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PubMed1989

Serum calcitriol and parathyroid hormone levels following prolonged infusion of calcitriol in vitamin D replete and depleted rabbits.

The objectives of this study are (1) to determine if serum calcitriol levels resulting from calcitriol infusion by subcutaneously implanted osmotic pumps are in proportion to dose, (2) to determine if such serum levels remain steady during the "pump-life" and (3) to determine if these increased calcitriol levels have an effect on serum parathyroid hormone (PTH) levels. A general objective of the study is to define a model whereby agents (calcitriol, and parathyroid hormone) suspected of enhancing absorption of metals other than calcium from the gastrointestinal tract could be evaluated individually by the levels of these hormones present in serum at a series of intervals during calcitriol infusion by osmotic pump. Calcitriol was infused into rabbits by subcutaneously implanted osmotic pumps at 3 different dosages (30, 60, and 100 IU/day) for 7 days and one dose (60 IU/day) for a 28 day period. The serum calcitriol levels initially rose markedly in all experimental rabbits in proportion to infused dosage and peaked at 3 days. The quantitative relationship between infused calcitriol and serum calcitriol at 3-5 days showed a correlation coefficient of 0.977 (P less than 0.005) for rabbits receiving the 7 day pumps with the 3 different dosages. There was subsequent decline of serum calcitriol which continued for the remainder of the pump-life, suggesting acceleration of degradation mechanisms. There was a sharp reduction in serum parathyroid hormone (PTH) levels 3-5 days after starting the calcitriol infusion, which was interpreted to result from direct suppression of PTH synthesis by calcitriol and/or the feedback effect of enhanced intestinal calcium absorption. Rabbits which had been depleted of vitamin D prior to implantation of the 28 day osmotic pumps showed a similar pattern of serum calcitriol and PTH. Multiple analyses within a single rabbit showed a reciprocal relationship between the serum calcitriol and PTH during the 28 days. There was a statistically significant negative correlation between these parameters (r = 0.635, P less than 0.05). The data indicate that despite a constant rate of infusion of calcitriol by osmotic pump, the levels of serum calcitriol and parathyroid hormone do not remain constant, but rather undergo marked changes. These findings demonstrate the necessity of monitoring blood levels, even in studies in which animals receive a constant infusion of calcitriol.

Animals↗
PubMed1986

Parathyrin (parathyroid hormone): metabolism and methods for assay.

Parathyrin (parathyroid hormone) radioimmunoassay is a commonly ordered endocrine assay. I discuss here of the metabolism of the hormone and the effect information on this metabolism has had on the development of radioimmunoassays for parathyrin. Although radioimmunoassay is the most widely accepted technique for the routine assay for parathyrin, "high-performance" liquid chromatography, cytochemical bioassay, and homologous bioassay have also been developed for this analyte. Accordingly, I briefly review the clinical utility of these assays in terms of their ability to assess the functional activity of the parathyroid gland.

Animals↗
PubMed1975

The metabolism of labeled parathyroid hormone. VII Attempts to modify hormone deposition.

Using a 125I-labeled parathyroid hormone with apparently full biological activity, a series of experiments was performed on rats to determine the effects of several physiological parameters on the deposition and metabolism of the hormone in the target tissues, liver, kidney and bone. Among the variables studied were: systemic phosphate levels, systemic calcium levels, calcitonin administration, pregnancy, and dosage (at low levels). Some small variations in deposition and tissue metabolism of the hormone were observed but the invariance of the pattern of deposition and the rapid automatic destruction by target tissues was most impressive.

Animals↗
PubMed1991

A five year audit of the role of parathyroid hormone assays and thallium-technetium isotope subtraction scanning in the preoperative investigation of primary hyperparathyroidism.

An audit has been performed of the value of parathyroid hormone assays and thallium-technetium isotope scanning in the pre-operative investigation of 67 hypercalcaemic patients referred for surgery over a 5 year period. Parathyroid hormone assay by region-specific technique was found to have a diagnostic sensitivity of 75% (n = 52) whilst the more recent assay for the intact molecule was 97% sensitive (n = 34). Thallium-technetium isotope scanning was only 64% sensitive overall (n = 59), due in part to the small size of adenomata now being referred for surgery. This study confirms the role of the intact parathyroid hormone assay but questions that of thallium-technetium isotope scanning in standard protocols of investigation for hypercalcaemia.

Adult↗
PubMed1976

A simplified assessment of response to parathyroid hormone in hypoparathyroid patients.

Hightly purified bovine parathyroid hormone (B.P.T.H) was given by injection and/or infusion to six normal volunteers and to patients with surgical hypoparathyroidism (five cases), idiopathic hyparathyroidism (five cases), or poeudo-hypoparathyroidism (six cases). Infusion and injection of B.P.T.H. produced very similar patterns of response in plasma adenosine 3' 5' cyclic monophosphate (cyclic A.M.P.) In all six normal volunteers and in the patients with surgical (five cases) or idiopathic (four cases) hypoparathyroidism who had injections of B.P.T.H., plasma-cA.M.P. had risen significantly within 5 min and the peak response was genereally observed 10 min after injection of hormone. In the five pseudohypoparathyroid patients who received injections of B.P.T.H., plasma-c?A.M.P. concentration increased only slightly or not at all after the hormone was administered. Unlike the traditional test for the investigation of hypocalcaemia, the test described here does not require collections of urine samples.

Adolescent↗
PubMedDate not supplied

Serum magnesium concentration is an independent predictor of parathyroid hormone levels in peritoneal dialysis patients.

BACKGROUND: Parathyroid hormone (PTH) is a cardinal factor in the pathogenesis of bone disease in the dialysis population. The spectrum of renal osteodystrophy has been reported to have changed during the past years, and adynamic bone disease has emerged as the most common bone disorder in these patients. Continuous ambulatory peritoneal dialysis (CAPD) is considered a risk factor for the development of this condition, and furthermore, the adynamic bone lesion is associated with a state of relative hypoparathyroidism (hypo-PTH). Calcium, vitamin D, and phosphorus play a key role in the control of parathyroid gland function in uremic patients. However, magnesium may also be able to modulate PTH secretion in a way similar to calcium. OBJECTIVE: The aims of this study were (1) to analyze the serum Mg concentration in a large group of CAPD patients, (2) to study the relationship between serum Mg and PTH levels, and (3) to investigate whether this relationship is independent of other factors, such as calcium, phosphorus, and calcitriol, that regulate parathyroid function. PATIENTS AND METHODS: We studied 51 stable patients, aged 23-77 years, under maintenance CAPD for more than 6 months (range 8-48 months). Calcium carbonate was used as a phosphate binder in all patients, and 9 subjects also received aluminum hydroxide. No patient had been previously treated with vitamin D. Biochemical parameters were prospectively evaluated over 6 months, and the mean values were computed. RESULTS: The mean serum Mg was 1.08 +/- 0.19 mmol/L, and hypermagnesemia, defined as a Mg level higher than 1.01 mmol/L, was found in 30 patients (59%). Thirty-one subjects (60%) had an intact PTH (iPTH) level lower than 120 pg/mL and were diagnosed as having relative hypo-PTH. Except for the values of iPTH and alkaline phosphatase, the only difference between the two groups was the serum Mg concentration, which was significantly higher in patients with hypo-PTH (1.16 +/- 0.15 mmol/L vs 0.91 +/- 0.14 mmol/L; p< 0.001). Furthermore, iPTH levels were lower in patients with hypermagnesemia than in subjects with normal serum Mg (69 +/- 49 pg/mL vs 190 +/- 89 pg/mL, p < 0.001). There was a significant correlation between serum Mg and PTH levels (r= -0.70, p< 0.01). After controlling for the effect of other variables by partial correlation analysis, a significant positive association between P and PTH (r= 0.25, p < 0.05), and a negative relationship between Mg and PTH (r= -0.57, p < 0.001) were evident. A forward stepwise multiple regression analysis showed that only P and Mg predicted PTH values (multiple r = 0.59, p < 0.001). CONCLUSIONS: Hypermagnesemia and hypoparathyroidism are frequent in CAPD patients. There is a significant inverse relationship between serum Mg concentration and iPTH levels. Furthermore, this association is independent of the most important factors regulating parathyroid gland function (calcium, phosphorus, and calcitriol). These results suggest that hypermagnesemia may have a suppressive effect on PTH synthesis and/or secretion. Therefore, elevated serum Mg levels may play a role in the pathogenesis of adynamic bone disease.

Adult↗
PubMed2006

Serum markers of bone turnover in dialyzed patients grouped by level of intact parathyroid hormone.

We evaluated serum markers of bone turnover (BT) in patients suspected to have low bone turnover (LBT) given their serum level of intact parathyroid hormone (iPTH). Studies were carried out in 30 dialyzed patients. In 9 patients, iPTH was below 100 pg/mL (LBT group), and in 21, it was above 100 pg/mL (non-LBT group). Other measured laboratory parameters included serum concentrations of cyclase inactivating parathyroid hormone (CAP), osteoprotegerin (OPG), OPG ligand (OPGL), inorganic phosphates, total calcium, creatinine, urea, serum alkaline phosphatase (ALP) activity, and blood pH. The LBT group showed significantly lower levels of iPTH (39.0 +/- 30.7 pg/mL), CAP (23.2 +/- 16.9 pg/mL), cyclase inactive parathyroid hormone (CIP: 15.8 +/- 15.0 pg/mL), and total ALP (83.9 +/- 26.2 IU/L) than did the non-LBT group (393 +/- 304 pg/mL, 268 +/- 216 pg/mL, 126 +/- 96 pg/mL, and 202 +/- 167 IU/L respectively). We observed no significant differences between the groups in the other examined parameters. When results were adjusted for sex, age, and dialysis modality and duration, differences remained significant only for iPTH and CIP. Our data indicate that a serum CIP concentration below 25 pg/mL has a significance similar to that of an iPTH concentration below 100 pg/mL in determining which dialyzed patients likely have LBT.

Biomarkers↗
PubMed1983

The role of parathyroid hormone and calcitonin in magnesium absorption in the rat small intestine.

We studied duodenal and ileal magnesium (Mg) absorption in intact, parathyroidectomized (PTX), thyroid-(TX) and thyroparathyroidectomized (TPTX) rats with iodine hormones replaced, and, additionally, in PTX rats receiving bovine parathyroid hormone 1-34 and 1,25-dihydroxyvitamin D3, respectively. Mg absorption was reduced after PTX and TPTX in the duodenum, but not in the ileum, whereas TX had no influence on duodenal or ileal Mg absorption. Both bovine parathyroid hormone 1-34 and 1,25-dihydroxyvitamin D3 increased Mg absorption in the duodenum and the ileum in PTX rats.

Animals↗
PubMed1986

Intact parathyroid hormone assay offers increased sensitivity over C-terminal assays in the study of parathyroid graft function.

Serum parathyroid hormone (PTH) levels in 6 patients who had received parathyroid tissue autografts were studied. Samples were taken from graft and non-graft arms both pre- and post-dialysis. Each sample was analysed using two PTH assays, one measuring C-terminal PTH and the other measuring the intact PTH molecule. For both pre- and post-dialysis samples an appreciably greater difference was seen between the graft and non-graft arms using the intact assay. A patient with suspected ectopic PTH production showed a very much reduced differential between the two sampling sites with both assays. We suggest that the intact PTH assay is of greater clinical utility in the localisation of ectopic glands and monitoring of graft function than the commonly used C-terminal assays.

Forearm↗
PubMed1976

Effect of diphosphonates on adenosine 3':5'-cyclic monophosphate in mouse calvaria after stimulation by parathyroid hormone in vitro.

1. The diphosphonates, disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) and disodium dichloromethylene diphosphonate (Cl2MDP), inhibit bone resorption in animals and in explanted bone in tissue culture. The possibility that these effects might be due to inhibition of skeletal adenylate cyclase has been studied. 2. EHDP and Cl2MDP, added for 30 min to the incubation medium at concentrations known to inhibit bone resorption, had no effect on basal content of adenosine 3':5'-cyclic monophosphate (cyclic AMP) of mouse calvaria incubated in vitro, nor did they inhibit the rise in cyclic AMP induced by bovine parathyroid hormone. 3. Pretreatment of mice for 3 days with Cl2MDP also had no effect on cyclic AMP under basal conditions or after incubation of explanted calvaria with parathyroid hormone in vitro. EHDP under similar conditions slightly inhibited the increase induced by parathyroid hormone but had no effect on basal concentrations of cyclic AMP. 4. It is suggested that the inhibition of adenylate cyclase is not an essential feature of the reduction of bone resorption by diphosphonates, which may act by direct inhibitory effects on the dissolution of hydroxyapatite and perhaps by other unidentified effects on bone cells. Key words: adenosine 3':5'-cyclic monophosphate, bone, dichloromethylene diphosphonate, diphosphonates, ethane-1-hydroxy-1,1-diphosphonate, parathyroid hormone.

Animals↗
PubMed1997

Parathyroid hormone (1-34)-mediated interleukin-6 induction.

Parathyroid hormone (PTH) functions in part by regulating osteoblast cytokine expression. We recently demonstrated that PTH induced a rapid and transient increase in interleukin-6 (IL-6) mRNA expression in rat bones in vivo. To determine the molecular basis of this effect, we analyzed the human IL-6 promoter fused (-1,179 to +9) with the chloramphenicol acetyltransferase (CAT) reporter gene in stable transfections into human osteoblast-like osteosarcoma SaOS-2 cells. We compared the effects of PTH on IL-6 expression with adenylate cyclase activator forskolin, PKC activator phorbol 12-myristate 13-acetate (PMA), calcium ionophore A23187, interleukin-1 alpha (IL-1 alpha), prostaglandin E-2 (PGE-2), RS-66271 (a parathyroid hormone-related peptide analog), and platelet-derived growth factor-BB (PDGF-BB). Analyses of cell clones showed that IL-6 promoter expression was extremely low in the unstimulated state. Exposure to PTH (0.001-100 nM) for 12 h stimulated CAT expression in a dose-dependent manner (200-500% of control). Treatment with IL-1 alpha was more potent than PTH in inducing transcription of the IL-6 promoter (900-1,000%). Activation of the cAMP-PKA pathway by treatment with forskolin induced a comparable level of induction with PTH. Together, the effects of PTH and forskolin were additive. RS-66271, previously shown to have PTH-like effects, induced a comparable level of IL-6 promoter expression. When examined together, PTH+RS-66271 effects were comparable to PTH effects alone. Exposure to PGE-2, PMA, PDGF-BB, or A23187 for 12 h did not significantly alter IL-6 promoter expression. These results demonstrate PTH, forskolin, the PTHrP analog RS-66271, and IL-1 alpha stimulate IL-6 expression by stimulating gene transcription. The response to forskolin suggests that the messenger system mediated by PKA is sufficient to induce IL-6 expression.

Becaplermin↗
PubMed1976

Effect of parathyroid hormone and cyclic AMP on protein phosphorylation in rabbit kidney cortex.

Suspensions of renal cortical tubules were incubated with 33Pi and exposed to parathyroid hormone (40 mlg/ml) or 1 mM dibutyryl cyclic AMP. In other experiments homogenates of renal cortex were assayed for protein kinase and phosphoprotein phosphatase activity using [gamma-32P]ATP with or without 5 mM cyclic AMP. Proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and phosphorylation of proteins measured by liquid scintillation counting of gel slices. The pattern of protein phosphorylation was similar in control tissue from both tubule suspensions and homogenates. In intact tubules, parathyroid hormone stimulated the phosphorylation of four proteins with molecular weights of approx. 150 000, 125 000, 100 000 and 50 000 by 28%, 24%, 13%, and 20%, respectively. Results with dibutyryl cyclic AMP were comparable but more variable. Stimulation of phosphorylation by cyclic AMP in homogenates was more generalized with the major effect on a 50 000 dalton protein (50% stimulation). No effect of cyclic AMP on dephosphorylation of proteins was observed. The results are interpreted as indicating that increased phosphorylation of cell proteins is part of the cyclic AMP-mediated response of the renal cortex to parathyroid hormone.

Animals↗
PubMed1987

Studies of the rapid effects of parathyroid hormone and prostaglandins on 45Ca uptake into chick and rat bone in vivo.

The rapid effects of parathyroid hormones and a variety of prostaglandins on net uptake of 45Ca into the skeleton have been investigated in chicks and, in a limited parallel study, in immature rats. Intravenous injection of bovine (b) parathyroid hormone(1-34) (bPTH(1-34)) or 16,16-dimethyl prostaglandin E2 (16,16-dimethyl PGE2) in a 45Ca-labelled vehicle, combined with subsequent microwave fixation of tissue isotope levels, resulted in rapid (3-15 min) net inhibition of 45Ca uptake into endochondral bone (femur) in chicks (12 days old) and rats (4 weeks old). Use of 125I-labelled albumin and [14C]mannitol indicated that these responses were not a reflection of gross changes in tissue vascular or extracellular space. In rats, bPTH(1-84) also caused significant net inhibition of 45Ca uptake into femur at 10 min. Both bPTH(1-34) and 16,16-dimethyl PGE2 produced generally smaller decreases in 45Ca uptake into chick dermal bone (calvarium) at 3-15 min. In rat calvarium, however, these agents stimulated net uptake of 45Ca at these times. When microwave fixation was omitted, inhibitory responses were reduced or disappeared, while the stimulatory response in rat calvarium was enhanced. Responses to natural prostaglandins (PGE1, PGE2, PGF2 alpha and PGI2) in chicks at 3 min were similar but less marked than those to 16,16-dimethyl PGE2; 45Ca uptake into femur and, to a lesser extent in calvarium, being inhibited. In rats, PGE1, PGE2 and PGF2 alpha showed a tendency to decrease 45Ca uptake into femur while PGE1 and PGE2 both increased 45Ca uptake into calvarium.

Animals↗
PubMed2001

Effect of aluminium load on parathyroid hormone synthesis.

BACKGROUND: Aluminium overload leads to parathyroid hormone (PTH) suppression. However, it is unclear whether a decrease in synthesis or release of the hormone is mainly involved. The aim of this study was to assess the effect of an acute administration of aluminium on PTH synthesis and release in rats with chronic renal failure and secondary hyperparathyroidism. METHODS: The study was performed using 100 adult male Wistar rats (body weight 443+/-54 g). 7/8 nephrectomy was performed and the rats were maintained on a high dietary phosphorous intake. Five weeks after surgery, the rats were randomly divided into two groups, one loaded with aluminium (AlCl3) and the other given placebo. Aluminium or placebo were administered i.p. for two consecutive days. The placebo group received saline at the same pH as the aluminium solution. After 2 weeks, serum calcium, phosphorous, creatinine, PTH, and aluminium were measured. The parathyroid glands were removed and PTH messenger RNA (mRNA) was measured by northern blot. Intact PTH was measured by IRMA (Rat PTH, Nichols Institute). RESULTS: No differences in serum PTH levels were found between the two groups after 5 weeks of renal failure. At the end of the study the rats given aluminium had higher aluminium levels than the placebo group and lower PTH levels. No significant differences were found for calcium, phosphorous, renal function, or body weight. PTH mRNA expression was lower in the aluminium group than in the placebo group. CONCLUSION: The administration of aluminium in rats with chronic renal failure resulted in reductions in serum PTH and PTH mRNA. Thus far, previous studies had demonstrated that aluminium suppressed PTH release. The present findings suggest that PTH synthesis is also reduced.

Aluminum↗
PubMedDate not supplied

The evolution of assays for parathyroid hormone.

Reliable measurements of the concentration of parathyroid hormone (PTH) in serum or plasma are crucial for the effective clinical management of patients with chronic kidney disease (CKD). New PTH assays that increase the specificity of such measurements are now available and are widely utilized. The current review summarizes key technical developments in the evolution of PTH assays. We also discuss the diagnostic value of various methods for measuring PTH in serum or plasma for the assessment of patients with renal bone disease.

Chronic Kidney Disease-Mineral and Bone Disorder↗
PubMed1990

[Parathyroid hormone stimulation of nerve cell calcium conduction].

Parathyroid hormone (PTH) has been studied for its effect on the voltage-sensitive calcium channels in voltage-clamp experiments on intracellularly perfused snail neurons. A two-stage action of the hormone on the calcium current (Ica) was shown. An initial stage was a short-term one and consisted in an increase of ICa by 7-10%. The second stage developed slowly for 60-70 min, ICa increased twice. The exogenous cAMP and cGMP did not produce such an effect as PTH did. It is suggested that the phosphoinositide pathway mediates the PTH effect.

Animals↗
PubMed1977

Effect of parathyroid hormone on urinary acidification.

The effect of parathyroid hormone (PTH) administration on urinary acidification was studied in intact and thyroparathyroidectomized dogs. PTH administration resulted in a significant increase in urine pH and HCO3 excretion. In dogs with maximally acid urine caused by Na2SO4 infusion PTH administration also led to a significant increase in urine pH and to a decrease in ammonium excretion. To examine the effect of PTH on H+ secretion in the distal nephron we measured the urine-blood (U-B) PCO2 gradient in dogs with maximally alkaline urine (urine pH greater than 7.8) before and after PTH administration. After infusion of the hormone, HCO3 excretion increased significantly but the U-B PCO2 gradient remained unchanged. The effects of PTH infusion on urinary acidification in animals with distal renal tubular acidosis caused by LiCl administration were also studied. PTH administration to these dogs increased HCO3 excretion to the same level seen in normal dogs. These data suggest that PTH does not inhibit distal H+ secretion but increases HCO3 excretion by depressing proximal HCO3 reabsorption.

Acid-Base Equilibrium↗