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hypervitaminosis a/crise epiléptica
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Acute hypervitaminosis A in a young lady.
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Acute vitamin A toxicity from a large dose has been reported to cause pseudotumour cerebri. Usually it is common in children. Herein we present the case of a young lady of 18 years old with the complaints of headache, vomiting, back pain and diplopia after ingestion of high dose (about 10 million
A lethal hypervitaminosis A syndrome in young monkeys (Macacus fascicularis) following a single intramuscular dose of a water-miscible preparation containing vitamins A, D2 and E.
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Large intramuscular doses of a water-miscible preparation of vitamin A (500,000 I.U. retinyl acetate/ml), vitamin E (50 I.U./ml) and vitamin D2 (50,000 I.U./ml) were administered to young monkeys (Macacus fascicularis) weighing 1-1.8 kg. At vitamin A doses equivalent to 200 mg retinol/kg or higher,
Drug-induced pseudotumor cerebri.
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Pseudotumor Cerebri (PTC) is an uncommon disorder whose etiology is largely unknown, although its association with steroid withdrawal, hypervitaminosis A, and the use of the tetracycline group of drugs has been well documented. We report here a case in which a patient on chronic divalproex therapy
Therapeutic effect of the arotinoid Ro 15-0778 on chemically induced rat mammary carcinoma.
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The arotinoid Ro 15-0778 (temarotene) is a third generation retinoid without a polar end-group. Established, palpable and measurable rat mammary tumours, chemically induced by oral administration of 12 mg/animal 7,12-dimethylbenz[a]anthracene, were treated with Ro 15-0778 as a feed-admix in daily
Neuromuscular adverse effects associated with systemic retinoid dermatotherapy: monitoring and treatment algorithm for clinicians.
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Although neuromuscular adverse effects represent significant clinical manifestations of hypervitaminosis A syndrome, surprisingly little attention has been paid to the potential neuromuscular toxicity of vitamin A derivatives (retinoids). Since isotretinoin and acitretin are currently the two most
Vitamin neurotoxicity.
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Vitamins contain reactive functional groups necessary to their established roles as coenzymes and reducing agents. Their reactive potential may produce injury if vitamin concentration, distribution, or metabolism is altered. However, identification of vitamin toxicity has been difficult. The only
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