The Experts below are selected from a list of 243 Experts worldwide ranked by ideXlab platform
Wendi D. Roe - One of the best experts on this subject based on the ideXlab platform.
-
Untargeted metabolic profiling of dogs with a suspected Toxic mitochondrial Myopathy using liquid chromatography-mass spectrometry.
Toxicon : official journal of the International Society on Toxinology, 2019Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. RoeAbstract:'Go Slow Myopathy' (GSM) is a suspected Toxic Myopathy in dogs that primarily occurs in the North Island of New Zealand, and affected dogs usually have a history of consuming meat, offal or bones from wild pigs (including previously frozen and/or cooked meat). Previous epidemiological and pathological studies on GSM have demonstrated that changes in mitochondrial structure and function are most likely caused by an environmental toxin that dogs are exposed to through the ingestion of wild pig. The disease has clinical, histological and biochemical similarities to poisoning in people and animals from the plant Ageratina altissima (white snakeroot). Aqueous and lipid extracts were prepared from liver samples of 24 clinically normal dogs and 15 dogs with GSM for untargeted liquid chromatography-mass spectrometry. Group-wise comparisons of mass spectral data revealed 38 features that were significantly different (FDR
-
untargeted metabolic profiling of dogs with a suspected Toxic mitochondrial Myopathy using liquid chromatography mass spectrometry
Toxicon, 2019Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. RoeAbstract:'Go Slow Myopathy' (GSM) is a suspected Toxic Myopathy in dogs that primarily occurs in the North Island of New Zealand, and affected dogs usually have a history of consuming meat, offal or bones from wild pigs (including previously frozen and/or cooked meat). Previous epidemiological and pathological studies on GSM have demonstrated that changes in mitochondrial structure and function are most likely caused by an environmental toxin that dogs are exposed to through the ingestion of wild pig. The disease has clinical, histological and biochemical similarities to poisoning in people and animals from the plant Ageratina altissima (white snakeroot). Aqueous and lipid extracts were prepared from liver samples of 24 clinically normal dogs and 15 dogs with GSM for untargeted liquid chromatography-mass spectrometry. Group-wise comparisons of mass spectral data revealed 38 features that were significantly different (FDR<0.05) between normal dogs and those with GSM in aqueous extracts, and 316 significantly different features in lipid extracts. No definitive cause of the Myopathy was identified, but alkaloids derived from several plant species were among the possible identities of features that were more abundant in liver samples from affected dogs compared to normal dogs. Mass spectral data also revealed that dogs with GSM have reduced hepatic phospholipid and sphingolipid concentrations relative to normal dogs. In addition, affected dogs had changes in the abundance of kynurenic acid, various dicarboxylic acids and N-acetylated branch chain amino acids, suggestive of mitochondrial dysfunction.
Mario Da Cunha Saporta - One of the best experts on this subject based on the ideXlab platform.
-
pearls oy sters hydroxychloroquine induced Toxic Myopathy mimics pompe disease critical role of genetic test
Neurology, 2019Co-Authors: Saurabh Shukla, Sakir Hume Gultekin, Mario Da Cunha SaportaAbstract:Chloroquine and hydroxychloroquine, commonly used for rheumatologic conditions, are rare yet very important causes of Toxic Myopathy with vacuolar changes on muscle biopsy.
-
Pearls & Oy-sters: Hydroxychloroquine-induced Toxic Myopathy mimics Pompe disease: Critical role of genetic test
Neurology, 2019Co-Authors: Saurabh Shukla, Sakir Hume Gultekin, Mario Da Cunha SaportaAbstract:Chloroquine and hydroxychloroquine, commonly used for rheumatologic conditions, are rare yet very important causes of Toxic Myopathy with vacuolar changes on muscle biopsy.
Lisa Christopher-stine - One of the best experts on this subject based on the ideXlab platform.
-
Statin-associated immune-mediated Myopathy: biology and clinical implications.
Current opinion in lipidology, 2017Co-Authors: Lisa Christopher-stine, Pari BasharatAbstract:Purpose of reviewIn the last 6 years, our understanding of statin-associated Myopathy expanded to include not only a Toxic Myopathy with limited and reversible side-effects but also an autoimmune variety in which statins likely induce an autoimmune Myopathy that is both associated with a specific au
-
Drug-related Myopathies of Which the Clinician Should Be Aware
Current Rheumatology Reports, 2010Co-Authors: Ritu Valiyil, Lisa Christopher-stineAbstract:Many drugs used for therapeutic interventions can cause unanticipated Toxicity in muscle tissue, often leading to considerable morbidity. A drug-induced, or Toxic, Myopathy is defined as the acute or subacute manifestation of myopathic symptoms such as muscle weakness, myalgia, creatine kinase elevation, or myoglobinuria that can occur in patients without muscle disease when they are exposed to certain drugs. A brief review of agents with a known association with myoToxicity and the proposed mechanisms linked to that Toxicity is outlined; however, the purpose of this review is to highlight recent discoveries and advances in the field of Toxic myopathies that have practical implications for practicing physicians. Because many drug-related myopathies are potentially reversible at early stages, it is important for clinicians to recognize Toxic myopathies early in their course to determine when to discontinue therapy and potentially prevent irreversible muscle damage.
-
Statin Myopathy: an update.
Current opinion in rheumatology, 2006Co-Authors: Lisa Christopher-stineAbstract:PURPOSE OF REVIEW Statin therapy has become the mainstay of treatment for lipid lowering, demonstrating cardiovascular risk reduction. Associated with statin popularity are misconceptions and fears of untoward side effects on muscle. This review clarifies the terminology relating to statin-related muscle disease; explores potential pathogenic mechanisms; reviews current estimates of statin Myopathy prevalence; and examines diagnosis and management. RECENT FINDINGS The fundamental mechanism of statin Myopathy remains elusive but is believed to be a class effect. The most common explanation for the cause of Toxic muscle injury invokes the deficiency of one of three main synthetic products in the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway. Recent studies have revealed several patients with statin-induced rhabdomyolysis who also have metabolic muscle defects, indicating that statin use may unmask presymptomatic metabolic myopathies. Although statin-related myoToxicity is believed to be a noninflammatory, Toxic Myopathy, experimental evidence suggests that it may be triggered by an autoimmune reaction or, conversely, initiate an autoimmune process. The precise mechanism is uncertain. SUMMARY As a class, statins appear to be usually safe, well tolerated agents with an excellent risk: benefit profile. The etiology and pathogenesis of statin Myopathy are poorly understood owing to the relative rarity of its existence.
H. Hunt - One of the best experts on this subject based on the ideXlab platform.
-
Untargeted metabolic profiling of dogs with a suspected Toxic mitochondrial Myopathy using liquid chromatography-mass spectrometry.
Toxicon : official journal of the International Society on Toxinology, 2019Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. RoeAbstract:'Go Slow Myopathy' (GSM) is a suspected Toxic Myopathy in dogs that primarily occurs in the North Island of New Zealand, and affected dogs usually have a history of consuming meat, offal or bones from wild pigs (including previously frozen and/or cooked meat). Previous epidemiological and pathological studies on GSM have demonstrated that changes in mitochondrial structure and function are most likely caused by an environmental toxin that dogs are exposed to through the ingestion of wild pig. The disease has clinical, histological and biochemical similarities to poisoning in people and animals from the plant Ageratina altissima (white snakeroot). Aqueous and lipid extracts were prepared from liver samples of 24 clinically normal dogs and 15 dogs with GSM for untargeted liquid chromatography-mass spectrometry. Group-wise comparisons of mass spectral data revealed 38 features that were significantly different (FDR
-
untargeted metabolic profiling of dogs with a suspected Toxic mitochondrial Myopathy using liquid chromatography mass spectrometry
Toxicon, 2019Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. RoeAbstract:'Go Slow Myopathy' (GSM) is a suspected Toxic Myopathy in dogs that primarily occurs in the North Island of New Zealand, and affected dogs usually have a history of consuming meat, offal or bones from wild pigs (including previously frozen and/or cooked meat). Previous epidemiological and pathological studies on GSM have demonstrated that changes in mitochondrial structure and function are most likely caused by an environmental toxin that dogs are exposed to through the ingestion of wild pig. The disease has clinical, histological and biochemical similarities to poisoning in people and animals from the plant Ageratina altissima (white snakeroot). Aqueous and lipid extracts were prepared from liver samples of 24 clinically normal dogs and 15 dogs with GSM for untargeted liquid chromatography-mass spectrometry. Group-wise comparisons of mass spectral data revealed 38 features that were significantly different (FDR<0.05) between normal dogs and those with GSM in aqueous extracts, and 316 significantly different features in lipid extracts. No definitive cause of the Myopathy was identified, but alkaloids derived from several plant species were among the possible identities of features that were more abundant in liver samples from affected dogs compared to normal dogs. Mass spectral data also revealed that dogs with GSM have reduced hepatic phospholipid and sphingolipid concentrations relative to normal dogs. In addition, affected dogs had changes in the abundance of kynurenic acid, various dicarboxylic acids and N-acetylated branch chain amino acids, suggestive of mitochondrial dysfunction.
Ralph W. Kuncl - One of the best experts on this subject based on the ideXlab platform.
-
Agents and mechanisms of Toxic Myopathy.
Current opinion in neurology, 2009Co-Authors: Ralph W. KunclAbstract:Purpose of review Mechanistic-based research has made possible a more pathophysiologic approach to certain drug-induced muscle disorders, especially those caused by the lipid-lowering statin family of drugs, but also myopathies caused by antimicrotubule drugs, mitochondrial toxins, foods, and purported nutriceutical remedies. This is a critical review of those syndromes that are most well founded on evidence of challenge/de-challenge/re-challenge, case-controls, or experimental controls. Recent findings Statins are well tolerated drugs with very high safety windows in skeletal muscle, and third-generation statins now under development offer the hope of even less risk of Toxic Myopathy. Toxicity is dose-related and time-related, and is due to intramyofiber cascades downstream from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG Co-A) reductase inhibition. A robust pathophysiologic animal model shows that statins decrease strength and increase cytosolic Ca 2+ by increasing both mitochondrial Ca 2+ permeability and Ca 2+ release from sarcoplasmic reticulum. As a result, the earliest pathologic change in statin myoToxicity is compatible with simple necrosis and intracellular membrane accumulation. Genome-wide searching has yielded a single nucleotide polymorphism in the SLCO1B1 gene for the organic anion-transporting polypeptide that regulates statin uptake. Drug-drug interactions dominate recent reports of all Toxic myopathies. The peculiar mitochondrial pathology of zidovudine-induced mitochondrial DNA depletion, cytochrome oxidase depletion, and mitochondrial proliferation has been confirmed in a rigorous animal model. Finally, recent interest has been piqued by putative lipid-lowering neutraceuticals like red yeast rice (Monascus purpureus) and edible mushrooms that can clearly cause Toxic Myopathy. Summary A principled approach to the diagnosis of Toxic myopathies, based on the consideration of currently known pathophysiologic mechanisms, biopsy pathology, the characteristic clearance properties of creatine kinase, the time course of muscle fiber regeneration, drug challenge/de-challenge/re-challenge, and differential diagnoses, rather than on mere temporal association, will reduce the healthcare costs of common diagnostic error.
-
Toxic neuropathies and myopathies
Current opinion in neurology, 1993Co-Authors: Ralph W. Kuncl, Edwin B. GeorgeAbstract:This review first considers Toxic neuropathies of recent interest, including those caused by antineoplastic and antiretroviral drugs, agents that affect methylation reactions, vitamin and herbal preparations, and certain occupational exposures. The discussion points out the interesting phenomenon of "coasting," the strategy of using neurotrophic factors to combat Toxic neuropathies, and the inapparent risks in "health foods." Second, it considers Toxic Myopathy syndromes, including zidovudine Myopathy and its differentiation from HIV-associated inflammatory Myopathy, cholesterol-lowering agent myopathies, acute Myopathy with selective loss of myosin filaments due to neuromuscular blocking agents and corticosteroids, the eosinophilia myalgia syndrome, and colchicine myoneuropathy. Some of these syndromes illustrate important Toxicologic principles about recognition of rare disorders, unanticipated temporal relationships with exposure, and risk factor assessment.