Felipedia

Vitamin E myopathy in cats

Vitamin E (alpha tocopherol) myopathies (variously termed white muscle disease, nutritional myopathy, and nutritional myodegeneration) have been reported in sheep, cattle, pigs, horses, and poultry (often in conjunction with selenium deficiency), but only rarely in dogs or cats. This myopathy is associated with low dietary levels of vitamin E , although similar clinical signs and pathology occur in dogs with experimental vitamin E and selenium deficiency. Selenium is an integral part of glutathione peroxidase and its function is closely involved with that of vitamin E. Clinical signs include of vitamin E (vitamin E/selenium) myopathy include weakness, dysphagia, sialosis, dysphonia, stiff stilted gait, difficulty in rising from a recumbent position, and inability to raise heads. Sudden death is reported in newborn puppies. Signs may be exacerbated with exercise. Serum muscle enzymes are often elevated, especially CK levels. Skeletal muscle lesions tend to be bilaterally symmetrical and may affect individual or several muscle groups. Grossly, the affected muscle is paler than normal and distinct chalky longitudinal striations may be visible. Pathological findings are characterized by necrosis, phagocytosis, proliferation of sarcolemmal nuclei, loss of striations, and fibre regeneration. Mineralization may be seen in necrotic muscle fibres. Myocardial necrosis is also a feature of vitamin E/selenium deficiency. Diagnosis is based on historical, clinical, and histopathological data. Animals usually recover rapidly after selenium and/or vitamin E replacement therapy.

A confirmed case of a myopathy due to a deficiency of vitamin E has been reported in a 2 year old female cat that was fed a diet consisting almost entirely of boiled Norwegian coley (fish). Muscles in the pelvic limbs were swollen, hot and very painful on palpation. Histological muscle changes were similar to those reported in dogs. Complete clinical recovery occurred within 14 days following correct dietary management and multivitamin supplementation (especially vitamin E additives). Recent studies suggest that vitamin E does not appear to play a role in sled dogs developing exertional rhabdomyolysis. For more information on vitamin E and the CNS, see vitamin E deficiency.