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

The effect of magnesium chloride or magnesium sulfate infusion on circulating levels of immunoreactive calcitonin (iCT) was evaluated on nine occasions in three patients with metastatic medullary carcinoma of the thyroid. One patient was normocalcemic and had normal circulating levels of immunoreactive parathyroid hormone (iPTH), one patient was hypocalcemic and had surgical hypoparathyroidism, and one patient had mild to moderate hypercalcemia associated with bone metastases. The basal serum iPTH levels were undetectable in the latter two patients. In every instance magnesium administration produced a rapid and striking fall in circulating iCT and usually a detectable fall in serum calcium. During the hypermagnesemic state, serum iPTH fell from normal to undetectable in the patient with normal parathyroid function, while serum iPTH levels remained undetectable in the hypoparathyroid patient and in the patient with hypercalcemia associated with bone metastases. The results of these studies indicate that: (a) contrary to what has been reported in normal experimental animals, magnesium administration lowers circulating iCT in human subjects with thyroid medullary carcinoma and (b) the calcium-lowering effect produced by magnesium in patients with medullary carcinoma may, in part at least, be due to a redistribution of body calcium that is not mediated by the actions of either parathyroid hormone or clacitonin.
 ...
PMID:Serum calcitonin-lowering effect of magnesium in patients with medullary carcinoma of the thyroid. 120 87

We have studied the production and release of cholecystokinin (CCK) forms by rat medullary thyroid cancer (MTC) in vivo. MTC cells were inoculated s.c. into 8 Wag-Rij rats. One month later, after i.v. injection of calcium plasma levels of CCK, calcitonin and tissue contents of gastrin and calcitonin were determined by radioimmunoassay (RIA), immunocytochemistry, and high-pressure liquid chromatography (HPLC). The tumors were passed 4 times to 8 rats in 1-month intervals fasting levels of CCK in control rats were unaffected by calcium stimulation, and in tumor-bearing rats, plasma CCK was elevated in 3 out of 4 passages, falling to normal levels at the end of passage 4. Hypercalcemia had no effect on plasma levels of CCK in tumor-bearing rats, but did stimulate the release of calcitonin in both control and some tumor-bearing rats in later passages. CCK-8 sulfate was found in all 4 tumor passages but not CCK-33/39. We conclude that rat MTC synthesizes and releases CCK-8, but unlike calcitonin, release of CCK appears unresponsive to calcium stimulation.
 ...
PMID:Expression of cholecystokinin forms by medullary thyroid cancer. 207 Dec 30

It has long been known that complex interactions occur between tumors and normal host immune cells. The human melanoma cell line A375 has been used previously as an indicator cell for tumor cell cytotoxicity mediated by monocytes. During other studies on this tumor cell line, we noted that the conditioned media harvested from A375 cultures induced both the human monocytoid cell line U937 and human blood monocytes to release the cytokine tumor necrosis factor (TNF). We characterized this tumor factor which induced TNF release by monocytic cells. Purification was performed using ammonium sulfate precipitation, ion exchange (DEAE) chromatography, gel filtration, and reversed-phase high performance liquid chromatography. The factor copurified with granulocyte-macrophage colony-stimulating factor (GM-CSF). The purified material caused the release of TNF by U937 cells and stimulated formation of granulocyte-macrophage colonies in methyl cellulose. TNF release by U937 cells in response to A375-conditioned medium was inhibited by neutralizing antibodies to GM-CSF. The TNF-inducing activity in A375-conditioned medium was completely removed by an anti-GM-CSF affinity column. Western blotting using antibodies to GM-CSF confirmed a single Mr27,000 band in A375-conditioned medium. We found that recombinant human GM-CSF stimulated TNF production by the same cells as the tumor-conditioned medium. These data show that A375 human melanoma cells produce GM-CSF, which in turn causes TNF production by cells in the monocyte lineage. The combination of GM-CSF production by the tumor and TNF production by immune cells may influence not only tumor growth but also some of the paraneoplastic syndromes associated with malignancy such as hypercalcemia, cachexia and leukocytosis.
 ...
PMID:Stimulation of tumor necrosis factor release from monocytic cells by the A375 human melanoma via granulocyte-macrophage colony-stimulating factor. 218 30

A 73-year-old man was admitted for evaluation of unexplained hypercalcemia and was found to have a large-cell non-Hodgkin's lymphoma with stage IV disease. Treatment with cyclophosphamide, doxorubicin (Adriamycin), vincristine sulfate, and prednisone chemotherapy returned his calcium levels to normal. Hypercalcemia with lymphoma is rare, and persistent evaluation for malignancy is essential.
 ...
PMID:Hypercalcemia as a clinical prodrome to lymphoma. 223 67

PTH-like proteins (PTHLP), which are associated with humoral hypercalcemia of malignancy, have recently been purified. Isolation of their corresponding cDNAs has revealed that they are derived from a single gene. In this report a synthetic gene encoding PTHLP-(1-141), a 141-amino acid protein corresponding to the most abundant PTHLP cDNA detected in human tumors, was expressed in bacteria and purified to homogeneity. Recombinant (r) PTHLP-(1-141) migrates with an aberrantly high mol wt on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, presumably as a result of its unusually basic pI. rPTHLP-(1-141), like PTH, induced hypercalcemia in rats, caused release of 45Ca from fetal rat bones, and stimulated the synthesis of cAMP by rat osteosarcoma cells and canine renal membrane preparations. A comparison of the abilities of rPTHLP-(1-141) and bovine PTH-(1-34) to stimulate cAMP synthesis indicated rPTHLP-(1-141) to be 5-fold more potent in the osteosarcoma assay, while nearly 30-fold less active in the renal membrane adenylate cyclase assay. Although 100-fold less potent than bovine PTH-(1-34) in promoting bone resorption, rPTHLP-(1-141) was a potent calcemic factor in vivo, inducing a rise in serum calcium from 10.4 to 14.5 mg/dl when infused into rats at 1.3 micrograms/h. These results support previous assumptions that PTHLP is the humoral factor responsible for humoral hypercalcemia of malignancy. In addition, they suggest substantial differences between PTHLP and PTH in the regulation of calcium homeostasis.
 ...
PMID:Synthesis of a gene encoding parathyroid hormone-like protein-(1-141): purification and biological characterization of the expressed protein. 253 1

In a 41-year-old hirsute woman, severe hypercalcemia led to the discovery of hyperparathyroidism related to the involvement (hyperplasia/or adenoma) of the 4 parathyroid glands. Plasma and urinary DHA, plasma DHA-sulfate and delta 5 steroid precursors were elevated. Steroid hormone hypersecretion was stimulated by hCG and ACTH, and exhibited a paradoxical rise during dexamethasone administration. Computerized tomography scanning as well as arteriography disclosed bilateral adrenal hyperplasia and left adrenal adenoma. Bilateral adrenal vein catheterization indicated a left/right gradient for delta 5 steroids and delta 5 steroid sulfates. At surgery a left brown adrenal encapsulated adenoma was removed with a hyperplastic adrenal gland. Results of in vitro studies (adrenal steroid content and incubation) together with postadrenalectomy hormonal results suggest that the left brown adrenal adenoma was the main source of excessive androgen production. The infrequent association of an androgen-producing adrenal adenoma with hyperparathyroidism raises the hypothesis of multiple endocrine neoplasia syndrome. However, evidence for this diagnosis is lacking in the absence of other glandular involvement and of family history.
 ...
PMID:Androgen producing adrenal adenoma. Report on a case associated with hyperparathyroidism. 289 90

Two new forms of BRP-2, a previously described bone resorptive protein, were purified from ascites fluids obtained from patients with hypercalcemia and metastatic bone cancer. The apparent molecular weights of BRP-2 and of these two proteins were 52,000, 48,000, and 46,000, respectively, as determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The three proteins have essentially the same amino acid compositions but differ with respect to their carbohydrate moieties. The amino-terminal amino acid sequences of the three glycoproteins were identical to each other as well as to human serum alpha 2HS-(human serum) glycoprotein. The relationship of the three forms of BRP-2 to alpha 2HS was also established immunochemically. The ascites proteins, as well as alpha 2HS, on a molar basis, were approximately one-tenth as potent as bovine parathyroid hormone fragment (1-34) in their abilities to stimulate calcium release from bone in vitro. This study describes for the first time a possible function for human serum alpha 2HS.
 ...
PMID:Three forms of BRP-2 (bone resorptive proteins) from human cancer ascites fluid and their relationship to human serum alpha-2 HS-glycoprotein. 311 44

This is a comparative study of the glycoprotein hormone, teleocalcin, from the corpuscles of Stannius of sockeye (Oncorhynchus nerka) and coho (O. kisutch) salmon. Coho teleocalcin was purified by the same procedures used previously to obtain sockeye teleocalcin and was obtained in a comparable yield. Both salmon teleocalcins had the same molecular weight as estimated by sodium dodecyl sulfate-electrophoresis and both appeared to have the structure of disulfide-linked oligomers. The two hormones were similar on the basis of amino acid and carbohydrate composition and shared 95% homology in the first 40 residues on the N-terminal. The salmon teleocalcins also shared 80% homology with the predicted 1-40 N-terminal sequence from Australian eels (Anguilla australis). Both teleocalcins had potent inhibitory effects on gill calcium uptake in intact rainbow trout (Salmo gairdneri). However, these effects were observed only at the peak in the calcium uptake cycle that is displayed by this species. In North American eels (A. rostrata), the acute administration of both teleocalcins caused significant inhibition of gill calcium uptake without any concomitant changes in plasma calcium levels or other plasma electrolytes. In 4- and 7-day stanniectomy (STX) eels, the acute administration of coho teleocalcin significantly reduced or completely abolished the accelerated gill calcium transport that occurs postoperatively, with no concomitant changes in plasma electrolytes or post-STX hypercalcemia. These experiments provide further evidence that teleocalcin is a regulator of gill calcium transport and has no acute hypocalcemic effects in fish.
 ...
PMID:Comparative biochemistry and physiology of teleocalcin from sockeye and coho salmon. 319 44

A patient is described in whom intravenous magnesium sulfate, administered for preeclampsia, successfully treated hypercalcemia associated with hyperparathyroidism. This single case suggests that magnesium sulfate might be an effective alternative to standard medical or surgical treatment of this condition.
 ...
PMID:Acute pancreatitis and primary hyperparathyroidism in pregnancy: treatment of hypercalcemia with magnesium sulfate. 362 3

A 58-year-old man was initially seen with fatigue and weight loss. Laboratory examination detected hypercalcemia, elevated 1,25-dihydroxycholecalciferol levels, low parathyroid hormone (PTH) concentrations, and subperiosteal bone resorption. The patient underwent subtotal parathyroidectomy for presumed hyperparathyroidism, but serum calcium and 1,25-dihydroxycholecalciferol levels remained elevated following surgery. Search for another cause of the hypercalcemia disclosed enlarged para-aortic lymph nodes, biopsy specimens of which demonstrated Hodgkin's disease. After treatment of the patient with two cycles of chemotherapy with mechlorethamine hydrochloride, vincristine sulfate, procarbazine hydrochloride, and prednisone, serum calcium, 1,25-dihydroxycholecalciferol, and PTH levels normalized. We speculate that the humoral hypercalcemia in this patient resulted from tumor production of 1,25-dihydroxycholecalciferol.
 ...
PMID:Humoral hypercalcemia in Hodgkin's disease. Association with elevated 1,25-dihydroxycholecalciferol levels and subperiosteal bone resorption. 383 28


1 2 3 Next >>