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PubMed1975

Perinatal primate parathyroid hormone metabolism.

Near-term fetal and neonatal parathyroid gland function has been studied in the Rhesus monkey. Fetal serum ionized calcium (Ca++) levels are significantly greater than simultaneously obtained maternal levels. Fetal serum parathyroid hormone (PTH) was undetectable both in the basal state and in association with EDTA-induced fetal hypocalcemia. Induced maternal hypocalcemia was associated with increased maternal serum PTH levels and no change in fetal basal serum Ca++ or PTH levels. Only a minimal decrease in simian neonatal serum Ca++ occurred over the first 48 h of life. Normal adult levels of serum PTH were present as early as 6 h of neonatal life. Induced hypocalcemia at 12 h of age resulted in a significant increase in serum PTH levels.

Animals↗
PubMed1982

Immunoreactive parathyroid hormone in early and advanced renal failure.

Immunoreactive parathyroid hormone (iPTH) was measured in the serum of 20 patients with early renal failure (ERF) using three assays with different specificity. Half of these patients had elevated iPTH in one or more assays, up to twice the upper limit of normal. In contrast, 36 patients with a creatinine clearance below less than 20 ml/min had an 80% elevated iPTH, up to 5 times the upper limit of normal. The patients with ERF and elevated iPTH had a lower serum calcium but no higher serum phosphate than those with normal iPTH. The differences in iPTH in early and end-stage renal failure can be explained by known differences in metabolism of different PTH forms in uremia.

Adolescent↗
PubMed1998

Parathyroid hormone activation of the 25-hydroxyvitamin D3-1alpha-hydroxylase gene promoter.

The DNA flanking the 5' sequence of the mouse 1alpha-hydroxylase gene has been cloned and sequenced. A TATA box has been located at -30 bp and aCCAAT box has been located at -79 bp. The gene's promoter activity has been demonstrated by using a luciferase reporter gene construct transfected into a modified pig kidney cell line, AOK-B50. Parathyroid hormone stimulates this promoter-directed synthesis of luciferase by 17-fold, whereas forskolin stimulates it by 3-fold. The action of parathyroid hormone is concentration-dependent. 1,25-Dihydroxyvitamin D3 does not suppress basal promoter activity and marginally suppresses parathyroid hormone-driven luciferase reporter activity. The promoter has three potential cAMP-responsive element sites, and two perfect and one imperfect AP-1 sites, while no DR-3 was detected. These results indicate that parathyroid hormone stimulates 25-hydroxyvitamin D3-1alpha-hydroxylase by acting on the promoter of the 1alpha-hydroxylase gene.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1994

Circulating intact parathyroid hormone levels in acute pancreatitis.

Serum levels of parathyroid hormone (PTH), calcium and albumin were measured daily for 5 days in 41 selected patients with moderate to severe acute pancreatitis. The PTH level was measured by means of a two-site immunoradiometric assay specific for the intact polypeptide. A rise in PTH level was observed more commonly in patients with a complicated or fatal outcome than in those with an uncomplicated course (14 of 16 versus six of 25 patients, P < 0.001). Although PTH levels were variable in the presence of hypocalcaemia, raised concentrations were found more frequently in patients with complications (seven of eight versus two of seven without complications, P = 0.035). This study confirms that an appropriate rise in PTH level occurs in response to the hypocalcaemic stimulus in patients with acute pancreatitis.

Acute Disease↗
PubMed1987

Reduction of serum parathyroid hormone levels during sympathetic stimulation in man.

The parathyroid glands contain sympathetic nerve endings and the parathyroid cells are endowed with beta-adrenergic receptors. The physiological role of the sympathoadrenal system for the secretion of parathyroid hormone (PTH) has, however, not been clarified. Using the technique of lower body negative pressure (LBNP), which is an established method to achieve sympathetic nerve activation, it was found in 17 healthy subjects that the venous serum levels of PTH were reduced by 7% within 20 min [from 0.79 +/- 0.12 (SD) to 0.74 +/- 0.11 arbU/l, p less than 0.01, paired t test]. The reduction corresponds to 30% of the maximal suppressibility of PTH by induced hypercalcemia or following parathyroidectomy when studied with the same PTH assay and with the short time period involved. After cessation of LBNP the PTH levels returned to baseline within 20 min. There were no concomitant changes of the plasma ionized calcium concentrations. The findings are compatible with a role for the sympathetic nervous system in the physiologic regulation of the secretion of PTH.

Adult↗
PubMed1991

Parathyroid hormone and myocardial performance in dialysis patients.

Whether parathyroid hormone (PTH) has a clinically important effect on myocardial performance is unclear. Previous investigations of cardiac function before and after parathyroidectomy have failed to control for ionized calcium, other biochemical parameters, or heart rate and cardiovascular loading conditions. We performed load- and rate-independent measurements of myocardial contractility in seven stable hemodialysis patients before and after surgical parathyroidectomy under identical conditions of blood ionized calcium (Ca2+), electrolytes, pH, PO2, and hematocrit. Mid-molecule PTH decreased from 44 +/- 8 to 2 +/- 1 ng/mL. Aortic systolic and diastolic pressures, left ventricular chamber dimensions, end systolic wall stress, left ventricular contractility at a common level of afterload, and contractile reserve evaluated with dobutamine were similar before and after parathyroidectomy. Thus, PTH appears not to have a direct effect on myocardial contractile state in dialysis patients.

Adult↗
PubMed1992

Differential effects of parathyroid hormone on chick growth plate and articular chondrocytes.

Parathyroid hormone (PTH) binds specifically to the hypertrophic region of growth plate cartilage [16]. This specific binding suggests a role for this hormone in chondrocyte maturation. Enzymatically isolated chick articular and growth plate chondrocytes grown in monolayer culture were used to assay the direct effects of PTH on chondrocytes. The articular chondrocytes were unresponsive to PTH. The growth plate chondrocytes, however, demonstrated a marked mitogenic response to PTH, with a 39-fold increase of [3H]-thymidine incorporation into DNA. PTH also affected matrix production by the growth plate chondrocytes causing a twofold stimulation of proteoglycan synthesis as determined by the rate of 35SO4 incorporated into matrix macromolecules. Furthermore, PTH depressed collagen synthesis as measured by [3H]-proline incorporation. PTH caused a 12-fold increase in intracellular cAMP in growth plate chondrocytes but no increase in the articular cells. This specificity of PTH for growth plate chondrocytes suggests a possible regulatory role in enchondral ossification.

Alkaline Phosphatase↗
PubMed1981

Urinary excretion of cyclic nucleotides and phosphate in response to parathyroid hormone and calcitonin in man.

The response to parathyroid hormone (PTH) and calcitonin (CT) was studied in eight children with various bone diseases by determining the serum calcium (Ca) and phosphate (P) concentration, urinary phosphate excretion rate, renal phosphate clearance, the percentage of filtered phosphate reabsorbed by the renal tubule (%TRP), creatinine clearance (Ccr), urinary cyclic adenosine 3',5' monophosphate excretion rate (UcGMPV). Administration of PTH caused no significant change in serum Ca and P values, whereas CT produced a decrease in Ca (delta Ca, -1.4 +/- 0.1 mg/100 ml) and P (delta P; -1.1 +/- 0.1 mg/100 ml). There was an increase in UcAMP V (delta UcAMP; 437 +/- 74 nmoles/min/100 ml Ccr) without any significant change in UcGMPV after administration of PTH. Phosphaturia was produced by both PTH (delta TRP, -18 +/- 3%) and CT (delta TRP, -13 +/- 2%). However, CT did not elicit any increase in either UcAMPV or UcGMPV.

Adolescent↗
PubMed1980

Parathyroid hormone: a coronary artery vasodilator.

Injection of synthetic bovine parathyroid hormone (the amino terminal peptide containing the first 34 amino acids) to the coronary circulation of the dog resulted in a marked coronary vasodilation. The vasodilatory response was dose-dependent and amounted to a 161 percent increase over the resting flow rate at a concentration of 1.0 unit per kilogram.

Animals↗
PubMed1991

Parathyroid hormone and enamel formation in rat maxillary incisors.

Parathyroid hormone (PTH) plays an important role in regulating calcium in serum. It is also known to affect bone and dentin formation. The purpose of this investigation was to evaluate enamel formation in normal rats receiving added PTH. It is in two parts: a pilot study where a known method was tested, followed by the main study where the rats were given different doses of PTH. The enamel was examined in both studies and in the main study the ameloblasts were also investigated. Contradictory results were seen. In the pilot study, severe enamel aberrations occurred, while no divergence from normal amelogenesis was noted in the main study. A factor causing the disparate results was the use of a hard tissue marker (oxytetracycline) in the pilot study. It can be concluded that injections of PTH in doses that affect bone and dentin did not cause any changes in normal enamel formation.

Acid Phosphatase↗
PubMed2005

Chronic glucocorticoid treatment alters spontaneous pulsatile parathyroid hormone secretory dynamics in human subjects.

OBJECTIVE: Spontaneous parathyroid hormone (PTH) secretory dynamics include tonic and pulsatile components. It is not known how glucocorticoids might alter these secretory dynamics. DESIGN: The aim of our study was to evaluate spontaneous fluctuations in serum PTH levels in six adult male patients (aged 31-64 years) receiving chronic (>6 months) therapy with glucocorticoids (daily dosage >7.5 mg of prednisone or dose equivalent of other corticosteroid) as compared with a control group of 10 age- and sex-matched normal subjects. METHODS: Peripheral venous blood sampling was performed every 3 min for 6 h from 0900 to 1500 h. Plasma PTH release profiles were subjected to deconvolution analysis, a method that resolves measured hormone concentrations into secretion and clearance components, and to an approximate entropy (ApEn) estimate, that in turn provides an integrated measure of the serial regularity or orderliness of the release process. RESULTS: In the glucocorticoid-treated group, the PTH tonic secretory rate was reduced (4.3+/-0.74 vs 8.8+/-1.4 pg/ml per min in controls, P = 0.017). There was, however, an increase in the fractional pulsatile PTH secretion (42+/-8.2 vs 18.3+/-3.9 pg/ml per min, P = 0.006) in glucocorticoid-treated vs normal subjects. Mean overall PTH concentration, as well as mean integrated area, was similar among normal and glucocorticoid-treated subjects. CONCLUSIONS: These results demonstrate, for the first time, that chronic glucocorticoid treatment induces a redistribution of spontaneous PTH secretory dynamics by reducing the amount released in tonic fashion and increasing the amount released as pulses.

Adult↗
PubMed2003

Parathyroid hormone protects against periodontitis-associated bone loss.

Parathyroid hormone (PTH) functions as a major mediator of bone remodeling and as an essential regulator of calcium homeostasis. In addition to the well-established catabolic effects (activation of bone resorption) of PTH, it is now recognized that intermittent PTH administration has anabolic effects (promotion of bone formation). The aim of this study was to investigate whether intermittent administration of PTH in rodents would block the alveolar bone loss observed in rats when a ligature model of periodontitis is used. Morphometric analysis showed that intermittent PTH administration (40 microg/kg) was able to protect the tooth site from periodontitis-induced bone resorption. In addition, there was a significant reduction in the number of inflammatory cells at the marginal gingival area in sections obtained from animals receiving PTH compared with control animals. These findings demonstrated that intermittent PTH administration was able to protect against periodontitis-associated bone loss in a rodent model.

Alveolar Bone Loss↗
PubMed1993

Effects of parathyroid hormone on pancreatic exocrine secretion.

The role of parathyroid hormone (PTH) and calcium on pancreatic exocrine secretion were observed using sham-operated and parathyroidectomized dogs. First, exocrine secretion of the pancreas stimulated with secretin and cholecystokinin octapeptide (CCK-8) was examined in vivo 3 weeks after parathyroidectomy. Secondly, perfusion experiments of isolated pancreas in the sham-operated and parathyroidectomized dogs were examined. In one experiment, volume of pancreatic juice and bicarbonate output, but not amylase output, was decreased in the parathyroidectomized dogs compared with those in the sham-operated dogs; no participation of calcium in exocrine secretion was revealed. In another experiment, high doses of PTH evoked increases of pancreatic juice and bicarbonate output without changing amylase output; as before, no participation of calcium in the exocrine secretion was observed. We conclude that (a) PTH increases volume of pancreatic juice and bicarbonate output, and (b) pancreatic exocrine secretion is modified by direct effect of PTH, and the pancreatic ductular cells, not the acinar cells, are the target for PTH.

Amylases↗
PubMed1988

Enhanced suppression of 1,25(OH)2D3 and intact parathyroid hormone in Graves' disease as compared to toxic nodular goiter.

1.25(OH)2D3, 25OHD3, and intact parathyroid hormone, as well as various parameters of calcium-phosphorus metabolism were measured in 38 patients with Graves' disease (GD) and in 24 patients with toxic nodular goiter (TNG). Plasma 1.25(OH)2D3 levels were lower in GD patients (82 +/- 29 pmol/liter) than in those with TNG (155 +/- 32 pmol/liter) (P less than 0.0005). The mean value of 1.25(OH)2D3 in 45 controls was intermediate between the two groups of patients (140 +/- 41) and the difference was statistically significant. GD patients before and after treatment had higher alkaline phosphatase (P less than 0.05), lower intact parathyroid hormone (PTH) (P less than 0.05), and lower 1.25(OH)2D3 levels (P less than 0.0005 in the hyperthyroid and P less than 0.01 in the euthyroid state) than TNG patients. We conclude that increased skeletal calcium resorption is due to elevated levels of T3 causing suppression of 1.25(OH)2D3 production and of PTH levels in both groups of patients albeit of different degrees. Furthermore, we postulate that the profound suppression of 1.25(OH)2D3 in GD is secondary to an immune-mediated phenomenon.

Calcitriol↗
PubMed1990

Comparison of different parathyroid hormone radioimmunoassays in uremic patients with secondary hyperparathyroidism.

Parathyroid hormone (PTH) levels of patients with chronic renal failure (CRF) were measured by three different radioimmunoassays (RIA); RIA for mid-region PTH by antibody CH9 (i-PTH) (1), RIA for intact fragments of PTH (intact PTH) and RIA for C-terminal fragments of PTH (PTH-C). PTH levels were higher in CRF patients undergoing hemodialysis therapy (hemodialysis patients) by all three methods. However, PTH levels measured only by i-PTH assay and intact PTH assay were significantly higher in patients with CRF who were not on dialysis (non-dialyzed CRF patients). PTH levels were above normal when creatinine clearance was below 45 ml/min in the intact PTH assay and 66 ml/min in the i-PTH assay. I-PTH levels were well correlated with the severity of osteitis fibrosa evaluated by the degree of periosteal resorption in the digits of hemodialysis patients. Since special handling of the sample is required for the intact PTH assay, i-PTH assay is the most suitable method for diagnosing secondary hyperparathyroidism in patients with CRF.

Bone Diseases, Metabolic↗
PubMed1981

The "calcium clamp": effect of constant hypocalcemia on parathyroid hormone secretion.

This report describes acute studies of parathyroid hormone (PTH) secretion and metabolism in conscious dogs, performed with a new technique, the "calcium clamp." Bolus injections and graded infusions of either calcium (Ca) or EGTA, respectively, increase or decrease plasma Ca to desired levels in 1-2 min; rapid determination of plasma Ca permits feedback control of the infusion rates to maintain the desired Ca concentration for prolonged periods. Using this technique, we have examined the effect in five dogs of a sustained (1 h) decrease in plasma Ca from 9.6 to 7.6 mg/dl on the secretion of PTH. Plasma immunoreactive PTH (IPTH) concentration in precaval blood increased within 1 min, peaked at 4-10 min (greater than 5 times control), but thereafter declined gradually to 57% of the maximum at 60 min, despite ongoing and constant hypocalcemia. Abrupt restoration of normocalcemia caused IPTH levels to decrease with an apparent half-time of 3.0 +/- 0.3 min (mean +/- SE). Thus, external feedback-regulated control of plasma Ca is possible in experimental animals. IPTH concentrations decline from the maximum during constant hypocalcemia, a new observation that suggests that PTH secretion and/or metabolism are altered progressively by the hypocalcemia.

Animals↗
PubMed2005

Calcimimetics: a remedy for all problems of excess parathyroid hormone activity in chronic kidney disease?

PURPOSE OF REVIEW: Cinacalcet is a calcimimetic agent that is now available for use clinically to manage secondary hyperparathyroidism among patients undergoing dialysis regularly. It acts as an allosteric activator of the calcium-sensing receptor, the molecular mechanism that controls parathyroid hormone secretion. This mechanism of action differs fundamentally from that of the vitamin D sterols, which heretofore have been the only definitive pharmacological intervention for treating secondary hyperparathyroidism. RECENT FINDINGS: The ability of calcimimetic agents to enhance signaling through the calcium-sensing receptor in parathyroid cells affects several important components of parathyroid gland function. Results from several large clinical trials demonstrate that cinacalcet effectively lowers plasma parathyroid hormone levels in dialysis patients with secondary hyperparathyroidism when used either alone or together with vitamin D. Unlike the vitamin D sterols, which generally raise serum calcium and phosphorus levels, treatment with cinacalcet is associated with modest reductions in serum calcium and phosphorus concentrations. The impact of these biochemical changes on renal bone disease and on soft-tissue and vascular calcification during long-term treatment has yet to be characterized fully. Cinacalcet also diminishes parathyroid hormone gene expression, and studies in experimental animals indicate that its use retards the progression of parathyroid gland hyperplasia and increases bone mass. If confirmed in future clinical trials in patients with secondary hyperparathyroidism, these features represent potentially important ancillary therapeutic benefits. SUMMARY: Calcimimetic agents have diverse effects on parathyroid gland function that may enhance the overall medical management of secondary hyperparathyroidism in patients undergoing dialysis regularly.

Animals↗
PubMed1993

Studies on the production of human parathyroid hormone by recombinant Escherichia coli.

Expression of human parathyroid hormone, hPTH(-1-84), by Escherichia coli N4830:pEX-PPTH was studied in controlled bioreactors. The hPTH is expressed as a fusion protein under control of the bacteriophage lambda PR promoter. In batch runs, low biomass concentrations but high specific hPTH productivities were obtained with complex TY (bactotryptone and yeast extract) medium whereas high biomass concentration and low specific productivities were found when fructose was used instead of bactotryptone (YF medium). The preinduction temperature was always 30 degrees C; the temperature shift to induce production of fusion protein was varied from 36 to 42 degrees C. Formation of hPTH passed a pronounced maximum as a function of induction temperature when using YF medium. However, the optimum temperature shift was 38 degrees C for both media used. For this temperature increase both media yielded about the same volumetric hPTH productivity (approx. 30 mg hPTH/1 per hour). By applying a fed-batch strategy for the YF medium, the productivity of the recombinant protein could be further increased more than fourfold. Compared to shake-flask experiments, the hPTH yield could be increased by a factor larger than 20.

Biotechnology↗