Cases reported "Hypercalcemia"

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1/14. lung, gastric, and soft tissue uptake of Tc-99m MDP and Ga-67 citrate associated with hypercalcemia.

    Metastatic calcifications are associated with chronic renal failure, hyperparathyroidism, metastatic neoplasms, hypervitaminosis D, and hypercalcemia of other origins. Bone scanning agents accumulate within these extraskeletal metastatic calcifications. The authors describe two patients with hypercalcemia associated with Tc-99m MDP uptake in the lungs, stomach, and soft tissues. Ga-67 scintigraphy was also performed and showed increased uptake in the same locations as those of Tc-99m MDP, suggesting the existence of an inflammatory process. Despite adequate treatment, only partial resolution of extraskeletal uptake was observed.
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2/14. Acne, hypervitaminosis a and hypercalcaemia. A case report.

    The ingestion of vitamin a, which is often prescribed for the treatment of acne, may lead to hypervitaminosis a. This syndrome has a wide spectrum of clinical features, hypercalcaemia being of special note since it has been reported in 4 previous cases only. hypervitaminosis a has been described as resulting from excess ingestion of vitamin a for prevention of sunburn and treatment of minimal brain dysfunction. With the present glut of health foods, this condition should be borne in mind when patients present with symptoms of hypercalcaemia and liver dysfunction.
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3/14. 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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4/14. The osteodystrophy of hypervitaminosis D: a metabolic study.

    A patient received 2.5 mg vitamin D2 daily for 10 years and presented with increasing skeletal pain and hypercalcaemia. The limbs were painful to touch especially at the insertions of ligaments and tendons, and radiographs showed osteosclerosis with calcification in the periosteum, blood vessels, tendoachilles and plantar fascia. Bone histomorphometry showed increased amounts of osteoid and defective mineralisation despite hypercalcaemia, hyperphosphataemia and raised serum concentrations of vitamin d metabolites. A negative external calcium balance was documented in the presence of enhanced intestinal calcium absorption and an increase in urinary hydroxyproline excretion. cortisone improved calcium balance and corrected the hypercalcaemia by reducing serum 1,25-dihydroxyvitamin D levels and urinary hydroxyproline excretion.
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5/14. 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.
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6/14. 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.
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7/14. Hypercalcaemia due to dihydrotachysterol treatment in patients with hypothyroidism after thyroidectomy.

    Hypercalcaemia is a recognised complication of hypothyroidism. We describe three patients who developed hypercalcaemia after thyroidectomy when thyroid supplements were discontinued. They were treated with thyroxine, dihydrotachysterol, and calcium after operation, and in all three cases serum calcium concentrations remained constant during combined treatment. thyroxine treatment was discontinued several weeks before a radioiodine scan was performed; dihydrotachysterol and calcium were continued throughout. serum calcium concentrations rose to hypercalcaemic levels in all cases. Elimination of dihydrotachysterol from plasma may be delayed in hypothyroidism, resulting in hypervitaminosis D. It is advisable to reduce the dose of dihydrotachysterol and to check serum calcium concentrations regularly in patients whose thyroid treatment is interrupted.
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8/14. Hypercalcaemia associated with cerebral vasospasm causing infarction.

    central nervous system disorders are not uncommon in patients with hyperparathyroidism and hypercalcaemia. Usually these consist of neuropsychiatric disturbances but acute encephalopathies and seizures may occur. A rare manifestation is cerebral infarction. A patient is presented with neuroradiological evidence of infarction caused by cerebral arterial spasm which appears related to hypercalcaemia due to hypervitaminosis D. Arterial spasm is suggested as a possible aetiological factor in focal neurological lesions associated with hypercalcaemia.
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9/14. Corticosteroid-responsive hypercalcemia with elevated serum 1-alpha, 25 dihydroxyvitamin D.

    A 51-year-old man has had absorptive hypercalciuria and corticosteroid-responsive hypercalcemia for at least 12 years. There has been no clinical or laboratory proof of primary hyperparathyroidism, hypervitaminosis D, or other known causes of hypercalcemia and absorptive hypercalciuria. hypercalciuria as well as the elevated serum level of calcium and 1 alpha, 25(OH)2D fell to normal during treatment with corticosteroids. The disturbed calcium metabolism in this patient is characteristic of that observed in sarcoidosis, but extensive studies have failed to uncover evidence of this condition.
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10/14. hypercalcemia and urologic malignancies.

    hypercalcemia may be a manifestation of a variety of disorders including hyperparathyroidism, hypervitaminosis D, sarcoidosis, multiple myeloma, hyperthyroidism, acute osteoporosis, metastatic bone disease, and a number of primary malignancies. hypercalcemia may be seen in as many as 1.5% of all patients with malignant disease, with or without bony metastases. The neoplasms most commonly associated with hypercalcemia include carcinoma of the lung (all cell types), breast cancer, squamous cell carcinomas, hematologic malignancies, and renal cell carcinoma. observation of a number of instances of hypercalcemia attendant on urologic malignancies prompts the brief report of 4 characteristic cases with documentation of response to therapy. Management of severe and debilitating hypercalcemia is emphasized. Urologists should be aware of new agents available for such treatment.
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