Vitamin A toxicosis
Vitamin A is an essential feline nutrient, and excesses leading to toxicosis are commonly seen in high liver intake or excessive supplementation in the cat's food.
Signs of vitamin A toxicosis, which usually develops from feeding the diet over a period of months or years, do not develop until the prolonged daily intake exceeds 17mg (57,000 IU)/kg BW.
Excesses of this fat-soluble vitamin are stored in the liver and a toxicity can lead to hepatic damage due to lipid infiltration. Clinically, the most recognizable, signs of hypervitaminosis A are those related to the skeletal changes that occur, particularly in the cervical vertebrae and the long bones of the forelimb. The periosteum appears to be particularly sensitive to high levels of vitamin A and subperiosteal hyperplasia occurs around the bony insertions of tendons and ligaments in response to physical forces exerted in these areas. Bony exostoses result and may invade joints, causing enlargement and ankylosis.
In kittens, vitamin A toxicosis is characterized by poor appetite, depression, dull coat and exophthalmos within 4 - 6 weeks of excessive intake.
Signs of a vitamin A deficiency in cats are similar to those in other species, except that classic xerophthalmia, follicular hyperkeratosis, and retinal degeneration are rarely seen and usually are associated with concomitant protein deficiency. Nonetheless, cats fed diets deficient in vitamin A exhibited conjunctivitis, xerosis with keratitis and corneal vascularization, retinal degeneration, photophobia, and slowed pupillary response to light. Certain of these alterations also result from the retinal degeneration that is seen in taurine deprivation.
Hypovitaminosis A in cats may exhaust vitamin A reserves of the kidneys and liver; affect reproduction causing stillbirths, congenital anomalies (hydrocephaly, blindness, hairlessness, deafness, ataxia, cerebellar dysplasia, intestinal hernia), and resorption of fetuses; and cause the same changes in epithelial cells noted in other animals.
Squamous metaplasia of the respiratory tract, conjunctiva, endometrium, and salivary glands has been noted. Changes such as subpleural cysts lined by keratinizing squamous epithelium and extensive infectious sequelae are frequent in the lungs and are occasionally noted in the conjunctiva and salivary glands. Focal dysplasia of pancreatic acinar tissue and marked hypoplasia of seminiferous tubules, depletion of adrenal lipid, and focal atrophy of the skin have been reported. Borderline deficiency is more common, especially in chronic ill health. Retinol at 9,000 IU/kg of diet should meet dietary needs for vitamin A during gestation and lactation and exceed the needs of the growing kitten. Excessive consumption of liver can lead to hypervitaminosis A, which is characterized by new bone formation without osteolysis. Vitamin A toxicosis produces skeletal lesions of deforming cervical spondylosis, ankylosis of vertebrae and large joints, osseocartilagenous hyperplasia, osteoporosis, epiphyseal plate damage, and a narrowing of the intervertebral foramina.
Initial signs may be of stiffness and pain, particularly of the neck and forelegs, and the owner may first observe the cat's reluctance to groom itself. This may be accompanied by anorexia, lethargy, weight loss and an unkempt appearance. The painful lesions may induce an affected cat to adopt a sitting 'kangaroo' posture in order to avoid weight bearing by the anterior regions.
Treatment consists primarily of dietary correction and the provision of a normal diet; supplementation with fish oils is strictly contraindicated. Non-steroidal anti-inflammatory drugs are useful in the initial stages for the control of pain, and food dishes may be elevated to facilitate eating and drinking. Early treatment may bring about a resolution of clinical signs and halt the progression of the disease, but established ankyloses are irreversible.
Unlike most other mammals, cats cannot convert β-carotene to vitamin A because they lack intestinal carotenase. Therefore, cats require a preformed source in their diet, such as that supplied by liver, fish liver oils, or synthetic vitamin A.
- Bufflington, CA (1994) Nutritional diseases and nutritional therapy. In: Sherding, RG (Ed). The cat: Diseases and clinical management. 2nd edition. WB Saunders, Philadelphia, pp:161-190
- Morgan, JP (1997) Radiographic and myelographic diagnosis of spinal disease: In August, JR (Ed): COnsultations in feline internal medicine. Vol 3. WB Saunders, Philadelphia. pp:425-428
- Norsworthy, GD (2003) Vitamin A toxicosis. In Norsworthy, GD et al (Ed): The feline patient: Essentials of diagnosis and treatment. 2nd edition. Lippincott, Willaims & Wilkins, pp:508-509