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PubMed2006

[Influence of quick intraoperative measurements of intact parathyroid hormone in the surgical management of primary hyperparathyroidism].

OBJECTIVE: To evaluate whether a quick parathyroid hormone assay that measures intact parathyroid hormone (iPTH) level intraoperatively has modified the surgical strategy for primary hyperparathyroidism in the Meixoeiro Hospital in Vigo (Pontevedra, Spain). DESIGN: An observational, analytic, historic cohort study was performed. Two study groups were established. In group 1 (n = 28) iPTH levels were not measured intraoperatively. In group 2 (n = 39) iPTH was measured intraoperatively. iPTH was monitored using blood samples from cannulated peripheral veins. A positive test was defined as a decrease in iPTH level of >or= 50% of the baseline preincision level at 10 minutes postexcision, even when the baseline value was outside the normal range. The dependent variables evaluated were operating time, the number of parathyroid glands visualized, the number of parathyroid glands biopsied, length of postoperative hospital stay, unilateral exploration, and the percentages of cure, persistence, and recurrence in each group. RESULTS: Group 2 showed a statistically significant decrease in operating time (144.7 +/- 62.1 versus 178.8 +/- 57.5 minutes; p = 0.025), the number of parathyroid glands visualized (1.9 +/- 0.9 versus 2.8 +/- 1.3; p = 0.002), the number of parathyroid glands biopsied (1.5 +/- 0.9 versus 2.2 +/- 1.4; p = 0.025), and the need for bilateral exploration (30.77% versus 85.72%) in comparison with group 1. No significant differences were observed in length of postoperative hospital stay or in the percentages of cure (94.8% versus 92.85%), persistence (5.12% versus 7.14%), and recurrence (2.56% versus 3.57%). CONCLUSIONS: In our hospital, intraoperative measurement of iPTH improved the surgical strategy of primary hyperparathyroidism and has therefore been included in our routine treatment protocol.

Female↗
PubMed1978

The role of cyclic AMP in parathyroid hormone action in the toad bladder.

Parathyroid hormone (PTH) inhibited active transport of inorganic phosphate and stimulated an increase in cyclic AMP concentration in the urinary bladder of the toad, Bufo marinus. Active transport of phosphate in the toad bladder was also inhibited by an analog of cyclic AMP (dibutyryl cyclic AMP) and by other drugs (pitressin and theophylline) which increase toad bladder intracellular cyclic AMP concentration. These data support the concept that cyclic AMP may be the mediator of PTH-induced phosphate transport inhibition in the toad bladder.

Animals↗
PubMed1981

Effect of age on serum immunoreactive parathyroid hormone and its biological effects.

Immunoreactive parathyroid hormone (iPTH) levels, nephrogenous cAMP (ncAMP), and tubular maximum phosphate reabsorption (TmP) were measured in 10 young and 12 healthy volunteers. The fasting urinary calcium to creatinine ratio (Ca:Cr) was also quantitated as an index of bone resorption. Aging was attended by increased iPTH levels (6.9 +/- 0.8 vs. 3.4 +/- 0.4 mu leq/ml; P less than 0.01) as well as increased ncAMP levels (2.48 +/- 0.28 vs. 1.12 +/- 0.21 nmol/100 ml glomerular filtrate; P less than 0.005) and decreased TmP (2.9 +/- 0.2 vs. 4.1 +/- 0.2 mg/100 ml glomerular filtrate; P less than 0.005), indicating that the increased iPTH levels reflected the biological effects of the hormone. A significant positive correlation of iPTH and ncAMP and a significant negative correlation of iPTH and TmP were observed. The Ca:Cr was increased in the older volunteers (0.10 +/- 0.02 vs. 0.05 +/- 0.01; P less than 0.05). The elderly subjects had significantly decreased daily calcium ingestion, serum phosphate and albumin, and creatinine clearance. Our findings suggest that the increased biological effects of PTH in the elderly subjects may contribute to the increases in Ca:Cr and bone loss that occur with age.

Adult↗
PubMed1995

Parathyroid hormone and the cellular immune system.

Parathyroid hormone (PTH) is the main hormone controlling calcium concentration in the extracellular fluid (ECF) through its biological activity on bone, kidney and intestine. However, data published over the last two decades indicate that PTH may act as an immunomodulator. The purpose of the present review is to summarize the effects of PTH on various immune functions. Polymorphonuclear leukocytes of patients with chronic renal failure (CRF) and elevated blood levels of PTH showed impaired migration, reduced phagocytic and bactericidal activity, and inhibited granulocyte chemotaxis. Antibody production and T and B lymphocyte proliferation are affected by PTH, both in vivo and in vitro. Possible implications of the involvement of PTH and its fragments in CRF are discussed.

Animals↗
PubMedDate not supplied

Pathogenesis of renal calculi in distal renal tubular acidosis. Possible role of parathyroid hormone.

Elevated circulating levels of immunoreactive parathyroid hormone (PTH), hypercalciuria and renal calculi were found in 3 patients with distal renal tubular acidosis (RTA). Treatment with alkali resulted in a fall of PTH toward normal and a reduction in urinary calcium, but the frequency of urolithiasis was unchanged. In one patient in whom prolonged follow-up was possible, a subtotal parathyroidectomy was performed. This was followed by virtual cessation of stone formation despite persistence of the acidification defect. This study suggests that RTA may be associated with secondary hyperparathyroidism and that the consequent elevation in PTH may play a contributory role in the pathogenesis of renal calculi.

Acidosis, Renal Tubular↗
PubMed2007

[Therapeutic agents for disorders of bone and calcium metabolism--Parathyroid hormone in weekly subcutaneous injection].

The parathyroid hormone (PTH) that is marketed outside Japan is for daily administration. It has been proven to increase bone mass and prevent fractures, and the effects are very strong. However, data suggest that daily administration of PTH increases bone resorption. By contrast, weekly administration of PTH, which is being developed in Japan, actually decreases bone resorption, and data suggest that this regimen maintains a good balance between bone formation (predominant) and bone resorption. Furthermore, it has been reported that weekly administration of PTH increases bone mass as much as every day administration of PTH, and as such, weekly administration of PTH has the potential to be a useful regimen with characteristics that are different from those of daily administration of PTH.

Animals↗
PubMed1991

Plasma cyclic AMP response to intravenous parathyroid hormone in pseudohypoparathyroidism.

Highly purified bovine parathyroid hormone (PTH) was given by intravenous bolus injection to patients being investigated for disorders of mineral metabolism, and to adult volunteer controls. Plasma cyclic AMP measured basally and at 10 min gave reliable discrimination between the normal response and cases of pseudohypoparathyroidism. Infants under 3 months of age tended to have higher basal levels of cAMP and a flatter pattern of response to the dose of PTH used. This simplified test procedure in children offers considerable advantages over previous tests of PTH responsiveness which involve urine collections and multiple blood sampling. It is suitable for selective screening of individuals suspected of pseudohypoparathyroidism on the basis of their family history or physical abnormalities.

Adolescent↗
PubMed2005

Delivery of parathyroid hormone for the treatment of osteoporosis.

Parathyroid hormone (PTH), along with its fragments and analogues, potently restores bone mass and biomechanical strength in animal models of osteoporosis, and reduces fractures by up to 65% in clinical trials in osteoporotic patients. Despite this demonstrated efficacy, patient acceptance and compliance with PTH is limited by the need for daily subcutaneous injections. The development of an equally efficacious, noninjectable form of PTH would significantly expand the present market. A challenge to the development of an alternative delivery system is the requirement for low-dose, daily, intermittent pulses of PTH to induce the anabolic actions on bone. In this review, recent basic and clinical efforts to deliver PTH by oral, buccal, sublingual, transdermal, nasal and pulmonary approaches will be addressed.

Animals↗
PubMed1986

Effect of parathyroid hormone and uremia on erythrocyte deformability.

Parathyroid hormone (PTH) caused a significant decrease in human erythrocyte filtration rate (EFR). This effect was Ca2+-dependent and was partially reversed by the Ca2+ blocker verapamil. It was mimicked by the Ca2+ ionophore A-23187. Mg2+ even at high concentrations could not substitute for Ca2+. There was a dose response between the filtration rate and Ca2+ or PTH concentrations. Serum ultrafiltrate of patients with chronic renal failure and secondary hyperparathyroidism caused significant inhibition similar to that seen with PTH extract. Ultrafiltrate from patients with chronic renal failure following parathyroidectomy and from healthy individuals did not cause this phenomenon. Erythroyctes deformability in uremic patients appears to be caused by high PTH levels. Our present findings agree with ones about the toxic effects of PTH on various biological systems.

Calcium↗
PubMed1988

Forskolin mimics the effects of calcitonin but not parathyroid hormone on bone resorption in vitro.

Parathyroid hormone (PTH) and calcitonin stimulate bone adenylate cyclase activity and increase bone cAMP content, but PTH enhances and calcitonin inhibits bone resorption. This study examined the effects of forskolin, a non-hormonal activator of adenylate cyclase, on bone resorption and cAMP accumulation in 19-day fetal rat limb bones. Forskolin (10(-9) to 10(-5) M) stimulated bone cAMP generation in a concentration-dependent manner. However, in contrast to bPTH(1-34), which also stimulated cAMP accumulation, forskolin did not stimulate bone resorption. Moreover, forskolin did not augment the bone-resorbing activity of PTH even though it potentiated PTH stimulation of bone cAMP levels. Rather, high doses of forskolin (10(-6) to 10(-5) M) exhibited a calcitonin-like effect to inhibit PTH-mediated bone resorption. These results support a second-messenger function of cAMP for the inhibitory effects of calcitonin, but not for the stimulatory effects of PTH on bone resorption.

Adenylyl Cyclases↗
PubMed1979

Increased RNA and heme synthesis in mouse erythroid precursors by parathyroid hormone.

The in vitro effect of parathyroid hormone (PTH) on RNA and heme synthesis by embryonic mouse liver erythroid precursors was examined. PTH produced a dose-dependent effect on RNA synthesis. A maximal increase of 60 +/- 16% (p less than 0.02) was observed with 1.0 U PTH/ml, whereas with higher concentrations a significant decline was found. Furthermore, PTH stimulated heme synthesis after 24 h of incubation. The maximal enhancement of 32 +/- 7% (p less than 0.01) was observed with 0.5 U PTH/ml, a lower effect was obtained with 1.0 U PTH/ml, while 2.0 U PTH/ml caused a pronounced decrease of heme synthesis. These data indicate that PTH affects directly the erythroid precursors by a mechanism similar to that of erythropoietin. The inhibitory effect on the RNA synthesis observed with large doses of PTH may explain at least one of the causes of the anemia reported in patients with primary hyperparathyroidism.

Animals↗
PubMed2001

Parathyroid hormone in the treatment of osteoporosis.

Parathyroid hormone (PTH), especially intact human PTH [hPTH(1-84)] and its various fragments [hPTH(1-31), (1-34), (1-36), (1-38) and their modifications], has been used for the treatment of osteoporosis over the last 10 years. Although chronic continuous excess of PTH markedly increases bone resorption, as seen in the typical example of primary hyperparathyroidism and osteitis fibrosa generalisata, intermittent PTH administration has been found to stimulate bone formation in animals, providing a basis for the use of PTH as a therapeutic agent for osteoporosis. In addition to dramatically increasing trabecular bone density and also sustaining cortical bone density, PTH administration increases bone strength and reduces the fracture rate, despite occasional increases in cortical porosity. Administration of PTH in combination with antiresorptive agents such as estrogen, calcitonin, vitamin D and bisphosphonates augments its effect. Because of its bone anabolic action, PTH is expected to be effective for osteoporosis in those of advanced age with suppressed bone remodelling, which might not respond favourably to antiresorptive agents.

Animals↗
PubMed1977

Circulatory and lipolytic effects of parathyroid hormone. An experimental study in dogs.

Parathyroid hormone (PTH) was given intravenously to anesthesized adult dogs. Blood flows were measured with electromagnetic probes in different vascular areas concomitant with analysis of glycerol, free fatty acid, calcium, glucose, sodium, potassium, albumin, carbon-dioxid and creatinine. PTH consistently caused an immediate increment in blood flow in the celiac vasculature and a following, less pronounced increase in the renal artery. These changes were effectuated by a vasodilatation. The degree and duration of the flow increments were dose dependent; The celiac artery was more sensitive to the effect of PTH than the renal artery. In celiac artery maximal increase above basal flow was 58 +/- 27% (Mean +/- S.D.), in renal artery 25 +/- 12%. A significant lipolytic action of PTH was consistently notable within minutes after the administration of PTH. The other parameters analysed in blood remained unchanged sixty to ninety minutes after the PTH injections. Then a hypercalcemic effect of PTH appeared. A lipolytic action of PTH could be demonstrated with PTH doses which did not induce hypercalcemia.

Animals↗
PubMed1980

[Evidence, in uremic man, of the role of beta 2 adrenergic receptors in the secretion of parathyroid hormone and calcitonin (author's transl)].

In order to determine the effect of beta-blocking agents on secretions of parathyroid hormone and calcitonin, 9 patients with renal failure were given single doses of propranolol (a blocker of the beta 1 and beta 2 receptors) or an equivalent amount of metoprolol (a beta 1 selective agent). Propranolol causes a decrease of plasma parathyroid hormone (p less than 0.02) as well as of calcitonin (p less than 0.05) whereas metoprolol has no effect on the plasma levels of these hormones. These findings suggest that parathyroid tissue and thyroid C cells have receptors that are exclusively of the beta 2 type which are modulating the secretion of parathyroid hormone and calcitonin.

Adult↗
PubMed1993

Parathyroid hormone increases cytosolic calcium of thymocytes.

Parathyroid hormone (PTH) has been implicated in the genesis of the abnormalities of the immune system in uremia. This action was attributed to the ability of PTH to augment entry of calcium and hence sustain an elevation of the basal level of cytosolic calcium ([Ca2+]i) in the cells of the immune system. However, direct evidence for such an action of the hormone on these cells is lacking. We examined whether PTH affects [Ca2+]i of rat thymocytes and the potential mechanisms of such an effect. 1-84 PTH (0.5, 1.0, 2.0 x 10(-7) M) increased [Ca2+]i in a dose-dependent manner by 31 +/- 2.6, 73 +/- 3.8, and 128 +/- 10.8 nM, respectively. 1-34 PTH had no effect. The various doses of PTH antagonist ([Tyr-34] bPTH (7-34)NH2) blocked the PTH-induced rise in [Ca2+]i by 41-67%. Dibutyryl adenosine 3',5'-cyclic phosphatase (cAMP), forskolin and phorbol ester 12-0-tetradecanoyl-phorbol 13-acetate (TPA) also produced a significant rise in [Ca2+]i of thymocytes. Verapamil blocked the PTH action by 44% but had no effect on the dibutyryl-cAMP-, forskolin- or TPA-induced rise in [Ca2+]i. Absence of calcium in the media abolished the PTH-induced increase in [Ca2+]i and significantly reduced that of dibutyryl cAMP. Staurosporine completely prevented the TPA-induced rise in [Ca2+]i but had no effect on that produced by PTH. 1-84 PTH in the presence of calcium in the medium produced a significant rise in thymocyte cAMP but had no effect in the absence of calcium in the media.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Recombinant full-length parathyroid hormone (1-84).

Full-length parathyroid hormone (PTH) 1-84 is a recombinant version of human PTH. It is approved in the EU for the treatment of postmenopausal women with osteoporosis who have a high risk of fractures. Once-daily subcutaneous administration of PTH(1-84) stimulates new bone formation and increases bone mass. In the pivotal, randomised, double-blind, multicentre, 18-month TOP trial in 2532 postmenopausal women with osteoporosis, subcutaneous PTH(1-84) 100 microg/day significantly reduced the incidence of new or worsened vertebral fractures relative to placebo (primary endpoint). Moreover, the increase from baseline in bone mineral density (BMD) at the lumbar spine, total hip, femoral neck and trochanter was also significantly greater than in the placebo group. In another well designed study (PaTH; n = 238), 1 year of subcutaneous PTH(1-84) 100 microg/day followed by 1 year of alendronate 10 mg/day resulted in significantly greater increases in total spine, femoral neck and total hip BMD at 24 months compared with patients who received placebo for the second year. During the first year, PTH(1-84) in combination with alendronate was no more effective than PTH(1-84) monotherapy in terms of increasing areal lumbar spine BMD. PTH(1-84) is generally well tolerated, although patients should be monitored for elevated serum calcium.

Animals↗
PubMed2001

Signaling pathway and chronotropic action of parathyroid hormone in isolated perfused rat heart.

Parathyroid hormone (PTH) activates both adenylyl cyclase and phospholipase C via the PTH-1 receptor. We previously reported that PTH increased heart rate and that this effect was mediated via the pacemaker current (I f ). However, it has been reported that PTH exerts its chronotropic effect via an interaction with adrenergic receptors or via L-type calcium channels. Thus, the objective of the study was to elucidate the exact mechanism of the chronotropic effect of PTH. We tested whether its chronotropic effects could be abolished by inhibitors of the following systems in isolated perfused rat hearts: alpha-adrenergic (prazosin); beta-adrenergic (propranolol); angiotensin II (CV11974); endothelin-1 (TAK044); calcium channel (verapamil); adenylyl cyclase (miconazole); phospholipase C (U73122) or I f (CsCl). In addition, we measured the cyclic adenosine monophosphate level of the heart after PTH administration. Whereas prazosin, propranolol, CV11974, TAK044, verapamil, and U73122 did not inhibit the chronotropic effect of PTH, CsCl or miconazole suppressed it significantly. PTH increased the cyclic adenosine monophosphate level of the atrium but not the left ventricle. These results indicate that the chronotropic actions of PTH are mediated via selective activation of adenylyl cyclase to increase the I f current.

Adenylyl Cyclases↗
PubMed2004

Parathyroid hormone: new assays, new receptors.

Accurate measurements of parathyroid hormone (PTH) in plasma are necessary for the assessment, monitoring, and therapy of disorders of bone and mineral metabolism including renal osteodystrophy. Assays for PTH have evolved to provide 2-site immunometric assays that are highly specific for the intact 84 amino-acid peptide, PTH (1-84). With the advent of such assays, it has been shown that the prior generation of assays, thought to measure intact PTH, in fact, also detected a PTH peptide that was truncated at the N-terminus and that appeared to be similar to PTH (7-84). There has been renewed interest in such circulating PTH fragments in view of the demonstration that PTH (7-84) (and other PTH peptides) might have biologic effects. These effects include an action to oppose the calcemic effect of PTH in vivo and to inhibit bone resorption and osteoclast generation in vitro. These effects appear to be mediated by actions of a receptor for PTH peptides with specificity for the C-terminal region of PTH and distinct from the PTH receptor known to be responsible for all of the classic actions of PTH. Although the C-PTH receptor has not yet been cloned, the observations have opened a new field of research in parathyroid physiology. Clinical applications of the assay of such PTH fragments in relation to the amount of circulating PTH (1-84) concentrations are being sought actively as the new PTH assay methodology is applied to the clinical arena and as the biology of the C-PTH receptor and C-terminal PTH fragments are investigated.

Chronic Kidney Disease-Mineral and Bone Disorder↗