Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Induction by 7,12-dimethylbenz(a)anthracene of mammary tumors was studied in analbuminemic rats, a mutant strain established from Sprague-Dawley rats which are characterized by the absence of serum albumin and hyperlipidemia. Twenty-three weeks after carcinogen administration, the incidence and average number of mammary tumors and the tumor weight per tumor-bearing rat were respectively 35.0%, 1.7 +/- 0.2 (S.E.) and 8.9 +/- 0.5 g in analbuminemic rats and 69.2%, 2.3 +/- 0.2 and 12.2 +/- 2.8 g in the controls. Associated with this lower mammary tumorigenic response, analbuminemic rats had significantly lower plasma prolactin levels than controls during proestrus at 7-8 weeks of age when carcinogen was given (176 +/- 62 vs 308 +/- 52 ng/ml).
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PMID:Mammary tumor induction in analbuminemic rats by 7,12-dimethylbenz(a)anthracene. 642 89

The free (unbound) concentration of drug in plasma is often an important determinant of pharmacological and toxicological effects. Unfortunately, studies examining the factors influencing the free fraction of quinidine in plasma have yielded inconsistent results. It is probable that differences in the type of blood collection tubes utilized and the analytical procedure employed biased some of these estimates of quinidine binding. The present study was executed in a manner free of factors now known to introduce artifacts into estimates of the free fraction of quinidine. In healthy volunteers, the free fraction of quinidine (1.0 microgram/mL) was 0.129 +/- 0.019 (mean +/- SD) and was constant throughout the therapeutic range. A high-affinity, low-capacity binding site (K = 1.17 X 10(5) M-1; nP = 3.49 X 10(-5) M) and a low-affinity, high-capacity binding site (K = 1.33 X 10(3) M-1; nP = 3.14 X 10(-3) M) were identified. The characteristics of quinidine binding in a 4.5-g/dL solution of human serum albumin (K = 3.05 X 10(3) M-1; nP = 1.36 X 10(-3) M) suggested that the low-affinity, high-capacity binding site was on this quinidine free fraction increased from 0.114 to 0.231. A lidocaine concentration of 250 micrograms/mL caused a similar increase. Patients suffering traumatic injury had a significant increase in alpha 1-acid glycoprotein concentration (197 mg/dL) and a decreased quinidine free fraction (0.075 +/- 0.019). Patients with hyperlipidemia had free fractions similar to those observed in healthy individuals (0.118 +/- 0.019).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting quinidine protein binding in humans. 649 48

Experiments on rabbits have shown hyperlipidemia to develop within the first 48 h after a single intravenous injection of bovine serum albumin (BSA, fraction V). The mean concentration of blood plasma triglycerides (TG) was considerably higher than normal (by 262% after 24 and by 625% after 48 h). The cholesterol content was also elevated (by 80 and 270%, respectively). Following 7 and 14 days the lipid concentration returned to normal. The plasma post-heparin lipoprotein lipase activity (PHP-LPL) was lower 24 h and 7 days after BSA injection and the hypotriglyceridemic effect of heparin was less pronounced. The data obtained support the hypothesis that hyperlipidemia provoked by a single intravenous injection of BSA to rabbits results from low PHP-LPL activity and possible changes in TG-rich lipoprotein substrate affinity for the enzyme.
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PMID:[Role of lipolytic enzymes in the development of hyperlipidemia induced by administration of heterologous albumin in rabbits]. 669 22

An analbuminemic rat colony (NAR, Nagase Analbuminemia Rat) was established from Sprague-Dawley rats. The Analbuminemia was inherited as an autosomal recessive trait. The rate of growth or propagation of the mutant rats was not different from those of normal rats. Biochemically the mutant was characterized by an extraordinarily low serum albumin and hyperlipidemia. Total protein level of the serum in the mutant rat was similar to that of control Sprague-Dawley rats and globulin increased compensatorily. Serum cholesterol concentration was inversely correlated with a decrease in albumin, its correlation coefficient was -0.92. NAR may serve as a model of human familial analbuminemia. It should be also useful in elucidating the functional roles of albumin.
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PMID:Albumin-deficient rat mutant: an animal model for analbuminemia. 739

Recently there has been a renewed interest in the possibility that lipoprotein(a)--Lp(a)--may be important in the pathogenesis of thrombosis-related disease. In nephrotic syndrome, hyperlipidemia is a common finding, and thrombosis is a major complication. With this regard, if Lp(a) levels increase concomitantly with low-density lipoprotein and/or very-low-density lipoprotein levels in nephrotic syndrome, this may be considered a thrombogenic factor. To probe this possibility and to corroborate the relationship between Lp(a) and fibrinolytic profiles, we measured the Lp(a) levels in patients with nephrotic syndrome (n = 43), in patients with chronic glomerulonephritis with less proteinuria than in nephrotic syndrome (n = 28), and in healthy controls (n = 50) and observed the relation between Lp(a) levels and tissue-type plasminogen activator (t-PA) activity, euglobulin fibrinolytic activity, and t-PA antigen. The Lp(a) levels were significantly higher in the patients with nephrotic syndrome as compared with both patients with chronic glomerulonephritis and healthy controls (p < 0.001). There was a direct correlation with serum cholesterol level (r = 0.780; p = 0.0001), triglyceride level (r = 0.445; p = 0.0001), and urine protein level (r = 0.675; p = 0.0001) and a reverse correlation with serum albumin levels (r = 0.566; p = 0.0001). The Lp(a) levels showed a reverse correlation with t-pA activity (r = 0.627; p = 0.0001), total fibrinolytic activity in euglobulin fraction (r = 0.458; p = 0.0001), and t-PA activity divided by the t-PA antigen (r = 0.567; p = 0.0001), but no correlation with t-PA antigen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein(a) levels and fibrinolytic activity in patients with nephrotic syndrome. 874 69

The effect of d-alpha-tocopherol on the progression of renal dysfunction was investigated in rats injected with adriamycin (ADR), a model of progressive glomerulosclerosis associated with the nephrotic syndrome. Treatment with d-alpha-tocopherol was started 1 day before or 1 day after ADR injections (BE-TOC or AF-TOC rats). When compared to rats without d-alpha-tocopherol treatment (ADR-CON rats), the serum total cholesterol and triglyceride levels were significantly lower in the BE-TOC and AF-TOC groups. In week 16, the LDL cholesterol level and the atherogenic index were both significantly lower in BE-TOC and AF-TOC rats than in ADR-CON rats. The urinary protein, serum creatinine, blood urea nitrogen, malondialdehyde, and systolic blood pressure levels as well as the glomerulosclerosis score were high in ADR-CON rats, and reduced in BE-TOC or AF-TOC rats. There were no significant differences in body weight and serum albumin between the three groups in week 16. It is concluded that d-alpha-tocopherol can improve hyperlipidemia and ameliorate glomerulosclerosis in rats with ADR-induced progressive renal failure. Thus, d-alpha-tocopherol may have the potential for clinical application to treat focal glomerulosclerosis.
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PMID:Alpha tocopherol improves focal glomerulosclerosis in rats with adriamycin-induced progressive renal failure. 783 58

Elevated serum levels of the atherogenic and thrombogenic lipoprotein (a) (Lp(a)) have been recognized as a feature of the nephrotic syndrome associated hyperlipidaemia. To examine a possible relationship between serum Lp(a) concentration and proteinuria, serum albumin, or blood pressure, we studied nine patients with nephrotic-range proteinuria both at baseline and after various forms of antihypertensive and antiproteinuric treatment. In fixed order, patients received conventional antihypertensive treatment (either alpha-methyldopa or clonidine), subsequently ACE-inhibition therapy (lisinopril), ACE inhibition combined with an NSAID (indomethacin), and finally NSAID plus conventional antihypertensive therapy. Measurements were performed at the end of each 2-month study period. When compared to controls (n = 29), proteinuric patients before treatment showed increased levels of total cholesterol, very-low and low-density lipoprotein (VLDL+LDL) cholesterol, triglycerides and apolipoprotein B (apoB), while high-density lipoprotein (HDL) HDL cholesterol was lower. Lp(a) was significantly higher in patients (107 (95% CI: 55-208) mg/l) as compared to controls (25 (13-49) mg/l, P < 0.01). Conventional antihypertensive treatment did not reduce proteinuria, while Lp(a) remained unaffected. ACE-inhibitor treatment lowered proteinuria, raised serum albumin, while La(a) tended to fall (-11 +/- 8%). Addition of an NSAID induced a further fall in proteinuria and a rise in serum albumin. Lp(a) now fell by 40 +/- 5% from baseline values (P < 0.01). Both serum total, HDL and VLDL+LDL cholesterol fell significantly. Finally, during subsequent single therapy with NSAID most parameters, including proteinuria and Lp(a), returned towards values obtained during single therapy with ACE inhibiton.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria. 805 29

Low-density lipoprotein apheresis (LDL-A) was performed for nine episodes of steroid-resistant nephrotic syndrome in eight patients. The clinical and immunohistological findings were analysed retrospectively. Six of the patients had focal glomerular sclerosis (FGS), one had minimal-change nephrotic syndrome (MCNS), and one had membranous nephropathy (MN) with FGS. The LDL-A treatment, carried out 2-13 times (mean 7.33 +/- 4.05) for one nephrotic episode, at average intervals of 3-16 days (mean: 8.5 +/- 5.1 days) and combined with steroid pulse therapy and the administration of an antihyperlipidaemic agent in some cases, led to rapid amelioration of hyperlipidaemia. In six nephrotic episodes (5 patients) more than 50% reduction of proteinuria occurred (less than 3.5 g/day) (response-group). A significant elevation of serum albumin (more than 3.0 g/dl) was obtained in five of these episodes. The other three patients were resistant (resistant-group). The number of and intervals between LDL-A treatments in the response group (5 +/- 2.8 times and 5.8 +/- 4.1 days) were significantly less than those in the resistant-group (12.0 +/- 0.8 times and 13.2 +/- 1.8 days) (P < 0.05). After LDL-A, significant reductions were observed in the serum total cholesterol (T-CHO), phospholipid (PL), triglyceride (TG), free-CHO (F-CHO), and beta-lipoprotein (beta-lipo) (P < 0.05). HDL-cholesterol (HDL-C) increased somewhat after LDL-A. Further, Ccr was elevated in all nephrotic episodes, except in one patient who manifested renal failure after 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does LDL-apheresis in steroid-resistant nephrotic syndrome affect prognosis? 805 31

The prevalence of hyperlipidemia in adolescents and young adults who are long-term survivors of pediatric renal transplantation with stable graft function has not previously been examined. We studied 33 renal transplant recipients aged 5 to 23 years, who were an average of 7.4 years (range 3 to 11 years) post-transplant. We found hypercholesterolemia in 17 (total cholesterol (TC) > 5.18 mmol/l). Both low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) levels were increased, such that the mean TC/HDL-C and apolipoprotein B/apolipoprotein A1 (Apo B/Apo A1) ratios were below levels associated with increased coronary artery disease risk. Subjects with hypercholesterolemia did not differ from those with normal cholesterol values in current age or age at transplant, serum creatinine, serum albumin, serum triglycerides, HDL-C, TC/HDL-C ratio, Apo B/Apo A1 ratio, prednisone dose, body mass index, gender, use of thiazides or beta blockers, or family history of premature atherosclerosis. Coronary risk factors appear to cluster in these patients, with hypertension in 53% of those with hypercholesterolemia. Lipid profiles were not different in patients treated with prednisone-azathioprine vs. prednisone-azathioprine-cyclosporine A immunosuppression. A significant correlation was found between prednisone dose (mg/m2) and TC, LDL-C and TC/HDL-C. According to National Cholesterol Education Program guidelines, 32% of these long-term survivors of pediatric renal transplantation warrant at least dietary intervention and 10% are candidates for treatment with lipid-lowering drugs. This proportion is likely to increase as the safety of lipid-lowering agents is established in younger children.
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PMID:Hyperlipidemia in long-term survivors of pediatric renal transplantation. 806 64

We treated hyperlipidemia in patients with nephrotic syndrome (NS) using pravastatin for more than one year. There were 7 cases consisting of 3 with minimal change nephrotic syndrome (MCNS), 1 with focal glomerulosclerosis (FGS), 1 with proliferative glomerulonephritis (PGN), 2 with membranous glomerulonephritis (MGN) and 1 of unknown origin. Three cases consisted of frequent relapsers, and 4 were steroid-resistant. Six randomly selected age- and sex-matched nephrotic patients were used as controls. The daily excretion of proteinuria was not decreased after pravastatin treatment, but, the serum albumin rose from 3.1 +/- 1.1 to 3.4 +/- 1.0 mg/dl. The serum total cholesterol level was significantly reduced from 401 +/- 174 mg/dl to 331 +/- 103 mg/dl in spite of an absence of marked change in the control group. However, there were no significant changes in the triglyceride and lipoprotein levels. The atherogenic index was 7.1 +/- 3.7 before and 2.8 +/- 1.7 after pravastatin treatment, respectively. Improvement of renal function defined by delta decrement of renal function per year (0.08 +/- 0.06 vs. 0.12 +/- 0.26) was observed after the discontinuation of pravastatin administration in 3 out of 4 intractable cases. We conclude that pravastatin has a potent effect in reducing the serum level of total cholesterol, but not triglyceride in NS. Furthermore, pravastatin can induce renal dysfunction especially in patients with intractable nephrotic syndrome.
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PMID:Pravastatin administration to hyperlipidemia in patients with nephrotic syndrome. 813 36


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