Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extensive generalized and subperiosteal bone resorption was demonstrated in a patient with adult T-cell lymphoma and marked hypercalcemia of unclear pathogenesis. Antibody to the human T-cell leukemia-lymphoma virus (HTLV) was present in the serum of the patient, consistent with the recently reported association of adult T-cell lymphoma, hypercalcemia, and HTLV. The unique feature of this case was the presence of bone radiographic and pathologic findings consistent with hyperparathyroidism, in the absence of elevated parathormone levels. These findings contrast with the few previously reported cases of adult T-cell lymphoma with hypercalcemia, which showed lytic, sclerotic, or osteoporotic bone lesions. The authors suggest that the patient's malignant T-lymphocytes may have produced an osteoclast-activating-factor-like substance or a parathormone-like substance, which caused the striking bone changes. The exact role of HTLV in the pathogenesis of such cases remains to be determined.
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PMID:Hypercalcemia, unusual bone lesions, and human T-cell leukemia-lymphoma virus in adult T-cell lymphoma. 298 Nov 52

The serum concentration of parathormone is usually normal in hypophosphatasia, a rare disease with a defect of bone mineralisation and low serum alkaline phosphatase activity. Nevertheless there are three cases in the literature presenting a hyperparathyroidism with or without hypercalcemia. No anomaly of parathyroid was found at autopsy. The authors describe the first cases of hypophosphatasia with low serum concentration of parathormone and raise the possibility of a trouble in the calcium-parathormone feed-back. They also emphasize the interest of the urinary pyrophosphate excretion. Its increase seem to be the most constant and the most specific biological disorder.
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PMID:[Inorganic pyrophosphates and parathormone in hypophosphatasia. Study of a family]. 300 10

Tumour extracts from two patients with humoral hypercalcaemia of malignancy contained material which stimulated adenylate cyclase in chick renal membranes and in rat osteosarcoma cells. Adenylate cyclase-stimulating activity in each system was inhibited by a specific parathyroid hormone (PTH) antagonist. Studies in two HPLC systems suggested that the adenylate cyclase-stimulating factors extracted from these tumours differed from each other and from synthetic human parathyroid hormone 1-34. The presence of similar PTH-like adenylate cyclase stimulating material(s) in oncogenic osteomalacia suggests that adenylate cyclase stimulating factor(s) may not be the direct or the sole cause of hypercalcaemia.
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PMID:Humoral hypercalcaemia of malignancy: report of two further patients with biochemical studies on tumour extracts. 301 3

In a 47-year-old woman with a pancreatic mass associated with hypercalcemia and mental confusion, medical measures failed to restore her serum calcium level to normal. To do so, radical resection of a locally invasive vascular neoplasm arising from the body and tail of the pancreas was necessary. The neoplasm was a pancreatic islet-cell tumour. Serum parathormone assays demonstrated abnormally high secretion of a parathormone-like substance. Ectopic secretion of such substances from islet-cell tumours should be considered in association with refractory metabolic disturbances. In view of the often indolent clinical course of islet-cell tumours and the potential for life-threatening hormonal effects, biopsy confirmation of adenocarcinoma should be obtained before resorting to palliative surgical management of pancreatic neoplasms.
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PMID:Pancreatic islet-cell neoplasia, with secretion of a parathormone-like substance and hypercalcemia. 303 May 25

A lipoadenoma of the parathyroid gland was discovered at autopsy as the result of a search for the cause of terminally detected hyperparathyroidism in an elderly man who had suffered cerebral infarction. It is the only case known to the authors in which this uncommon cause of hyperparathyroidism was found at post-mortem examination after hypercalcemia and raised levels of serum immunoreactive parathormone were documented during life.
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PMID:Functioning lipoadenoma of the parathyroid gland. 307 74

A case of fatal hepato-renal failure occurring during mithramycin treatment is reported. A 64 year-old female patient was admitted to hospital in a state of acute renal failure. She also presented with hypercalcaemia and bilateral pulmonary metastases. She had been operated on 10 years previously of a parathyroid cancer. Despite treatment with mithramycin (total dose 8.25 mg) and haemodialysis, the hypercalcaemia returned; it was then decided to remove the secretory lung metastases (parathormone 420 micrograms X ml-1). 48 hours before surgery, the patient was again given 1.25 mg mithramycin. Immediately after surgery, she developed hepatic failure with massive cell destruction and anuria. The patient died 48 h after the operation. The hepatic and renal complications of mithramycin are discussed.
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PMID:[Acute fatal hepatorenal failure during treatment with mithramycin]. 316 Feb 68

Two-site immunoradiometric assay for human parathyrin (PTH1-84) is specific for the intact, secreted, biologically active 84 amino peptide. This system incorporates two-different polyclonal antibodies to human intact PTH and has several technical advantages for use. This assay could detect a wide range of PTH in patients with hypo-, hyperparathyroidism, chronic renal failure and hypercalcemia with malignancy, especially distinguishing the level of human intact PTH in hypoparathyroidism from in normal.
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PMID:[Basic studies on an immunoradiometric assay system for human parathyrin (intact PTH1-84)]. 317 64

The authors report two cases of hyperparathyroidism presenting mainly with muscular weakness. In the first case, a 74 year old woman had become completely bed-ridden and muscular recovery was obtained in 18 months. In the second case, a 24 year old sportsman had to stop all competition. Hypercalcaemia was suspected after finding radiological muscular calcification; the patient was able to start his sporting activities again two months after excision of the adenoma. After a review of the literature the authors discuss the principal physiopathogenic mechanisms; a direct action of parathormone is the probable cause but this has not been proved. Muscular forms of hyperparathyroidism are rare but this "pseudo-myopathic" presentation justifies the systematic exclusion of hyperparathyroidism in all cases of unexplained muscle weakness.
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PMID:[Neuromuscular forms of hyperparathyroidism. Apropos of 2 cases]. 319 71

We evaluated musculoskeletal complaints related to arthropathy in 28 patients with end stage renal failure receiving maintenance dialysis. Twenty-three of 28 patients had arthritic complaints and 14 had an arthropathy. Six of 14 patients with arthropathy had a pattern resembling calcium pyrophosphate dihydrate deposition (CPPD) disease, 4 patients had moderately severe osteoarthritis, 3 had calcific periarthritis, and 1 patient had acute arthritis with intermittent pain and swelling. Factors which predispose to metabolic arthropathies were observed as follows: 29% elevated ferritin; 39% history of hyperparathyroidism; 68% elevated parathormone; 54% hyperphosphatemia; 36% hypercalcemia, 29% HLA haplotypes A3, B7, or B14; and 60% hyperaluminemia. The arthropathy group had more abnormalities per patient (mean 3.6) than the group without arthropathy (mean 2.7) (p less than 0.05). Our data suggest that (1) arthritic complaints occur frequently in patients receiving dialysis; (2) arthropathy accounted for 61% of the complaints; (3) 43% of patients with arthropathy had CPPD-type; (4) renal osteodystrophy caused 17% of arthritic complaints; and (5) in patients receiving dialysis, there is a high incidence of metabolic abnormalities that are known to be associated with arthropathy.
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PMID:Musculoskeletal symptoms related to arthropathy in patients receiving dialysis. 323 May 70

Content of vitamin D, evaluated by the level of 25(OH]D2 (calcidiol), was decreased in 68 patients with chronic kidney insufficiency, among which 16 patients required hemodialysis, 52 patients exhibited a terminal step of chronic kidney insufficiency and were treated with programme-assigned hemodialysis. Content of the vitamin was more distinctly decreased in the patients, kidney insufficiency of which developed simultaneously with congenital and hereditary kidney diseases. Phosphorus-calcium metabolism in the patients was corrected using both high doses of vitamin D2 (20,000 IU) and I alpha-hydroxycholecalciferol (oxidevite) combined with small doses of vitamin D2 (2,000 IU). The later procedure was more effective. After the treatment calcidiol was normalized within a month and maintained within a year at a level close to normal values. Blood calcium was normalized within 2 months, while normalization of parathormone and thyrocalcitonine occurred within a year. After treatment with vitamin D2 at a dose of 20,000 IU distinct hypercalcediolemia as observed in all the patients within 4 months. In 25% of the patients we noted hypercalcemia, which might lead to metastatic calcification.
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PMID:[Vitamin D deficiency and its correction in children with terminal stage of chronic kidney failure]. 326 96


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