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| COMMENTARY |
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| Year : 2013 | Volume
: 5
| Issue : 8 | Page : 494-495 |
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Severe vitamin D deficiency, myopathy, and rhabdomyolysis
Charles J Glueck, Brandon Conrad
Cholesterol Center, Jewish Hospital of Cincinnati, Cincinnati, Ohio, USA
| Date of Web Publication | 30-Aug-2013 |
Correspondence Address:
Charles J Glueck
Cholesterol Center, Jewish Hospital, 2135 Dana Ave, Suite 430, Cincinnati 45207
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1947-2714.117325
How to cite this article:
Glueck CJ, Conrad B. Severe vitamin D deficiency, myopathy, and rhabdomyolysis. North Am J Med Sci 2013;5:494-5 |
In the report by Rasheed et al., [1] a 33-year-old female developed proximal myopathy and rhabdomyolysis associated with very low serum 25 (OH) vitamin D (4 ng/mL, laboratory lower normal limit 31 ng/mL). Rasheed et al., [1] noted that serum 25 (OH) vitamin
D levels <20 ng/mL can cause increased body sway, while <10 can lead to inability to rise from a chair, or ascend stairs, coupled with muscle pain.
We have recently assessed exercise-induced severe rhabdomyolysis in a thin, athletic, dark-skinned (Meztizo), highly conditioned, nondiabetic young man, occurring in the setting of a 5 K race. He was subsequently found to have severe 25 (OH) vitamin D deficiency (6 ng/mL). Rhabdomyolysis, myoglobinemia, and even mild renal failure can occur as sequelae of marathon races, military recruit training, strength training, and endurance athletics. [2] Often this muscle damage resolves without incident or treatment and may be detected only upon laboratory testing. [2] We speculate that subjects with preexisting low serum 25 (OH) vitamin D are selected out for exertional rhabdomyolysis during strenuous activities. In subjects not receiving statins, low serum 25 (OH) D levels have been associated with myositi [3] and reduced muscle function. [4] Vitamin D may improve muscle strength through a highly specific nuclear receptor in muscle tissue. [5] Serum 25 (OH) D is related to physical performance. [6]
Since myositis-myalgia is the major cause of statin intolerance, [7] and the tripartite association of serum 25 (OH) vitamin D deficiency, statins, and myositis-myalgia has physiologic plausibility, [3],[4],[6],[8],[9] resolution of vitamin D deficiency interacting with statins to produce myositis-myalgia would have significant clinical importance, allowing reinstitution of statins to optimize low-density lipoprotein (LDL) cholesterol and prevent cardiovascular disease (CVD). Recently, we prospectively studied 150 hypercholesterolemic patients, unable to tolerate ≥1 statin because of myositis-myalgia, selected by low (<32 ng/mL) serum 25 (OH) vitamin D. [10] On no statins, 50,000 units of vitamin D was given twice a week for 3 weeks and then continued once a week. After 3 weeks on vitamin D, statins were restarted. On vitamin D supplementation plus reinstituted statins for a median of 8.1 months, 131 of 150 patients (87%) were free of myositis-myalgia and tolerated reinstituted statins well. Serum 25 (OH) vitamin D increased from median 21 to 40 ng/mL (P < 0.001), and normalized (≥32 ng/mL) in 117 (78%) of 150 previously vitamin D deficient, statin-intolerant patients. Median LDL cholesterol decreased from 146 to 95 mg/dL, P < 0.001. We concluded [10] that symptomatic myositis-myalgia in hypercholesterolemic statin-treated patients with concurrent serum 25 (OH) vitamin D deficiency may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle causing myalgia.
We believe vitamin D deficiency places subjects at higher risk for rhabdomyolysis, which develops during severe exertion. We suggest that when exercise-induced rhabdomyolysis develops, after full recovery and back at normal nutrition, serum 25OH vitamin D be measured. We suggest that when very low vitamin D is documented, it be normalized before major prolonged exertion. We hypothesize that normalization of vitamin D before heavy exertion could perhaps prevent severe muscle damage events and sequelae, which may occur in previously asymptomatic athletes.
| References | |  |
| 1. | Rasheed K, Sethi P, Bixby E. Severe vitamin D deficiency induced myopathy associated with rhabydomyolysis. N Am J Med Sci 2013;5:334-6. 
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| 2. | Clarkson PM. Exertional rhabdomyolysis and acute renal failure in marathon runners. Sports Med 2007;37:361-3.
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| 3. | Erkal MZ, Wilde J, Bilgin Y, Akinci A, Demir E, Bödeker RH, et al. High prevalence of vitamin D deficiency, secondary hyperparathyroidism and generalized bone pain in Turkish immigrants in Germany: Identification of risk factors. Osteoporos Int 2006;17:1133-40.
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| 4. | Shinchuk LM, Holick MF. Vitamin d and rehabilitation: Improving functional outcomes. Nutr Clin Pract 2007;22:297-304.
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| 5. | Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, et al. Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr 2004;80:752-8.
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| 6. | Bunout D, Barrera G, Leiva L, Gattas V, de la Maza MP, Avendaño M, et al. Effects of vitamin D supplementation and exercise training on physical performance in Chilean vitamin D deficient elderly subjects. Exp Gerontol 2006;41:746-52.
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| 7. | Thompson PD, Clarkson P, Karas RH. Statin-associated myopathy. JAMA 2003;289:1681-90.
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| 8. | Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr 2006;84:18-28.
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| 9. | Lips P. Vitamin D physiology. Prog Biophys Mol Biol 2006;92:4-8.
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| 10. | Glueck CJ, Budhani SB, Masineni SS, Abuchaibe C, Khan N, Wang P, et al. Vitamin D deficiency, myositis-myalgia, and reversible statin intolerance. Curr Med Res Opin 2011;27:1683-90.
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