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)

A 52-year-old Indian woman with underlying diabetes mellitus and hyperlipidemia, presented with generalized musculoskeletal pain and oliguria for three days. The patient was taking 80 mg of simvastatin initiated 20 days earlier after cardiac catheterization for an inferior myocardial infarction. Laboratory investigations revealed the following serum levels: creatine kinase 81,620 U/L, aspartate aminotransferase 2497 U/L, alanine aminotransferase 1304 U/L, blood urea nitrogen 21.7 mmol/L, creatinine 447 micromol/L, Free T4 12.6 pmol/L, and thyroid stimulating hormone (TSH) 22.7 microIU/L. Simvastatin was discontinued and the patient received forced alkaline diuresis. Her hypothyroidism was treated with thyroxin, which was continued upon discharge, and her renal function recovered within two months. This case report discusses the incidence of rhabdomyolysis in a patient with primary hypothyroidism receiving large doses of simvastatin.
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PMID:Severe rhabdomyolysis and acute renal failure secondary to use of simvastatin in undiagnosed hypothyroidism. 1911 32

A 75-year-old woman with diabetes mellitus, hypertension, and hyperlipidemia came to the emergency department with generalized and upper-extremity weakness; she had experienced a fall 2 months earlier. On admission, her drug therapy included lovastatin 40 mg/day, controlled-release diltiazem 240 mg/day, and glimepiride 1 mg/day. Nineteen days earlier, sitagliptin 100 mg/day had been started; it was discontinued 2 weeks later, and glimepiride was begun. A cardiology consultation performed on the day of admission determined that a markedly elevated creatine kinase-myocardial band isoenzyme level and borderline-high troponin I level were diagnostic of rhabdomyolysis secondary to statin use. Because the patient had been taking lovastatin for the past 12 years, the possibility that the rhabdomyolysis may have been caused by a drug interaction between lovastatin and a concomitant drug was evaluated. As it had been 10 months since her last dosage adjustment of diltiazem, it was unlikely that the statin-induced rhabdomyolysis was precipitated by diltiazem. Use of the Drug Interaction Probability Scale to determine the strength of a lovastatin-sitagliptin interaction indicated a possible association (score of 4). Multiple drug interactions have been reported with lovastatin. To our knowledge, however, this is the first case report of a possible sitagliptin-lovastatin interaction that may have caused rhabdomyolysis. Studies must be performed to further evaluate the in vivo effect of sitagliptin on the cytochrome P450 3A4 enzyme system and to elucidate other mechanisms that may potentiate such a drug-drug interaction. In the meantime, however, clinicians should be aware of this possible drug interaction.
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PMID:Rhabdomyolysis caused by a potential sitagliptin-lovastatin interaction. 1924 53

A 66 year-old woman with no history of renal or liver disease presented with progressive asthenia and diffuse myalgia. She cited 5 months history of mild hyperlipidemia under treatment with rosuvastatin (10 mg/day). Clinical examination documented both an increase in liver size and proximal muscle weakness, with difficulty in raising arms above the head. Blood tests showed the presence of renal, liver and muscle failure, with no evidence of virological, immunological or haematological diseases. Rosuvastatin treatment was stopped and blood values normalised within five days; but because of an increase in cholesterol plasma levels, rosuvastatin (10 mg/day) was restarted. Two days later, the patient returned to our observation due to the development of asthenia and muscle weakness, with an increase in creatine phosphokinase, 12,165 U/l. Rosuvastatin was discontinued and replaced with pravastatin (40 mg/day) with a complete resolution of clinical and laboratory findings in about six days. Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.
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PMID:Rosuvastatin-induced rhabdomyolysis probably via CYP2C9 saturation. 1935 2

The major component, called curcumin, of turmeric (Curcuma longa L.) (Family Zingiberaceae) powder is responsible for its biological actions. The present study aimed to prove the protective effect of turmeric extract against doxorubicin (DOX)-induced cardiac, hepatic, and renal toxicity as evaluated in rats. Body weight and urine volume of the animal groups under investigation were recorded daily throughout the experimental period. Also, the cardiac, hepatic, and renal toxicities were determined by estimating the changes in serum activities of the enzymes lactate dehydrogenase (LDH) and creatine kinase (CK), serum levels of alanine aminotransferase, aspartate aminotransferase, nitric oxide, albumin, and calcium, and kidney and liver tissue activities of superoxide dismutase and glutathione peroxidase, as well as the contents of glutathione and malondialdehyde. Hyperlipidemia was also determined, and protein and albumin changes in urine were estimated. Biochemical and histopathological findings demonstrate that turmeric extract has multiple therapeutic activities that are beneficially protective, and it has an ameliorative effect against DOX-induced cardiac toxicity and hepatotoxicity and blocks DOX-induced nephrosis. Similarly, turmeric extract inhibited the DOX-induced increase in plasma cholesterol, LDH, and CK. The present findings conclude that the turmeric extract has multiple therapeutic activities that block the cardiac, hepatic, and renal toxicities induced by DOX, and it also possibly acts as a free radical scavenger.
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PMID:The role of Curcuma longa against doxorubicin (adriamycin)-induced toxicity in rats. 1945 43

Statins are regarded as a well-tolerated class of drugs, particularly when compared with some of the older lipid-modifying agents, which have poor rates of compliance. Despite some early concern, the incidence of lens opacities observed in clinical studies involving statin use is no different from that in a normal ageing population. Similarly, the occurrence of insomnia with lipophilic agents appears to have been overemphasised and is not a clinically significant problem, irrespective of the statin under study. Fluvastatin is the newest representative of this class of agents; it has already been evaluated in thousands of patients who have hyperlipidaemia with and without additional risk factors. In controlled clinical studies, the incidence of the majority of adverse events observed with fluvastatin therapy is no higher than that seen with placebo, with the exception of gastrointestinal disturbances (known to be common to all stains). Nonetheless, the incidence of these effects seen with fluvastatin treatment is noted to be lower than that associated with cholestyramine or fibrate use. Elevations in levels of liver transaminases (aspartate aminotransferase and alanine aminotransferase) have been reported with fluvastatin therapy but have led to discontinuation of treatment with the same frequency as with placebo. Elevations in creatine kinase levels as a cause of discontinuing fluvastatin are not more frequent than with placebo. Myopathy and rhabdomyolysis have not been reported with fluvastatin therapy, and myalgia does not occur more frequently than with placebo. In terms of drug interactions, fluvastatin does not interfere with the efficacy of antihypertensive agents. In controlled clinical trials, the overall reported discontinuation rate due to adverse events noted with fluvastatin therapy is 3.3%, which is not significantly distingushable from the rate associated with placebo (3.5%)2.
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PMID:Safety profile of fluvastatin. 872 86

Hyperlipidemia is regarded as an independent risk factor in the development of ischemic heart disease, and it can increase the myocardial susceptibility to ischemia/reperfusion (I/R) injury. Ischemic postconditioning (Postcon) has been demonstrated to attenuate the myocardial injury induced by I/R in normal conditions. But the effect of ischemic Postcon on hyperlipidemic animals is unknown. Hypoxia inducible factor-1 (HIF-1) has been demonstrated to play a central role in the cardioprotection by preconditioning, which is one of the protective strategies except for Postcon. The aim of this study was to determine whether Postcon could reduce myocardial injury in hyperlipidemic animals and to assess whether HIF-1 was involved in Postcon mechanisms. Male Wistar rats underwent the left anterior descending coronary occlusion for 30 min followed by 180 min of reperfusion with or without Postcon after fed with high fat diet or normal diet for 8 weeks. The detrimental indices induced by the I/R insult included infarct size, plasma creatine kinase activity and caspase-3 activity. Results showed that hyperlipidemia remarkably enhanced the myocardial injury induced by I/R, while Postcon significantly decreased the myocardial injury in both normolipidemic and hyperlipidemic rats. Moreover, both hyperlipidemia and I/R promoted the HIF-1alpha expression. Most importantly, we have for the first time demonstrated that Postcon further induced a significant increase in HIF-1alpha protein level not only in normolipidemic but also in hyperlipidemic conditions. Thus, Postcon reduces the myocardial injury induced by I/R in normal and hyperlipidemic animals, and HIF-1alpha upregulation may involve in the Postcon-mediated cardioprotective mechanisms.
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PMID:Hyperlipidemia does not prevent the cardioprotection by postconditioning against myocardial ischemia/reperfusion injury and the involvement of hypoxia inducible factor-1alpha upregulation. 1972 23

A 52-year-old Indian woman with underlying diabetes mellitus, hyperlipidemia and undiagnosed hypothyroidism presented with generalized musculoskeletal pain and oliguria for three days. The patient was taking 80 mg of simvastatin (initiated 20 days before) after cardiac catheterization for an inferior myocardial infarction. Laboratory evaluation revealed the following serum levels: creatine kinase, 81,660 U/L; aspartate aminotransferase, 2,497 U/L; alanine aminotransferase, 1,304 U/L; blood urea nitrogen, 88 mg/dL; creatinine, 5.1 mg/dL; free thyroxine (FT(4)), 12.6 Pmol/L and thyroid stimulating hormone, 22.7 uIU/L. Simvastatin was discontinued and the patient was administered forced alkaline diuresis. Her hypothyroidism was treated with thyroxine, which was continued after discharge. Her renal function recovered within two months. This case report discusses the higher incidence of rhabdomyolysis in patients with undiagnosed hypothyroidism receiving large doses of simvastatin.
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PMID:Severe rhabdomyolysis and acute renal failure secondary to the use of simvastatin in undiagnosed hypothyroidism. 2036 19

Ischemic preconditioning (IPC) produces cardioprotection by phosphorylation of glycogen synthaes kinase-3beta (GSK-3beta) that inhibits the opening of mitochondrial permeability transition pore (MPTP), and this cardioprotective action of IPC is attenuated by hyperlipidaemia. The present study investigated the role of GSK-3beta in attenuation of cardioprotective effect of IPC, by hyperlipidaemia in the rat heart. Hyperlipidaemia was produced in rat by feeding high fat diet for six weeks. Isolated perfused rat heart was subjected to 30 min of ischemia followed by 120 min of reperfusion. Myocardial infarct size was estimated by triphenyltetrazolium chloride (TTC) staining and lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) was analyzed from coronary effluent. IPC significantly decreased the myocardial infarct size and the release of LDH and CK-MB from normal rat heart. IPC induced myocardial protection was attenuated in hyperlipidaemic rat heart. However, cardioprotective effect of pharmacological preconditioning with GSK-3beta inhibitors i.e. Lithium Chloride (LiCl) (20mM), Indirubin - 3 Monooxime (1 microM) and 3-(2, 4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2, 5-dione (SB216763) (3 microM), was not attenuated. This differential attenuation by hyperlipidaemia, of IPC and pharmacological preconditioning induced cardioprotection is a new finding in our study. GSK-3beta inhibition is reported to increase the threshold of opening for MPTP during reperfusion. Administration of atractyloside (20 microM), an opener of MPTP, significantly attenuated the cardioprotective effect of IPC in normal heart, and pharmacological preconditioning in the hyperlipidaemic rat heart. Thus, the attenuation of cardioprotective effect of IPC in hyperlipidaemic heart may be due to inhibition of protective signaling pathways upstream of GSK-3beta and inhibition of opening of MPTP.
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PMID:Modulation of the cardioprotective effect of ischemic preconditioning in hyperlipidaemic rat heart. 2059 82

The telomere length and subtelomeric methylated status of peripheral blood leukocytes has been reported to be correlated with many kinds of pathophysiological conditions. However, the correlation between the telomeric parameters and clinical laboratory data in metabolic disorders is not well known. This study investigated the correlation between the telomere length and subtelomeric methylated status in peripheral leukocytes and the laboratory data of male outpatients with combined metabolic disorders and no clinical history of cardiovascular or cerebrovascular event were assessed, to find good clinical laboratory markers reflecting the biological aging. The laboratory data were collected in 26 Japanese male outpatients with diabetes mellitus and hyperlipidemia, and no history of cardiovascular or cerebrovascular event, and the telomeric parameters in their peripheral leukocytes were determined by Southern blot with methylation-sensitive and insensitive isoschizomers. Any correlations between the laboratory data and the telomeric parameters were assessed. The patients showed a significant negative correlation among the bilirubin and creatine phosphokinase with the aging-associate change of the telomeric and subtelomeric parameters. Lowered serum bilirubin and creatinine phosphokinase level correlated to genomic aging represented by telomere attrition of patients with metabolic disorders.
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PMID:The correlation between clinical laboratory data and telomeric status of male patients with metabolic disorders and no clinical history of vascular events. 2067 Jan

Ocimum sanctum (OS) has a lipid-lowering action in both normal and diabetic animals. Because OS leaves are rich in oil, the present study was conducted to explain the anti-hyperlipidemic and organ-protective effect of OS fixed oil in rats fed with a high fat (HF) diet. OS fixed oil was extracted by hexane and the fatty acids composition identified by GC-MS. Four groups of male Wistar rats included a normal control group, a high fat fed-diet (HF) group, a HF group treated with OS fixed oil, and a HF group treated with a reference drug simvastatin. The results show that OS fixed oil contains five kinds of fatty acids, of which alpha-linolenic acid was the major fatty acid. OS fixed oil depressed high serum levels of total cholesterol, triglyceride, LDL-C, and AI, whereas no significant effect on HDL-C was observed. OS fixed oil also suppressed high levels of liver cholesterol and triglyceride with no significant effect on both lipids in feces. In addition, OS fixed oil normalized the high serum levels of LDH and CK-MB but no significant effect on high serum levels of ALT, AST, and ALP was obtained. We conclude that treatment with OS fixed oil during the last three weeks of HF diet feeding decreased the high serum lipid profile and expressed antiartherogenic and cardioprotective actions against hyperlipidemia. The anti-hyperlipidemic action of OS fixed oil was mainly resulted from the suppression of liver lipid synthesis. Linolenic acid and linoleic acid contained in OS fixed oil were possibly responsible for both lipid-lowering and cardiac protective action against hyperlipidemia.
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PMID:Anti-hyperlipidemic and cardioprotective effects of Ocimum sanctum L. fixed oil in rats fed a high fat diet. 2130 53


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