The Effect of Stanol-Sterol on the Lipid Profile of Patients Who Have Undergone Renal Transplantation - Assignment Example

6. DISCUSSION The aim of the current study is to study the effect of stanol/sterol, alone or in addition to other agents, on the lipid profile of patients who have undergone renal transplantation and to assess their acceptability as a treatment alternative or adjunct to statin therapy. The study assumes significance because of the fact that dyslipidaemia is common in patients with renal disease and is a recognized risk factor for in the general population and occur in a majority of patients with renal disease (Weiner, 2004). The reported prevalence of dyslipidemia in renal transplant patients ranges from 16-72%. Renal transplantation is now widely acknowledged as the treatment of choice for patients in ESRF. The pathogenesis of changes in lipid pattern in transplant patients appears to be multifactorial. There is circumstantial evidence that lipid disorders in patients following renal transplantation play a major role in the pathogenesis of atherosclerosis and chronic renal allograft rejection (Wanner, 2000). The National Kidney Foundation has recently released guidelines suggesting a low-density-lipoprotein (LDL) cholesterol goal of < 100 mg/dL in renal transplant patients. Statins and diet therapy are recommended as first-line agents for achieving goal LDL cholesterol levels in this population. But a potential pharmacokinetic interaction with cyclosporine and a resultant increase in the risk of myopathy or rhabdomyolysis and also reduced renal elimination influence the dose to be used. It was shown by two large pioneering interventions that it is possible to reduce the incidence of CVD by dietary means only (Miettinen, 2004). In those long-term controlled studies, with up to 8- and 12-year follow-up periods, two dietary variables were changed; the amount of dietary cholesterol was reduced by approximately 40%, and fat intake was modified to contain less saturated and more unsaturated fatty acids. The incidences of end-points - coronary death, and nonfatal and fatal myocardial infarction and manifestations of atherosclerosis in cerebral and peripheral arteries - were significantly lower in the experimental groups than in the control groups. Therefore it has been suggested that adjunctive use of foods fortified with stanol/ sterol can facilitate dosage adjustments of statins and other lipid lowering agents without compromising the therapeutic efficacy. They do this by reducing the absorption of cholesterol from the gut by competing for the limited space for cholesterol in mixed micelles (the "packages" in the intestinal lumen that deliver mixtures of lipids for absorption into the mucosal cells). This reduced absorption lowers serum cholesterol despite the compensatory increase in cholesterol synthesis which occurs in the liver and other tissues. Plant sterols are potentially atherogenic like cholesterol but atherogenesis does not occur because so little of the plant sterols are absorbed. Since the mechanism of action stanol/sterol is different from that of statins and other lipid lowering agents, and since the compensatory increase in cholesterol synthesis caused by stanol esters is neutralised and eliminated by statins there is a potential for additive or synergistic action when used in combination. In the current study both, control and intervention groups had mean values of cholesterol and LDL which were outside the acceptable value of 5mmol/. Furthermore, both groups had triglycerides (TG) which were approaching the upper limit of the acceptable values or were above them. Thus hHypertriglyceridaemia associated with the nephrotic syndrome may results from impaired catabolism of triglyceride-rich lipoproteins. The importance of elevated TG's in patients of with a renal transplant stems from a hypothesis that increased serum TG levels have been implicated as the most consistent predictor of chronic allograft failure (Guijjaro, 1995). There is also aA definite correlation between serum cholesterol and TG and the duration of transplant has previously been shown. The levels of both of these lipid components decrease over the first 2-3 years of after transplantation (Baliga, 2003). Since the lipid profile in the first 8-12 months after transplantation is variable, it should not form the basis of therapy. The decision to treat hyperlipidaemia should be based on the lipid levels and the presence of positive risk factors for CAD including age > 45 years in males, age >55 years in females, family history of premature CAD, current cigarette smoking, blood pressure >140/90 mm Hg despite antihypertensive therapy, HDL-C Read More