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)

Costs of providing a particular medical service can be measured, but it is more difficult to assess whether the service provides good value for the money spent. Rigorous trials have demonstrated the health benefits connected with interventions for treatment and prevention of cardiovascular disease (CVD), and in-depth analyses of the costs associated with many of those interventions have been performed. Careful use of terminology clearly differentiating among cost-minimization (relative costs of proved equivalent therapeutics), cost-effectiveness (lives saved or years of life added), and cost-benefit (total net effect in monetary terms) analyses is warranted. Although trials commonly assess clinical effectiveness as reductions in mortality or CVD-specific outcomes, improvement in quality of life may be equally important and is expressed in quality-adjusted life-years. Comparisons between therapies can be assessed as a cost-effectiveness ratio. Extensive cost-effectiveness studies have been conducted on many important cardiovascular therapies: (1) beta-blockers and diuretics for multiple CVD outcomes, mortality, and prevention of recurrent myocardial infarction (MI); (2) statins for both primary and secondary prevention of CVD; (3) enalapril for prevention and treatment of congestive heart failure; (4) tissue plasminogen activator treatment of acute MI; (5) coronary artery bypass graft for left main, single-, and 2-vessel coronary artery disease, or severe angina; (6) physician counseling for smoking; and (7) radiofrequency ablation therapy for Wolff-Parkinson-White syndrome. Therapies considered economically attractive include (1) secondary prevention with statins in hyperlipidemia, (2) smoking cessation programs, (3) primary prevention in treatment of high blood pressure with diuretics and beta-blockers, (4) primary prevention with regular exercise programs, (5) secondary prevention with cardiac rehabilitation, and (6) postinfarction treatment with beta-blockers and angiotensin-converting enzyme (ACE) inhibitors. A recent cost-minimization analysis has been performed showing aspirin to be a "best buy" therapy for secondary prevention of CVD. The Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) and Telmisartan Randomized Assessment Study in ACE-I Intolerant Patients with Cardiovascular Disease (TRANSCEND) program provide potential opportunities for both cost-minimization and cost-effectiveness analyses.
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PMID:How cost-effective are new preventive strategies for cardiovascular disease? 1278 5

We studied the effect of an eight-week treatment with telmisartan (5 mg kg(-1)day(-1)) on cardiovascular complications that are associated with type 2 diabetes in a neonatal rat model. Type 2 diabetes was induced by the administration of 90 mg/kg streptozotocin (STZ), ip, in two-day-old rats. The development of diabetes was checked 12 weeks after STZ administration, and the animals were divided into different groups. Telmisartan treatment was given for eight weeks. At the end of the eight-week treatment, various biochemical and cardiac parameters were measured. Diabetic rats exhibited hyperglycemia, hyperinsulinemia, hyperlipidemia, increased blood pressure and heart rate, increased creatinine, cardiac enzyme and C-reactive protein (CRP) levels, a reduction in the rate of pressure development and decay, cardiac hypertrophy and oxidative stress. Chronic treatment with telmisartan significantly prevented STZ-induced hypertension and tachycardia and elevated fasting glucose and insulin levels. It significantly prevented the dyslipidemia and significantly reduced the elevated creatinine and CRP levels and the levels of other cardiac enzyme markers, like lactate dehydrogenase and creatinine kinase, in diabetic rats. There was an increase in rate of blood pressure development and decay with telmisartan treatment. Telmisartan also produced beneficial effects by preventing cardiac hypertrophy, which was evident from left ventricular collagen levels, the cardiac hypertrophy index and the left ventricular hypertrophy index in diabetic rats. Telmisartan successfully prevented oxidative stress, which was evidenced by a decrease in malondialdehyde and an increase in glutathione, catalase, superoxide dismutase levels. In conclusion, our data suggest that telmisartan prevented STZ-induced metabolic abnormalities and cardiovascular complications in type 2 diabetes.
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PMID:Beneficial role of telmisartan on cardiovascular complications associated with STZ-induced type 2 diabetes in rats. 2200 83

Anastrozole is a selective non-steroidal aromatase inhibitor that blocks the conversion of androgens to estrogens in peripheral tissues. It is used as adjuvant therapy for early-stage hormone-sensitive breast cancer in postmenopausal women. Significant side effects of anastrozole include osteoporosis and increased levels of cholesterol. To date, seven case reports on anastrozole hepatotoxicity have been published. We report the case of an 81-year-old woman with a history of breast cancer, arterial hypertension, type 2 diabetes mellitus, hyperlipidemia, and chronic renal insufficiency. Four days after switching hormone therapy from tamoxifen to anastrozole, icterus developed along with a significant increase in liver enzymes (measured in the blood). The patient was admitted to hospital, where a differential diagnosis of jaundice was made and anastrozole was withdrawn. Subsequently, hepatic functions quickly normalized. The observed liver injury was attributed to anastrozole since other possible causes of jaundice were excluded. However, concomitant pharmacotherapy could have contributed to the development of jaundice and hepatotoxicity, after switching from tamoxifen to anastrozole since several the patient's medications were capable of inhibiting hepatobiliary transport of bilirubin, bile acids, and metabolized drugs through inhibition of ATP-binding cassette proteins. Telmisartan, tamoxifen, and metformin all block bile salt efflux pumps. The efflux function of multidrug resistance protein 2 is known to be reduced by telmisartan and tamoxifen and breast cancer resistance protein is known to be inhibited by telmisartan and amlodipine. Moreover, the activity of P-glycoprotein transporters are known to be decreased by telmisartan, amlodipine, gliquidone, as well as the previously administered tamoxifen. Finally, the role of genetic polymorphisms of cytochrome P450 enzymes and/or drug transporters cannot be ruled out since the patient was not tested for polymorphisms.
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PMID:Drug-induced liver injury after switching from tamoxifen to anastrozole in a patient with a history of breast cancer being treated for hypertension and diabetes. 3324 Apr 77