Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolism of lipids in CAPD has not been fully elucidated. To further clarify the behavior of dyslipidemia in this setting we followed the values of total cholesterol (TC), HDL-cholesterol (HDL-C) and apolipoprotein (apo) parameters over time (12-24 months) in 40 patients and correlated these values and their ratios with clinical (age, gender, race, weight, diabetes, etc.) and biochemical (multiphastic screen) information. Mean HDL-C was lower in men (p less than 0.04), in whites, (p less than 0.03) and in diabetic patients (p less than 0.05), but there were no group differences for mean total cholesterol, mean apolipoprotein values, the atherogenic risk ratio TC/HDL-C, or the anti-atherogenic ratio apo A-I/apo B. Total months on CAPD was found to correlate positively with TC/HDL-C (p less than 0.05), an atherogenic risk factor, and to correlate negatively with HDL-C (p less than 0.02), an anti-atherogenic index. There was also a negative correlation with another anti-atherogenic index, apo A-I/apo B, which did not reach statistical significance (r = -0.41, p = NS). Counterbalancing this apparently increased atherogenic risk is the stability of individual parameters for each patient over time in this study. In fact, the good news appears to be that TC, HDL-C, apolipoproteins and the risk ratios TC/HDL-C and apo A-I/apo B all remained stable over 12-24 months (p = NS by paired t-test for all). Thus, we find no evidence for worsening of the uremic dyslipidemia over time with CAPD treatment.
Adv Perit Dial 1990
PMID:The impact of CAPD treatment on lipid metabolism and cardiovascular risk. 198 15

Dyslipidemia is an important risk factor for atherosclerotic vascular disease. Serum lipoprotein (a) [Lp(a)] has been implicated as an independent atherogenic risk factor. We measured serum (Lp(a) levels in our patients and studied its correlations with other lipoproteins and clinical parameters. All stable patients on continuous ambulatory peritoneal dialysis (CAPD) for more than one month were enrolled in the study. Fasting serum Lp(a), total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, apolipoprotein-A and apolipoprotein-B levels were measured on entering the CAPD program and at 3 monthly intervals. One hundred and nine patients (M/F: 65/44, mean age +/- SD: 59.5 +/- 12.0 years) were studied. Fifty-two patients had diabetes mellitus. Age- and sex-matched normals were used as controls. Serum Lp(a) levels were raised in 54.5% of CAPD patients compared to 18.6% of controls (p < 0.01). There was no significant change in Lp(a) levels over time. Serum Lp(a) levels showed positive and negative correlations with LDL-cholesterol and triglycerides, respectively, but not with age, sex, diabetic status, and serum total cholesterol and albumin levels. Thirty-six of 54 (66.7%) patients with serum Lp(a) levels greater than 30 mg/dL had either coronary, cerebral, and/or peripheral vascular disease compared to 30/55 (54.5%) of patients with serum Lp(a) levels less than 30 mg/dL (p = NS). In conclusion, serum Lp(a) levels were raised in a significant proportion of CAPD patients, but there was no significant association with vascular disease.
Adv Perit Dial 1995
PMID:Lipoprotein (a) levels and clinical correlations in CAPD patients. 853 86

We compared the lipid-lowering effects of simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, and gemfibrozil, a fibric acid derivative, in 22 continuous ambulatory peritoneal dialysis patients whose serum total cholesterol and/or triglyceride levels were > or = 220 mg/dL after a standard diet for six months. The study group was first treated with gemfibrozil (600 mg/b.i.d.) for three months (stage 1). After a wash-out period of two months, during which no treatment was given, all of the patients became hyperlipidemic again and, therefore, were given simvastatin (10 mg/day) for three months (stage 2), which was followed by another two-month wash-out period. A control group, which served to evaluate the natural progression of pharmacologically untreated dyslipidemia, was followed during the same period. Blood determinations of triglyceride, total cholesterol, and high-density lipoprotein (HDL) cholesterol were performed after each step. Low-density lipoprotein (LDL) cholesterol and HDL ratio were calculated from the measured values. Both gemfibrozil and simvastatin improved all parameters of the lipid profile, but the effect of simvastatin was better than that of gemfibrozil (-69 vs -39 mg/dL for triglyceride and -95 vs -64 mg/dL for cholesterol), while their actions on LDL and HDL cholesterol were of equal magnitude. Two months after discontinuation of simvastatin, significant decreases of total cholesterol (-46 mg/dL) and triglyceride (-60 mg/dL) were still present, while these values had returned to pretreatment levels after stopping gemfibrozil. The HDL ratio remained markedlyhigher (p < 0.05) during the wash-out period after simvastatin, while it decreased to pretreatment values after gemfibrozil was stopped. The lipid profile of the control group did not change during the follow-up. Both drugs were well tolerated, and no serious side effects occurred.
Adv Perit Dial 1996
PMID:Lipid-lowering effects of simvastatin and gemfibrozil in CAPD patients: a prospective cross-over study. 886 16

All uremic patients have multiple risk factors for CAD including in many, the conditions that caused their ESRD--for example, diabetes and hypertension. conventional risk factors--for example, dyslipidemia and hyperhomocysteinemia. risk factors that are unique to uremia--for example, calcium and phosphate abnormalities. PD patients have particular risk with respect to their lipid status and hyperinsulinemia. Many of these risks are potentially modifiable, but evidence does not exist to assess the impact of treatment on clinical outcomes. Therefore, current decisions for therapy directed at risk factor modification must be made on an individual basis.
Perit Dial Int 2000
PMID:Major and minor risk factors for cardiovascular disease in peritoneal dialysis. 1091 62

Hormone replacement is an integral part of therapies to prevent osteoporosis in postmenopausal women and may be considered a component in the treatment of dyslipidemia, cardiovascular disease, and possibly cognitive function. The indications for, and efficacy and prescription of, hormone replacement therapy in postmenopausal women with ESRD have been infrequently studied and less than 10% of postmenopausal women on dialysis are receiving hormone replacement. Small studies suggest that hormone replacement therapy is valuable in treating the dyslipidemia of women on dialysis, but indicate that a reduction in the dosage of hormone replacement may be needed. A potential role for hormone replacement therapy in the treatment and/or prevention of osteoporosis and sexual dysfunction in postmenopausal women on dialysis exists as well.
Semin Dial
PMID:Hormone replacement therapy in postmenopausal women with end-stage renal disease: a review of the issues. 1142 14

Studies in the uremic rat indicate that insulin resistance and glucose intolerance leading to dyslipidemia are associated with a hyperparathyroid-induced increase in cytosolic calcium ([Ca++i]). These alterations are reversed with verapamil, but recur after discontinuation of the drug, suggesting that increased [Ca++i] is responsible for the metabolic derangement. To our knowledge, no similar studies have been conducted in humans. We retrospectively examined, over 12-year period, the effects of factors that lower [Ca++i] on total serum cholesterol and triglycerides in 176 peritoneal dialysis (PD) patients. Because the study was retrospective, detailed lipid profiles were not available. We therefore relied on the morbidity and mortality outcome related to atherosclerotic vascular disease. Diabetic patients were excluded from the study, because their dyslipidemia and vascular disease are mediated via a different mechanism. The patients were classified into four groups. Group I [high parathyroid hormone (PTH) in the absence of calcium channel blockers (CCBs), n = 56] represented the highest [Ca++i]. Group II (high PTH in the presence of CCBs, n = 43) and group III (lower PTH in the absence of CCBs, n = 37) represented intermediate [Ca++i]. Group IV (lower PTH in the presence of CCBs, n = 40) represented the lowest [Ca++i]. High PTH was defined as > or = 3.0 times normal; lower PTH, as < 3.0 times normal. Lower [Ca++i] was achieved through the use of CCBs, or through lower PTH, or both. Lower PTH was achieved by parathyroidectomy or calcitriol administration. The four groups showed no differences in age, sex, race, weight, dialysis duration, or primary disease. Group I showed a mean serum cholesterol of 358 +/- 27 mg/dL and serum triglycerides of 469 +/- 41 mg/dL. Group II showed mean serum cholesterol of 198 +/- 21 mg/dL and serum triglycerides of 147 +/- 17 mg/dL. Group III showed a mean serum cholesterol of 205 +/- 20 mg/dL and serum triglycerides of 174 +/- 16 mg/dL. Group IV showed mean serum cholesterol of 184 +/- 10 mg/dL (p = 0.008) and serum triglycerides of 103 +/- 8 mg/dL (p = 0.005). The cardiovascular morbidity and mortality incidences were: group I, 64%; group II, 27%; group III, 31%; and group IV, 20% (p = 0.002). We conclude that, in non diabetic PD patients, dyslipidemia is related to a hyperparathyroid-induced increase in cytosolic calcium [Ca++i]. Lowering [Ca++i] by decreasing the parathormone level (via parathyroidectomy or calcitriol administration), or by blocking calcium entry into cells (via CCBs), or both, is associated with less dyslipidemia and improved long-term morbidity and mortality related to atherosclerotic vascular disease.
Adv Perit Dial 2001
PMID:Factors modulating cytosolic calcium. Role in lipid metabolism and cardiovascular morbidity and mortality in peritoneal dialysis patients. 1151 Feb 92

Patients with end-stage renal disease (ESRD) are at extreme cardiovascular risk. At least half of all patients starting dialysis therapy have overt cardiovascular disease (CVD). In addition, recent studies suggest annual incidence rates for new-onset cardiac failure, peripheral vascular disease, ischemic heart disease (IHD), and stroke of approximately 7%, 7%, 5%, and 1%, respectively. High-level exposure to traditional risk factors, such as smoking and dyslipidemia, hemodynamic overload factors, such as anemia and hypertension, and a myriad of metabolic factors related to uremia are all likely to play a role. There has been explosive growth in observational studies and a heartening, if less dramatic, increase in risk factor intervention trials, suggesting that risk factor modification can lead to meaningful benefit.
Semin Dial
PMID:Clinical epidemiology of cardiac disease in dialysis patients: left ventricular hypertrophy, ischemic heart disease, and cardiac failure. 1264 74

Individuals with chronic kidney disease (CKD) are at increased risk for the development and progression of cardiovascular disease (CVD). The increased risk is due to a higher prevalence of both traditional risk factors as well as nontraditional risk factors. In this review we focus on individuals at all stages of CKD and discuss modifiable traditional risk factors, namely hypertension, dyslipidemia, diabetes mellitus and poor glycemic control, smoking, and physical inactivity. The prevalence of each risk factor and its relationship with CVD is described. Treatment recommendations are provided using evidence available from populations with CKD or evidence extrapolated from the general population when there are insufficient data on individuals with CKD.
Semin Dial
PMID:Traditional cardiac risk factors in individuals with chronic kidney disease. 1264 76

Growing evidence has been gathered over the last 15 years regarding the role of nontraditional or uremia-related risk factors in the pathogenesis of atherosclerosis in subjects with renal failure. Among those factors, dyslipidemia, inflammation, hyperhomocysteinemia, and oxidant stress have been extensively studied. However, the clinical significance of many of these factors remains controversial in light of reported studies. In this article, the existing evidence regarding the role of uremia-related risk factors in the pathogenesis of atherosclerosis is reviewed, with special emphasis on prevalence, cardiac risk, and management in patients with chronic kidney disease (CKD). Consensus treatment recommendations are provided for risk factors for which there is evidence to support preventive or therapeutic interventions.
Semin Dial
PMID:Uremia-related metabolic cardiac risk factors in chronic kidney disease. 1264 80

The medical, social, and financial burdens posed by end-stage renal disease (ESRD) are many and growing rapidly. People generally reach ESRD as a result of chronic progressive kidney disease. Advancing kidney disease is associated with several treatable complications, which if poorly managed reduce the length and quality of life. In addition, there are strong links between chronic kidney disease (CKD) and cardiovascular disease (CVD). Many people with less advanced CKD will die or suffer complications of CVD before reaching ESRD. Efficacious interventions, such as lowering blood pressure and treating dyslipidemia, can substantially reduce the progression of both kidney and cardiovascular disease. Careful management of these complex and interrelated diseases and risk factors requires detailed longitudinal and focused care which does not seem to be optimally delivered by health service practitioners organized in traditional ways. A disease management approach offers promise in this setting, but requires further study of clinical and economic impact.
Semin Dial
PMID:Applying multiple interventions in chronic kidney disease. 1264 81


1 2 3 4 5 Next >>