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Drug-Related Muscular Pain
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Coenzyme Q10 deficiency is the most common associated muscle defect. CoQ10 is an essential cofactor in mitochondrial respiration pathways in the electron transport chain.1 Moreover, carnitine palmityl transferase (CPT) II deficiency is a mitochondrial abnormality most likely acquired as a result of exposure to statins opposed to a genetic inheritance. CPT II is located in the mitochondrial membrane where it facilitates the transport of long-chain fatty acids into the mitochondrion.1
Leigh Syndrome (Encephalopathy)
Published in Charles Theisler, Adjuvant Medical Care, 2023
Biotin: Specific therapy via biotin administration is appropriate for three forms of Leigh-like syndrome: biotin-thiamine-responsive basal ganglia diseasebiotinidase deficiencycoenzyme Q10 deficiency due to PDSS2 mutation4
Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Mitochondrial diseases: Leigh's syndrome (LS) (multiple genes).Familial striatal lucencies with Leber's optic atrophy.Coenzyme Q10 deficiency.
Statin-associated muscle symptoms in coronary patients: design of a randomized study
Published in Scandinavian Cardiovascular Journal, 2019
John Munkhaugen, Nils Tore Vethe, Morten Wang Fagerland, Toril Dammen, Joep Perk, Erik Gjertsen, Jan Erik Otterstad, Lars Gullestad, Stein Bergan, Einar Husebye
It remains unclear how statins may produce muscle symptoms and reliable biomarkers for the prediction or diagnosis of SAMS are lacking [6,7]. Individual variations in statin pharmacokinetics, mitochondrial dysfunction or coenzyme Q10 deficiency are suggested mechanisms for SAMS [15]. A few studies indicate that pharmacokinetic alterations in statin metabolites may contribute to SAMS [16–18]. The lactone metabolites of statins seem to be more potent in inducing myotoxic effects compared to the corresponding acid metabolites. Plasma concentrations of atorvastatin lactones have been associated with clinical muscle symptoms [17,18]. Accordingly, the lactones inhibit the mitochondrial complex III enzyme activity, thereby reducing the respiratory capacity in muscle cells [19]. We have recently developed and validated a fast, sensitive, and reliable liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for precise quantification of atorvastatin and its major lactone and acid metabolites in blood [20]. The acyl glucuronide of atorvastatin is also included because acyl glucuronide metabolites of drugs are associated with toxicity [21]. Atorvastatin or metabolite levels have previously not been investigated as diagnostic markers of SAMS, under randomized, blinded and placebo-controlled conditions.
Effect of coenzyme Q10 supplementation on clinical features of migraine: a systematic review and dose–response meta-analysis of randomized controlled trials
Published in Nutritional Neuroscience, 2020
Mohammad Parohan, Payam Sarraf, Mohammad Hassan Javanbakht, Sakineh Ranji-Burachaloo, Mahmoud Djalali
We systematically searched online medical databases including ISI Web of Science, PubMed, Cochrane library and Scopus to identify eligible studies published in English up to April 2018. The following search keywords were used: (‘Migraine Disorders’ OR Migraine* OR Headache OR Migraineur*) AND (‘coenzyme Q10’ OR ‘ubiquinol-10’ OR ‘Coenzyme Q10 Deficiency’ OR ‘co-enzyme Q10’ OR ubiquinone OR ubidecarenone OR CoQ10 OR semiquinone OR ubisemiquinone OR ubiquinol). The reference lists of eligible articles also were checked. All search results including titles and abstracts were downloaded into EndNote (version X8) to merge retrieved citations, remove duplicated, and simplify the review process.