Low Vitamin D as a Risk Factor for the Development of Myalgia in Patients Taking High-Dose Simvastatin: A Retrospective Review

Mergenhagen, Kari A.; Ott, Michael; Heckman, Kerry; Rubin, Lisa M.; Kellick, Kenneth

doi:10.1016/j.clinthera.2014.02.023

Cited by 42 publications

(30 citation statements)

References 12 publications

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“…They suggested that correction of 25-hydroxyvitamin D levels before statin therapy initiation may mitigate one risk factor in the development of statin-related myalgia. [16] In our study, we found myopathy only in patients with Vitamin D deficiency and patients with adequate Vitamin D levels did not develop myopathy but due to the limited number of patients in which Vitamin D levels were measured, we cannot conclude with certainty regarding the risk of myopathy attributed to Vitamin D deficiency. However, Vitamin D estimation in all 200 subjects could have demonstrated more strongly the risk potential of Vitamin D deficiency with respect to atorvastatin-induced myopathy.…”

Section: Discussionmentioning

confidence: 59%

“…who reported muscle-related symptoms in 39% patients ( n = 106) but did not find any significant difference in Vitamin D level among patients with or without myalgia. [16] In a retrospective medical record review done by Margenhagen et al ., they have reported lower incidence of adverse muscle events in the patients treated with high-dose simvastatin (80 mg) who also had a higher Vitamin D level. They suggested that correction of 25-hydroxyvitamin D levels before statin therapy initiation may mitigate one risk factor in the development of statin-related myalgia.…”

Section: Discussionmentioning

confidence: 99%

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Myopathy in patients taking atorvastatin: A pilot study

Manoj

Jain

Madhu

2017

Indian J Endocr Metab

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Aim:This study aims to investigate the prevalence and risk factors of statin-induced myopathy.Subjects and Methods:A total of 200 patients aged ≥ 40 years and taking atorvastatin 10 mg/day or more for at least 2 weeks were recruited in the study. A detailed history of participants and anthropometry of study participants was recorded, and features of myopathy were explained. Biochemical investigations along with thyroid stimulating hormone (TSH) and Vitamin D were done in all patients.Results:Mean age of study population was 54.81 ± 9.10 years. Sixty-five percent (65.5%) of atorvastatin users had coronary heart disease, 62.5% were hypertensive, 38% had diabetes. Thirty-five percent (35.5%) patients were taking 10 mg/day atorvastatin, 45% were taking 20 mg/day, and 19.5% were taking 40 mg/day. The overall frequency of myopathy among statin users was 7.5% which was significantly higher with increasing dose of atorvastatin (1.4% in 10 mg/day group, 10% in 20 mg/day group, and 12.8% in 40 mg/day, P < 0.05). The frequency of atorvastatin-related myopathy was higher in females 8.65% compared to 6.25% in males. Serum TSH levels in patients with myopathy were 4.05 ± 7.76 μIU/ml while in those without myopathy were 3.13 ± 2.88 μIU/ml (P = 0.649). Serum 25-hydroxy Vitamin D levels were measured in 66 patients randomly. Mean levels in patients with myopathy were 15.98 ± 12.94 ng/ml and without myopathy were 10.20 ± 5.64 ng/ml (P = 0.285).Conclusion:The present study demonstrates that a significantly higher number of patients taking atorvastatin develop myopathy in real life clinical condition. The frequency of myopathy increases with increase in atorvastatin dose.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Myopathy in patients taking atorvastatin: A pilot study

Manoj

Jain

Madhu

2017

Indian J Endocr Metab

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“…Cholesterol is used to synthesize 7-dehydrocholesterol (7-DHC), the precursor to vitamin D3 (cholecalciferol), but studies to date have shown that statin therapy either has no effect on vitamin D (22, 23), or, conversely, increases vitamin D levels in asymptomatic adults (24, 25). Despite these latter findings, several studies and systematic reviews (7–9, 26, 27) have linked low vitamin D levels to SAMS, and consequently vitamin D supplementation to mitigation of muscle symptoms (10, 28), although other investigations have not supported this association (11, 12, 29). In the current report, we found no association between vitamin D levels, pre- and post-statin therapy, or clinical vitamin D deficiency and insufficiency, on the development of SAMS.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies and meta-analyses have found a higher prevalence of low vitamin D levels in patients with SAMS (7, 8) and that low Vitamin D is a risk factor for SAMS (9). In addition, vitamin D supplementation may mitigate SAMS (10), but other studies have found no relationship between low vitamin D levels and SAMS (11, 12).…”

Section: Introductionmentioning

confidence: 99%

Low vitamin D does not predict statin associated muscle symptoms but is associated with transient increases in muscle damage and pain

et al. 2017

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Background and aims Low vitamin D (VITD) may contribute to statin-associated muscle symptoms (SAMS). We examined the influence of baseline and change in VITD in patients with verified SAMS. Methods SAMS was verified in 120 patients with prior statin muscle complaints using 8-week randomized, double-blind crossover trials of simvastatin (SIMVA) 20 mg/d and placebo. 25 (OH)vitamin D was measured at each phase of the trial. Results Forty-three patients (35.8%) experienced muscle pain on SIMVA but not placebo, exhibiting confirmed SAMS. VITD (mean ± standard deviation) prior to SIMVA treatment were not different between patients who did (31.7 ± 12.1 ng/mL, n=43) or did not (31.6 ± 10.3 ng/mL, n=77) develop SAMS and did not predict SAMS (p=0.96). The change in VITD with SIMVA treatment was not different between patients with and without SAMS (0.3 ± 5.9 vs. 0.2±8.3 ng/mL, respectively) and did not predict SAMS (p=0.96). The proportion of patients classified as VITD deficient (<20 ng/mL) did not differ between patients with (n=16) and without (n=10) SAMS (χ2=1.45; p=0.23), nor did the proportion of patients classified as VITD insufficient (<30 ng/mL) (n=42 vs. 48; χ2<0.01 and p=0.94). Both baseline and on-statin VITD were inversely related to the change in creatine kinase (CK) with statin therapy (p=0.01 and 0.02, respectively), independent of SAMS (p=0.36 and 0.35). Conclusions Baseline VITD, VITD deficiency/insufficiency and changes in VITD with statin therapy do not predict SAMS in patients with rigorously verified SAMS. However, low VITD may exacerbate statin-induced muscle injury and could contribute to SAMS development with a longer duration of statin treatment.

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“…There is a possible relationship between vitamin D deficiency and statin-induced myalgia (34). It is important to be aware of this with regard to certain groups of immigrants whose level of vitamin D may be very low (35). After a treatment break during which the vitamin D level is normalised, the treatment can in many cases be resumed without the pain recurring (34,36).…”

Section: Lipid-lowering Agentsmentioning

confidence: 99%