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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:The recognition and treatment of hypervitaminosis A. 267 24

A 22-year-old man, had ingested more than 300 10(6) I.U. of vitamin A over a 2-year period. He presented with diffuse arthralgia, weight loss, low-grade fever, dryness and peeling of the skin, hair loss, liver enlargement with ascites and pleural effusion. He had a raised E.S.R., hypercalcemia and acute renal failure. Plasma levels of vitamin A and retinol-binding-protein were in the normal range. All symptoms disappeared after withdrawal of vitamin A except for the liver enlargement. Iliac bone biopsy showed cortical thickening, numerous resorptive lacunae and no index of bone formation. Liver biopsy showed obliteration of the space of Disse by swollen fat-storing cells (Ito cells). Tissue levels of vitamin A were very high in the liver. A second biopsy, 6 months later, showed a decrease of fat storage in the Ito cells but the development of a fibrosis.
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PMID:[A systemic-like disease: chronic vitamin A poisoning]. 371 19

In 42 myeloma patients our results confirm the association of light chain proteinuria and renal damage, but suggest that while the amount of light chain excreted is an important factor, only some light chains are nephrotoxic. The excretion of the proximal tubular cell lysosomal enzyme N acetyl B D glucosaminidase was a sensitive index of tubular injury, while the presence of low molecular weight proteinuria (Retinol Binding Protein and Lysozyme) was shown to indicate tubular dysfunction in a kidney sufficiently damaged to produce an impaired GFR. Isolated defects of distal tubular function (acid load response and concentrating ability) were rare. Such changes were seen mainly as part of global renal impairment and were usually associated with such specific pathophysiological conditions as plasma hyperviscosity or tubular crystal deposition. Hypercalcemia had a specific effect on the concentrating ability independent of any impairment of renal acidification.
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PMID:Tubular function in multiple myeloma. 393 70

Serum vitamin A concentrations were measured in 38 patients undergoing haemodialysis, 24 of whom were taking multivitamin preparations containing vitamin A. Vitamin A concentrations were significantly higher in patients undergoing haemodialysis than in 28 normal controls (p less than 0.001). Patients taking vitamin A supplements had significantly higher vitamin A concentrations than those not taking them (p less than 0.05), and hypercalcaemic patients had higher concentrations than normocalcaemic patients (p less than 0.005). Withdrawal of vitamin A supplements in seven patients caused significant falls in serum vitamin A concentrations and plasma calcium concentrations (p less than 0.01 at two and three months in both cases) and in plasma alkaline phosphatase concentrations (p less than 0.01 at two months). Vitamin A toxicity can contribute to hypercalcaemia in patients undergoing haemodialysis, probably by an osteolytic effect. Multivitamin preparations containing vitamin A should therefore be prescribed with caution in these patients.
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PMID:Vitamin A toxicity and hypercalcaemia in chronic renal failure. 678 64

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.
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PMID:Hypervitaminosis A unmasked by acute viral hepatitis. 719 70

Parathyroid gland is the overall regulatory organ within the systemic calcium homeostasis. Through cell surface bound calcium-sensing receptors external calcium inversely regulates release of parathyroid hormone (PTH). This mechanism, which is voltage independent and most sensitive around physiologic calcium concentrations, is regulated through a 120 kDa calcium sensing receptor, CaR. Inherited inactivation of this receptor is the cause for familial hypocalciuric hypercalcemia (FHH). Parallel research identified the 550 kDa glycoprotein megalin, which also is expressed on the parathyroid cell surface, as another potential calcium sensing protein. Although this protein expresses numerous calcium binding sites on its external domain, its main function may be calcium sensitive binding and uptake of steroid hormones, such as 25-OH-vitamin D3 (bound to vitamin D binding protein) and retinol. In hyperparathyroidism (HPT), excessive PTH is secreted and the calcium sensitivity of the cells reduced, i.e. the set-point, defined as the external calcium concentration at which half-maximal inhibition of PTH release occurs, shifted to the right. Pathological cells have reduced expression of both CaR and megalin, and reduced amount of intracellular lipids, possibly including stored steroid hormones. A number of possible genetic disturbances have been identified, indicating multifactorial reasons for the disease. In postmenopausal women, however, the individual group with highest incidence of disease, a causal relation to reduced effect of vitamin D is possible. An incipient renal insufficiency with age, lack of sunshine in the Northern Hemisphere, and an association to the baT haplotype of the vitamin D receptor supports this theory. This review summarizes data on regulation of PTH release, dysregulation in HPT, as well as proliferation of parathyroid cells.
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PMID:Pathophysiology of primary hyperparathyroidism. 1080 83

An 86-year-old woman presented with anorexia, thirst and nycturia. Laboratory results revealed a hypercalcaemia with renal failure. The patient used 1-6 vitamin A-D tablets daily (1 tablet contains 600 IU retinol palmitate and 200 IU cholecalciferol). The diagnosis was: hypercalcaemia due to chronic vitamin A ingestion. This diagnosis was supported by the finding of the elevated vitamin A concentration in the patient's serum and the exclusion of other causes of hypercalcaemia. In chronic vitamin A ingestion risk factors for vitamin A toxicity are age, body weight and renal insufficiency. The hypercalcaemia caused by chronic vitamin A ingestion is explained through the up-regulation of osteoclasts by retinol metabolites.
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PMID:[Hypercalcemia due to chronic vitamin A use by an elderly patient with renal insufficiency]. 1122 64

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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PMID:Hypercalcemia caused by iatrogenic hypervitaminosis A. 1563 57

Vitamin A intoxication secondary to over-the-counter nutritional supplements and from its use in acne treatment has been described. However, there have been very few case reports of chronic hypervitaminosis A leading to hypercalcemia in the pediatric population. This paper describes a boy with hypercalcemia secondary to chronic vitamin A intoxication in the context of vitamin A usage for therapy of autism. In addition to discontinuation of vitamin A, hyperhydration, and furosemide, the hypercalcemia in this patient required the use of prednisone and pamidronate to normalize the calcium.
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PMID:Case of hypercalcemia secondary to hypervitaminosis a in a 6-year-old boy with autism. 2293 83

Vitamin A toxicity is a well-described medical condition with a multitude of potential presenting signs and symptoms. It can be divided into acute and chronic toxicity. Serum vitamin A concentrations are raised in chronic renal failure even with ingestion of less than the usual toxic doses. Hypercalcaemia can occasionally be associated with high levels of vitamin A but it is rare. In this report, we describe a 67- year old female patient with chronic kidney disease who was taking vitamin A supplements for approximately 10 years. The patient had worsening of her chronic kidney disease over the last years and developed chronic hypercalcaemia. Her vitamin A level was elevated with a daily intake of 7000 IU. The vitamin A supplement was stopped. A few months later, vitamin A level diminished substantially and serum calcium levels returned to normal.
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PMID:Hypercalcaemia secondary to hypervitaminosis a in a patient with chronic renal failure. 2530 2


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