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)

A patient with Hodgkin's disease spontaneously developed steroid-responsive hypercalcaemia during two consecutive summers. Administration of 3000 U/day of vitamin D, while he was normocalcaemic, caused a sharp increase in serum 1,25(OH)2D3 (from 59 pg/ml to 142 pg/ml) and subsequently hypercalcaemia while serum 25(OH)D3 rose moderately within the normal range (from 2.8 ng/ml to 10 ng/ml). During a spontaneous episode of hypercalcaemia which was accompanied by increased circulating 1,25(OH)2D3 concentrations, administration of hydrocortisone decreased serum 1,25(OH)2D3 rapidly (from 115 pg/ml to 62 pg/ml) and eventually led to normocalcaemia while serum 25(OH)D3 remained unchanged. Thus the disturbances of mineral metabolism found in this patient with Hodgkin's disease are very similar to those previously described in sarcoidosis.
Postgrad Med J 1990 Sep
PMID:Intermittent hypercalcaemia and vitamin D sensitivity in Hodgkin's disease. 223 11

A 10-year-old boy with leukaemia-associated hypercalcaemia was treated with aminohydroxypropylidene biphosphonate (AHPrBP previously APD) in a total dosage of 60 mg over 5 days, when the condition failed to respond to rehydration and frusemide and no sustained effect was produced by haemodialysis with a calcium (Ca)-free dialysate. Bone films showed no lytic lesions, and AHPrBP, which is a potent inhibitor of osteoclast-mediated bone resorption was well tolerated and induced a rapid and sustained fall in plasma Ca (from 3.42 to 2.07 mM in 5 days). Plasma magnesium and alkaline phosphatase remained normal. The results could have been affected by other drugs [vincristine, cyclophosphamide, zorubicin (Rubidazone) L-asparaginase and prednisone] which were simultaneously administered. However, the observation that: (1) the response curve of plasma Ca was similar to that reported when AHPrBP was used alone, (2) there was complete inhibition of urinary Ca excretion and (3) hypocalcaemia occurred suggests that AHPrBP was the major cause of the reduction in plasma Ca. AHPrBP should be considered a potential therapy for hypercalcaemia in childhood malignancy.
Pediatr Nephrol 1990 Sep
PMID:Leukaemia-associated hypercalcaemia in a 10-year-old boy: effectiveness of aminohydroxypropylidene biphosphonate. 224 18

A 59 years old woman, born in Fukuoka Prefecture, was admitted to our hospital in Aug, 1988 because of diarrhea, fever and skin eruption. Physical examination revealed systemic lymphadenopathy and hepatosplenomegaly. The white blood cell count was 11,200/microliters with 28% atypical lymphocytes with convoluted nuclei. Mild anemia, thrombocytopenia and hypercalcemia were also observed. Antibody against the adult T-cell leukemia (ATL) associated antigen in serum was positive. OKT 4/8 ratio was high. A diagnosis of ATL was made. Because of the complications of pneumonia and herpes simplex, systemic chemotherapy was not given, and interferon (IFN)-alpha-2b was intramuscularly injected daily from Oct, 1988, resulting in the disappearance of atypical lymphocytes and improvement of skin lesions. The effect of IFN therapy lasted for three months, followed by increase of atypical lymphocytes. Although the patient became refractory to systemic IFN therapy, local injection of IFN into a buccal tumor infiltrated with atypical lymphocytes resulted in its regression of size. In spite of continued administration of IFN, the patient died of pneumonia in Jan, 1989.
Rinsho Ketsueki 1990 Sep
PMID:[Successful treatment of adult T-cell leukemia with interferon-alpha-2b by systemic and local administration]. 224 35

The endocrine abnormalities associated with acquired immunodeficiency syndrome (AIDS) are reviewed. These include adrenal insufficiency, hyporeninemic hypoaldosteronism, panhypopituitarism, hypogonadism, and alterations in thyroid function tests. AIDS-related infections or neoplasms may lead to hypercalcemia, whereas malabsorption may cause hypocalcemia. The possibility that AIDS-associated cachexia and hypertriglyceridemia may be caused by cachectin (tumor necrosis factor) is discussed, along with possible therapy for cachexia with megestrol acetate. Ketoconazole, sulfonamides, and pentamidine have specific, potentially deleterious metabolic effects when used in AIDS patients. Because treatment of endocrinological abnormalities of AIDS is often effective, improved diagnosis and appropriate therapy of these abnormalities will result in improved quality of life and, possibly, longer survival of patients with AIDS.
Mt Sinai J Med 1990 Sep
PMID:Endocrinologic and metabolic manifestations of the acquired immunodeficiency syndrome. 224 1

We report two patients with non-Hodgkin's lymphoma in whom hypercalcemia and elevated 1,25 dihydroxyvitamin D (1,25-(OH)2D3) levels developed in the absence of any lytic bone lesions. Hypercalcemia responded only transiently to glucocorticoids which were ill tolerated. Intravenous APD administration was needed to circumvene hypercalcemia. Humoral hypercalcemia of malignancy is discussed. Our cases confirm that hypercalcemia associated with elevated 1,25-(OH)2D3 may occur in malignant lymphoma.
Clin Rheumatol 1990 Sep
PMID:1,25-Dihydroxyvitamin D-related hypercalcemia in lymphoma: two case reports. 226 43

31 cases of primary hyperplasia and neoplasms of the parathyroid gland are reported. Among them, 23 cases were parathyroid adenoma, 6 cases parathyroid hyperplasia, one case adenoma associated with hyperplasia, and one case of parathyroid adenocarcinoma. Follow-up study demonstrated that prognosis in the adenoma group is better than that in the hyperplasia group, and one carcinoma patient died from metastasis. Regarding differential diagnosis, adenoma is usually single, with frequent presence of oppressed parathyroid tissue next to the tumor capsule; and cell atypical hyperplasia is often seen microscopically, which is usually multiple in sites, and some residual adipose tissue can be found under the microscope. Clinically, both groups manifested hypercalcemia and hypophosphatemia, especially in those cases with chief cell hyperplasia. Capsule infiltration and vascular embolism are emphasized as the differential features between benign and malignant parathyroid tumours.
Zhonghua Bing Li Xue Za Zhi 1990 Sep
PMID:[A clinico-pathologic study of 31 cases of parathyroid hyperplasia and tumours]. 227 14

We treated a hypoparathyroid woman with calcitriol during pregnancy and did not reduce the dosage after delivery. Despite lactation, the serum calcium level increased to 15.4 mg/dL 11 days postpartum. We treated two other hypoparathyroid women during four pregnancies with either calcitriol or dihydrotachysterol. In all five pregnancies, requirements for the vitamin D preparations increased beginning at the 20-28th week of gestation. Hypercalcemia did not occur in the two women who did not breast-feed and in whom we reduced the dose of calcitriol or dihydrotachysterol after delivery. We conclude the following: 1) Calcitriol is effective for treating hypoparathyroidism during pregnancy; 2) the dose usually needs to be increased during the latter half of gestation; 3) the calcitriol dose should be reduced during lactation; and 4) both mother and infant should be monitored to detect hypercalcemia during breast-feeding. We speculate that low serum estrogen levels associated with breast-feeding promote bone resorption and diminish calcitriol needs in lactating hypoparathyroid women.
Obstet Gynecol 1990 Sep
PMID:Hypercalcemia in a calcitriol-treated hypoparathyroid woman during lactation. 238 32

The Rice H500 rat Leydig cell tumor is a well characterized model of humoral hypercalcemia of malignancy (HHM). Circulating concentrations of PTH-related protein (PTHRP) have not been reported in this or any other animal model of HHM. Taking advantage of the marked N-terminal amino acid homology between rodent and human PTHRPs, we have adapted a sensitive two-site immunoradiometric assay developed for measurement of human PTHRP for use in measuring rat PTHRP. Circulating calcium and PTHRP concentrations were serially measured after sc passage of the Leydig cell tumor in rats. Significant hypercalcemia and elevation of PTHRP occurred on day 9 after tumor inoculation. When grouped by tumor size, both plasma calcium and PTHRP levels were significantly elevated in animals with tumor burdens greater than 10 cc. The PTHRP concentration was strongly correlated with both serum calcium (r = 0.88) and tumor size (r = 0.80). Circulating rat PTHRP averaged 12.8 pM on day 9 and 27.5 pM on day 10 or 11. PTHRP was undetectable in the plasma of 19 control rats. In 3 rats, plasma calcium returned to normal, and PTHRP became undetectable within 24 h after tumor excision. Rat milk displayed a PTHRP concentration of 2000 pM, while acid-urea extract of the rat tumor contained 0.32 pmol/mg protein. Dilutions of rat plasma, milk, and tumor extract displayed response curves that were parallel to the human PTHRP-(1-74) standard in the assay. This two-site immunoradiometric assay is a sensitive and easily performed means of measuring rat PTHRP. It should be useful in studying this animal model of HHM and the function of PTHRP in normal tissues.
Endocrinology 1990 Sep
PMID:Measurement of circulating parathyroid hormone-related protein in rats with humoral hypercalcemia of malignancy using a two-site immunoradiometric assay. 238 60

Adult T cell leukemia (ATL) is associated with human T cell leukemia virus type 1 (HTLV-1) infection, and almost all ATL patients have the complication of hypercalcemia. To understand the mechanism of the high incidence of hypercalcemia in ATL, we studied the expression of a parathyroid hormone-related protein (PTHrP) gene that has been proposed as a causative factor of hypercalcemia in some solid tumors. The polymerase chain reaction coupled with reverse transcription of mRNA was applied to RNA from peripheral blood mononuclear cells. Cells from all 13 ATL patients examined showed abundant expression of the PTHrP gene, while cells from uninfected normal subjects did not. Significant expression of PTHrP gene was also detected in HTLV-1 carriers without any symptoms and in patients with HTLV-1-associated myelopathy or tropical spastic paraparesis. PTHrP mRNA levels correlated with the number of infected cells that were estimated by the integrated HTLV-1 DNA. These results suggest that HTLV-1-infected cells are expressing the PTHrP gene. This concept was further supported by the finding that the HTLV-1 trans-activator, the tax gene product, caused trans-activation of the PTHrP gene promoter linked to the CAT gene. These observations might explain the general expression of the PTHrP gene in ATL patients and the high incidence of hypercalcemia in ATL.
J Exp Med 1990 Sep 01
PMID:Constitutive expression of parathyroid hormone-related protein gene in human T cell leukemia virus type 1 (HTLV-1) carriers and adult T cell leukemia patients that can be trans-activated by HTLV-1 tax gene. 238 34

We investigated the possible involvement of parathyroid hormone-related protein (PTHrP) in 2 cases of metastatic pancreatic neuro-endocrine tumors associated with severe hypercalcemia. Both patients displayed biochemical alterations in renal tubular reabsorption of calcium and phosphate, as well as in urinary cAMP excretion, similar to those encountered in primary hyperparathyroidism, although plasma levels of parathyroid hormone were within the normal range. Tumor protein extracts stimulated cAMP production, which was inhibited by the PTH-antagonist (8,18 Nle, 34 Tyr)bPTH-(3-34)amide, in the PTH-responsive osteoblastic cell line UMR-106. Northern blot analysis of tumor extracts revealed the presence of PTHrP mRNA transcripts, while PTH mRNA was undetectable. In contrast, neither PTHrP mRNA(s) nor cAMP-stimulating activity was detectable in other neuroendocrine tumors not accompanied by hypercalcemia. These results demonstrate that certain pancreatic neuroendocrine tumors associated with hypercalcemia can synthesize and release PTHrP.
Int J Cancer 1990 Sep 15
PMID:Parathyroid hormone-related protein and hypercalcemia in pancreatic neuro-endocrine tumors. 239 7


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