| Coverage Policy Manual | |
| Policy #: | 2013020 |
| Category: | Laboratory |
| Initiated: | July 2013 |
| Last Review: | December 2023 |
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| Genetic Test: Statin-Induced Myopathy (SLCO1B1) | |
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| Description: |
HMG-CoA reductase inhibitors, or statins, which are widely used to treat hypercholesterolemia, can cause muscle-related adverse events. Serious myopathy (i.e., myositis or rhabdomyolysis) can also occur and may be associated with variants in the SLCO1B1 gene. Commercially available tests for the presence of SLCO1B1 variants are currently marketed for use in predicting the risk of myopathy for patients taking statins.
Background
HMG-CoA reductase inhibitors, or statin drugs, are the primary pharmacologic treatment for hypercholesterolemia throughout the world. In the United States, there are an estimated 38 million individuals taking statins as of 2008 (Vladutiu, 2008). Use of statins is associated with an approximately 30% reduction in cardiovascular events across a wide variety of populations (Maggo, 2011). A variety of socioeconomic disparities in cardiovascular outcomes and implementation of risk-reducing measures, including use of statins and other agents for managing hypercholesterolemia, have been identified. Women with coronary artery disease are less likely to be receiving a statin than men, and those taking statins are less likely to have therapy intensified and to achieve lipid control compared to men taking statins (Arnold, 2011; Virani, 2011; Aggarwal, 2022). Black individuals at high risk of atherosclerotic cardiovascular disease are significantly less likely to be prescribed statins compared to similar White individuals, and rates of lipid control are lower among Black and non-White Hispanic individuals taking statins compared to White individuals taking statins (Dorsch, 2019; Aggarwal, 2022). These observations are mediated in part through disparities in social determinants of health, such as income, insurance, and immigration status (Guadamuz, 2020; He, 2021).
Commercially Available SLCO1B Molecular Diagnostic Tests
Several commercial and academic labs offer genetic testing for statin-induced myopathy (SLCO1B1) variants, including Boston Heart Diagnostics™ and Arup Laboratories.
Other labs offer panel tests for drug metabolism that include the SLCO1B1 gene.
Regulatory Status
Clinical laboratories may develop and validate tests in-house and market them as a laboratory service; laboratory-developed tests must meet the general regulatory standards of the Clinical Laboratory Improvement Amendments. The Boston Heart Statin Induced Myopathy (SLCO1B1) Genotype test and ARUP Laboratories Statin Sensitivity SLCO1B1 are available under the auspices of the Clinical Laboratory Improvement Amendments. Laboratories that offer laboratory-developed tests must be licensed by the Clinical Laboratory Improvement Amendments for high-complexity testing. To date, the U.S. Food and Drug Administration has chosen not to require any regulatory review of this test.
Coding
There is no specific CPT code for genetic testing for SLCO1B1.
Effective July 1, 2013, code 81400 Molecular pathology procedure, Level 1 (e.g., identification of single germline variant [e.g., SNP] by techniques such as restriction enzyme digestion or melt curve analysis) – will include testing for SLCO1B1 (solute carrier organic anion transporter family, member 1B1) (e.g., adverse drug reaction), V174A variant.
For testing of variants other than V174A, the unlisted molecular pathology procedure code 81479 would be reported.
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Policy/ Coverage: |
Does Not Meet Primary Coverage Criteria Or Is Investigational For Contracts Without Primary Coverage Criteria
Genetic testing for the presence of variants in the SLCO1B1 gene for the purpose of identifying patients at risk of statin-induced myopathy does not meet member benefit certificate primary coverage criteria that there be scientific evidence of effectiveness.
For members with contracts without primary coverage criteria, genetic testing for the presence of variants in the SLCO1B1 gene for the purpose of identifying patients at risk of statin-induced myopathy is considered investigational. Investigational services are specific contract exclusions in most member benefit certificates of coverage.
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| Rationale: |
A literature search was performed for the period of January 1, 2000 through May 15, 2013. Published articles were selected that reported on the analytic validity, clinical validity, and clinical utility of genetic testing for statin-induced myopathy.
Analytic Validity
One lab (Boston Heart Diagnostics™) performs the test by real-time polymerase chain reaction (PCR). This technique allows detection and amplification of DNA fragments to be performed simultaneously. While this is an accepted method for genetic analysis and generally has high accuracy, no published information was found on the accuracy of this technique for detecting genetic variants associated with statin-induced myopathy.
Clinical Validity
There are no studies that report the sensitivity or specificity of genetic testing for statin-induced myopathy. Studies were identified that report the degree of risk for myopathy associated with the SLCO1B1 genetic variants. These include genome-wide association studies, case-control studies, cohort analyses, and clinical trials. Representative types of each study are included below.
Genome-wide association (GWA) studies have reported that SLCO1B1 variants are associated with statin-induced myopathy. The SEARCH study group published a GWA study in 2008 based on data from the SEARCH trial (Link, 2008). This was a randomized controlled trial (RCT) of 12,064 individuals with a prior myocardial infarction randomized to 80 mg simvastatin or 20 mg simvastatin. Of the 6,031 patients in the 80-mg-statin group, 48 (0.8%) had an elevation of serum CK level more than 10 times normal, and an additional 48 patients (0.8%) had a creatinine kinase (CK) level that was more than 3 times normal and more than 5 times the baseline level. These subjects were matched with 96 control subjects without CK elevations, matched for gender, age, renal function, and ancillary medication use. Adequate DNA was available for 85 patients with myopathy and 90 controls, and these patients formed the study group for derivation of the genome associations.
The SLCO1B1 locus was the single single nucleotide polymorphism (SNP) that had a strong association with myopathy, at a corrected p value of 0.001. The estimated odds ratio for myopathy in patients with a single C allele was 4.3 (95% confidence interval [CI]: 2.5-7.2), and the estimated odds ratio for patients homozygous for the C allele was 17.4 (95% CI: 4.8-62.9). Based on these data, the cumulative risk of developing myopathy after 6 years of treatment with 80 mg simvastatin was 0.6% for patients with the T/T allele, 3% for patients with the T/C allele, and 18% for patients with the C/C allele. Other clinical factors that predicted a risk of myopathy were female gender (relative risk [RR]: 1.8, 95% CI: 1.1-2.8), age >65 (RR 2.2, 95% CI 1.4-3.4), impaired renal function (RR 2.2, 95% CI 1.4-3.4), use of amiodarone (RR 6.4, 95% CI: 3.4-12.1), use of calcium antagonists (RR: 1.7, 95% CI: 1.2-2.6), and diabetes mellitus (RR: 1.7, 95% CI: 1.0-2.9).
The SEARCH investigators replicated the association of the SLCO1B1 with myopathy in 16,664 patients from a separate RCT, the Heart Protection Study. In this study, all patients were treated with 40 mg of simvastatin, and 23 (0.1%) were identified with CK levels greater than 10 times normal. SLCO1B1 variants were also strongly associated with myopathy in this replication study, with a corrected p value of 0.004). The estimated odds ratio for the presence of one C allele was 2.6 (95% CI: 1.3-5.0).
The STRENGTH (Statin Response Examined by Genetic Haplotype Markers) study was a randomized trial that examined statin response and safety by dose of statin, type of statin, and by presence of genetic markers (Voora, 2009). A total of 509 patients were randomized to various doses of pravastatin or simvastatin and followed for the presence of adverse events, including myopathy. The presence of at least one variant on the SLCO1B1 gene was associated with an increased rate of adverse events (37% vs. 25%, p=.03). There was also evidence for a “dose-response” effect, with the risk of adverse events being 19% with no variant alleles, 27% with one variant allele, and 50% with two variant alleles (p=0.01 for trend).
A case-control study reporting on the risk of myopathy associated with SLCO1B1 variants was reported in 2012 (Brunham, 2012). This study identified cases with statin-induced myopathy, defined as muscle symptoms with a CK elevation at least 10 times normal, from two large lipid clinics in the Netherlands. Twenty-five cases of myopathy were identified from 9,000 total patients, for a prevalence of 0.26%. These patients were matched for age, gender, statin type, and statin dose, with 84 patients who did not have myopathy. In the whole cohort of patients taking any statin, there was a non-significant trend toward an increase in myopathy for patients with a SLCO1B1 variant (odds ratio [OR]: 1.5, 95% CI: 0.58-3.69, p=.21). When restricted to patients on simvastatin, the association was stronger but did not quite reach statistical significance (OR: 3.2, 95% CI: 0.83-11.96, p=.06).
Clinical Utility
There were no studies identified that reported direct evidence on the clinical utility of genetic testing for statin myopathy. Indirect evidence includes the predicted number of patients who avoid statin myopathy as a result of genetic testing. This number is uncertain because there are a number of actions that can be taken as a result of genetic testing. Statins can be stopped or not started, a lower dose can be used, and other risk factors can be avoided, such as use of amiodarone. Despite the uncertainty in the precise number of events avoided, the number will necessarily be low due to the low underlying rate of serious events.
When statin use is reduced or eliminated, the reduction in statin myopathy needs to be weighed against the increased cardiovascular events that may occur as a result of this change. In patients with a moderate to high risk of cardiovascular events, the probability of myocardial infarction (MI) over a 10-year period may be in the range of 10-20%. This event rate is substantially higher than the probability of serious myositis and rhabdomyolysis. As a result, if statin drugs are avoided because of genetic testing, the number of MIs that will result may exceed the number of myopathy episodes avoided, and net harm may result. Since there are no alternative agents that can reduce the rate of cardiovascular events to the extent as do statins, it may not be possible to ameliorate this net harm by a change to an alternate lipid-lowering strategy.
Summary
Statin muscle symptoms are the most common side effect of statins, and serious myopathy or rhabdomyolysis occurs in a very small number of patients treated with statins. An association between genetic variants of the SLCO1B1 gene and statin myopathy has been reported. This association has been found in genome-wide association studies that indicate a several-fold risk of statin myopathy associated with genetic variants. Evidence from case-control studies and clinical trials also show a possible association, but the quantity of evidence is small and the association has not been demonstrated to be strong. Statins are associated with a definite decreased risk of cardiovascular events such as myocardial infarction (MI), and this benefit of reduced cardiovascular events is likely to far outweigh the risk of myopathy, even in patients with the highest risk of myopathy, i.e., two abnormal SLCO1B1 alleles. Therefore, there is a possibility of harm if the results of genetic testing for statin-induced myopathy are used as part of the decision-making process for prescribing statins.
2014 Update
A literature search conducted using the Medline database through June 2014 did not reveal any new literature that would prompt a change in the coverage statement.
Carr et al reported results from a similar case-control study evaluating the risk of statin-induced myopathy associated with SLCO1B1 variants (Carr, 2013). The authors identified 77 statin-induced myopathy patients (serum CK greater than 4 times the upper limit of normal) and 372 statin-tolerant controls from a large database of anonymous longitudinal medical records in the UK. In multiple logistic regression analyses to determine statin-associated myopathy risk, the presence of the C allele in the SLCO1B1 gene was significantly associated with myopathy: for all myopathy, the adjusted OR per C-allele was 2.08 (95% CI, 1.3 to 3.32); for severe myopathy, the adjusted OR per C-allele was 4.47 (95% CI, 1.84 to 10.84). When the analysis was restricted to only those patients receiving simvastatin (n=281), there was a significant association between the SLCO1B1 gene status and myopathy (adjusted OR per C-allele=2.13; 95% CI, 1.29 to 3.54; p=0.014). In contrast, when the analysis was restricted to only those patients receiving atorvastatin (n=121), no significant association was found. Variations in the COQ2 gene were not associated with statin-induced myopathy.
Some evidence, including the Carr et al results, suggest that the association between myopathy and SLCO1B1 genotype is most pronounced for simvastatin. Danik et al evaluated the role of SLCO1B1 polymorphisms as effect modifiers for clinical myalgia in the Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial, which randomly allocated subjects to rosuvastatin (20 mg/day) or placebo (Danik, 2013). Among the 4404 subjects allocated to rosuvastatin, there was no significant association between SLCO1B1 gene status and either muscle symptoms or a diagnosis of rhabdomyolysis, myopathy, or myositis.
In a subanalysis of a prospective population-based cohort study of chronic diseases in the elderly population, deKeyser et al evaluated whether SLCO1B1 polymorphisms modified the risk of adverse drug reactions during statin therapy among 2080 patients who received simvastatin or atorvastatin and had SLCO1B1 genotype available (de Keyser, 2014). The study’s primary outcome was reduction in statin dose or switch to another statin-lowering drug as an indicator for an adverse drug reaction. Among simvastatin users, the T®C polymorphism was significantly associated with the primary outcome. Patients who had the CC genotype had a hazard ratio for dose decrease or switch of 1.74 (95% CI, 1.05 to 2.88). A similar association was not seen among atorvastatin users.
Ferrari et al conducted a case-control study among patients treated with atorvastatin, rosuvastatin, or simvastatin to assess the contribution of polymorphisms in the SLCO1B1, ABCB1, andABCG2 genes to the risk of statin-induced myopathy (Ferrari, 2014). Cases (n=33) included patients with statin-induced elevations in serum CK of greater than 3 times the upper limit of normal and were compared to 33 matched controls. Patients with increased CK levels had significantly increased odds for the SLCO1B1 C allele or the ABCB1 T allele: OR of 8.86 (p<0.01) and 4.67 (p<0.05), respectively. Patients with increased CK levels did not have a significantly increased odds of having the ABCG2 genotype.
Clinical Utility
There were no studies identified that reported direct evidence on the clinical utility of genetic testing for statin myopathy. Direct evidence for clinical utility in this setting would come from studies that demonstrate that using SLCO1B1 genotype to inform statin therapy (statin dose or choice of specific drug) has positive outcomes in terms of lower rates of myopathy with adequate lipid control and tolerability of alternative treatments. Indirect evidence includes the predicted number of patients who avoid statin myopathy as a result of genetic testing. This number is uncertain because there are a number of actions that can be taken as a result of genetic testing. Statins can be stopped or not started, a lower dose can be used, and other risk factors can be avoided, such as use of amiodarone. Despite the uncertainty in the precise number of events avoided, the number will necessarily be low because of the low underlying rate of serious events.
Several institutions have implemented electronic medical record-based clinical decision support systems to guide statin dosing and follow-up for patients started on a statin based on patients’ SLCO1B1 status, including Vanderbilt University Medical Center(Wilke, 2012) and St. Jude Children’s Research Hospital (Hoffman, 2014). However, studies that demonstrate that such systems are associated with improved clinical outcomes are lacking.
Ongoing Clinical Trials
A search of the database ClinicalTrials.gov on April 1, 2014, using the term “SLCO1B1” identified 1 comparative study evaluating the utility of genetic testing in preventing statin-induced myopathy:
2015 Update
A literature search conducted through June 2015 did not reveal any literature that would prompt a change in the coverage statement. There were no new published studies assessing the clinical utility of genetic testing for the presence of variants in the SLCOB1 gene.
One review assessing the tests clinical validity (Canestaro, 2014) was identified. Canestaro et al conducted a systematic review of studies evaluating the association between a number of genetic variants, including SLCO1B1, and statin serum concentrations and subsequent myopathy (Canestaro, 2014).Thirteen studies were identified, which evaluated 7 genes in classes of genes: 3 cytochrome p450 enzymes (CYP2D6, CYP3A4, CYP3A5), the mitochondrial enzyme glycine amidinotransferase (GATM), SLCO1B1, and the cell efflux transporters ABCB1 and ABCG2. The STRENGTH and SEARCH studies, along with the Brunham et al study, were included in the systematic review. The authors concluded that
the evidence for an association between the *5 allele of SLCO1B1 and statin-related myopathy is strong and replicated in multiple studies, particularly for simvastatin.
In 2012, the Clinical Pharmacogenetics and Pharmacogenomics Implementation Consortium issued guidelines for SLCO1B and simvastatin-induced myopathy, which were updated in 2014 (Ramsey, 2014). These guidelines provide recommendations for patient management for various SLCO1B genotypes, including prescribing a lower dose or considering an alternative statin and considering routine creatinine kinase surveillance, in patients with SLCO1B genotypes consistent with intermediate or low statin metabolism.
2017 Update
A literature search conducted through May 2017 did not reveal any new information that would prompt a change in the coverage statement.
2018 Update
A literature search was conducted through November 2018. There was no new information identified that would prompt a change in the coverage statement. The key identified literature is summarized below.
Randomized Controlled Trials
Vassy et al conducted a systematic review of SLCO1B1 testing of patient and clinical outcomes (Vassy, 2018). They identified 5 pilot studies and an RCT by Voora that studied how SLCO1B1 test results influence patient outcomes (Voora, 2017). Voora recruited patients who had discontinued statin therapy due to suspected side effects (73% reported myalgia, 25% of patients were SLCO1B1*5 carriers). Patients were randomized to immediate or delayed results of SLCO1B1 testing, stratified based on SLCO1B1*5 genotype (carriers vs noncarriers) and clinic site. The primary outcome was adherence as assessed by the Morisky Medication Adherence Scale. Secondary outcomes included low-density lipoprotein cholesterol, Brief Pain Inventory, and 12-Item Short-Form Health Survey. Voora reported a significant difference between groups in low-density lipoprotein cholesterol at 3 months, but not in other outcome measures. Limitations in trial design might have affected adherence to medications and self-reporting on questionnaire.
2021 Update
Annual policy review completed with a literature search using the MEDLINE database through November 2021. No new literature was identified that would prompt a change in the coverage statement. The key identified literature is summarized below.
The Integrating Pharmacogenetics in Clinical Care (I-PICC) Study, conducted by Vassy et al, assessed the effect of SLCO1B1 testing in statin-naive patients eligible for statin therapy due to cardiovascular disease risk factors (Vassy, 2020). The study was conducted at 8 Veterans Affairs primary care facilities. Similar to the Voora et al RCT, participants were randomized to either immediate SLCO1B1 testing or delayed testing after 12 months. In the immediate testing group, SLCO1B1 test results were delivered to treating physicians via the patient's electronic health record, but it was left to the discretion of the physician regarding when (or if) test results were communicated to the patient. Ultimately, only 15.5% of physicians documented communicating SLCO1B1 test results to patients. The primary outcome of the study was change from baseline in LDL-C after 12 months follow-up. Physician assessed statin-associated muscle symptoms were a secondary outcome. After 12 months, there was less LDL lowering in the immediate group than the delayed group (between-group difference -1.1 mg/dL, 90% CI -4.1 to 1.8). This mean difference between groups was within the prespecified noninferiority margin of 10 mg/dL, indicating that SLCO1B1 testing did not cause harm to patients in this study, nor did it provide benefit. There was no difference between groups in physician-reported statin-associated muscle symptoms (1% vs. 1.4%; p>.99). This study was limited by the low uptake of statin prescriptions in statin-eligible patients in both the immediate and delayed groups (40% and 34.8%, respectively).
2022 Update
Annual policy review completed with a literature search using the MEDLINE database through November 2022. No new literature was identified that would prompt a change in the coverage statement. The key identified literature is summarized below.
A number of variant alleles with impacts on expression and/or function of SLCO1B1 have been identified and arranged by the Clinical Pharmacogenetics Implementation Consortium into phenotypic categories, including poor, decreased, normal, and increased transporter function phenotypes (Cooper-DeHoff, 2022). Poor and decreased function phenotypes frequently involve the well-studied rs4149056 c.521T>C variant found in the SLCO1B1*5 and *15 haplotypes; these variants are estimated to occur in 15% of the population and are associated with increased risk of statin-induced myopathy (Link, 2008). The estimated prevalence of poor and decreased function phenotypes is highest in individuals of Native American (42%), North African or Middle Eastern (36%), European (31%), East Asian (22%), and Central/South Asian (13%) descent (Cooper-DeHoff, 2022).
In 2012, the Clinical Pharmacogenetics and Pharmacogenomics Implementation Consortium issued guidelines for SLCO1B genotypes and simvastatin-induced myopathy, which were updated in 2014 and again in 2022 (Cooper-DeHoff, 2022). The 2022 guideline update reorganized genotype-phenotype categories and expanded upon recommendations for statin selection and dosing recommendations according to phenotype, statin intensity according to 2018 American College of Cardiology/American Heart Association guidelines, and strength of supportive data
The purpose of genetic testing for SLCO1B1 variants in patients who are taking statin drugs is to inform a decision whether patients identified as at risk for statin-associated myopathy should continue taking specific statin drugs. Genome-wide association studies have found that SLCO1B1 variants are associated with statin-induced myopathy. The Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine ( SEARCH) was an RCT of 12,064 patients assigned to simvastatin 20 mg or 80 mg (Armitage, 2010). A genome-wide association study was conducted using data for the 1.4% of patients assigned to the 80 mg simvastatin group in SEARCH, who experienced myopathy (defined by elevations in creatine kinase levels with or without muscle symptoms) and who had adequate DNA available for genomic analysis, with matched controls (Link, 2008). The noncoding rs4363657SLCO1B1single-nucleotide variant was the sole variant that had a strong association with myopathy. Further analysis indicated the identified variant was in near-complete linkage disequilibrium with the rs4149056 c.521T>C variant. The cumulative risk of developing myopathy after 6 years of treatment with simvastatin 80 mg was 0.6% for patients with the rs4149056 T/T genotype, 3% for patients with the T/C genotype, and 18% for patients with the C/C genotype. The investigators replicated the association of the SLCO1B1rs4149056 c.521T>C variant with myopathy in 16,664 patients from the Heart Protection Study. In this trial, all patients were treated with simvastatin 40 mg; 0.1% were identified with creatine kinase levels greater than 10 times normal. The rs4149056 c.521T>CSLCO1B1 variant was strongly associated with myopathy in this replication analysis.
Some evidence has suggested that the association between myopathy and SLCO1B1 genotype is most pronounced for simvastatin. The Statin Response Examined by Genetic Haplotype Markers study was a randomized trial that examined statin response and safety by the dose of statin, statin type, and presence of genetic markers (Voora, 2008). A total of 509 patients were randomized to various doses of atorvastatin, pravastatin, or simvastatin and followed for adverse events, including myopathy. The presence of at least 1 variant on the SLCO1B1 gene was associated with an increased rate of adverse events with the risk of adverse events being 19% with no variant alleles, 27% with 1 variant allele, and 50% with 2 variant alleles (p=.01 for trend). The association between SLCO1B1 gene status and adverse event rates did not appear to be present for patients who received pravastatin.
Large retrospective studies indicate an association between the rs4149056 c.521T>C variant and likelihood of statin discontinuation or surrogate markers (such as myalgia-related diagnosis codes or new statin allergies) of statin-induced myopathy (Turkmen, 2022; Voora, 2022).
2023 Update
Annual policy review completed with a literature search using the MEDLINE database through November 2023. No new literature was identified that would prompt a change in the coverage statement. The key identified literature is summarized below.
Other genes have been studied, including ABCB1, which encodes ATP-binding cassette (ABC) transporters subfamily B member1 (ABCB1/P-glycoprotein 1), ABCG2, which encodes ABC transporters subfamily G member 2 (ABCG2/breast cancer resistance protein), and the coenzyme Q2 (COQ2) homolog gene. Other studies have evaluated the association between variants in the GATM gene and statin-induced myopathy (the GATM gene encodes a glycine amidinotransferase that is the rate-limited enzyme in creatine biosynthesis). However, it should be noted that the association between variants has not been consistently replicated (Luzum, 2015).
In their meta-analysis, Xiang et al (2018) assessed the association between SLCO1B1 T521C and 521T alleles and the risk of statin-induced myopathy (Xiang, 2018). Fourteen cohort and case-control studies were included, with a total of 3265 myopathy patients and 7743 controls. Findings of several studies suggested that 521TT carries a statistically significant lower risk of statin-induced myopathy compared to the other genotypes studied (ie, 521CC, 521TC, 521CC + TC). In addition, 521C was also associated with a greater risk of statin-induced myopathy than 521T. These studies all had significant heterogeneity. The authors also evaluated the association of SLCO1B1 T521C and the risk of myopathy when taking different types of statins. They found a statistically significant risk for 521CC + TC individuals on simvastatin (odds ratio [OR], 2.35; 95% CI, 1.08 to 5.12; p=.032) or rosuvastatin (OR, 1.69; 95% CI, 1.07 to 2.67; p=.024) compared with 521TT. The 521C allele was also associated with a greater risk of myopathy from taking cerivastatin (OR, 1.95; 95% CI, 1.47 to 2.57; p<.001). The heterogeneity among studies of statin types for SLCO1B1 T521C and myopathy risk was not statistically significant. Publication bias could not be ruled out in several comparisons.
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| References: |
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