Fatal and Widespread Skeletal Myopathy Confirmed Morphologically Years After Initiation of Simvastatin Therapy

Boltan, David Demitry; Lachar, Whitney A.; Khetan, Anita; Bouffard, John-Paul; Roberts, William C.

doi:10.1016/j.amjcard.2006.11.071

Cited by 10 publications

(3 citation statements)

References 15 publications

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“…Research suggests possible associations between suboptimal levels of vitamin D and development of various diseases, including pulmonary disorders (Black and Scragg 2005 ; Sita-Lumsden et al 2007 ; Camargo et al 2007 ; Devereux et al 2007 ; Litonjua and Weiss 2007 ) chronic rhinitis (Abuzeid et al 2012 ), tonsillar hypertrophy, (Nunn et al 1986 ; Reid et al 2011 ), metabolic syndrome (Botella-Carretero et al 2007 ), type 2 diabetes (Mattila et al 2007 ), hypertension (Forman et al 2007 ), cancers of the breast, colon, and prostate (Garland et al 2006 ), poor stress resilience (Bracha et al 2004 ), depression (Berk et al 2007 ), and cognitive decline (Przybelski and Binkley 2007 ). Vitamin D appears to be necessary for skeletal muscle as well and its deficiency has been associated with nonspecific musculoskeletal pain (Plotnikoff and Quigley 2003 ), chronic pain (Turner et al 2008 ), low back pain (Lotfi et al 2007 ), and myopathy (Boltan et al 2007 ; Goldstein 2007 ; Prabhala et al 2000 ). Some researchers have even suggested a link between vitamin D deficiency and all-cause mortality (Giovannucci 2007 ).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D deficiency and fatigue: an unusual presentation

Johnson

Sattari

2015

SpringerPlus

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Fatigue is a vague but common complaint that is poorly characterized by physicians as well as patients. While fatigue may result from a number of different etiologies, at the present time, a comprehensive approach to each patient with fatigue does not include routine measurement of serum vitamin D levels. A 61-year-old man was evaluated for excessive daytime fatigue. No features characteristic for depression, sleep apnea, or narcolepsy were present. A comprehensive work-up, including thyroid function tests and testosterone levels, did not reveal any abnormalities. However, serum 25-hydroxyvitamin D level was low, at 18.4 ng/mL. Vitamin D supplementation was initiated. At follow-up in 3 and 12 months, the patient reported complete resolution of daytime fatigue, corresponding to an increase in his vitamin D levels. Possible mechanisms for clinical improvement include effects of vitamin D on components of inflammatory cascades, including tumor necrosis factor-alpha and prostaglandin D2, which result in decrease in central nervous system homeostatic sleep pressure. While more research is needed to determine if patients presenting with fatigue should be routinely screened for vitamin D deficiency, clinicians should consider obtaining vitamin D levels in patients with unexplained fatigue, nonspecific musculoskeletal pain, and risk factors for vitamin D deficiency.

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Section: Introductionmentioning

confidence: 99%

Vitamin D deficiency and fatigue: an unusual presentation

Johnson

Sattari

2015

SpringerPlus

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“…Sixth, with the caveat that it is difficult to extrapolate from cell culture to intact animals and man, the present study addresses an important question regarding the potential cardiac effects of statins in the setting of conditions associated with increased NO. There is little doubt that statins are of benefit in the reduction of morbidity and mortality from atherosclerotic cardiovascular disease, just as there is little doubt that they have definite adverse effects which in some patients is manifested as a skeletal muscle myopathy or rhabdomyolysis that can be fatal [59,60] . Although our study did not examine skeletal muscle, it is noteworthy that recent data make a compelling case for cell death of skeletal muscle myofibres as the key element in the pathophysiology of statin-induced myopathy [60] , suggesting that our data may be relevant to consideration of skeletal muscle myopathy as well.…”

Section: Discussionmentioning

confidence: 99%

Interaction of the HMG-CoA Reductase Inhibitor Lovastatin and Nitric Oxide in Cardiomyocyte Cell Death

Rabkin

Tsang²

2008

Pharmacology

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Aim: The objective of this study was to examine the interaction ofa 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) with a nitric oxide (NO) donor from the perspective of the impact on cardiomyocyte cell viability. Methods: Embryonic chick cardiomyocytes in culture were treated with a wide range of concentrations of sodium nitroprusside (SNP), which releases NO and also generates toxic reactive nitrogen species. SNP was combined with the HMG-CoA reductase inhibitor lovastatin and cell viability was assessed by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. Results: SNP and lovastatin each produced a significant (p < 0.01) concentration-dependent increase in cell death. Using SNP concentrations at or below the ED₅₀, SNP (0.01, 0.1 or 0.5 mmol/l) increased the amount of cell death when combined with lovastatin (1, 10, 50 and 100 µmol/l). At lovastatin concentrations of 50 µmol/l and less, the amount of cell death was consistently similar to the arithmetic sum of SNP and lovastatin, suggesting that there was an additive and not synergistic relationship between SNP and lovastatin. In combination with lovastatin (100 µmol/l), however, the amount of cell death was consistently lower than the calculated expected value and suggested saturation of a common mechanism. The combination of SNP and lovastatin produced the characteristic microscopic changes of apoptosis. Considering that both SNP and lovastatin can activate caspase-3, cells were treated with the caspase-3 inhibitor Ac-DEVD-CHO. This inhibitor produced a significant (p < 0.05) and consistent 30% reduction in the amount of cell death induced by SNP and lovastatin. Conclusion: These data suggest that the cardiomyocyte toxicity from NO continues to be evident uninterrupted by and not accentuated by the presence of an HMG-CoA inhibitor. The cardiac adverse effect of each of these agents utilizes a common pathway involving caspase-3 so that their cardiotoxicity can be blunted by a caspase-3 inhibitor.

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“…[16][17][18] Vitamin D appears to be necessary for optimum functioning of skeletal muscle as well, with deficiency associated with increased risk for falls 19 and disability 20 among elderly patients, as well as chronic pain, 21 low back pain, 22 and cases of overt painful myopathy. [23][24][25] In one study of patients admitted to a Minneapolis hospital, 93% of those complaining of nonspecific musculoskeletal pain were found to have significant vitamin D deficiency. 26 Recent publications point to a potential link between vitamin D deficiency and the metabolic syndrome, 27 type 2 diabetes, 28 incident hypertension, 29 as well as a possible association with cancers of the breast, colon, and prostate.…”

Section: Abbreviationsmentioning

confidence: 99%

Resolution of Hypersomnia Following Identification and Treatment of Vitamin D Deficiency

McCarty

2010

Journal of Clinical Sleep Medicine

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Fatal and Widespread Skeletal Myopathy Confirmed Morphologically Years After Initiation of Simvastatin Therapy

Cited by 10 publications

References 15 publications

Vitamin D deficiency and fatigue: an unusual presentation

Vitamin D deficiency and fatigue: an unusual presentation

Interaction of the HMG-CoA Reductase Inhibitor Lovastatin and Nitric Oxide in Cardiomyocyte Cell Death

Resolution of Hypersomnia Following Identification and Treatment of Vitamin D Deficiency

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