Histopathologic findings in the sacrocaudalis dorsalis medialis muscle of horses with vitamin E-responsive muscle atrophy and weakness.
키워드
요약
OBJECTIVE
To characterize clinical findings, outcomes, muscle characteristics, and serum or muscle concentrations of α-tocopherol for horses with vitamin E-responsive signs of muscle atrophy and weakness consistent with signs of equine motor neuron disease (EMND).
METHODS
Retrospective case-control study.
METHODS
8 affected (case) adult horses with acute (n = 3) or chronic (5) gross muscle atrophy that improved with vitamin E treatment and 14 clinically normal (control) adult horses with adequate (within reference range; 8) or low (6) muscle concentrations of α-tocopherol.
METHODS
Medical records were reviewed, serum and muscle concentrations of α-tocopherol were measured, and frozen biopsy specimens of sacrocaudalis dorsalis medialis muscle and gluteal muscle were histologically evaluated for pathological changes. Fiber type composition and fiber diameters were assessed in gluteal muscle specimens.
RESULTS
A myopathy that was histologically characterized by redistribution of mitochondrial enzyme stain (moth-eaten appearance) and anguloid atrophy of myofibers was evident in sacrocaudalis dorsalis medialis muscle fibers of the 8 affected horses that had low serum (6/8) or skeletal muscle (5/5) concentrations of α-tocopherol; these histopathologic changes were not found in muscle specimens of control horses with low or adequate muscle concentrations of α-tocopherol. All affected horses regained strength and muscle mass within 3 months after initiation of vitamin E treatment and dietary changes.
CONCLUSIONS
A vitamin E-deficient myopathy characterized histologically by a moth-eaten appearance in the mitochondria and anguloid myofiber atrophy in frozen sections of sacrocaudalis dorsalis medialis muscle biopsy specimens was found in horses with clinical signs of EMND that were highly responsive to vitamin E treatment. This myopathy may be a specific syndrome or possibly precede the development of neurogenic muscle fiber atrophy typical of EMND.
