Disorders of the Musculoskeletal System

Valberg, Stephanie J.

doi:10.1016/b978-0-323-44329-6.00010-3

Cited by 8 publications

(4 citation statements)

References 156 publications

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“…The most common muscle disorder in QHs, rhabdomyolysis, shares the characteristic of increased serum creatine kinase (CK) activity with IMM . Causes of rhabdomyolysis range from toxins such as hypoglycin A to genetic disorders such as type 1 polysaccharide storage myopathy (PSSM1) and malignant hyperthermia (MH) . However, in many cases of rhabdomyolysis, the specific etiology is unrecognized .…”

Section: Introductionmentioning

confidence: 99%

An E321G MYH1 mutation is strongly associated with nonexertional rhabdomyolysis in Quarter Horses

Valberg

Henry

Perumbakkam

et al. 2018

Veterinary Internal Medicne

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BackgroundAn E321G mutation in MYH1 was recently identified in Quarter Horses (QH) with immune‐mediated myositis (IMM) defined by a phenotype of gross muscle atrophy and myofiber lymphocytic infiltrates.Hypothesis/ObjectivesWe hypothesized that the MYH1 mutation also was associated with a phenotype of nonexertional rhabdomyolysis. The objective of this study was to determine the prevalence of the MYH1 mutation in QH with exertional (ER) and nonexertional (nonER) rhabdomyolysis.AnimalsQuarter Horses: 72 healthy controls, 85 ER‐no atrophy, 56 ER‐atrophy, 167 nonER horses selected regardless of muscle atrophy.MethodsClinical and histopathologic information and DNA was obtained from a database for (1) ER > 2 years of age, with or without atrophy and (2) nonER creatine kinase (CK) ≥ 5000 U/L, <5 years of age. Horses were genotyped for E321G MYH1 by pyrosequencing.ResultsThe MYH1 mutation was present in a similar proportion of ER‐no atrophy (1/56; 2%) and in a higher proportion of ER‐atrophy (25/85; 29%) versus controls (4/72; 5%). The MYH1 mutation was present in a significantly higher proportion of nonER (113/165; 68%) than controls either in the presence (39/42; 93%) or in absence (72/123; 59%) of gross atrophy. Lymphocytes were present in <18% of muscle samples with the MYH1 mutation.Conclusions and Clinical ImportanceAlthough not associated with ER, the MYH1 mutation is associated with atrophy after ER. The MYH1 mutation is highly associated with nonER regardless of whether muscle atrophy or lymphocytic infiltrates are present. Genetic testing will enhance the ability to diagnose MYH1 myopathies (MYHM) in QH.

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Section: Introductionmentioning

confidence: 99%

An E321G MYH1 mutation is strongly associated with nonexertional rhabdomyolysis in Quarter Horses

Valberg

Henry

Perumbakkam

et al. 2018

Veterinary Internal Medicne

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“…The most conspicuous blood parameters were marked elevations in CK, AST and lactate dehydrogenase (LDH) activities. Creatine kinase is the most sensitive indicator for an acute muscle injury with a peak concentration of 4–6 h after the muscular insult (Valberg 2018). Cardiac troponin I, a biomarker for myocardial disease (Peacock et al .…”

Section: Discussionmentioning

confidence: 99%

Complete AV block in a neonatal foal suffering from nutritional myodegeneration

Conze

Falkenau

Goehring

et al. 2021

Equine Veterinary Education

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This case report concerns a 1-day-old, full-term Quarter Horse colt presented due to a progressive inability to rise and nurse. Besides the general weakness, a marked bradycardia was evident, which was caused by a third-degree atrioventricular (AV) block. Subsequently, the diagnosis of acute nutritional myodegeneration (NMD) was made based on clinical signs, elevated muscle enzymes, ECG findings, as well as low serum selenium and vitamin E values. Despite intensive care and supportive therapy, the foal´s condition deteriorated, and euthanasia was elected. Necropsy confirmed the diagnosis of NMD and revealed diffuse necrosis and inflammatory infiltration of the skeletal and myocardial musculature, as well as the cardiac conduction system which might have resulted in complete AV block.

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“…Supplementation of vitamin E (Nano E™): 10 iu/kg PO SID and selenium (Selenavite E™): 0.2 g/kg PO SID was implemented in case of nutritional myodegeneration whilst awaiting serum vitamin E and glutathione peroxidase levels. Glutathione peroxidase is a selenium‐dependent enzyme which is formed in red blood cells during erythropoiesis and provides an estimation of body selenium status (Valberg, 2018). In this case neither vitamin E nor glutathione peroxidase levels were supportive of nutritional myodegeneration, however, it is possible that the antioxidant activity of supplementation may have been beneficial for the myopathy irrespective of cause.…”

Section: Treatmentmentioning

confidence: 99%

Masseter myodegeneration in the horse: Suggested approach to diagnosis and treatment

Wilson

Talbot

Crosby-Durrani

et al. 2022

Equine Veterinary Education

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Summary A descriptive case report of the management of a miniature pony presenting to a UK equine veterinary hospital with marked trismus and increased masseter muscle size. Diagnosis of masseter myodegeneration (MM) was aided by the use of computed tomography and excisional biopsy. Hyperlipaemia was diagnosed as a sequelae of MM. Treatment included nonsteroidal anti‐inflammatories, parenteral nutrition and fluid therapy in addition to supportive care. The gelding was discharged from the hospital 30 days after admission, having made a full recovery. MM in the horse is a rare condition that appears to be physiologically distinct from canine masticatory muscle myositis which is primarily immune mediated.

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Disorders of the Musculoskeletal System

Cited by 8 publications

References 156 publications

An E321G MYH1 mutation is strongly associated with nonexertional rhabdomyolysis in Quarter Horses

An E321G MYH1 mutation is strongly associated with nonexertional rhabdomyolysis in Quarter Horses

Complete AV block in a neonatal foal suffering from nutritional myodegeneration

Masseter myodegeneration in the horse: Suggested approach to diagnosis and treatment

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