucial for Hcycatabolism. Hcy is ultra filtrated in glomeruli, almost completely absorbed in tubules, and degraded in kidneytissue by Transmethylation and Transsulphuration in the activated methyl cycle 16 . It has been shown thatmetabolism in kidney tissue accounts for a major fraction of total renal clearance of plasma Hcy and the loss ofcapacity for Hcy degradation might explain the increase in plasma Hcy seen in end-stage renal disease.Diabetes Mellitus, Vascular ComplicationsHHcy may accelerate vascular damage related to diabetes. Some studies re-searching the relationshipbetween plasma Hcy and diabetes have shown that type 2 diabetic patients have a higher prevalence of HHcy thancontrol subjects. There are still controversial studies with respect to the association between plasma Hcy andmacro vascular complications or micro vascular complications.Hoogeveen et, al 17found that diabetic patients with HHcy had an increased risk for developingcardiovascular disease compared with those with normohomocysteinemia. Moreover one of the prospective studiesindicated that HHcy was related to 5-year mortality independent of other major risk factors and appeared to be astronger (1.9-fold) risk factor for mortality in type 2 diabetic patients than in non diabetic subjects. For each5µmol/l increase in Hcy, the risk of 5- year mortality rose by 17% in the non diabetic and by 60% in the diabeticsubjects. Faisal I. Mohammad et al., have concluded that plasma level of Homocysteine is significantly elevated indiabetic coronary heart disease female patients above 50 years old and significantly elevated in non diabeticcoronary heart disease males and female patients, thus non diabetic coronary heart disease male and femalepatients and diabetic coronary female patients are at high risk of vascular diseases. It is recommended that thesepatients may take supplementation of folate and vitamin B12 to reduce the level of Homocysteine 18 .IJPT | Dec-2010 | Vol. 2 | Issue No.4 | 551- 564Page 557
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