11/22. Chance discovery of hepatic fibrosis in patient with asymptomatic hypervitaminosis a.A liver biopsy specimen was obtained from a 50-year-old patient whose clinical and functional liver tests showed no abnormalities but who had for some time a high vitamin a intake (109 X 10(6) IU over four years). liver architecture was normal. Sinusoids were slightly dilated in zone 2. Perisinusoidal cells were numerous and enlarged. On Sirius red staining, there was mild fibrosis of the central veins, portal tracts, and terminal portal venules and perisinusoidal fibrosis in zone 1 of the acinus. liver vitamin a level was increased. By electron microscopy, perisinusoidal cells filled with numerous lipid droplets had slightly dilated rough endoplasmic reticulum, numerous minute filament condensations below the plasma membrane, and stellate-shaped processes giving them the appearance of fibroblast-myofibroblast-like cells. Numerous collagen bundles, fibrils, amorphous material, and fragments of basement membrane-like material were identified in Disse's space. Immunocytochemistry showed increased amounts of collagen types I, III, IV, laminin, and fibronectin. This observation suggests that vitamin a per se, and not the cellular damage often seen in hypervitaminosis a, is responsible for fibrosis.- - - - - - - - - - ranking = 1keywords = hypervitaminosis (Clic here for more details about this article) |
12/22. 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.- - - - - - - - - - ranking = 1keywords = hypervitaminosis (Clic here for more details about this article) |
13/22. Increased risk for vitamin a toxicity in severe hypertriglyceridemia.A 48-year-old woman with malabsorption and type V hyperlipoproteinemia developed hypervitaminosis a with a total plasma vitamin a level of 871 micrograms/dL during therapy with an oral dosage of 18,000 retinol equivalents (60,000 IU) daily. Twelve percent of the total plasma retinol was found to be transported in the chylomicron-very low density lipoprotein (VLDL) fraction, which does not contain retinol-binding protein. For comparison, concentrations of retinyl esters and retinol were determined in nine patients with type V hyperlipoproteinemia and nine control subjects, none of whom were using vitamin a supplements. Both retinyl esters and retinol were significantly elevated in the group with hyperlipoproteinemia (p less than 0.0005 in both cases). Eight of these nine patients had retinol present in the chylomicron-VLDL fraction, whereas retinol was not detectable in this fraction in any of the nine normal controls. The data suggest that patients with severe hypertriglyceridemia associated with type V hyperlipoproteinemia are at increased risk for hypervitaminosis a.- - - - - - - - - - ranking = 0.4keywords = hypervitaminosis (Clic here for more details about this article) |
14/22. Scintigraphic dissociation of reticuloendothelial and hepatocyte function in chronic vitamin a hepatotoxicity.A discordant hepatic uptake between Tc-99m sulfur colloid and Ga-67 citrate has occurred in an adult patient with hepatotoxicity due to hypervitaminosis a. The authors believe this is a scintigraphic phenomenon related to the characteristics of the radiopharmaceuticals used and does not necessarily represent a true dissociation of various cellular functions of the liver.- - - - - - - - - - ranking = 0.2keywords = hypervitaminosis (Clic here for more details about this article) |
15/22. vitamin a toxicity and hypercalcemia.A patient hospitalized with hypercalcemia and a history of chronic vitamin a ingestion was studied in order to investigate the rarely reported association between elevated serum calcium and vitamin a toxicity. The clinical presentation marked by profound weight loss, a psychiatric disturbance, total body alopecia, erosive dermatitis, and liver disease, was compatible with hypervitaminosis a. The diagnosis of vitamin a toxicity was established by elevated total vitamin a levels and the component due to retinyl esters. Other etiologies for hypercalcemia were excluded. In view of these results and the well-known effects of vitamin a on bone metabolism, it is concluded that the most likely etiology of the hypercalcemia in this patient was vitamin a toxicity.- - - - - - - - - - ranking = 0.2keywords = hypervitaminosis (Clic here for more details about this article) |
16/22. Fatal hypervitaminosis a in a neonate.Although hypervitaminosis a is not uncommon, fatal cases are rare. We describe a neonate who died after having ingested more than 60 times the suggested dose of vitamin a per day, for 11 days. His hospital course was marked by hypercalcemia, hyperphosphatemia, a bleeding disorder, and pulmonary insufficiency. An autopsy showed extensive calcifications of the alveolar septa and bronchioles. Metastatic calcifications were also present in the kidneys, stomach, soft tissue, and skin. The skeleton showed prominent alteration of the endochondral bone formation. There was also evidence of accelerated resorption of bone, which is presumably responsible for the development of hypercalcemia and metastatic calcification.- - - - - - - - - - ranking = 1keywords = hypervitaminosis (Clic here for more details about this article) |
17/22. Chronic hypervitaminosis a.A case of chronic hypervitaminosis a in a 51-year-old female is discussed. The patient was ingesting 27,500--35,000 international units of vitamin a daily for 30 years. The patient displayed the classic symptoms of the disease, including skin and hair changes, esophageal varices and extensive liver disease. vitamin a products were discontinued and the patient's dietary intake of the vitamin was minimized. Previous reports and studies of hypervitaminosis a are reviewed. Social factors causing increased consumption of vitamin a and regulations governing the sale of vitamin a are discussed. By being aware of the factors influencing vitamin a consumption, hypervitaminosis a can be detected and prevented more readily.- - - - - - - - - - ranking = 1.4keywords = hypervitaminosis (Clic here for more details about this article) |
18/22. 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.- - - - - - - - - - ranking = 0.2keywords = hypervitaminosis (Clic here for more details about this article) |
19/22. hypervitaminosis a unmasked by acute viral hepatitis.A case of acute hypervitaminosis a complicating viral hepatitis is reported. Twenty days after presenting with hepatitis b, a 42-yr-old vegetarian developed acute hypervitaminosis a in the absence of recent, massive exposure to the vitamin. Findings included headache, confusion, skin desquamation, and hypercalcemia. Prior to developing hepatitis, he had ingested supplemental vitamin a without recognized ill effect. liver and serum vitamin a without recognized ill effect. liver and serum vitamin a levels were both elevated; the liver biopsy showed abundant, lipid-filled Ito cells and perisinusoidal fibrosis. This case demonstrates that patients with excessive hepatic stores of vitamin a may develop hypervitaminosis a during acute, intercurrent liver disease. Levels of retinol binding protein are reduced in hepatitis. This phenomenon may account for the findings in this case, since vitamin a is more toxic when not specifically bound to retinol binding protein. The size of the population at risk for this complication of hepatitis in unknown, but presumably it is growing with the widespread use of supplemental vitamin a.- - - - - - - - - - ranking = 0.6keywords = hypervitaminosis (Clic here for more details about this article) |
20/22. hypervitaminosis a in two hemodialysis patients.We present two cases of hemodialysis patients developing vitamin a toxicity related to excessive consumption of nutritional supplements containing large quantities of vitamin a. In one patient, severe hypercalcemia was the lone presenting sign; in the other, hypercalcemia was associated with unusual neurologic manifestations. We will discuss the reason why hemodialysis patients are at special risk for the development of hypervitaminosis a and review the mechanism leading to the associated hypercalcemia.- - - - - - - - - - ranking = 0.2keywords = hypervitaminosis (Clic here for more details about this article) |
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