Myopathy in horses with pituitary pars intermedia dysfunction (Cushing's disease)

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Fifteen horses with pituitary pars intermedia dysfunction were studied. The horses were of various breeds and between 15 and 28 years of age. Control horses matched for breed and age were studied for comparison. Evaluations included complete blood cell count and serum biochemical analysis, electromyography, and gluteus medius muscle biopsies for histochemical, morphometric, and ultrastructural analysis. No differences were found between groups of horses on routine laboratory analysis or electromyography. We demonstrated that muscle wasting in diseased horses was the result of atrophy of types 2A and 2B muscle fibers and loss of type 2B myofibers. Mild non-specific non-inflammatory myopathic alterations such as myofiber size variation, internal nuclei, perimysial, endomysial and sarcoplasmic fat accumulation were observed. At the ultrastructural level, subsarcolemmal mitochondrial accumulation and increased lipid droplets were evident. Similar to other species, this study confirmed atrophy of type 2 fibers as the cause of muscle mass loss in horses with Cushing's disease.

Original languageEnglish (US)
Pages (from-to)737-744
Number of pages8
JournalNeuromuscular Disorders
Volume16
Issue number11
DOIs
StatePublished - Nov 2006

Fingerprint

Intermediate Pituitary Gland
Pituitary ACTH Hypersecretion
Muscular Diseases
Horses
Muscles
Blood Cell Count
Electromyography
Atrophy
Wasting Syndrome
Fats
Biopsy
Serum

Keywords

  • Cushing's disease
  • Equine
  • Myopathy
  • Pituitary
  • Steroids

ASJC Scopus subject areas

  • Clinical Neurology
  • Pediatrics, Perinatology, and Child Health
  • Developmental Neuroscience
  • Neurology

Cite this

Myopathy in horses with pituitary pars intermedia dysfunction (Cushing's disease). / Aleman, Monica R; Watson, Johanna L; Williams, D. C.; Lecouteur, Richard A; Nieto, Jorge; Shelton, G. D.

In: Neuromuscular Disorders, Vol. 16, No. 11, 11.2006, p. 737-744.

Research output: Contribution to journalArticle

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AU - Shelton, G. D.

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