McArdle disease with rhabdomyolysis induced by rosuvastatin: case report

Lorenzoni, Paulo José; Silvado, Carlos Eduardo; Scola, Rosana Hermínia; Luvizotto, M L; Werneck, Lineü Cesar

doi:10.1590/s0004-282x2007000500020

Cited by 19 publications

(5 citation statements)

References 14 publications

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“…On contrary, the present diminution in glycogen's muscle content disagrees with Lorenzoni et al, (2007) who reported a case of 35-years old man who acquired rosuvastatin-induced rhabdomyolysis and investigations cleared that in muscle biopsy, subsarcolemmal and central acummulation of glycogen were noticed.…”

Section: Discussioncontrasting

confidence: 99%

Effect of Simvastatin on Male Albino Rats, Cytogenetic and Histochemical Studies

Shalaby

Rashed

Foda

et al. 2018

Journal of Scientific Research in Science

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Introduction: Simvastatin belongs to statins drugs that are used globally for lowering blood cholesterol level in cardiovascular patients. Simvastatin can be considered as life threatening agent, since prolonged usage may cause myotoxicity. Materials & methods: The present study was performed on 20 adult male rats which were divided into: Group I which was the control group that did not receive any treatments, and Group II which was the treated group that received 80 mg/kg b.wt/day of simvastatin for 46 days. All rats were submitted to bone marrow collection for the cytogenetics tests and gastrocnemoius muscles' biopsied were taken for the histochemical tests. Results: statistical analysis showed a non-significant increase in the mean of chromosomal aberrations (CAs) in the treated rats' cells comparing to the control samples. On the other hand, an observed non-significant decrease in the mean of total proteins (TP) content in rats' gastrocnemius muscles of Group II when compared to the control group. Whereas, noticed significant reduction in the mean of glycogen (Glyc.) content in rats' gastrocnemius muscles of the same group when compared to the control group. Conclusion: Simvastatin may lead to an increase in the incidence of (CAs) in bone marrow cells, and determination of TP and Glyc. content in skeletal muscle biopsies can be considered as indicators for muscle necrosis incidence. Recommendations: Simvastatin has to be prescribed carefully in patients suffering from hypercholesterolemia, precautions have to be taken into consideration since it may affect skeletal muscles' health and lead to muscle toxicity on the short or long run of usage.

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Section: Discussioncontrasting

confidence: 99%

Effect of Simvastatin on Male Albino Rats, Cytogenetic and Histochemical Studies

Shalaby

Rashed

Foda

et al. 2018

Journal of Scientific Research in Science

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“…Some genetic conditions have been associated with a higher risk for developing statin myotoxicity. Notably, patients with myoadenylate deaminase deficiency or palmitoyltransferase II deficiency, as well as those with McArdle disease, might be at higher risk for having statin-induced myalgias than the general population (Vladutiu et al 2006;Lorenzoni et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Manifesting heterozygotes in McArdle disease: a myth or a reality—role of statins

Núñez-Manchón

Ballester-Lopez

Koehorst

et al. 2018

J of Inher Metab Disea

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McArdle disease is an autosomal recessive condition caused by deficiency of the PYGM gene-encoded muscle isoform of glycogen phosphorylase. Some cases of "manifesting" heterozygotes or carriers (i.e., patients who show some McArdle-like symptoms or signs despite being carriers of only one mutated PYGM allele) have been reported in the literature but there is controversy, with misdiagnosis being a possibility. The purpose of our study was to determine if there are actually "manifesting" heterozygotes of McArdle disease and, if existing, whether statin treatment can trigger such condition. Eighty-one relatives of McArdle patients (among a total of 16 different families) were studied. We determined whether they were carriers of PYGM mutations and also collected information on exercise tests (second wind and modified Wingate anaerobic test) and statin intake. We found 50 carriers and 31 non-carriers of PYGM mutations. Although we found existence of heterozygotes manifesting some exercise-related muscle problems such as exacerbated myalgia or weakness, they only accounted for 14% of the carriers and muscle symptoms were milder than those commonly reported in patients. Further, no carrier (whether reporting symptoms or not) showed the second wind phenomenon or a flat blood lactate response to maximal-intensity exercise, both of which are hallmarks of McArdle disease. On the other hand, statin myotoxicity was not associated with muscle symptom onset.

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“…Both patients with definite McArdle disease and asymptomatic heterozygotes with MPD developing statin myopathy have been reported previously [74][75][76][77]. In various settings, the advanced age at diagnosis plus the absence of prior symptoms suggest that the statins could uncover the genetic defect in these kind of patients.…”

Section: Glycogen Storage Disordersmentioning

confidence: 98%

Role of Genetic Factors in Statins Side-Effects

Scarpini

Cappellone²,

Auteri³

et al. 2012

CHDDT

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Statins are relevant drugs involved in the reduction of cardiovascular events both in primary and secondary prevention. Related muscular side-effects are the most common cause of withdrawal and statins discontinuation could induce a negative rebound effect in terms of vascular events. Among factors in association with statins side-effects the combination with other drugs and the female sex are established conditions. However recent data suggest a specific genetic influence in intolerance development, at least for some statins. Indeed a genome-wide study in patients treated with simvastatin found an impressive association between single-nucleotide polymorphisms (SNPs) located within SLCO1B1 gene on chromosome 12 and established myopathy. Furthermore, the association between the SLCO1B1*5 variant and side-effects was found also in patients treated with atorvastatin but not, apparently, with pravastatin and categorized as carriers of mild-myopathy. Recently a similar evidence has been suggested in type 2 diabetic patients treated mainly with simvastatin. However another relevant issue is that, apart from genetic influence in liver transporters influencing drug levels, the complexity of mechanisms involved in the muscular side effects of statins has been addressed by the evidence of other influencing pathways such as the variant within the COQ2 gene involved in Coenzyme Q(10) mild-asymptomatic deficiency and skeletal muscle drug transporters expression. In conclusion, the picture of putative pharmacogenetic modulation of statins safety is reaching a growing body of evidence for translation into clinical practice but more specific studies for each single statin, in different clinical settings, both from genome-wide or competitive candidate genes evaluation, are needed before describing a definitive class-risk profile.

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McArdle disease with rhabdomyolysis induced by rosuvastatin: case report

Cited by 19 publications

References 14 publications

Effect of Simvastatin on Male Albino Rats, Cytogenetic and Histochemical Studies

Effect of Simvastatin on Male Albino Rats, Cytogenetic and Histochemical Studies

Manifesting heterozygotes in McArdle disease: a myth or a reality—role of statins

Role of Genetic Factors in Statins Side-Effects

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