Cases reported "Hypervitaminosis A"

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1/43. vitamin a toxicity secondary to excessive intake of yellow-green vegetables, liver and laver.

    We report a case of sudden onset of vitamin a poisoning. A 20-year-old Japanese woman had been eating pumpkin and only a very limited amount of other foods on a daily basis for 2 years. She was overly concerned about weight reduction. Aurantiasis cutis and abnormal liver function tests were noted by her family doctor in 1995 when she was 18 years old. At that time, she stopped eating pumpkin. However, she secretly continued an excessive intake of other beta-carotene-rich vegetables, liver and laver for about 2 years. Two and one-half years after being seen by her family physician, she experienced sudden onset of low-grade fever, limb edema, cheilitis, dry skin, and headache. These symptoms worsened daily. A liver needle biopsy was performed, and it showed a normal portal tract along with fat-laden Ito cells in the space of Disse. A final diagnosis of vitamin a poisoning and hepatic injury secondary to an eating disorder was made. Her symptoms and serum beta-carotene levels returned to normal with successful adjustment of her diet. ( info)

2/43. 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. ( info)

3/43. 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. ( info)

4/43. 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. ( info)

5/43. 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. ( info)

6/43. vitamin a abuse: development of cirrhosis despite cessation of vitamin a. A six-year clinical and histopathologic follow-up.

    We report the case of a 35-year-old man who contracted vitamin a-induced liver cirrhosis. Five years before, he had been investigated for vitamin a-induced non-cirrhotic portal hypertension. In this case, the clinical and histopathologic evolution from non-cirrhotic portal hypertension to cirrhosis was documented. In spite of the cessation of pharmaceutical vitamin a intake, the disease progressed. Therapy with colchicine and phenobarbital apparently did not influence evolution to cirrhosis. This suggests that vitamin a can trigger largely unknown mechanisms of liver fibrosis which seem to be self-perpetuating. ( info)

7/43. Can carrots be addictive? An extraordinary form of drug dependence.

    The paper describes three cases of dependence on carotenoids with typical symptoms of irritability and nervousness accompanying their abstinence, with a long-term dependence, and an inability to simply discontinue. Three patients (a man and two women) all being smokers, evaluated this dependence as very similar to that on tobacco. The limitation of further use had the same effect in both cases. The women evaluate the dependence as stronger than that on cigarettes, the man as somewhat weaker. The former patient--a woman--even relapsed, and recently found herself in danger of further relapse. This, however, she nipped in the bud. Laboratory enzyme examinations revealed a disorder in the enzymatic outfit affecting the auto-immunity and the neurovegetative system. ( info)

8/43. 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. ( info)

9/43. 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. ( info)

10/43. Epiphyseometaphyseal cupping of the distal femur with knee-flexion contracture.

    An 11-year-old child with a history of receiving megadoses of vitamin a as an infant, and a 4-year-old child with a history of fulminant staphylococcal septicemia with multiple joint involvement presented with recalcitrant knee-flexion contractures. Roentgenography revealed epiphyseometaphyseal cupping (ie, epiphyseal invagination) of the distal femur. osteotomy resulted in only temporary correction. Our experience suggests that in the skeletally immature child, skin traction, physical therapy, splinting, and, in some instances, two-pin tibial traction should be the treatments of choice. ( info)
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