Vitamin A toxicity presenting as bone pain.

A 4-year-old boy presented with severe bone pains, refusal to walk, diffuse bony swelling of forelimbs, skin changes and abdominal pain, with symptoms evolving over 6 weeks. Blood screening tests were normal except for raised aspartate aminotransferase (AST). Radiographs revealed thickened periosteum, widening of the diaphyses of long bones and lifted periosteum in mid-shaft of ulnae and right femur. Skeletal scintigraphy showed a high uptake of radionuclide at clinically affected and unaffected sites, suggestive of multifocal osteoblastic skeletal lesions. After repeated enquiries, his parents admitted to giving him massive doses of preformed vitamin A for over 3 months as 'health tablets'. Surprisingly, he did not have overt liver disease typically found with much smaller doses, although the dermal changes and musculoskeletal pathology were florid. He made a full clinical recovery within 2 months of cessation of vitamin A.

Hypervitaminosis A-induced hepatic fibrosis in a cat.

RATIONALE: The excessive intake of vitamin A in the form of vitamin concentrate, supplement or vitamin-rich liver can result in hypervitaminosis A in man and animals. Although osteopathologies resulting from chronic vitamin A intoxication in cats are well characterized, no information is available concerning feline hypervitaminosis A-induced liver disease. CLINICAL SUMMARY: We report the first case of hepatic stellate cell lipidosis and hepatic fibrosis in a domestic cat that had been fed a diet based on raw beef liver. Radiographic examination revealed exostoses and ankylosis between vertebrae C1 and T7, compatible with deforming cervical spondylosis. Necropsy showed a slightly enlarged and light yellow to bronze liver. Microscopic and ultrastructural analyses of liver tissues revealed diffuse and severe liver fibrosis associated with hepatic stellate cell hyperplasia and hypertrophy. These cells showed immunopositive staining for α-smooth muscle actin and desmin markers. The necropsy findings of chronic liver disease coupled with osteopathology supported the diagnosis of hypervitaminosis A. PRACTICAL RELEVANCE: As in human hepatology, if there is dietary evidence to support increased intake of vitamin A, then hypervitaminosis A should be considered in the differential diagnosis of chronic liver disease in cats.

The effects of hypervitaminosis A in sheep following intramuscular administrations of vitamin A.

Ten ewe lambs (median age 11 months and average weight 29.2+/-2.5 kg) were used in the present study. They were divided into two groups: test (n=5) and control (n=5). Housing and all diets were identical. In the test group vitamin A was injected into the thigh muscle at a daily dose of 5000 IU/kg body weight for 16 days. The average final body weight of sheep in the test group was significantly (P<0.05) less than the control group. All animals were slaughtered at day 17. The lambs' feet were X-rayed to evaluate any difference for radiographic signs between test and control groups. No significant differences were seen for PCV, WBC, differential leukocyte count, and total serum protein between groups. There were no significant differences for serum AST, ALT, and ALP activities and serum calcium, inorganic phosphate, and magnesium concentrations between groups. Histological examination revealed an increased number of lipid droplets in the cytoplasm of the stellate cells of the liver in the test group. The results showed that daily administrations of vitamin A approximately 150 times greater than the daily requirement were well tolerated by sheep.

Central physeal arrests as a manifestation of hypervitaminosis A.

Vitamin A is necessary for synthesis of visual pigments and required in appropriate amounts for membrane stability. Acute hypervitamin A intoxication can lead to increased intracranial pressure, vomiting, and lethargy. Chronic excessive intake of vitamin A can lead to pruritus, muscle and bone tenderness, and failure to thrive. Reported effects of hypervitamin A intoxication on bone include osteoporosis, fracture, cortical thickening, and metaphyseal irregularity. We are reporting on a case of central physeal arrest in the distal femur, proximal tibia, and distal tibia after excessive intake of vitamin A.

Hypervitaminosis A in the cat: a case report and review of the literature.

A case of hypervitaminosis A with secondary entrapment and compression of the left brachial plexus nerve roots is described. A 9-year-old male castrated domestic shorthair, fed a home-made diet based on raw pork liver, was submitted for examination for a left forelimb lameness that evolved to paralysis over a 2-month period. Clinical examination revealed a flaccid paralysis and atrophy of all left forelimb muscles. An ipsilateral Horner's syndrome was also noted. Radiological examination of the cervical and thoracic spine showed massive new bone formation at the ventral aspect of the second cervical to sixth thoracic vertebra. The diagnosis of hypervitaminosis A was made, based on the clinical and radiographic findings, as well as the determination of serum vitamin A concentration, which was 630 microg/dl, three times above the upper normal limit for this species. Despite the unfavourable initial prognosis, the cat progressively regained function of the affected limb approximately 6 months after the diet was changed to a commercial canned food.

Radiographic features of feline joint diseases.

Feline joint disorders are often overlooked, possibly because cats are extremely agile and appear to cope with pathologic changes within their joints better than their canine counterparts. There is a growing awareness that osteoarthritis occurs more frequently than previously anticipated in cats, and recently we have seen the emergence of hip dysplasia as an entity of concern in some purebred cats. There are also several poorly understood conditions that affect the joints of cats, such as synovial osteochondromatosis, that invite further study. In recent years we have seen an expansion in the knowledge of immune-mediated and infectious arthropathies and their inter-relationship with infective agents. This article describes the radiographic changes seen in many of the currently recognized joint disorders of domestic cats.

Local disappearance of epiphyseal growth plates in rats with hypervitaminosis A.

Epiphyseal growth plates of proximal tibiae in rats with high doses of vitamin A (V-A) were observed. Of 4 groups, each consisting of 5 rats, three groups were given V-A at doses, IU/100 g by body weight/day, of 50,000, 100,000, and 150,000, respectively. The other group rats were given no V-A (control). Rats were administered V-A for the 5 days from 4 weeks after birth and sacrificed at 12 weeks after birth. Three rats of the 150,000 IU group died during the period of observation. The decalcified sections were stained with hematoxylin-eosin or toluidine blue. In the ground sections, microradiography, backscattered electron imaging, and energy-dispersive X-ray microanalysis were performed. These observations suggest that the local disappearance of epiphyseal growth plates under high doses of V-A goes in the order of the increased doses through the process of (1) calcified cartilage areae appearing in the resting cell zone, (2) some of the calcified areae extending in the growth plate towards the diaphysial side, (3) bone tissue replacing the calcified areae, and (4) the local disappearing of the growth plate. Such a local disappearance may be formed in the stressed proximal regions of tibiae.

Hypervitaminosis A as a complication of treatment for neuroblastoma.

A case of hypervitaminosis A (HVA) as a complication of therapy for stage-IV neuroblastoma is presented. The patient was randomized to a trial of 13-cis -retinoic acid (a vitamin A-related compound) after completing routine chemotherapy. This acid was given as a means of maturing potential minimal residual disease. A routine follow-up bone scan revealed areas of increased activity, initially along the midshaft of the right ulna and subsequently bilaterally, which were ultimately found to be due to HVA. Hypervitaminosis A has not been previously reported in this setting, and awareness of the condition is important in centers where this treatment is contemplated.

Hypervitaminosis A in a cat.

A 10-year-old cat that was kept on a diet consisting largely of raw liver was evaluated because of lethargy, partial anorexia, and weight loss of several months' duration. The cat's head and neck were rigidly extended, and a hard mass was palpable in the ventral cervical region. Cervical and thoracic radiography revealed proliferative bony lesions of the cervical and thoracic vertebrae as well as of the sternum and costal cartilages. Serum vitamin A concentration was 4 times normal. For reasons unrelated to hypervitaminosis A, euthanasia and necropsy were performed 6 months after evaluation. The skull and the cervical and first few thoracic vertebrae were rigidly fused, and the vertebral architecture was altered by deposition of new bone. The sternum and costal cartilages were similarly affected. The historical, physical, radiographic, laboratory, and postmortem findings were consistent with the diagnosis of hypervitaminosis A. On the basis of findings in this cat, hypervitaminosis A should be suspected in any sick cat fed a diet consisting partly or completely of raw liver.