Cases reported "Hypervitaminosis A"

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11/16. liver damage with reversible portal hypertension from vitamin a intoxication: demonstration of Ito cells.

    A patient with sudden onset of ascites and hepatosplenomegaly made a complete recovery after vitamin a was withdrawn. fluorescence microscopy on embedded tissue provided a simple method of demonstrating the accumulation of fat storage (Ito) cells in the liver.
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12/16. pleural effusion and ascites: unusual presenting features in a pediatric patient with vitamin a intoxication.

    The usual presenting features of vitamin a intoxication are pseuotumor cerebri, skeletal pain, desquamative dermatitis, and hepatic inflammation. Our patient was a nine-year-old female who had increasing cough, dyspnea, and abdominal distention for a short time prior to admission. She was said to have been treated with 10,000 units of vitamin a per day for skin rashes. Radiographic studies revealed a very large right sided pleural effusion, ascites, demineralized bones, and retarded skeletal maturation. The diagnosis of hypervitaminosis a was made. More detailed medical history confirmed that the child had, in actuality, received up to 300,000 units/day of vitamin a plus desiccated liver pills and carrot juice for the previous year. Clinical symptoms completely abated following acute medical treatment for ascites and cessation of vitamin a intake. Several months later, a sample of liver, obtained and preserved at the time of exploratory laparotomy, was homogenized and extracted with ethanol/hexane. The retinyl palmitate level was significantly elevated and consistent with vitamin a poisoning.
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13/16. Chronic vitamin a intoxication in infants fed chicken liver.

    Twin female infants were fed 120 gm of chicken liver homogenate daily for four months. They developed irritability, vomiting, and bulging anterior fontanelles. Computed tomograms of the brain revealed enlarged ventricles in both infants and dilated subarachnoid spaces in one. plasma vitamin a concentrations were elevated. After all sources of vitamin a intake were stopped, the infants recovered without sequelae. The chicken liver homogenate contained 36,000 IU of vitamin a per 120 gm. Since infants often receive 4,000 units of vitamin a daily from fortified milk and vitamin supplements, they probably cannot be fed 60 gm of chicken liver safely more often than once weekly.
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14/16. Chronic vitamin a intoxication. A multisystem disease that could reach epidemic proportions.

    Two patients seen in a six-month period had a diffuse, multisystem disorder characterized by edema of the extremities and face, rash, bone pain and tenderness, symptoms of increased intracranial pressure, and hypercalcemia. Both had been receiving extraordinarily high doses of vitamin a for some time. serum vitamin a concentrations were markedly elevated, and serum vitamin d concentrations were normal. The history of excessive vitamin administration was only elicited following the detection of hypercalcemia. This is a potential complication of the administration of unregulated food supplements, stressing the need for complete dietary histories in the evaluation of multisystem disorders, with or without hypercalcemia.
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15/16. Reduced vitamin a tolerance in a hyperlipidaemia patient with rapid destructive and hyperostotic osteoarthritis of the hip.

    A 59-year-old patient suffering from hyperlipidaemia developed a chronic vitamin A intoxication syndrome after ingestion of 30000 IE retinol/daily over a period of six years. Functional disability of the right hip was caused by radiologically documented hyperostosis of the acetabular circumference. Finally, a prosthesis had to be implanted because of rapid destructive osteoarthritis of the right hip. Implications of vitamin a for rheumatological management are discussed.
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16/16. Hyperostotic and destructive osteoarthritis in a patient with vitamin a intoxication syndrome: a case report.

    The authors present a case report of a 59-year-old female suffering from hyperlipidemia who developed chronic vitamin a intoxication syndrome after ingestion of 30,000 IU retinol/daily over a period of six years. The patient's main complaints included severe headaches, morning nausea, myalgias and disability around the hip, knee, and ankle joints. Radiologically, hyperostosis of the acetabular circumference and the spine was demonstrated. Because of rapidly increasing pain, total hip replacement was performed. histology of cross sections from the femoral head revealed destructive osteoarthritis. Since no other causative reason was found, retinol may not only be responsible for hyperostotic bone and soft tissue formations but may perhaps also account for rapid progressing of degenerative joint disease. Despite the cessation of vitamin a intake the clinical symptoms persisted due to hyperlipidemia. The enlarged number of chylomicrons and the higher fraction of very low density lipoproteins may represent a second retinyl ester pool in case of overloaded fat storing Ito-cells in the liver. Therefore, rheumatological treatment reducing risk factors such as hyperlipidemia is mandatory.
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