Rosuvastatin for lowering lipids

BACKGROUNDNo published studies have assessed the efficacy and safety of rosuvastatin generics.OBJECTIVESPrimary objective to assess the safety and efficacy of a generic rosuvastatin in reducing plasma low-density-lipoprotein cholesterol (LDL-C) in Lebanese dyslipidemic patients. Changes in high-density lipoprotein cholesterol, triglycerides and adverse effects were secondary objectives.DESIGNProspective, observational, non-comparative.SETTINGMultiple outpatient clinics in Lebanon.PATIENTS AND METHODSDyslipidemic patients requiring statin therapy were followed for 2 months after prescription of a generic rosuvastatin at the physician’s discretion. Efficacy and safety measurements were collected from medical records.MAIN OUTCOME MEASURE(S)Efficacy was assessed based on the evaluation of mean and percent change in LDL-C between baseline and week 8 as well as the proportion of patients reaching target LDL-C levels. Safety was assessed based on the evaluation of the incidence of adverse events (AEs) during the study period.RESULTSTwo months after initiation of generic rosuvastatin, LDL-C levels in the 313 eligible patients who completed the study significantly decreased from 4.3 (0.8) mmol/L (168.2 [31.3] mg/dL) at baseline to 2.7 (0.7) mmol/L (105.9 [25.5] mg/dL) (P<.001). The mean percent change in LDL-C level was highest in subjects receiving generic rosuvastatin at a dose of 40 mg/day (−47.4%), followed by 20 mg/day (−36.8%), and 10 mg/day (−31.4%); 82.5% of patients reached the target LDL-C level as set by their physician at baseline. Thirteen patients (4%) reported six AEs during treatment: abdominal pain, headache, stomach ache, insomnia, musculoskeletal pain/myalgia and nausea. No clinically significant changes in serum creatinine, serum creatine kinase, or liver function tests were reported. One patient withdrew because of an adverse event.CONCLUSIONSGeneric rosuvastatin was efficacious and safe in reducing LDL-C levels and helping the majority of patients achieve LDL-C targets after a short treatment period.LIMITATIONSThe observational nature, and a control group, and the relatively short duration of follow-up limit the generalizability of results. The authors received fees for study activities at patient visits from an independent clinical research organization subcontracted by the sponsor.

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“…This difference can be due to the relatively low baseline TG levels in our study compared to those usually reported in trials. 31 …”

Section: Discussionmentioning

confidence: 99%

Efficacy and safety of a generic rosuvastatin in a real-world setting: prospective, observational clinical study in Lebanese patients

Betto

Fares

Saliba

et al. 2017

Annals of Saudi Medicine

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“…The critical role played by LDL-C in atherosclerosis has prompted the development of rational strategies to counter the pathogenic effects of hypercholesterolemia. The use of statins (inhibitors of HMG-CoA reductase, the rate-controlling enzyme of the mevalonate, and cholesterol synthesis pathways) as a pharmacological approach to lower cholesterol levels is one of the most widely used therapies in the treatment of atherosclerosis and acute coronary syndromes, as these drugs show consistent clinical event reductions with a very good safety profile (Adams et al, 2014). Other clinical studies reveal that the use of ezetimibe (an inhibitor of intestinal cholesterol absorption) considerably reduces LDL-C blood levels when combined with statins (Catapano et al, 2016).…”

Section: Importance Of Cardiopulmonary Diseasesmentioning

confidence: 99%

“…Other clinical studies reveal that the use of ezetimibe (an inhibitor of intestinal cholesterol absorption) considerably reduces LDL-C blood levels when combined with statins (Catapano et al, 2016). An alternative approach is the administration of fibrates, a particular class of agonists of the peroxisome proliferator-activated receptor α (PPAR-α) a regulator of lipoprotein metabolism, showing a good effect in lowering TG levels as mono-therapy, even though the results are not as promising as for the statins (Adams et al, 2014). Recently, a large multi-scale and multiethnic study was undertaken to better understand the role of genetic and environmental factors in CVD and to identify genetic variants associated to blood lipids levels (Klarin et al, 2018).…”

Section: Importance Of Cardiopulmonary Diseasesmentioning

confidence: 99%

Metabolic Alterations in Cardiopulmonary Vascular Dysfunction

Smolders

Zodda

Quax

et al. 2019

Front. Mol. Biosci.

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Cardiovascular diseases (CVD) are the leading cause of death worldwide. CVD comprise a range of diseases affecting the functionality of the heart and blood vessels, including acute myocardial infarction (AMI) and pulmonary hypertension (PH). Despite their different causative mechanisms, both AMI and PH involve narrowed or blocked blood vessels, hypoxia, and tissue infarction. The endothelium plays a pivotal role in the development of CVD. Disruption of the normal homeostasis of endothelia, alterations in the blood vessel structure, and abnormal functionality are essential factors in the onset and progression of both AMI and PH. An emerging theory proposes that pathological blood vessel responses and endothelial dysfunction develop as a result of an abnormal endothelial metabolism. It has been suggested that, in CVD, endothelial cell metabolism switches to higher glycolysis, rather than oxidative phosphorylation, as the main source of ATP, a process designated as the Warburg effect. The evidence of these alterations suggests that understanding endothelial metabolism and mitochondrial function may be central to unveiling fundamental mechanisms underlying cardiovascular pathogenesis and to identifying novel critical metabolic biomarkers and therapeutic targets. Here, we review the role of the endothelium in the regulation of vascular homeostasis and we detail key aspects of endothelial cell metabolism. We also describe recent findings concerning metabolic endothelial cell alterations in acute myocardial infarction and pulmonary hypertension, their relationship with disease pathogenesis and we discuss the future potential of pharmacological modulation of cellular metabolism in the treatment of cardiopulmonary vascular dysfunction. Although targeting endothelial cell metabolism is still in its infancy, it is a promising strategy to restore normal endothelial functions and thus forestall or revert the development of CVD in personalized multi-hit interventions at the metabolic level.

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“…Rosuvastatin is the most powerful widely‐prescribed statin worldwide; due to its rapid absorption, achieving peak plasma concentration within three hours. Moreover, its lipid‐lowering effect is not influenced by the time‐of‐day by which it is administered; due to the comparatively long half‐life of 20 hours [ 16 , 17 ]. Accordingly, the current study has been initiated to investigate, on mechanism-based, the possible therapeutic effects of rosuvastatin when combined with androgen deprivation in metastatic prostate cancer patients.…”

Section: Introductionmentioning

confidence: 99%

The prognosis of lipid reprogramming with the HMG-CoA reductase inhibitor, rosuvastatin, in castrated Egyptian prostate cancer patients: Randomized trial

et al. 2022

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Aim The role of surgical castration and rosuvastatin treatment on lipid profile and lipid metabolism related markers was evaluated for their prognostic significance in metastatic prostate cancer (mPC) patients. Methods A total of 84 newly diagnosed castrated mPC patients treated with castration were recruited and divided into two groups: Group I served as control (statin non-users) while group II treated with Rosuvastatin (20 mg/day) for 6 months and served as statin users. Prostate specific antigen (PSA), epidermal growth factor receptor (EGFR), Caveolin-1 (CAV1), lipid profile (LDL, HDL, triglycerides (TG) and total cholesterol (TC)) and lipid metabolism related markers (aldoketoreductase (AKR1C4), HMG-CoA reductase (HMGCR), ATP-binding cassette transporter A1 (ABCA1), and soluble low density lipoprotein receptor related protein 1 (SLDLRP1)) were measured at baseline, after 3 and 6 months. Overall survival (OS) was analyzed by Kaplan-Meier and COX regression for prognostic significance. Results Before castration, HMG-CoA reductase was elevated in patients <65 years (P = 0.009). Bone metastasis was associated with high PSA level (P = 0.013), but low HMGCR (P = 0.004). Patients with positive family history for prostate cancer showed high levels of EGFR, TG, TC, LDL, alkaline phosphatase (ALP), but low AKR1C4, SLDLRP1, CAV1 and ABCA-1 levels. Smokers had high CAV1 level (P = 0.017). After 6 months of castration and rosuvastatin administration, PSA, TG, LDL and TC were significantly reduced, while AKR1C4, HMGCR, SLDLRP1, CAV1 and ABCA-1 were significantly increased. Overall survival was reduced in patients with high baseline of SLDLRP1 (>3385 pg/ml, P = 0.001), PSA (>40 ng/ml, P = 0.003) and CAV1 (>4955 pg/ml, P = 0.021). Conclusion Results of the current study suggest that the peripheral lipidogenic effects of rosuvastatin may have an impact on the treatment outcome and survival of castrated mPC patients. Trail registration This trial was registered at the Pan African Clinical Trial Registry with identification number PACTR202102664354163 and at ClinicalTrials.gov with identification number NCT04776889.

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Rosuvastatin for lowering lipids

Cited by 45 publications

References 208 publications

Efficacy and safety of a generic rosuvastatin in a real-world setting: prospective, observational clinical study in Lebanese patients

Efficacy and safety of a generic rosuvastatin in a real-world setting: prospective, observational clinical study in Lebanese patients

Metabolic Alterations in Cardiopulmonary Vascular Dysfunction

The prognosis of lipid reprogramming with the HMG-CoA reductase inhibitor, rosuvastatin, in castrated Egyptian prostate cancer patients: Randomized trial

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