Comparison of the effects of atorvastatin or fenofibrate on nonlipid biochemical risk factors and the LDL particle size in subjects with combined hyperlipidemia

Melenovský, Vojtěch; Malík, Jan; Wichterle, Dan; Simek, J; Písaříková, A.; Škrha, J; Poledne, R.; Stávek, P.; Češka, Richard

doi:10.1016/s0002-8703(02)00142-4

Cited by 56 publications

(35 citation statements)

References 27 publications

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“…These findings are in agreement with the small number of studies evaluating the influence of statin therapy on homocysteine levels. [21][22][23][24][25] However, it has been reported that higher doses of simvastatin (i.e., 80 mg daily) produce a significant reduction in total serum homocysteine levels. 21 Interestingly, in a pilot study run for the Study Evaluating Additional Reduction in Cholesterol and Homocysteine (SEARCH) trial, simvastatin (80 mg daily) combined with vitamin B12 and folic acid produced a similar reduction in homocysteine levels to vitamin supplementation alone.…”

Section: Discussionmentioning

confidence: 99%

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Comparative Effects of Atorvastatin, Simvastatin, and Fenofibrate on Serum Homocysteine Levels in Patients with Primary Hyperlipidemia

Milionis

Papakostas

Kakafika

et al. 2003

The Journal of Clinical Pharma

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Hyperhomocysteinemia is regarded as an independent risk factor for cardiovascular disease. Lipid-lowering agents, such as fibrates, can modify homocysteine levels. However, less is known about the effect of statin therapy on homocysteine. The authors compared the effects of atorvastatin (40 mg/day), simvastatin (40 mg/day), and micronized fenofibrate (200 mg/day) on the serum concentrations of total homocysteine, vitamin B12, and folic acid in patients with primary hyperlipidemia. A total of 128 patients with primary hyperlipidemia (total cholesterol > 240 mg/dL and triglycerides < 350 mg/dL) were assigned to atorvastatin, simvastatin, or fenofibrate. Serum lipid and metabolic parameters were measured at baseline and at 6 and 12 weeks of treatment. Homocysteine correlated positively with serum creatinine and uric acid levels and inversely with serum folic acid levels. All treatment modalities reduced total, low-density lipoprotein (LDL) cholesterol, and triglyceride concentrations. High-density lipoprotein (HDL) cholesterol levels significantly increased only in the fenofibrate-treated patients (47.9 +/- 12.5 vs. 50.7 +/- 12.6 vs. 51.2 +/- 12.8 mg/dL, p < 0.01). Atorvastatin and fenofibrate treatment resulted in a significant reduction of serum uric acid levels (5.3 +/- 1.6 vs. 4.9 +/- 1.4 vs. 4.8 +/- 1.4 mg/dL, p < 0.0001 for atorvastatin; 5.6 +/- 1.6 vs. 4.3 +/- 1.4 vs. 4.4 +/- 1.4 mg/dL, p < 0.0001 for fenofibrate). Homocysteine levels were significantly increased only by fenofibrate (10.3 +/- 3.3 vs. 14.1 +/- 3.8 vs. 14.2 +/- 3.6 microU/L, p < 0.001) but did not change from baseline following statin treatment. Neither statins nor fenofibrate had any effect on serum vitamin B12 and folic acid levels. In contrast to fenofibrate, therapeutic dosages of atorvastatin and simvastatin have a neutral effect on serum homocysteine levels, which is in favor of their "cardioprotective" properties.

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Section: Discussionmentioning

confidence: 99%

“…[13][14][15][16][17][18][19][20] However, less is known about the effect of statin therapy on homocysteine levels. [21][22][23][24][25] We compared the effects of a synthetic and a natural statin (i.e., atorvastatin, simvastatin) and a fibrate (fenofibrate) on serum concentrations of total CLINICAL STUDIES J Clin Pharmacol 2003;43:825-830…”

mentioning

confidence: 99%

Comparative Effects of Atorvastatin, Simvastatin, and Fenofibrate on Serum Homocysteine Levels in Patients with Primary Hyperlipidemia

Milionis

Papakostas

Kakafika

et al. 2003

The Journal of Clinical Pharma

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“…On the other hand, several pharmacolagic molecules have been showed to reduce CRP levels. Lipid-modulating medications, including 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), fi brates and niacin, have been found to infl uence directly, beyond lipid lowering properties, infl ammatory serum factor levels (Blake and Ridker 2002;Melenovsky et al 2002;Kashyap et al 2002). Statins reduced CRP concentrations through a direct action on hepatocyte intracellular signalling pathways (Ridker et al 1999;Arnaud et al 2005).…”

Section: Therapeutic Strategies To Reduce Crp Levelsmentioning

confidence: 99%

New evidences for C-reactive protein (CRP) deposits in the arterial intima as a cardiovascular risk factor

Montecucco

Mach

2008

CIA

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Infl ammatory processes are orchestrated by several soluble molecules, which interact with cell populations involved. Cytokines, chemokines, acute-phase reactants, and hormones are crucial in the evolution of several infl ammatory disorders, such as atherosclerosis. Several evidences suggest that C-reactive protein (CRP) started to be considered as a cardiovascular risk factor, since CRP directly induces atheroslerosis development. The recent demonstration of CRP production not only by the liver, but also within atherosclerotic plaques by activated vascular cells, also suggests a possible dual role, as both a systemic and tissue agent. Although more studies are needed, some therapeutic approaches to reduce CRP levels have been performed with encouraging results. However, given the strong limitations represented by its low specifi city and still accordingly with the American Heart Association, there is no need for high sensitivity CRP screening of the entire adult population as a public-health measure. The measure of serum CRP might be useful only for patients who are considered at intermediate risk.

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“…51 The same uric-acid-lowering effect of atorvastatin was not observed in patients with combined hyperlipidaemia. 52 Fenofibrate, but not other fibrates, has been shown to enhance renal uric acid clearance and reduce SUA concentrations. 53 In patients treated for gout with allopurinol or benzbromarone, the addition of fenofibrate results in additional uric acid reduction.…”

Section: Treatment Of Associated Conditionsmentioning

confidence: 99%

Emerging therapies in the long‐term management of hyperuricaemia and gout

Stamp¹,

O’Donnell²,

Chapman³

2007

Internal Medicine Journal

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Gout is a common chronic arthritis that can lead to significant disability. Gout is one of the few rheumatological conditions that can be diagnosed with certainty, has a known cause and can be cured with appropriate therapy. Hypouricaemic agents reduce uric acid concentrations through inhibiting uric acid production (allopurinol) or enhancing uric acid excretion (probenecid, benzbromarone). Allopurinol is the most commonly used hypouricaemic agent but at recommended doses often fails to reduce adequately uric acid concentrations and prevent acute attacks of gout. The use of probenecid is limited by lack of efficacy in renal impairment. In the last few years, new agents in the management of hyperuricaemia and gout have become available. Febuxostat, a new xanthine oxidase inhibitor, is an effective hypouricaemic agent although further data are required for patients with renal impairment and other significant medical conditions. Rasburicase, a recombinant uricase (which catalyses the conversion of uric acid to the more readily excreted allantoin) is available for prevention of tumour lysis syndrome. However, its repeated use, as would be required in chronic gout, is limited by antigenicity. A less antigenic PEGylated uricase can rapidly reduce serum uric acid concentrations and promote resorption of tophi. However, further information with regard to the long-term risks and benefits of these agents is required. These agents may ultimately be used in the short term to rapidly deplete urate stores (induction therapy) followed by long-term therapy with an alternative hypouricaemic agent to prevent subsequent accumulation of uric acid (maintenance therapy).

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Comparison of the effects of atorvastatin or fenofibrate on nonlipid biochemical risk factors and the LDL particle size in subjects with combined hyperlipidemia

Cited by 56 publications

References 27 publications

Comparative Effects of Atorvastatin, Simvastatin, and Fenofibrate on Serum Homocysteine Levels in Patients with Primary Hyperlipidemia

Comparative Effects of Atorvastatin, Simvastatin, and Fenofibrate on Serum Homocysteine Levels in Patients with Primary Hyperlipidemia

New evidences for C-reactive protein (CRP) deposits in the arterial intima as a cardiovascular risk factor

Emerging therapies in the long‐term management of hyperuricaemia and gout

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