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Lipid-modifying Therapy (lipid-modifying + therapy)
Selected AbstractsInterpreting clinical trials of diabetic dyslipidaemia: new insightsDIABETES OBESITY & METABOLISM, Issue 3 2009A. S. Wierzbicki Current treatment guidelines highlight the importance of aggressive lipid-modifying therapy in reducing cardiovascular risk in patients with type 2 diabetes. Statins are established as the cornerstone of dyslipidaemia management in diabetic patients, based on their efficacy in lowering levels of low-density lipoprotein cholesterol (LDL-C). However, statins fail to address the high residual cardiovascular risk in treated patients, some of which may be attributable to low HDL cholesterol (HDL-C) and elevated triglycerides and to a preponderance of small, dense LDL particles, indicating the need for further intervention. Fibrates are effective against all components of atherogenic dyslipidaemia associated with type 2 diabetes. Clinical studies, most notably the Fenofibrate Intervention and Event Lowering in Diabetes, indicate that fibrates, most likely in combination with a statin, have a secondary role in reducing cardiovascular risk in patients with type 2 diabetes, particularly in those without prior cardiovascular disease or patients with low HDL-C. Results are awaited from the ongoing Action to Control Cardiovascular Risk in Diabetes trial to fully evaluate the outcome benefits of this combination strategy. [source] Nicotinic acid/laropiprant: a new lipid-modifying therapyFUTURE PRESCRIBER, Issue 1 2009MRPharmS Medical Writer, Steve Chaplin MSc Cardiovascular disease (CVD) is a leading cause of death in the UK.1 Blood choleserol levels are a key risk factor for CVD, and can be modified by both drug treatment and lifestyle changes. In this article, Steve Chaplin considers the available clinical data on a new lipid-modifying therapy, a modified-release formulation of nicotinic acid and laropiprant; and Marc Evans comments on its potential contribution to reducing the risk of CVD. Copyright © 2009 John Wiley & Sons, Ltd. [source] LIPID-LOWERING IMPROVES ENDOTHELIAL FUNCTION IN NEPHROTIC RANGE PROTEINURIANEPHROLOGY, Issue 3 2000G. Dogra OBJECTIVE: To determine whether lipid-modifying therapy with atorvastatin improves impaired endothelial function in patients with nephrotic range proteinuria (NRP). METHODS: A sequential, open-label study of the effects of atorvastatin on dyslipidaemia and endothelial dysfunction in 9 patients with NRP. Endothelial function was assessed at baseline, after 12 weeks of atorvastatin treatment and after an 8 week wash-out period. Brachial artery endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) using ultrasonography. Endothelium- independent, glyceryl trinitrate (GTN) mediated vasodilatation was also measured. RESULTS: At baseline, median serum albumin was 31g/L (range 20-40) and 24 hour protein excretion was 4.7g (1.0-16.23). There was no significant change in serum creatinine and 24 hour protein excretion during the study. Total cholesterol (TC) and triglycerides (TG) were significantly lower following treatment with atorvastatin 20mg (20-40): TC 8.1mmol/L (5.9-14.9) vs. 5.2 (4.0-8.6), TG 2.9mmol/L (1.3-15.0) vs. 1.6 (1.0-3.5), both p < 0.05. Brachial artery FMD improved significantly following atorvastatin treatment: 2.1% (-1.2- 5.2%) to 4.7% (0.8-16.3%), p < 0.05. At the end of the 8 week wash-out, FMD had significantly deteriorated to 3.2% (-2.8-8.2), p < 0.05 vs. week 12 FMD, and was similar to pre-treatment values. GTN mediated dilatation was unchanged through the study. CONCLUSION: Atorvastatin significantly reduced the hyperlipidaemia of NRP. This was associated with improved conduit artery endothelial function after 12 weeks of treatment. This is consistent with the hypothesis that dyslipoproteinaemia is the primary cause of endothelial dysfunction in NRP. [source] | ||||||||||