Cases reported "Hypervitaminosis A"

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1/16. 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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2/16. Hepatic hyper-vitaminosis A: importance of retinyl ester level determination.

    We report the case of a 32-year-old man with portal hypertension without cirrhosis due to chronic vitamin a intoxication. Portal hypertension revealed by oesophageal varice rupture progressively worsened and ascites occurred 5 years after the patient stopped vitamin a intake. Initially, serum retinyl palmitate concentration was increased whereas serum retinol concentration was normal. There was no hepatic fibrosis on light microscopic examination of liver biopsy specimens. Five years after the patient stopped excessive vitamin a intake, serum retinol and retinol-binding protein concentrations were below the normal range even though there was an increased hepatic retinyl ester content. This was attributed to the late development of peri-sinusoidal fibrosis. This case mainly shows the importance of retinyl ester level determination: serum retinyl palmitate should be measured immediately after intoxication and hepatic retinyl esters should be measured initially and particularly later. Indeed, later serum and hepatic retinol levels in chronic hyper-vitaminosis A may be normal and lead to under-estimation of liver vitamin a overload.
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3/16. 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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4/16. 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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5/16. Excess vitamin a injures the liver.

    Chronic vitamin a intoxication in a 56-year-old female is reported. Some abnormal blood chemistries included elevated transaminase and alkaline phosphatase, increased cerebrospinal fluid and portal pressure, and elevated vitamin a in blood and liver. A liver biopsy indicated histologic evidence of perisinusoidal collagen deposition and noncoalescent fat droplets in Ito cells. Caution against the misdiagnosis of alcoholic cirrhosis for vitamin a intoxication is recommended.
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6/16. Severe hypervitaminosis a in siblings: evidence of variable tolerance to retinol intake.

    A 2-year-old boy had signs and symptoms of chronic hypervitaminosis a. A course of increasing severity led to eventual death. A younger brother later had similar clinical features. Chicken liver spread containing up to 420 IU/g vitamin a was the likely source of intoxication. Markedly elevated circulating retinyl ester levels have persisted in the surviving sibling for 3 subsequent years despite severe restriction of vitamin a intake. A therapeutic trial of the carbohydrate-derived complexing agent 2-hydroxypropyl-beta-cyclodextrin was initiated. Circulating retinyl esters transiently increased during the infusion (from 407 to 4791 micrograms/dL), and urinary total vitamin a excretion, undetectable before infusion, increased to 23 micrograms/dL after infusion. The frequency of hypervitaminotic episodes has decreased somewhat in the 2 years since the infusion, probably related to dietary vitamin a restriction. The occurrence of this syndrome in two brothers, while a sister ingesting the same diet remains completely healthy, suggests an inherited variance in tolerance to vitamin a intake.
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7/16. plasma lipoprotein abnormalities associated with acquired hepatic triglyceride lipase deficiency.

    Two enzymes, lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL), are released into human plasma after intravenous injection of heparin. LPL is the major enzyme responsible for initiating catabolism of chylomicrons and very-low-density lipoproteins (VLDL). The physiological role of HTGL is less certain. HTGL has been postulated to be an alternate enzyme to LPL in hydrolysis of triglyceride in VLDL and to be an important enzyme for removal of phospholipid from both low-density lipoproteins (LDL) and high-density lipoproteins (HDL). In this latter role, this enzyme would convert larger, lighter lipoprotein particles to smaller denser particles. HTGL deficiency has been found in severe liver disease and with a genetic deficiency of this enzyme. A unique patient is described with acquired hepatic triglyceride lipase deficiency and vitamin a intoxication. This patient developed hypercholesterolemia with an increase in both LDL and HDL. An increased proportion of lighter LDL (LDL1) and HDL (HDL2) was noted. In addition, after administration of heparin there was no shift in the distribution of apoE in plasma fractionated using a column containing 4% agarose. These findings are consistent with a postulated role of HTGL in metabolism of light LDL and HDL particles and some classes of apoE containing lipoproteins.
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8/16. Massive vitamin a intoxication with ascites and pleural effusion.

    vitamin a intoxication was diagnosed in a 14-year-old girl who presented with massive exudative ascites and right pleural effusion, impaired liver enzymes, and hypertriglyceridemia. Electron microscopy of liver biopsy material demonstrated numerous perisinusoidal lipid-filled Ito cells. The patient had taken 100-200,000 I.U. vitamin a per day for 15 months. serum vitamin a level remained elevated for 4 months after vitamin discontinuation. The unusual severity of portal hypertension was documented by a high wedged hepatic vein pressure level. The ascites occurred 2 months after vitamin a had been discontinued, probably owing to particularly slow mobilization of large hepatic stores of vitamin a. Portal hypertension disappeared after a 6-month low vitamin a diet, but the liver biopsy failed to demonstrate any decrease in number or size of Ito cells, suggesting that lipid venous obstruction is unlikely to be the only mechanism responsible for portal hypertension in vitamin a-induced liver disease.
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9/16. Megavitamins for minimal brain dysfunction. A potentially dangerous therapy.

    vitamin a intoxication as a consequence of megavitamin therapy for minimal brain dysfunction occurred in a 4-year-old boy. An early clue to diagnosis was provided by an abnormal bone scan.
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10/16. Unusual presentation of vitamin a intoxication.

    A 10.5-year-old boy was admitted to hospital because of a focal motor seizure. He had suffered from impaired attention span and emotional instability from the age of 6 years. From the age of 5 years he received daily a multivitamin preparation containing 5,000 IU vitamin a. The cause of his symptoms was found to be vitamin A intoxication, with an unusual acute presentation of microscopic hematuria, electroencephalographic abnormalities, and convulsions.
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ranking = 0.625
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