McArdle's disease diagnosed following statin-induced myositis

Livingstone, Callum; Riyami, Said Al; Wilkins, P.; Ferns, Gordon A.

doi:10.1258/0004563041201554

Cited by 33 publications

(15 citation statements)

References 10 publications

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“…Interestingly, Hansen et al, 20 after having evaluated the clinical course and outcome in 45 patients with statinassociated myopathy, recently reported that all patients experienced full resolution of muscle pain and other clinical symptoms after cessation of statin therapy (mean period of recovery, 2.3 months; range, 0.25-14 months). These findings when combined with the observations of our group and other investigators [3][4][5] imply that the resolution of muscular symptoms after statin discontinuation (which may also be followed by substantial reduction of increased CK levels) could assist the clinician to differentiate statinassociated myopathy from a latent neuromuscular disorder that was potentially disclosed by the intake of 3-hydroxy-3-methylglutaryl coenzyme A inhibitors.…”

Section: Commentsupporting

confidence: 68%

“…The reported disclosure of a metabolic myopathy following statin prescription in case 2 has also been recognized lately in 2 other patients with myophosphorylase deficiency 3,4 and 2 individuals with acid maltase deficiency. 3,5 As in our patient, statin therapy had triggered muscular symptoms and serum CK level elevation that did not resolve after its discontinuation. The treating physicians were alerted, and further diagnostic workup was performed leading to the eventual diagnosis of the underlying disorders.…”

Section: Commentmentioning

confidence: 52%

“…21,22 It should also be kept in mind that measurement of ␣ glucosidase activity in leucocytes or skin fibroblasts may disclose a latent acid maltase deficiency that may become symptomatic during statin treatment. 3,5 Finally, since asymptomatic CK elevations are common, the present clinical observation underscores the importance of the currently recommended pretreatment measurements of CK levels, which might be helpful in the diagnostic evaluation and optimal management of more complex cases with elevated serum CK levels and muscular symptoms. 23 In conclusion, latent neuromuscular disorders can be disclosed by statin therapy in presymptomatic patients.…”

Section: Commentmentioning

confidence: 74%

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Presymptomatic Neuromuscular Disorders Disclosed Following Statin Treatment

Tsivgoulis¹,

Spengos²,

Karandreas³

et al. 2006

Arch Intern Med

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It is well recognized that statins affect muscular tissue adversely and that their use is associated with clinically important myositis, rhabdomyolysis, mild elevation of serum creatine kinase (CK) levels, myalgias, muscle weakness, muscle cramps, and persistent myalgias or serum CK level elevations after statin treatment is discontinued. The association between statins and the disclosure of presymptomatic metabolic myopathy is another underrated phenomenon related to statin therapy that was recently recognized in rare cases. The purpose of this report is to provide additional support for this association and to report other neuromuscular disorders that have also been seen following statin intake. The present case series illustrates that statins may act as unmasking agents in asymptomatic patients with a latent neuromuscular disorder. Thus, it may be postulated that statin intake may be a sufficient insult to precipitate neuromuscular symptoms and substantially increase muscle enzymes in presymptomatic patients with an abnormal neuromuscular substrate. In conclusion, muscular symptoms or increased serum CK levels persisting after statin treatment discontinuation should alert the clinician to pursue further diagnostic evaluations for the detection of potential underlying neuromuscular diseases.

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Section: Commentsupporting

confidence: 68%

Section: Commentmentioning

confidence: 52%

Section: Commentmentioning

confidence: 74%

See 1 more Smart Citation

Presymptomatic Neuromuscular Disorders Disclosed Following Statin Treatment

Tsivgoulis¹,

Spengos²,

Karandreas³

et al. 2006

Arch Intern Med

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“…20 The mechanisms of lipid-lowering drug-induced myotoxicity are unknown although there has been considerable speculation in this regard. 3,4,46 Few reports exist regarding associations with inherited 5,11,29 and acquired metabolic myopathies 2 or with peripheral neuropathies. 17,40 We suggest that a substantially larger number of individuals than expected in the general population with lipid-lowering drug-induced myopathies will have underlying metabolic myopathies triggered by the drugs.…”

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confidence: 99%

Genetic risk factors associated with lipid‐lowering drug‐induced myopathies

et al. 2006

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Lipid-lowering drugs produce myopathic side effects in up to 7% of treated patients, with severe rhabdomyolysis occurring in as many as 0.5%. Underlying metabolic muscle diseases have not been evaluated extensively. In a cross-sectional study of 136 patients with drug-induced myopathies, we report a higher prevalence of underlying metabolic muscle diseases than expected in the general population. Control groups included 116 patients on therapy with no myopathic symptoms, 100 asymptomatic individuals from the general population never exposed to statins, and 106 patients with non-statin-induced myopathies. Of 110 patients who underwent mutation testing, 10% were heterozygous or homozygous for mutations causing three metabolic myopathies, compared to 3% testing positive among asymptomatic patients on therapy (P = 0.04). The actual number of mutant alleles found in the test group patients was increased fourfold over the control group (P < 0.0001) due to an increased presence of mutation homozygotes. The number of carriers for carnitine palmitoyltransferase II deficiency and for McArdle disease was increased 13- and 20-fold, respectively, over expected general population frequencies. Homozygotes for myoadenylate deaminase deficiency were increased 3.25-fold with no increase in carrier status. In 52% of muscle biopsies from patients, significant biochemical abnormalities were found in mitochondrial or fatty acid metabolism, with 31% having multiple defects. Variable persistent symptoms occurred in 68% of patients despite cessation of therapy. The effect of statins on energy metabolism combined with a genetic susceptibility to triggering of muscle symptoms may account for myopathic outcomes in certain high-risk groups.

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“…In addition, the onset of CK rise in his serum was late, more than two and a half years after the statin was initiated. Raised plasma CK due to previously undiagnosed glycogen storage disease has been reported during treatment with statins, but it involved symptomatic patients and the CK elevation was noted early during treatment [4,5]. While baseline CK measurement prior to statin therapy is recommended, routine CK monitoring is currently considered of little value in asymptomatic patients [1].…”

mentioning

confidence: 99%