Subclinical myopathy associated with hyperadrenocorticism in the dog.
One of seven dogs with clinical signs of hyperadrenocorticism had clinical evidence of neuromuscular disorder. Clinical diagnosis of hyperadrenocorticism was confirmed by plasma cortisol concentrations before and after adrenocorticotrophin hormone and dexamethasone administration. Electromyographic studies showed bizarre, high frequency discharges in all dogs. Examination of muscle biopsies taken from the biceps femoris muscle from each dog revealed mild degenerative changes of fiber size variation, focal necrosis and fiber splitting. Ragged red fibers were prominent and appeared to be related to mitochondrial aggregates. Significant (P less than 0.05) type 1 and 2 fiber atrophy was found in all dogs. Fiber grouping was present in four dogs. Studies of fascicular biopsies of the peroneal nerve showed thinly myelinated fibers, onion-bulb formation, segmental demyelination and short intercalated internodes. These findings suggested a glucocorticoid-related myopathy in hyperadrenocorticism that also may have a neurogenic component.
D000303:Adrenal Cortex Diseases / Q000150:complications / Q000473:pathology / Q000662:veterinary*; D000818:Animals; D004283:Dog Diseases / Q000473:pathology*; D004285:Dogs; D005260:Female; D008297:Male; D009132:Muscles / Q000648:ultrastructure; D009135:Muscular Diseases / Q000150:complications / Q000473:pathology / Q000662:veterinary*