Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An assessment of free and total calcium measurements was made in 691 patients with suspected hypercalcemia or disorders often associated with hypercalcemia. In 18.9% of the 1049 specimens analyzed from nine different patient groups, a different impression of hypercalcemia was obtained depending on whether the free or total calcium was considered. Analysis of the ratio of free to total calcium indicated that there are two main factors which influence the distribution of calcium in the serum of hypercalcemic patients: the concentrations of albumin and parathyroid hormone. A lowered albumin concentration accounted for the altered distribution of calcium in patients with malignancies and partially accounted for the altered distribution in patients postrenal transplantation. In patients with confirmed primary hyperparathyroidism a higher ratio of free to total calcium was found, which could not be explained by alterations in protein, albumin, pH, or CO2 content but was related to parathyroid hormone concentration. Free calcium appears to be a slightly better indicator of elevated calcium states than total calcium. Measurements of free calcium should be particularly useful in patients with altered albumin concentration, with multiple myeloma in whom a calcium-binding protein could be present, after renal transplantation, and with suspected hyperparathyroidism and normal or slightly elevated total calcium values.
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PMID:Relationship of free and total calcium in hypercalcemic conditions. 42 92

Intracellular calcium ([Ca(2+)](i)) is the most relevant modulator of parathyroid hormone (PTH) secretion. Uniquely, an increase in [Ca(2+)](i) results in an inhibition of PTH secretion, and it probably exerts its function via calcium-binding protein pathways. The ubiquitous calcium-binding proteins, calmodulin and calmodulin-dependent protein kinase II (CaMKII), have well-established roles in regulated exocytosis in neurons and neuroendocrine cells. However, their roles in parathyroid cells and PTH secretion are still unclear. Using reverse transcription-PCR and western blot analysis, we have demonstrated the expression of calmodulin and CaMKII in human normal parathyroid and parathyroid chief cell adenomas. Blocking of calmodulin and CaMKII activity by the specific antagonists calmidazolium and KN-62 respectively caused a rise in PTH secretion from parathyroid adenoma cells in spite of increased [Ca(2+)](i). The inhibitory effect of Ca(2+) calmodulin on PTH secretion may be due to the absence of synaptotagmin 1 protein in parathyroid adenomas, as demonstrated by western blot analysis. An increased extracellular calcium level acutely lowered the amount of active phosphorylated CaMKII (pCaMKII) in adenoma cells in vitro, indicating the physiological importance of this pathway. Moreover, a negative correlation between the levels of pCaMKII in parathyroid adenomas and serum calcium was found in 20 patients with primary hyperparathyroidism. Taken together, these results show that calmodulin negatively contributes to the regulation of PTH secretion in parathyroid adenoma, at least partially via a CaMKII pathway.
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PMID:Calmodulin and calmodulin-dependent protein kinase II inhibit hormone secretion in human parathyroid adenoma. 2097 37