Cases reported "Hypervitaminosis A"

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1/22. Acute fish liver intoxication: report of three cases.

    The livers of some larger fish such as shark, tuna and seabass have been reported to be responsible for a peculiar poisoning causing headaches and desquamation. This type of poisoning can also be induced by ingestion of the livers of the sea whale, the polar bear and the seal. Since these animals contain an extremely large quantity of vitamin A in their livers and the symptoms of poisoning in the patients resembled those of patients with acute hypervitaminosis a, the poisoning was believed to have been caused by excessive vitamin A intake. We observed an episode of acute fish liver intoxication in which 3 man experienced dizziness, headache, blurred vision, nausea, vomiting, fever, and desquamation after ingesting the liver of the grouper fish Cephalopholis boenak (C. boenak). One of the patients had full-blown symptoms and presented with a high fever, headache, dizziness, generalized aching pain, and superficial vesicles and bullae of the skin. The treatment was mainly supportive. In the follow-up period, he subsequently developed hair loss and diffuse peeling of the skin on his palms and soles. Acute fish liver intoxication is rare, especially in subtropical regions. Symptomatologically, the clinical pictures of these patients were comparable to acute hypervitaminosis a or retinoid intoxication. The average vitamin A content in the grouper (C. boenak) is high enough to cause acute vitamin A intoxication. Moreover, ethanol may play a potentiating role in this type of event.
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2/22. infant hypervitaminosis a causes severe anemia and thrombocytopenia: evidence of a retinol-dependent bone marrow cell growth inhibition.

    Vitamin A is a pivotal biochemical factor required for normal proliferation and differentiation as well as for specialized functions, such as vision. The dietary intake of 1500 IU/day is recommended in the first year of life. Here, we report the case of an infant who had been given 62 000 IU/day for 80 days. The infant showed several clinical signs of retinol intoxication, including severe anemia and thrombocytopenia. bone marrow showed a remarkably reduced number of erythroid and megakaryocytic cells. The interruption of vitamin A treatment was immediately followed by clinical and biochemical recovery. To clarify whether the effects of retinol are due to a direct action on bone marrow cell proliferation, we investigated the activity of retinol (both the drug and the pure molecule) on the growth of K-562, a multipotent hematopoietic cell line, and on bone marrow mesenchymal stem cells. We observed that vitamin A strongly inhibited the proliferation of the cells at concentrations similar to those reached in vivo. Subsequent biochemical analyses of the cell cycle suggested that the effect was mediated by the up-regulation of cyclin-dependent kinase inhibitors, p21(Cip1) and p27(Kip1). These are the first findings to demonstrate that infant hypervitaminosis a causes a severe anemia and thrombocytopenia and that this is probably due to the direct effect of the molecule on the growth of all bone marrow cellular components. Our data also suggest potential bone marrow functional alterations after excessive vitamin A intake because of emerging social habits.
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3/22. Benign intracranial hypertension due to A-hypervitaminosis in adults and adolescents.

    Three new cases of chronic vitamin A intoxication are reported and a review of the literature with special reference to chronic intoxication in adolescents and adults is presented. The most prominent features are intracranial hypertension, skin and hair deviations, pain in the musculoskeletal system, and fatigue. intracranial hypertension occurs in 50% of chronic intoxications, but is not invariably linked with the other symptoms. Young women are the major age group represented. There seems to be no relation between the severity of the clinical picture and the vitamin A serum level. Discontinuance of vitamin A intake is sufficient for cure.
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4/22. Overdosage of vitamin A supplements in a child.

    hypervitaminosis a in a one-year-old child resulted from overfeeding of daily vitamin supplements by a caretaker. Most cases of chronic hypervitaminosis a are the result of self-medication or health food faddism. The signs and symptoms of overdosage of vitamin A are reviewed.
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5/22. hypercalcemia caused by iatrogenic hypervitaminosis a.

    Vitamin A toxicity produces protean clinical manifestations involving a wide variety of tissues and systems. hypercalcemia can occasionally be associated with high vitamin A levels, but is rare. In this report we describe a patient who was receiving a commercially prepared enteral feeding formula for 2 years. He developed asymptomatic hypercalcemia and had serum vitamin A levels several fold above normal. Subsequently, a custom-made enteral feed was used which contained negligible amounts of vitamin A. Several months later, vitamin A levels diminished substantially and serum calcium levels returned to normal.
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6/22. Hepatic hypervitaminosis a: a familial observation.

    Four siblings with hepatic fibrosis are described. The liver damage in these patients was secondary to chronic ingestion of massive doses of vitamin A for congenital ichthyosis. Although the extrahepatic manifestations were helpful in the diagnosis of hypervitaminosis a, the distinctive features of hepatic histopathology were confirmatory. The plasma concentrations of vitamin A and retinol-binding protein were misleading. The recovery from the liver damage in these patients was slow despite a complete withdrawal of the vitamin A intake. These cases show the importance of hepatic vitamin A assessment in the diagnosis of hepatic fibrosis.
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7/22. hypervitaminosis a following long-term use of high-dose fish oil supplements.

    The use of various dietary supplements containing fish oils has become popular as a method of reducing the risk of developing cardiovascular disease. However, consumption of large amounts of these substances may pose some potential hazards. Described herein is a patient who developed hypervitaminosis a after prolonged fish oil supplement ingestion.
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8/22. Vitamin A in cystic fibrosis: case report and review of the literature.

    Much has been learned about vitamin A physiology in the last 50 years, yet few changes have been made in therapy. Unfamiliarity with vitamin A bioavailability and distribution may inadvertently result in toxicity. A literature search demonstrates that hypovitaminosis A has rarely been reported in patients with cystic fibrosis, and may manifest very differently in children of different ages. Furthermore, hypervitaminosis a may present with similar features, and can result from correction of deficiency. We report such a case in a 4.5-month-old infant, newly diagnosed with cystic fibrosis, who suffered first from vitamin a deficiency and then vitamin A toxicity. A brief review of vitamin A physiology, deficiency, and toxicity is presented.
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9/22. The recognition and treatment of hypervitaminosis a.

    The increasing incidence of vitamin A toxicity is related to vitamin A supplementation for unfounded reasons. This article describes the common symptomatology of vitamin A toxicity, including hypercalcemia, hepatomegaly, and dermatological and neurological effects. Retinol supplements, but not carotene supplements, become toxic when free retinol circulates. Responsibilities of health professionals include questioning vitamin use when taking health histories, educating themselves with scientifically based nutritional studies and applying RDAs (recommended daily allowances) when advising clients.
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10/22. Hepatic and dermatologic manifestations of chronic hypervitaminosis a in adults. Report of two cases.

    Chronic hypervitaminosis a in adults is a clinical syndrome that can develop over varying periods of time depending on the average daily intake of vitamin A. Two adult cases of chronic hypervitaminosis a are described and illustrate this diverse dosage-duration relationship. Hepatic cirrhosis developed as a manifestation of vitamin A toxicity in one of the patients; this appears to be the first reported case of chronic hypervitaminosis a in an adult induced by the long-term frequent ingestion of beef liver.
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