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PubMed1989

Calcium-dependent release of N-terminal fragments and intact immunoreactive parathyroid hormone by human pathological parathyroid tissue in vitro.

The regulation of PTH secretion by extracellular calcium was studied in parathyroid tissue obtained from patients with hyperparathyroidism (adenoma or hyperplasia) using both an amino (N)-terminal RIA as well as an immunoradiometric assay (intact assay) specific for the intact hormone. The parathyroid glands separated into three major groups when examined in terms of absolute amounts of PTH secreted, degree of suppressibility, and set-point for calcium (the concentration of calcium causing half-maximal inhibition of PTH release). In cell preparations from group A (two different adenomas, two hyperplastic glands from a patient with renal failure, and a hyperplastic gland from a patient with hypophosphatemic rickets), both assays showed comparable PTH release (agreeing within 2-fold), similar degrees of suppressibility and similar, if not identical, set-points. In group B (two adenomas and one hyperplastic gland from a patient with renal failure), PTH secretion, as measured in the N-terminal assay, was 3- to 6-fold more than that measured in the intact assay. The set-points and maximal degrees of suppressibility were, however, still comparable. In group C [two adenomas and one gland from a patient with hypophosphatemic rickets (the sister of the patient in group A)], no suppressibility was observed when PTH release was measured using the intact assay (i.e. less than 50% suppression of PTH release at 2-3 mM Ca2+). In one of these three glands, the N-terminal assay was used in addition to the intact assay, and no suppressibility was present with either assay. Thus, in general, the effects of extracellular Ca2+ on PTH secretion from pathological parathyroid tissue were similar when assessed with both an N-terminal and an intact assay, at least with respect to setpoint and maximal suppressibility. In a few cases, maximal PTH release was greater when measured with the N-terminal assay, consistent with substantial release of N-terminal fragments in addition to intact PTH. In addition, nonsuppressible glands were not uncommon when PTH release was measured by the intact assay, confirming previous studies with less specific assays.

Adolescent↗
PubMed1996

Persistent elevated serum levels of intact parathyroid hormone after operation for sporadic parathyroid adenoma: evidence of detrimental effects of severe parathyroid disease.

BACKGROUND: A significant number of patients with primary hyperparathyroidism (pHPT) who are surgically treated have increased serum levels of intact parathyroid hormone (PTH) during long-term follow-up despite normocalcemia. The cause and significance of this finding remain to be established. METHODS: A total of 82 patients operated on for sporadic parathyroid adenoma were investigated before and at 8 weeks and 1 year after operation with serum levels of intact PTH, bone mineral content, and biochemical variables known to reflect PTH activity. RESULTS: All patients had low or normal serum levels of calcium during follow-up. At 8 weeks after operation 20 (24%) patients had increased serum levels of PTH. These patients had severe parathyroid disease and low levels of 25(OH) vitamin D before operation. In contrast to patients with normal levels of PTH after operation, they did not have an elevated bone mineral content but had elevated levels of serum creatinin. At 1 year after operation 13 patients had elevated serum levels of PTH. Compared with patients with normal serum levels of PTH, they were older and had an increased frequency of cardiovascular disease and biochemical indications of compromised renal function. They did not have an elevated bone mineral content. CONCLUSIONS: Persistently increased serum levels of PTH indicate harmful effects of pHPT even after surgical cure, especially in elderly patients with severe disease before operation. The results in this investigation therefore favor early treatment of pHPT.

Adenoma↗
PubMed1987

The effect of vincristine on parathyroid hormone release and on the parathyroid cell microtubular structures in the intact rat.

The effect of vincristine on immunoreactive parathyroid hormone (iPTH) release and parathyroid cell microtubular structures was evaluated in intact, unanaesthetized, and unrestrained rats with indwelling catheters. In overnight fasted rats, blood samples were collected before and at 30, 60 and 120 min after iv vincristine administration in low dosage (0.15 mg/kg) or in higher dosage (0.5 mg/kg) or vehicle (controls) for serum iPTH and calcium determinations. Mean baseline serum iPTH and calcium concentrations were similar in the vincristine-treated and the control rat. Following the low dose vincristine treatment, serum iPTH slightly but significantly declined to 89 +/- 5% at 30 min and remained at this low level at 60 and 120 min as compared to those observed in control rat. Similarly, iPTH concentrations after higher doses of vincristine were also significantly decreased to 87 +/- 4% at 30 min and to 83 +/- 4% at 60 min, and 86 +/- 7% at 120 min as compared to those observed in the control rat. Serum calcium concentrations were similar in the vincristine-treated and control rats. In the next study, each of the rats received vincristine and vehicle in a random order, 10 days apart. In this study also, mean serum iPTH significantly declined to 85 +/- 7% at 60 and 120 min during vincristine treatment as compared with those observed during the vehicle treatment in the same rats. Parathyroid glands were removed from rats between 60 and 120 min after vincristine or vehicle treatments for electron microscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Transient rise in intact parathyroid hormone concentration after surgery for parathyroid adenoma.

OBJECTIVE: Our goal was to describe the course of parathyroid hormone (PTH) after surgery for primary hyperparathyroidism (PHPT). PTH levels drop to low values after parathyroidectomy for PHPT. However, in some patients, a rebound transient increase in PTH concentrations can occur. Study design and setting A prospective study included 72 patients who underwent surgical exploration for PHPT. A single adenoma was found in 57 patients (79.1%), 2 adenomas were found in 2 (2.7%), and parathyroid hyperplasia was found in 13 (18.05%). The postoperative PTH secretion was studied in those patients who had an adenoma excised. RESULTS: This phenomenon was noted in 18 (31.6%) patients between 4 and 12 weeks, although total calcium concentrations were normal (9.3 +/- 0.6 mg/dL). Before surgery these patients had a more remarkable hyperparathyroidism (clinical and biochemical) than the others, but differences were not significant. CONCLUSION: Postoperative increases in PTH concentration can occur after successful parathyroidectomy. These increases are transient and do not indicate persistent or recurrent disease.

Adenoma↗
PubMed1993

Parathyroid hormone: regulation of synthesis and secretion.

Calcium homeostasis is essential for survival and is primarily achieved through the actions of parathyroid hormone. Parathyroid hormone secretion and synthesis are primarily regulated by serum calcium levels, although other factors such as vitamin D and neurotransmitters play a role. This review is intended to provide the reader with up to date information on the current state of basic cell regulation research into parathyroid function. While some mention of disease states is made, the focus of this review is on the calcium regulation of parathyroid hormone secretion at the molecular level. Individual sections will discuss calcium-sensing, signal transduction by calcium and other secretagogues, regulation of parathyroid hormone synthesis, and strategies of regulation of parathyroid hormone secretion by calcium. Particular emphasis is given to the calcium-stimulated degradation of parathyroid hormone within the parathyroid as one of the major pathways by which circulating levels of bioactive hormone are controlled.

Amino Acid Sequence↗
PubMed1997

[Cushing's syndrome due to small cell lung cancer with ectopic production of adrenocorticotropic and parathyroid hormone].

A 72-year-old man was admitted to our hospital because of a tumor-like shadow on a chest X-ray film. At the initial examination, he had clinical signs of Cushing's syndrome: moon face, central obesity, and hypertension. A computed tomographic scan of chest showed an abnormal shadow in the lung (5 x 6 cm) with involvement of the right paratracheal and anterior tracheal lymph nodes, and a right-sided pleural effusion. Small cell lung cancer (extended disease; T2N2M6 stage IV) was diagnosed after a transbronchial biopsy. The concentrations of adrenocorticotropic hormone, cortisol, and parathyroid hormone in plasma were markedly elevated, and there was no circadian rhythm (336 pg/ml. more than 60.1 micrograms ml. and 805 pg/ml, respectively). Fluid obtained by thoracentasis had malignant cells, and the levels of adrenocorticotropic hormone and parathyroid hormone in the effusion (1120 pg/ml and 1810 pg/ml, respectively) were higher than those in serum, which indicates that these hormones were produced by the tumor cells. The patient received chemotherapy and responded well, but he died of respiratory failure 26 months later. The response rate to chemotherapy in elderly patients with lung cancer is said to be comparable to that in younger patients, but treatment may be difficult because of poor performance status and diminished physical capacity. Although patients with lung cancer complicated by Cushing's syndrome have a poor prognosis, this patient survived for more than 2 years after the disease was diagnosed.

Adrenal Cortex Hormones↗
PubMed1997

Comparison of the abilities of human parathyroid hormone(1-31)NH2 and human parathyroid hormone-related protein(1-31)NH2 to stimulate femoral trabecular bone growth in ovariectomized rats.

N-terminal fragments of PTH and PTHrP, such as hPTH-(1-34) and hPTHrP-(1-34), are sufficiently similar with respect to amino acid sequence, location of functional domains, and higher order configuration to activate the same PTH/PTHrP receptor and the same two signal enzymes, adenylyl cyclase and phospholipase-Cbeta. Therefore, it was expected that hPTHrP-(1-31)NH2 would stimulate bone growth in ovariectomized rats as strongly as hPTH-(1-31)NH2. Like hPTH-(1-31)NH2, hPTHrP-(1-31)NH2 stimulated adenyly cyclase in ROS 17/2 osteosarcoma cells as strongly as the standard hPTH-(1-34) and like hPTH-(1-31)NH2, triggered a large drop in mean blood pressure when injected intravenously. Unlike hPTH-(1-31)NH2, however, hPTHrP-(1-31)NH2 could not stimulate trabecular growth in the distal femurs of young, sexually mature, ovariectomized rats.

Adenylyl Cyclases↗
PubMed1988

[The measurement of parathyroid hormone in sera of hemodialysis patients with renal insufficiency by employing the various kinds of parathyroid hormone kits].

This study focussed on elucidating difference of blood PTH levels, by employing the various kinds of PTH kits. We carried out the measurements of PTH levels in sera of the hemodialysis patients with renal insufficiency presumably inactivated PTH degradative regulation in kidney. Our results showed the remarkable significant relationships among blood PTH levels of carboxyl and mid-region PTH and intact PTH in hemodialysis patients and was deduced that the difference of PTH levels by using various kinds of PTH kits was responsible of PTH cleavage effect in the kidney.

Adult↗
PubMed1999

Hyperphosphatemia accelerates parathyroid cell proliferation and parathyroid hormone secretion in severe secondary parathyroid hyperplasia.

We studied the role of phosphorus retention in parathyroid cell proliferation and parathyroid hormone (PTH) oversecretion in severe secondary parathyroid hyperplasia. Mice transplanted with human parathyroid tissue from a patient who had undergone parathyroidectomy for severe secondary hyperparathyroidism were divided into four groups; each group was given a diet with a different phosphorus content (0.4, 0.7, 1.0, and 1.2%) to alter serum phosphorus concentrations. Histologic examinations of grafts by hematoxylin-eosin or by bromodeoxyuridine (BrdU) immunohistochemical staining were performed to assess parathyroid cell proliferation. Changes in serum phosphorus concentrations unidirectionally affected PTH secretion from the graft, because human PTH did not cross-react with mouse PTH. Serum phosphorus concentrations of 1.0P and 1.2P groups were significantly higher than those of 0.4P and 0.7P groups (p<0.05). Serum phosphorus concentrations were significantly correlated with the gradient of human PTH elevation with a coefficient of 0.48 and a p<0.05. Furthermore, serum phosphorus concentrations and the gradient of human PTH elevation were significantly higher in mice with BrdU-immunoreactive cells in the parathyroid graft than in mice without immunoreactive cells in the graft. These results indicate that uncontrolled hyperphosphatemia may accelerate the proliferation of parathyroid cells, exacerbating PTH oversecretion.

Animals↗
PubMed1975

Selective proteolysis of the receptor for parathyroid hormone in skeletal tissue.

Parathyroid hormone, calcitonin, and prostaglandin E2 activate the adenylate cyclase-cyclic AMP system in fetal-rat calvaria. These agents presumably interact with the tissue at separate receptor sites. When calvaria were preincubated with trypsin, 500 mug/ml for 45 min, the subsequent increase in 3',5'-AMP in response to parathyroid hormone was markedly diminished, whereas the response to calcitonin and prostaglandin E2 were not altered significantly. The effect was attributable to an action of the enzyme on the tissue and not to hydrolysis of the hormone. Similarily, preincubation of calvaria with trypsin prior to homogenization and preparation of a crude plasma membrane fraction decreased PTH-sensitive adenylate-cyclase activity by 58% but did not alter the degree of stimulation of the enzyme in response to calcitonin, prostaglandin E2, or sodium fluoride. These studies support the hypothesis that the actions of parathyroid hormone and calcitonin on bone are mediated through distinct receptor sites, and the receptors for parathyroid hormone can be altered selectively with trypsin.

Adenylyl Cyclases↗
PubMed1983

Aspiration of enlarged parathyroid glands for parathyroid hormone assay.

Enlarged parathyroid glands were percutaneously aspirated under computed tomographic (CT) control in 7 patients, and levels of parathyroid hormone (PTH) and human thyroglobulin (HTg) were measured. All 7 patients had high levels of PTH in at least 1 specimen. It is concluded that the measurement of high concentrations of PTH in the aspirate from a cervical or mediastinal mass, with CT documentation of needle position, provides absolute localization of parathyroid masses.

Adenoma↗
PubMed1995

Proparathyroid hormone is preferentially cleaved to parathyroid hormone by the prohormone convertase furin. A mass spectrometric study.

Parathyroid hormone (PTH), an 84-amino acid peptide, is the major regulator of blood calcium homeostasis. Its mRNA, in addition to encoding the mature peptide, also encodes a "pre" sequence of 25 amino acids and a basic "pro" hexapeptide. To assess which of the subtilisin-like prohormone convertases can process proPTH to PTH we coinfected cells with a vaccinia virus construct expressing human preproPTH and vaccinia virus constructs expressing furin, PC1 or PC2. BSC-40 cells, having a constitutive secretory pathway, and GH4C1 cells, having a regulated secretory pathway, were used. PTH biosynthetic products in cell extracts and media were purified by high performance liquid chromatography, identified by radioimmunoassay, and unambiguously defined as either proPTH or PTH by ion-spray mass spectrometry. In both cell types, furin was the most effective in processing proPTH to PTH. In all cases only PTH was released into the medium. In addition, partially purified furin and PC1 were tested for their ability to appropriately cleave a tridecapeptide spanning the prohormone cleavage site found in proPTH. Here too furin was much more effective at cleaving at the correct site. Northern blot analysis and in situ hybridization showed that furin and preproPTH mRNA are co-expressed in the parathyroid, whereas PC1, PC2, and PC5 are not and PACE4 is expressed only at very low levels. Taken together these studies strongly suggest that furin is the enzyme responsible for the physiological processing of proPTH to PTH.

Amino Acid Sequence↗
PubMed1975

[Parathyroid response to EDTA: effect of the immune heterogeneity of the parathyroid hormone].

The parathyroid response to EDTA infusion was measured in 23 patients with hypo- or hyperparathyroidism using two different antisera, one predominantly anti COOH-terminal (GP 62) and the other predominantly anti NH2-terminal (WC), and was compared with the responses observed in 16 controls for GP 62 and 18 controls for WC. In primary hyperparathyroidism elevated basal PTH values were found more frequently with GP 62 (6 of 10 cases) than with WC (3 of 9 cases). However, WC more frequently exhibited exaggerated responses to EDTA (8 of 9 cases) than GP 62 (7 of 10 cases). In hypoparathyroidism the basal values were not distinguishable from the normals. However, the EDTA test showed absent or low responses in 10 of 11 cases studied with GP 62. Antiserum WC showed normal responses in 4 cases with postoperative hypoparathyroidism, revealing some residual PTH secretion but not response in the 2 cases with idiopathic hypoparathyroidism. Since one of them had a normal response when measured with GP 62, secretion of an immunologically abnormal PTH may be suspected. In chronic renal failure normal responses can be observed despite an abnormal basal PTH level, since it is falsely elevated by the accumulation of COOH-terminal fragments.

Acids↗
PubMed1977

Beta-adrenergic stimulation of cyclic AMP content and parathyroid hormone release from isolated bovine parathyroid cells.

The effects of beta-adrenergic agonists and antagonists on cyclic AMP (cAMP) accumulation and parathyroid hormone (PTH) release from isolated bovine parathyroid cells have been determined. Beta-adrenergic agonists markedly stimulate cAMP production and PTH release with an order of potency (-) isoproterenol greater than (-)epinephrine greater than greater than (-) norepinephrine, suggesting a beta2-type adrenergically mediated process. Both effects are blocked by the beta-blocker propranolol with the strict stereospecificity expected for a beta-adrenergic response. Low calcium concentrations also stimulate cAMP accumulation, but the cyclic nucleotide response under these conditions is only 3% of that obtained with isoproterenol, raising the possibility that factors other than cAMP may control low calcium-mediated PTH release. The release of PTH by low calcium is also not blocked by propranolol, confirming the independence of the response to low ambient calcium from the beta-adrenergic receptor. These studies substantiate further the utility of the isolated parathyroid cell preparation for studying secretagogue-mediated alterations in cyclic nucleotides and hormone secretion. Isolated cells also also make feasible the direct identification of beta-adrenergic receptors in parathyroid cell membranes and whole cells.

Adrenergic beta-Agonists↗
PubMed2001

The evolution of assays for parathyroid hormone.

Recent progress in the assay of parathyroid hormone has revealed that commercially available assays for intact parathyroid hormone also measure additional parathyroid hormone peptides that appear to be truncated at the amino-terminal region and have the elution position on high-performance liquid chromatography of parathyroid hormone 7-84. Specific assays have been developed that measure only the true or 'whole', 84-amino-acid peptide. Such 'whole' parathyroid hormone assays have led to the discovery of new findings that suggest that parathyroid hormone fragments such as parathyroid hormone 7-84, which have hitherto been considered to be biologically inactive, may actually have biologic effects. These data, coupled with the emerging discovery of additional receptors for parathyroid hormone peptides, suggest that parathyroid hormone fragments might have potentially important actions, at least in the setting of renal failure.

Animals↗
PubMed1986

Parathyroid cell surface autoantibodies that inhibit parathyroid hormone secretion from dispersed human parathyroid cells.

Serum autoantibodies directed toward antigenic determinants on the surface of human parathyroid cells (PTAb-CS) have been demonstrated in a subset (8 of 23) of adult patients with idiopathic hypoparathyroidism (IHP). In sera from 3 of 8 patients with PTAb-CS, binding of these autoantibodies to their respective parathyroid cell surface antigen(s) resulted in marked inhibition of parathyroid hormone (PTH) secretion in an in vitro dispersed human parathyroid cell (dPTC) system. In 1 subject evaluated longitudinally, circulating levels of PTAb-CS, and the magnitude of the inhibitory effect on PTH secretion, temporally correlated with the clinical course of the hypoparathyroidism. These findings suggest a causative role for antibodies directed against cell surface antigens in parathyroid dysfunction in some cases of "autoimmune" hypoparathyroidism.

Aged↗