Context: The present review aimed at reviewing the effects of different statins on lipid profile, particularly in Asians. Evidence Acquisition: PubMed searches were conducted using the keywords 'statin, effect, and lipid profile' from database inception through March 2016. In this review, 718 articles were retrieved from the primary search. After reviewing the titles, abstracts, and full texts, we found that 59 studies met our inclusion criteria. These also included subsequent reference searches of retrieved articles. Results: CURVES study compared the effect on lipid profile between atorvastatin and other statins. This study demonstrated that low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TG) were reduced more with atorvastatin compared to simvastatin, pravastatin, lovastatin, and fluvastatin. However, simvastatin provided a greater elevation of high-density lipoprotein cholesterol (HDL-C) compared to atorvastatin. The STELLAR trial was based on dose-to-dose comparisons between atorvastatin and rosuvastatin efficacy in reducing LDL-C. Te present study also revealed that as the doses of rosuvastatin, simvastatin, and pravastatin increased, HDL-C also increased, with rosuvastatin having the greatest effect. However, HDL-C levels decreased as the dose of atorvastatin increased. The DISCOVERY study involving the Asian population revealed that the percentage of patients achieving the European goals for LDL-C and TC at 12 weeks was higher in rosuvastatin group compared to atorvastatin group. Conclusions: The effects of statins on lipid profile are dose dependent. Most studies showed that rosuvastatin has the best effect on lipid profile. Prescribing lower doses of statins in Asians seems necessary.
Event Abstract Back to Event A Pilot Study on the Association between SLCO1B1 rs4363657 Polymorphism and Muscle Adverse Events in Adults with Newly Diagnosed Dyslipidaemia who were Prescribed a Statin: The Malaysian Primary Health Care Cohort Meor Fairuz Rizal Meor Anuar Shuhaili1, Boon How Chew2, Intan Nureslyna Samsudin1, Hejar Abdul Rahman3, Johnson Stanslas4, Shariful Hasan4, Zalinah Ahmad1 and Subashini C. Thambiah1* 1 Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Malaysia 2 Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Department of Family Medicine, Malaysia 3 Department of Community Health, Faculty of Medicine and Health Sciences, Putra Malaysia University, Malaysia 4 Department of Medicine, Faculty of Medicine and Health Sciences, University Putra Malaysia, Malaysia Background Statin, the first-line treatment for dyslipidaemia, may have suboptimal adherence due to its associated muscle adverse events. This data however, remains limited, due to under-reporting, mis/underdiagnoses or statin-associated muscle adverse events are generally rare. The aim of this study is to determine the association of serum creatine kinase (CK) and rs4363657 polymorphism of SLCO1B1 gene with statin-associated muscle adverse events among dyslipidaemia subjects. Methods This was a prospective cohort study at government health clinics involving newly diagnosed adults with dyslipidaemia. Muscle adverse events were recorded based on the patient’s complaint after a month on statin (lovastatin or simvastatin). Biochemical analyses including CK, fasting lipid profile, apo A1, apo B were taken at baseline and follow-up. Genetic profiling was performed for rs4363657 polymorphism of SLCO1B1 gene. Results A total of 118 subjects participated. Majority were Malay (72%) males (61%) with a mean age of 49 ± 12.2 years old and prescribed lovastatin (61.9%). There was a significant association between types of statin and muscle adverse events (p = 0.0327); frequency of muscle adverse events was higher with lovastatin (15.2%). No significant association noted between CK and muscle adverse events (p = 0.5637). The rs4363657 polymorphism of SLCO1B1 gene was significantly associated with muscle adverse events (p < 0.0001). The frequency of muscle adverse events was highest in CC genotype (100%); TC and TT (wild type) genotypes were 42.31% and 3.57%, respectively. Subjects with TC and CC genotypes were 26.24 and 357.96 times more likely to exhibit muscle adverse events compared to subjects with normal SLCO1B1 gene, respectively (p < 0.0001). Conclusion Statin-associated muscle adverse events were significantly higher in subjects on lovastatin compared to simvastatin. rs4363657 polymorphism of SLCO1B1 gene was a significant risk factor for statin-associated muscle adverse events in this study. Keywords: Dyslipidemia, statin, muscle adverse events, SLCO1B1, rs4363657, Creatine Kinase, Simvastatin, Lovastatin Conference: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”, Putrajaya, Malaysia, 3 Dec - 5 Feb, 2019. Presentation Type: Poster Presentation Topic: Metabolic diseases Citation: Meor Anuar Shuhaili M, Chew B, Samsudin I, Abdul Rahman H, Stanslas J, Hasan S, Ahmad Z and C. Thambiah S (2019). A Pilot Study on the Association between SLCO1B1 rs4363657 Polymorphism and Muscle Adverse Events in Adults with Newly Diagnosed Dyslipidaemia who were Prescribed a Statin: The Malaysian Primary Health Care Cohort. Front. Pharmacol. Conference Abstract: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”. doi: 10.3389/conf.fphar.2018.63.00003 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 11 Oct 2018; Published Online: 17 Jan 2019. * Correspondence: Dr. Subashini C. Thambiah, Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor Daruh Ehsan, Selangor, 43400, Malaysia, subashini@upm.edu.my Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Meor Fairuz Rizal Meor Anuar Shuhaili Boon How Chew Intan Nureslyna Samsudin Hejar Abdul Rahman Johnson Stanslas Shariful Hasan Zalinah Ahmad Subashini C. Thambiah Google Meor Fairuz Rizal Meor Anuar Shuhaili Boon How Chew Intan Nureslyna Samsudin Hejar Abdul Rahman Johnson Stanslas Shariful Hasan Zalinah Ahmad Subashini C. Thambiah Google Scholar Meor Fairuz Rizal Meor Anuar Shuhaili Boon How Chew Intan Nureslyna Samsudin Hejar Abdul Rahman Johnson Stanslas Shariful Hasan Zalinah Ahmad Subashini C. Thambiah PubMed Meor Fairuz Rizal Meor Anuar Shuhaili Boon How Chew Intan Nureslyna Samsudin Hejar Abdul Rahman Johnson Stanslas Shariful Hasan Zalinah Ahmad Subashini C. Thambiah Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
Introduction: Statins have several pleiotropic effects including its primary effect of lipid lowering that is important to prevent cardiovascular disease (CVD). Subjects often have heterogeneous responses to statin. This study aims to determine the biochemical effects of statins on lipid parameters among newly diagnosed dyslipidaemia subjects. Methods: This was a prospective observational study involving 118 newly diagnosed adults with dyslipidaemia from three government health clinics in Selangor, Malaysia. Biochemical analyses including fasting lipid profile [triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C)] and apolipoproteins (apoA1, apoB) were taken at baseline and follow-up after a month on statin. Results: Majority of subjects (61.9%) were prescribed with lovastatin, with the rest on simvastatin. At baseline, the median values for all lipid profile parameters (TC, LDL-C, HDL-C) and non-conventional lipid parameters (LDL-C:HDL-C ratio, non-HDL-C, TC:HDL-C ratio, apoB:apoA1 ratio) were deranged except for TG and apoA1. On follow up, all parameters showed median values within the reference range except for HDL-C, non-HDL-C and TC:HDL-C ratio. There was significant difference in the effect of statins on lipid parameters including predictors of cardiovascular risk, simvastatin having better effects. Conclusions: Different statins have varying effects on lipid parameters. Simvastatin showed significantly better effects compared to lovastatin. Non-HDL value should be included in the standard lipid profile report given its ease of use and implementation as it’s both a marker of coronary artery disease (CAD) risk stratification as well as an established determinant of goal attainment during therapy.
Introduction: Statin, the first-line treatment for dyslipidaemia, may have suboptimal adherence due to its associated muscle adverse events. These data, however, remain limited. Aim: To determine the association of serum creatine kinase (CK) and SLCO1B1 rs4363657 polymorphism with statin-associated muscle adverse events (SAMAE) among dyslipidaemia participants. Methods: This was a prospective cohort study at government health clinics involving newly diagnosed adults with dyslipidaemia. SAMAE were recorded based on the patient's complaint after a month on statin. CK was taken at baseline and follow-up. Genetic profiling was performed for SLCO1B1 rs4363657 polymorphism. Results: Among 118 participants, majority were Malay (72%) males (61%) with a mean age of 49 ± 12.2 years old and prescribed lovastatin (61.9). There was a significant association between statin types (lovastatin and simvastatin) and SAMAE (p = 0.0327); no significant association noted between CK and SAMAE (p = 0.5637). The SLCO1B1 rs4363657 polymorphism was significantly associated SAMAE (p < 0.0001). Conclusions: In this first pilot study of a multiethnic Malaysian population, the incidence of SAMAE was 18.6%. SAMAE were significantly higher in subjects on lovastatin compared to simvastatin. SLCO1B1 rs4363657 polymorphism was a significant risk factor for SAMAE.
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