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)

Changes in calcium concentration were induced by an infusion of disodium-EDTA or calcium in 2 members of a family suffering from hypocalciuric hypercalcaemia ( FHH ) associated with interstitial lung disease. These changes in calcium demonstrated an inverse linear relationship with the changes in serum parathyroid hormone (PTH). Infusion of EDTA in control subjects and in patients with an adenoma or hyperplasia of the parathyroid glands also showed inverse relationships between calcium and PTH. The correlation between serum calcium and serum PTH was significant over the range observed during the induced hypo- and/or hypercalcaemia in controls and in patients with FHH or adenoma. The regressions were, however, shifted relative to each other: in comparison with controls, the FHH was displaced upwards and to the right, although not as far as the adenomas. These findings suggest the existence of an elevated set point for extracellular calcium (or calciostat ) in FHH .
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PMID:Altered parathyroid set point to calcium in familial hypocalciuric hypercalcaemia. 642 23

Maternal and fetal parathyroidd hormone (PTH) responsiveness to hypocalcemia induced by EDTA infusion (50 mg/kg over 2 h) was studied in rhesus monkeys in late pregnancy. Although baseline serum total calcium (Ca) levels in the fetus exceeded those in the mother (4.83 +/- 0.13 vs. 4.28 +/- 0.15 meq/liter; P < 0.001), PTH values were not significantly different (5.62 +/- 0.37 vs. 6.18 +/- 0.33 muleq/ml; P > 0.05). EDTA infusion directly to five fetuses produced significant hypocalcemia (maximal decline averaging 19 +/- 2%) and PTH response (maximal increase averaging 46 +/- 5%). In contrast, in four control studies involving fetal saline infusion, there were no significant changes in fetal Ca or PTH levels. Four maternal control infusions produced no significant changes in either Ca or PTH levels. A comparison of maternal and fetal PTH responses indicated considerable similarity, although fetal PTH levels tended to return to baseline somewhat more gradually after cessation of the hypocalcemic stimulus than did maternal levels. These studies indicate that fetal PTH secretion, both baseline and in response to hypocalcemia, is quantitatively similar to that of the adult, and thus, the fetal parathyroid does not appear to be suppressed by the relative hypercalcemia of late fetal life.
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PMID:Maternal and fetal parathyroid hormone responsiveness in pregnant primates. 677 97

The stability of plasma parathyroid hormone-related protein (PTHrP) as measured by the Nichols Institute assay at room temperature was assessed over a period of 72 h in blood samples collected in protease inhibitor tubes and EDTA tubes at 0, 6, 24, 48 and 72 h from 10 patients with hypercalcaemia of malignancy. Mean plasma PTHrP concentrations in blood samples collected in protease inhibitor tubes remained stable for up to 48 h but had decreased by 10% at 72 h. The mean EDTA plasma PTHrP at zero time was 67% of the protease inhibitor tube value and this had fallen to 39% at 72 h. The stability of parathyroid hormone (PTH) in separated blood samples was also assessed by collection into heparin and plain tubes as well as EDTA and protease inhibitor tubes. Serum PTH concentrations progressively declined throughout the 72 h study period although the zero time values were significantly higher than corresponding plasma PTH concentrations. Plasma PTH concentrations appeared to be stable when blood was collected in heparin, EDTA and protease inhibitor tubes during the 72 h period, except in one subject with markedly elevated plasma amylase activity.
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PMID:Stability of parathyroid hormone-related protein and parathyroid hormone at room temperature. 753 Apr 39

In view of previous animal studies showing that pamidronate (Aredia) can cause renal damage, and human data indicating that pamidronate in doses of 60-90 mg is more effective in the control of tumor-induced hypercalcemia than when given at lower doses, we decided to investigate whether pamidronate 90 mg infused over 60 minutes at weekly intervals had any adverse effects on renal function in patients with bone metastases. Twelve patients, 7 female (all with breast cancer) and 5 male (4 with prostate cancer, 1 with bladder cancer) were entered into the trial. Each patient received weekly intravenous infusions of pamidronate 90 mg in 250 ml normal saline over 60 minutes for 4 weeks. 51Cr-EDTA clearances showed no significant changes in renal function. Urinary N-acetyl-B-D-glucosaminidase/creatinine ratios fluctuated considerably, but no consistent changes were found. No patient with a normal level of urinary beta 2-microglobulin had elevated levels at the end of the trial. Serum creatinine levels did not change significantly, though 1 patient had a corrected serum calcium level of < 2 mmol/L on a single occasion on day 8. No evidence of renal toxicity was detected. However, the possibility that neprohtoxicity would ultimately appear cannot be excluded, and these favourable short-term results cannot be extrapolated to patients with impaired renal function.
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PMID:Intravenous pamidronate: infusion rate and safety. 787 59

The local surgical manipulation of sympathetic and parasympathetic nerves innervating the thyroid-parathyroid territory was employed to search for the existence of a peripheral neuroendocrine link controlling parathyroid hormone (PTH) and calcitonin (CT) release. From 8 to 24 h after superior cervical ganglionectomy (SCGx), at the time of wallerian degeneration of thyroid-parathyroid sympathetic nerve terminals, an alpha-adrenergic inhibition, together with a minor beta-adrenergic stimulation, of hypercalcemia-induced CT release, and an alpha-adrenoceptor inhibition of hypocalcemia-induced PTH release were found. In chronically SCGx rats PTH response to EDTA was slower, and after CaCl2 injection, serum calcium attained higher levels in face of normal CT levels. SCGx blocked the PTH increase found in sham-operated rats stressed by a subcutaneous injection of turpentine oil, but did not affect the greater response to EDTA. The higher hypocalcemia seen after turpentine oil was no longer observed in SCGx rats. The effects of turpentine oil stress on calcium and CT responses to a bolus injection of CaCl2 persisted in rats subjected to SCGx 14 days earlier. Interruption of thyroid-parathyroid parasympathetic input conveyed by the thyroid nerves (TN) and the inferior laryngeal nerves (ILN) caused a fall in total serum calcium, an increase of PTH levels and a decrease of CT levels, when measured 10 days after surgery. Greater responses of serum CT and PTH were detected in TN-sectioned, and in TN- or ILN-sectioned rats, respectively. Physiological concentrations of CT decreased, and those of PTH increased, in vitro cholinergic activity in rat SCG, measured as specific choline uptake, and acetylcholine synthesis and release. The results indicate that cervical autonomic nerves constitute a pathway through which the brain modulates calcium homeostasis.
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PMID:Influence of the autonomic nervous system on calcium homeostasis in the rat. 792 Sep 72

Cholinergic nerve fibers can be traced to the vicinity of C- and parathyroid cells. The objective of this study was to examine the changes in circulating calcium, parathyroid hormone (PTH) and calcitonin levels after a bilateral surgical section of thyroid (TN) or inferior laryngeal nerves (ILN) in rats. Parasympathetic surgical section decreased significantly thyroid and parathyroid neuronal [3H]choline uptake. A significant fall in total serum calcium and a significant increase in serum PTH were observed 10 days after TN and ILN sections, while calcitonin levels decreased significantly after ILN sections only. When parathyroid sensitivity to a hypocalcemic challenge was assessed, a significantly larger serum PTH response to EDTA was detectable in TN- or ILN-sectioned rats. A significantly smaller hypocalcemia after EDTA was observed in TN-sectioned rats only. Following calcium chloride injection, the increase in serum calcitonin was greater, and the increase in serum calcium levels smaller, in TN-sectioned rats as compared to sham-operated controls. In ILN-sectioned rats, the secretory response of calcitonin and the hypercalcemia achieved after a calcium chloride challenge was significantly greater than in controls. The results indicate that ILN or TN sections induced hypocalcemia and increased serum PTH levels in rats, as well as bringing about a greater secretory response of PTH and calcitonin when challenged with an appropriate stimulus. An inhibitory parasympathetic influence parathyroid and C-cell secretion can be envisioned.
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PMID:Parasympathetic control of parathyroid hormone and calcitonin secretion in rats. 802 17

This study analyzes the parathyroid function in four dogs before and after 2 years of a low-calcium, high-sodium, vitamin D-deficient diet and the involution of the same function following (1) correction of dietary calcium deficiency and administration of i.v. 1,25-(OH)2D (0.25 micrograms twice per day) during 1 month, (2) after an additional month of normal dog chow supplemented with oral vitamin D (25 micrograms per day), and, finally, (3) after 5 and 17 months of a diet with normal levels of calcium and vitamin D. The parathyroid function was evaluated through i.v. infusion of CaCl2 and Na2 EDTA with measurement of intact (I) and carboxyl-terminal (C) immunoreactive parathyroid hormone (iPTH). The C-iPTH/I-iPTH ratio was calculated to assess the modulation of molecular forms of iPTH induced by the various treatments. The 2 years of calcium and vitamin D deprivation lowered ionized calcium (1.23 +/- 0.04, p < 0.05) and 25-OHD (4.02 +/- 2.06 nM, p < 0.005) and tended to decrease 1,25-(OH)2D (80.8 +/- 8.6 pM); it increased basal I- and C-iPTH levels approximately eightfold (I-iPTH, 40.2 +/- 20.7, p < 0.05; C-iPTH, 185.4 +/- 94.9, p < 0.05) and stimulated I-iPTH (60.2 +/- 23.0 pM, p < 0.05) and C-iPTH (239.6 +/- 80.7 pM, p < 0.05) fivefold. A greater rise in nonsuppressible I-iPTH levels than in C-iPTH levels led to a decreased C-iPTH/I-iPTH ratio in hypercalcemia (12.5 +/- 2.8 versus 27.8 +/- 6.05 pM, p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of involution of hyperplastic parathyroid glands in dogs: adaptation via a decrease in the calcium stimulation set point and a change in secretion profile. 805 90

Hypocalcemia is a common finding during stress. The objective of this study was to examine: (a) the changes in circulating calcium, parathyroid hormone (PTH) and calcitonin (CT) concentration in rats stressed by being given a subcutaneous injection of turpentine oil, and (b) the involvement of the sympathetic cervical pathway in stress-induced changes of calcium homeostasis. Four hours after receiving turpentine oil or vehicle, rats were subjected either to hypocalcemia, by being given EDTA intraperitoneally, or to hypercalcemia, by being injected CaCl2 intraperitoneally. Significant changes in serum calcium (10% decrease), serum PTH (28% increase) and CT levels (40% decrease) were observed in stressed rats. EDTA administration brought about a significantly greater hypocalcemia, and a higher PTH secretory response in turpentine oil-stressed rats. During stress, the increase of serum calcium after CaCl2 was significantly smaller, and the rise of CT was greater than in controls. In the case of CT the changes were still observed in rats subjected to superior cervical ganglionectomy (SCGx) 14 days earlier. In the case of PTH, the increase found in stressed rats, but not the augmented response after EDTA, was blunted by SCGx. The potentiation of hypocalcemia brought about by turpentine oil was no longer observed in SCGx rats. In vehicle-treated controls, SCGx delayed PTH response to hypocalcemia, but did not affect the increased response of CT to CaCl2 challenge. The results indicate that a number of changes in calcium homeostasis arise during turpentine oil stress in rats. SCGx was effective to modify the set point for PTH release, but played a minor role in affecting the augmentation of CT release during stress.
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PMID:Involvement of the cervical sympathetic nervous system in the changes of calcium homeostasis during turpentine oil-induced stress in rats. 832 9

Calcium infusion in normal men decreases immunoreactive PTH (iPTH). Intact iPTH (I) shows the greatest decline, and there is a greater decrease in carboxyl-terminal iPTH (C) than in midcarboxyl-terminal iPTH (M); thus, C/I, M/I, and M/C ratios are increased. To verify whether this adaptive mechanism to hypercalcemia was present in patients with primary hyperparathyroidism (PHP), we measured total serum calcium (Ca), I, C, and M as well as C/I, M/I, and M/C ratios in 32 normocalcemic normal subjects (NN), in the same normal subjects made hypercalcemic (HN), in 31 patients with PHP, and in 12 patients with nonparathyroid hypercalcemia (NPHN). Eight patients with PHP and the 32 NN were submitted to CaCl2 and Na2 EDTA infusions to evaluate their parathyroid function. Ca was lower (P < 0.005) in NN (2.21 +/- 0.06 mmol/L) than in PHP (2.80 +/- 0.25 mmol/L) or NPHN (2.83 +/- 0.20 mmol/L). The HN Ca value (2.80 +/- 0.18 mmol/L) was similar to those in PHP and NPHN subjects. C, M, and I were increased in PHP compared to the other groups (P < 0.005). PHP had C/I and M/I ratios of 2.03 +/- 0.72 and 9.04 +/- 7.69, values similar to NN (2.29 +/- 0.55 and 8.70 +/- 3.0), but lower than HN (5.36 +/- 2.48 and 25.93 +/- 13.86; P < 0.005) and NPHN (11.91 +/- 13.06 and 18.69 +/- 10.81; P < 0.005). NPHN also had a lower M/C ratio than HN (2.76 +/- 2.02 vs. 4.99 +/- 1.81; P < 0.05). PHP and NN could increase their C/I ratio to the same maximum (4.71 +/- 1.26 vs. 5.70 +/- 2.94), but PHP did so at a much higher set-point (2.67 +/- 0.19 vs. 2.24 +/- 0.10 mmol/L; P < 0.005). PHP also had higher set-points for M/I, and M/C ratios even if they failed to increase the ratios to the high values in NN [M/I 11.6 +/- 6.4 vs. 29.3 +/- 18.3 (P < 0.005); M/C, 2.16 +/- 1.20 vs. 5.0 +/- 1.93 (P < 0.005)]. Thus, carboxyl-terminal fragments are not secreted preferentially in PHP as they are in other hypercalcemic conditions. This relates to a higher set-point for the regulation of C/I and M/I ratios, permitting the secretion of more intact hormone relative to C or M fragments. The lower M/C ratio in NPHN and in PHP made more hypercalcemic compared to HN suggests a lower production or a higher clearance of midcarboxyl-terminal fragments in chronic hypercalcemia.
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PMID:Carboxyl-terminal fragments of parathyroid hormone are not secreted preferentially in primary hyperparathyroidism as they are in other hypercalcemic conditions. 834 45

The introduction of assays for the intact parathyrin (parathyroid hormone) has dramatically improved the diagnosis and follow-up of patients with primary hyperparathyroidism. However, in some patients with mild or intermittent hypercalcaemia, when plasma concentrations of intact parathyrin may be within the normal reference concentrations, the diagnosis of primary hyperparathyroidism may still be problematic. In these patients, the EDTA-infusion test is of potential value, as it also might be in patients with equivocal operative findings.
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PMID:Potential clinical use of the EDTA-infusion test. 836 62


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