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Association of vitamin D and incident statin induced myalgia--a retrospective cohort study
Ghanshyam Palamaner Subash Shantha1, Julio Ramos1, Linda Thomas-Hemak1
1Department of Internal Medicine, The Wright Center for Graduate Medical Education, Scranton, Pennsylvania, United States of America.
Insights
Low vitamin D levels increase the risk of statin-induced myalgia (SIM). A vitamin D level of 15 ng/ml or lower is highly predictive of developing SIM in patients starting statin therapy.
Area of Science:
- Endocrinology
- Pharmacology
- Primary Care Medicine
Background:
- Conflicting evidence exists regarding vitamin D's role in statin-induced myalgia (SIM).
- Previous studies were limited by cross-sectional designs and patient samples from cardiology clinics.
Purpose of the Study:
- To assess the association between vitamin D levels and SIM in a primary care setting.
- To establish a serum vitamin D cutoff level for identifying patients at risk of SIM.
Main Methods:
- Retrospective cohort study of 5526 patients from a primary care practice (2005-2012).
- Vitamin D (25-hydroxy cholecalciferol) levels at statin initiation were categorized into quartiles.
- SIM was identified based on patient self-report.
Main Results:
- Of 1160 patients on statins, 276 (24%) developed SIM.
- The lowest quartile of vitamin D (≤10 ng/ml) was independently associated with a higher hazard of SIM.
- A vitamin D cutoff of ≤15 ng/ml demonstrated high predictive accuracy for SIM (LR+ 5.1).
Conclusions:
- Low vitamin D levels at statin initiation are significantly associated with SIM.
- A serum vitamin D level ≤15 ng/ml is a strong predictor of SIM.
- Further randomized controlled trials are warranted to confirm these findings.
Background And Objectives:
Evidence is conflicting with regards to the role of vitamin D in statin induced myalgia (SIM). Studies so far have assessed cross-sectional association and were limited by study sample selected predominantly from cardiology clinics. In this retrospective cohort study we assessed the association between vitamin D and SIM and attempted to establish a serum vitamin D cutoff to identify patients at risk for developing SIM.
Methods:
Medical charts of 5526 consecutive patients from a primary care practice in Scranton, Pennsylvania from 2005-2012 were reviewed. Vitamin D level (25-hydroxy cholecalciferol) at statin initiation was considered "Exposure level". Vitamin D levels were categorized into quartiles (≤ 10, 11-20, 21-30, >30 ng/ml). SIM was identified by patient report.
Results:
1160 out of 5526 patients were treated with statins. The mean age was 55.9 years. 276 (24%) developed SIM. Unadjusted 7-yr cumulative incidences of SIM for quartiles 1-4 of vitamin D were 32.3, 21.5, 18.3 and 14.6% respectively. The lowest quartile of vitamin D was independently associated with 1.21 times the hazard of the fourth quartile for developing SIM (95% CI: 1.09, 1.33; P-trend = 0.001). Vitamin D cut-off ≤15 ng/ml, showed a positive predictive value, negative predictive value, likelihood ratio (LR) + and LR- of 81, 90, 5.1 and 0.1, respectively for predicting SIM.
Conclusions:
Low vitamin D level at statin initiation is associated with SIM, levels ≤15 ng/ml have a high predictive accuracy for SIM. Randomized controlled trials are needed to validate our results.
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