{"title":"Relationship Between Statin-associated Muscle Symptoms, Serum Vitamin D and Low-density Lipoprotein Cholesterol - A Cross-sectional Study.","authors":"Harsheen Kaur, Jagjit Singh, Jeet Ram Kashyap, Ravi Rohilla, Harmanjit Singh, Shivani Jaswal, Rajiv Kumar","doi":"10.17925/EE.2020.16.2.137","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Statin-associated muscle symptoms (SAMS) can lead to medication non-adherence among statin users. There is a complex relationship between SAMS, vitamin D and low-density lipoprotein cholesterol (LDL-C). The objective of this study was to evaluate the relationship between vitamin D, LDL-C and occurrence of SAMS.</p><p><strong>Methods: </strong>This was a cross-sectional study in patients using statins. Thorough patient histories were taken, a clinical examination was conducted and SAMS were recorded. Levels of vitamin D, creatine phosphokinase (CPK) and LDL-C were measured. These parameters were compared amongst statin users with SAMS and those without SAMS. Levels of vitamin D and LDL-C were converted into percentiles and their relationship with SAMS was evaluated in terms of odds ratio. Receiver operating characteristics (ROC) were drawn, taking vitamin D and LDL-C as predictors of SAMS.</p><p><strong>Results: </strong>A total of 121 statin users were enrolled in this study. Thirty-eight patients (31.4%) presented with SAMS. Significantly lower levels of serum vitamin D were observed amongst statin users with SAMS compared with those without SAMS (19.8 ± 9.67 ng/mL versus 25.0 ± 14.6 ng/mL; 95% confidence interval -10.4 to -0.07; p=0.04). With vitamin D levels less than or equal to 5th, 10th and 25th percentile, the chances of occurrence of SAMS were significantly higher, but not at the 50th percentile (corresponding vitamin D level of 20.21 ng/mL). LDL-C did not show any conclusive relationship with SAMS. ROC curves showed a significant discrimination for vitamin D levels, but not for LDL-C.</p><p><strong>Conclusion: </strong>Statin users with low levels of vitamin D are at increased risk of developing SAMS. However, LDL-C status of statin users failed to predict any meaningful association with SAMS. Given the small sample size of this study, these results should be regarded as preliminary.</p>","PeriodicalId":38860,"journal":{"name":"European Endocrinology","volume":"16 2","pages":"137-142"},"PeriodicalIF":0.0000,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7572163/pdf/euendo-16-137.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Endocrinology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.17925/EE.2020.16.2.137","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/10/6 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: Statin-associated muscle symptoms (SAMS) can lead to medication non-adherence among statin users. There is a complex relationship between SAMS, vitamin D and low-density lipoprotein cholesterol (LDL-C). The objective of this study was to evaluate the relationship between vitamin D, LDL-C and occurrence of SAMS.
Methods: This was a cross-sectional study in patients using statins. Thorough patient histories were taken, a clinical examination was conducted and SAMS were recorded. Levels of vitamin D, creatine phosphokinase (CPK) and LDL-C were measured. These parameters were compared amongst statin users with SAMS and those without SAMS. Levels of vitamin D and LDL-C were converted into percentiles and their relationship with SAMS was evaluated in terms of odds ratio. Receiver operating characteristics (ROC) were drawn, taking vitamin D and LDL-C as predictors of SAMS.
Results: A total of 121 statin users were enrolled in this study. Thirty-eight patients (31.4%) presented with SAMS. Significantly lower levels of serum vitamin D were observed amongst statin users with SAMS compared with those without SAMS (19.8 ± 9.67 ng/mL versus 25.0 ± 14.6 ng/mL; 95% confidence interval -10.4 to -0.07; p=0.04). With vitamin D levels less than or equal to 5th, 10th and 25th percentile, the chances of occurrence of SAMS were significantly higher, but not at the 50th percentile (corresponding vitamin D level of 20.21 ng/mL). LDL-C did not show any conclusive relationship with SAMS. ROC curves showed a significant discrimination for vitamin D levels, but not for LDL-C.
Conclusion: Statin users with low levels of vitamin D are at increased risk of developing SAMS. However, LDL-C status of statin users failed to predict any meaningful association with SAMS. Given the small sample size of this study, these results should be regarded as preliminary.