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)

Muscle weakness and tenderness together with a rise in serum creatine kinase (C.K.) were noted in five uraemic patients treated with 1-2 g of clofibrate ('Atromid-S') daily. Excessive accumulation of both total and free serum chlorophenoxyisobutyric acid (C.P.I.B.), the active circulating metabolite after clofibrate therapy, was found in three patients in whom it was sought. It is suggested that chronic renal failure should be regarded as a contraindication to the use of clofibrate for the treatment of any coexisting hyperlipidaemia. If such therapy is contemplated it must be cautiously instituted at low dosage and the patient monitored by regular assessment of serum C.K. and levels of both total and free C.P.I.B.
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PMID:Clofibrate-induced muscle damage in patients with chronic renal failure. 5

The pharmacokinetics of the hypolipidemic agent, clofibrate have been studied in anuric patients on intermittent hemodialysis. In addition we have tried to determine whether the treatment of hyperlipidemia of chronic renal failure with clofibrate was safe and efficacious. Seven healthy volunteers and five uremic patients received a single dose of 25 mg/kg body weight of clofibrate. Mean peak plasma levels of clofibrate were comparable in both groups and were reached 3.5 hr after drug ingestion in the control subjects and after 6.5 hr in the uremic patients. The mean plasma half-life of clofibrate was 16.7 hr and 68.4 hr in the control subjects and in the patients, respectively (P less than 0.001). Following a short loading period a daily oral maintenance dose of 5 mg/kg body weight was given leading to a plasma clofibrate level of 75-100 microgram/100 ml. Five hyperlipidemic uremic patients received this dose for 3 months. Their plasma clofibrate and creatine kinase levels were constantly monitoried to detect clofibrate myotoxicity which we have observed in uremic patients at plasma levels generally considered safe in patients with normal renal function. Significant decreases in serum total lipid, triglyceride, and cholesterol levels were observed when compared to pretreatment values. In two of the 5 patients serum lipids remained decreased for 10 and 14 months. It is concluded that clofibrate treatment of hyperlipidemia in uremic patients, when carefully monitored, is safe and efficacious.
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PMID:Clofibrate treatment of hyperlipidemia in chronic renal failure. 59 55

The clinical laboratory furnishes information valuable not only in the diagnosis of myocardial infarction (MI), but also in screening for possible causes of ischemic heart disease through definition of the lipid status of individuals. Accordingly, the panels used in the study of hyperlipidemia as a possible cause of ischemic heart disease are reviewed, including the determination of serum cholesterol, triglycerides, and electrophoretic development of the lipoprotein pattern. The results of an on-going study of more than 500 patients admitted to the emergency room of a general hospital with symptoms of "chest pain" are presented--including the electrocardiogram, enzyme tests, and isoenzyme patterns, in conjuction with the clinical picture. The relative diagnostic value of test procedures is considered, convering the pre-enzymatic period, current test panels, and possible future approaches. It is concluded that the laboratory's position in providing data for diagnosis of MI would be enhanced through development of procedures with as great or greater specificity than the isoenzyme patterns of creatine kinase and lactate dehydrogenase, currently the most specific indicators of MI, but which have results available in two to five minutes.
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PMID:The cardiac profile. 64 63

Case 1, a 60-year-old man and case 2, a 70-year-old man had several year history of chronic renal failure with hypertension and hyperlipidemia due to diabetes mellitus. Treatment of hyperlipidemia was started by oral bezafibrate intake 1,200 mg per day in case 1 and 400 mg per day in case 2 respectively. Three to fourteen days later, both patients noticed symmetrical muscle pain and weakness. Then the symptoms worsened and they were hospitalized. At the time of admission, both patients revealed weakness in the proximal muscles of their upper and lower limbs and the serum creatine kinase and myoglobin levels were remarkably elevated. Myoglobinuria was also noted. Routine light microscopic examination of biopsied quadriceps femoris muscles of two patients showed scattered necrotic muscle fibers, some of which were under phagocytosis. The symptoms of the patients were immediately resolved after the drug was discontinued. Serum concentration of bezafibrate was remarkably elevated during treatment. Thus the diagnosis was established as having bezafibrate induced myopathy and, as far as we know, this is the first report of bezafibrate induced myopathy in Japan. On the basis of the above description, bezafibrate may induce muscle damage if dose is excess over the renal capacity. Extreme caution is warranted when the patient is placed on bezafibrate and has renal dysfunction. Strict dose adjustment is necessary in taking account of renal function to avoid muscle damage including rhabdomyolysis.
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PMID:[Bezafibrate myopathy in two patients with chronic renal failure]. 129 Nov 64

Hypercholesterolemia (type II hyperlipidemia) after cardiac transplantation is common and may play a role in the accelerated rate of coronary atherosclerosis seen following the procedure. However, conventional cholesterol-lowering drugs are either ineffective or contraindicated for use in transplant recipients. The presence of type II hyperlipidemia was identified in 11 cardiac transplant recipients during a mean follow-up period of 15 months (range 3 to 41) after transplantation. Lovastatin, at an initial dosage of 20 mg/day, was administered for a period of 1 year. The maximal dosage of lovastatin was 60 mg/day. All patients received maintenance dosages of immunosuppressive agents, including cyclosporine-A, prednisone and, in some instances, azathioprine. Lipid profiles, hepatic transaminases, serum creatinine, creatine kinase and cyclosporine-A serum trough levels were measured quarterly. Total cholesterol decreased by 27% (354 +/- 50 vs 258 +/- 36 mg/dl, p less than 0.01) after 3 months and remained stable thereafter. Similarly, low density lipoprotein cholesterol decreased by 34% (221 +/- 51 vs 146 +/- 40 mg/dl, p less than 0.01) after 3 months and remained constant. Triglycerides, high density lipoprotein, hepatic transaminases, creatinine, creatine kinase and trough cyclosporine-A levels remained stable during the 1-year follow-up period. Lovastatin was uniformly well tolerated in this study group. When given in modest dosages, lovastatin appears to be a safe, effective and well-tolerated therapy for hypercholesterolemia in cardiac transplant recipients.
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PMID:Lovastatin therapy for hypercholesterolemia in cardiac transplant recipients. 267 84

A total number of 30 native breed cows were used in this investigation. Ten animals were clinically healthy and kept as control, while 20 diseased cows were selected according to rectal findings. At the beginning of the disease, the cows appeared obese with marked deposition of fat in the subcutaneous tissue at the lumbosacral area, later on they became emaciated. Additional signs were digestive disturbance in form of diarrhea or constipation and tympany. Rectal examination revealed hard irregular masses of various size which were palpated in the pelvis, the perirenal area around the colon and the rectum. More information about the nature and character of the lesions were taken from slaughtered cows. Biochemical analysis, including total lipids, cholesterol triglycerides and creatine kinase, were carried out in both healthy and diseased cows. In advanced cases of bovine lipomatosis hyperlipemia and hypercholesterolemia as well as increased creatine kinase values were constant findings. The aetiology of this disease is still unknown.
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PMID:[Accumulated occurrence of lipomatosis in a cattle herd in Assiut (Egypt)]. 322 88

Hyperlipidemia, particularly hypercholesterolemia, occurs in cardiac transplant recipients both as a preexisting condition and as a consequence of immunosuppressive therapy. Lovastatin (Mevacor) has emerged as an agent that may effectively manage this condition. Few serious side effects of this drug have been observed. We describe two cardiac transplant recipients treated with lovastatin in conjunction with their other medications, including cyclosporine, who developed acute renal failure and rhabdomyolysis. Resolution of muscle damage followed discontinuation of cyclosporine and lovastatin therapy. We postulate that hepatic dysfunction secondary to cyclosporine predisposed these patients to lovastatin-induced muscle damage. Use of this drug in cardiac and other organ transplant recipients should be accompanied by close surveillance of creatine kinase, hepatic transaminases, and cyclosporine levels.
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PMID:Rhabdomyolysis and renal injury with lovastatin use. Report of two cases in cardiac transplant recipients. 329 May 20

The clinical and echocardiographic variables related to postinfarction angina were evaluated in 54 patients with acute myocardial infarction. All patients underwent 2D echocardiography at 2-3 weeks after infarction. Wall motion analysis was quantified with a wall motion score index (WMSI) based on 16 left ventricular wall segments. Among the 54 patients with acute myocardial infarction 23 (42.6%) had early postinfarction angina. Multiple regression analysis demonstrated no significant difference between the patients with and without postinfarction angina in age, sex, location of infarction, Killip classification, previous angina, hypertension, hyperlipidemia, diabetes mellitus, creatine kinase level and left ventricular ejection fraction. In comparison with patients without postinfarction angina, patients with postinfarction angina had higher WMSI. It indicates that postinfarction angina appears to be related more to myocardial ischemia rather than to the infarct of myocardium.
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PMID:[Analysis of risk factors in postinfarction angina]. 788 38

In this preliminary report of a 20-week trial, 66 patients with non-insulin-dependent diabetes mellitus (NIDDM) and hyperlipidaemia who remained eligible after an 8-week dietary stabilization phase were randomly allocated to receive 20 mg of fluvastatin or placebo once daily for 6 weeks. Fluvastatin was subsequently increased to 20 mg twice daily and administered according to the same schedule, versus placebo, for a further 6 weeks. Both dosages of fluvastatin substantially improved serum lipid profiles compared with baseline and placebo. Both dosages of fluvastatin significantly reduced low-density- and very-low-density-lipoprotein (LDL, VLDL), cholesterol and triglyceride (TG) compared with placebo, and both dosages significantly elevated high-density-lipoprotein (HDL) cholesterol. The ratio of LDL to HDL was also significantly decreased. Amongst the 58 patients who completed the study, there was no evidence either of myopathy or of hepatotoxicity; mean creatine kinase values remained stable in the fluvastatin arm. Fasting glucose, glycosylated haemoglobin, and fructosamine levels were not markedly affected by active treatment. No serious adverse events attributable to the drug were reported. In conclusion, both dosages of fluvastatin appear to be effective and safe in the management of hyperlipidaemia in this outpatient, maturity-onset, diabetic population.
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PMID:Efficacy and safety of fluvastatin in hyperlipidaemic patients with non-insulin-dependent diabetes mellitus. 798 2

A 61-year-old woman with hyperlipidemia was treated with gemfibrozil. She also had insulin-treated diabetes mellitus and chronic renal failure and was admitted because of severe chest pain. The ST segment was depressed and creatine kinase levels were elevated. The original diagnosis was acute myocardial infarction. In the presence of increasing chest pain, the onset of limb muscle tenderness, and increasing levels of creatine kinase, the diagnosis of myopathy secondary to gemfibrozil therapy was made and the drug was discontinued. All symptoms then subsided and creatine kinase levels returned to normal. Myopathy is a well-known complication of blood lipid-lowering drugs, especially in patients with renal failure.
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PMID:[Gemfibrozil-induced myopathy]. 825 19


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