Managing the underestimated risk of statin-associated myopathy

Rallidis, Lοukianos S.; Fountoulaki, Katerina; Anastasiou-Nana, Maria

doi:10.1016/j.ijcard.2011.07.048

Cited by 87 publications

(66 citation statements)

References 78 publications

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“…This confirmed by grading of degeneration of muscle fibers. This was in agreement with Rallidis et al, [14] who reported that in clinical practice 5-10% of patients receiving statins develop myopathy, and this myopathy was dose dependent. Also this was in line with the study of Silva et al [15] who reported a 10-fold increase in myopathy in patients taking a high dose of atorvastatin or simvastatin compared to patients on a lower dose.…”

Section: Discussionsupporting

confidence: 93%

“…Different statins can induce apoptosis in skeletal muscle [41]. This result was explained by Rallidis et al, [14] who reported that statin induced myotoxicity through the depletion of isoprenoids that control the rate of myofiber apoptosis. Isoprenoids are linked to proteins by either farnesylation or geranylgeranylation.…”

Section: The Morphometric Resultsmentioning

confidence: 93%

“…This will cause production of free radicals, which affect the nerve cells [25]. In contrast, many studies reported that the serum coenzyme Q10 levels decrease during statin treatment but its myocyte levels are not consistently decreased [14].…”

Section: The Morphometric Resultsmentioning

confidence: 99%

See 2 more Smart Citations

Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

Mokhmer¹,

Saber²,

Hamouda³

et al. 2017

J Cytol Histol

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Section: Discussionsupporting

confidence: 93%

Section: The Morphometric Resultsmentioning

confidence: 93%

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Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

Mokhmer¹,

Saber²,

Hamouda³

et al. 2017

J Cytol Histol

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show abstract

“…Those aspects corroborate with the risk factors indicated by the literature as influencing the occurrence of muscle side effects by statins (1,5,26) . The fact of free available statins in the health system of the city to be restricted to simvastatin and atorvastatin, high to intermediate risk classes for the occurrence of muscle discomfort (5,27) could have contributed to the occurrence of those side effects.…”

Section: Resultsmentioning

confidence: 99%

Adherence to statin treatment and associated factors in female users from the Unified Health System (SUS)

Bonfim

Hansen

Turi

et al. 2014

Rev. esc. enferm. USP

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Objective: To identify the adherence rate of a statin treatment and possible related factors in female users from the Unified Health System. Method: Seventy-one women were evaluated (64.2 ± 11.0 years) regarding the socio-economic level, comorbidities, current medications, level of physical activity, self-report of muscular pain, adherence to the medical prescription, body composition and biochemical profile. The data were analyzed as frequencies, Chi-Squared test, and Mann Whitney test (p<0.05). Results: 15.5% of women did not adhere to the medical prescription for the statin treatment, whose had less comorbidities (p=0.01), consumed less quantities of medications (p=0.00), and tended to be younger (p=0.06). Those patients also presented higher values of lipid profile (CT: p=0.01; LDL-c: p=0.02). Musculoskeletal complains were not associated to the adherence rate to the medication. Conclusion: The associated factors to adherence of dyslipidemic women to statin medical prescription were age, quantity of comorbidities and quantity of current medication.

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“…This provoked muscular damage, as was verified by biochemical tests. [3][4][5] However, hypothyroidism and hyperaldosteronism, with consequent hypokalemia and hypocalcemia, can all have contributed to statin-induced myopathy. [6][7][8] Our patient underwent total thyroidectomy 16 years ago because of Graves's disease.…”

Section: Discussionmentioning

confidence: 99%

A dangerous mixture

Piva¹,

Filippi²,

Simioni³

2014

Ital J Med

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Emilia, a 59-year old woman was hospitalized due to fatigue, cramps and paresthesias involving her arms with a spontaneous Trousseau sign (spasm of the wrist and metacarpophalangeal joints, extension of distal and proximal interphalangeal joints, adduction of the fingers). 1,2 Urgent biochemical tests showed hypernatremia (150 mmol/L), hypokalemia (2.3 mmol/L), hypocalcemia (total calcium 7.3 mg/dL, ionized calcium 0.89 mmol/L).Her medical history included: thyroidectomy for Graves's disease, now treated with levothyroxine, vitiligo, mild carotid arteries atherosclerosis treated with acetylsalicylic acid, recently diagnosed hypercholesterolemia treated with simvastatin, started the previous month.On admittance to hospital the patient was alert and collaborative; general examination did not show any particular alteration except for vitiligo and mild hyperreflexia. Blood pressure was high (140/100 mmHg) and other vital parameters were normal.Routine laboratory tests confirmed hypernatremia, hypocalcemia and hypokalemia and showed: metabolic alkalosis (pH 7.50, pCO 2 44 mmHg, HCO 3 34 mmol/L); mild hypomagnesemia (1.54 mg/dL; n.v. 1.58-2.55); albuminemia, phosphatemia, blood urea nitrogen and creatinine were normal, but with slightly increased urinary protein excretion (0.29 g/24 h); urinary excretion of calcium was low (31.2 mg/24 h; n.v. 100-320); urinary sodium excretion was elevated (290 mmol/24 h; n.v. 40-220); urinary excretion of phosphate and potassium was normal; muscle enzymes were very elevated (creatine kinase 2509 U/L; myoglobin 466 ng/mL; aldolase 34.9 UI/L); cortisol and aldosterone level were normal, plasma renin activity was low (0.5 pg/mL in orthostatism and 1.5 pg/mL in clynostatism), thyroid-stimulating hormone (TSH) level was high (22.9 uUI/mL) with normal free thyroxine (FT4) (0.92 ng/dL); parathyroid hormone (PTH) level was high (70.8 pg/mL; n.v. 7-53); vitamin D3 was low (19.2 nmol/L; n.v. 75-100). Blood cell count, plasma osmolarity, C-reactive protein, cholesterol and triglycerides levels were normal.Electrocardiogram (EKG) showed sinus rhythm with normal heart rate (60 bpm), prolongation of QT interval. Chest X-ray was regular, upper and lower limbs electromyography showed only a mild A dangerous mixture ABSTRACTA 59-year old woman was admitted for fatigue and arm paresthesias with Trousseau sign. Her medical history included thyroidectomy and hypercholesterolemia recently treated with simvastatin. Laboratory tests showed severe hypokalemia and hypocalcemia, severe increase in muscle enzymes, metabolic alkalosis; low plasma renin activity, increased thyroid-stimulating hormone, normal free thyroxine, increased parathyroid hormone, decreased vitamin D3; alterations in electrolyte urinary excretion, cortisol and aldosterone were excluded. Hypothesizing a statin-related myopathy, simvastatin was suspended; the patient reported use of laxatives containing licorice. Electrolytes normalized with intravenous supplementation. Among many biochemical alterations, none stands out as a major cause f...

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Managing the underestimated risk of statin-associated myopathy

Cited by 87 publications

References 78 publications

Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

Adherence to statin treatment and associated factors in female users from the Unified Health System (SUS)

A dangerous mixture

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