DECREASED PARATHYROID FUNCTION IN HYPERTHYROIDISM: INTERRELATIONSHIPS BETWEEN SERUM PARATHYROID HORMONE, CALCIUM-PHOSPHORUS METABOLISM AND THYROID FUNCTION

1977 ◽  
Vol 84 (3) ◽  
pp. 566-575 ◽  
Author(s):  
Leif Mosekilde ◽  
Merete Sanvig Christensen
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Excretion ◽  
Serum Calcium ◽  
Elevated Serum ◽  
Serum Levels ◽  
Urinary Calcium ◽  
Albumin Concentration ◽  
Parathyroid Function ◽  
Calcium Phosphorus ◽  
Calcium And Phosphorus

ABSTRACT Serum immunoreactive parathyroid hormone (S-iPTH) was measured together with serum and urinary calcium and phosphorus in 45 hyperthyroid patients in order to assess parathyroid function. Serum calcium and phosphorus were increased and positively correlated to the degree of hyperthyroidism. The prevalence of hypercalcaemia was 51.1 % using serum calcium values corrected for individual variations in serum albumin concentration compared to 15.6% using the uncorrected calcium values. S-iPTH was decreased and inversely correlated to serum calcium (corrected). Subnormal levels of S-iPTH were found in 28.9 % of the patients. The urinary excretion of calcium and phosphorus was increased and positively correlated to the degree of hyperthyroidism. The tubular reabsorption of calcium (TRCa %) was decreased, positively correlated to S-iPTH and inversely correlated to serum calcium. Increased mobilisation of bone mineral in hyperthyroidism is suggested mainly to be responsible for the elevated serum levels and increased urinary excretion of calcium and phosphorus and for the decreased parathyroid function.

EFFECT OF ANTITHYROID TREATMENT ON CALCIUM-PHOSPHORUS METABOLISM IN HYPERTHYROIDISM I: CHEMICAL QUANTITIES IN SERUM AND URINE

1978 ◽  
Vol 87 (4) ◽  
pp. 743-750 ◽  
Author(s):  
Leif Mosekilde ◽  
Merete Sanvig Christensen ◽  
Flemming Melsen ◽  
Niels Schwartz Sørensen
Keyword(s):  
Medical Treatment ◽  
Serum Calcium ◽  
Serum Alkaline Phosphatase ◽  
Elevated Serum ◽  
Total Serum ◽  
Albumin Concentration ◽  
Phosphorus Metabolism ◽  
Total Serum Calcium ◽  
Antithyroid Treatment ◽  
Calcium Phosphorus

ABSTRACT The effect of antithyroid treatment on the disturbed calcium-phosphorus metabolism in hyperthyroidism was studied in 16 patients. Elevated serum concentrations and urinary excretions of calcium and phosphorus were almost normalized 4 weeks after the start of medical treatment. Serum immunoreactive parathyroid hormone was decreased in the hyperthyroid state and became normal after medical treatment. Serum alkaline phosphatase levels were elevated throughout the study with an increase to a maximum peak after 8 weeks of antithyroid treatment. Urinary hydroxyproline excretion was initially markedly increased and fell rapidly during therapy. The observed changes suggest decreased bone resorption and increased bone formation with deposition of bone mineral after antithyroid treatment. Alterations in the serum albumin concentration during the investigation period influenced the total serum calcium concentration. Using albumin adjusted serum calcium values no hypocalcaemia was found during medical treatment or after a subsequent subtotal thyroidectomy.

TEMPORAL EFFECTS OF PARATHYROID HORMONE ON SERUM AND URINARY CALCIUM IN THE HAMSTER

1972 ◽  
Vol 55 (2) ◽  
pp. 377-385
Author(s):  
D. M. BIDDULPH ◽  
L. B. GALLIMORE
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Excretion ◽  
Short Duration ◽  
Intravenous Injection ◽  
Serum Calcium ◽  
Hormone Replacement ◽  
Urinary Calcium ◽  
Single Intravenous Injection ◽  
Temporal Effects ◽  
Temporal Aspects

SUMMARY The temporal aspects of calcium addition to blood and renal conservation of calcium were compared in fasted, parathyroidectomized (PTX) hamsters after a single, intravenous injection of parathyroid hormone (PTH). Injection of 110 units of hormone rapidly stabilized urinary excretion of calcium at normal (sham-PTX) levels during a following 3-h period in contrast to the progressive and rapidly occurring hypercalciuria in animals without hormone replacement. Serum calcium concentrations increased rapidly after hormone replacement, rising 3 mg/100 ml within the first 2 h. No further increase was detected after 2 h with a significant decrease in concentration apparent between 3 and 4 h after injection of hormone. Nephrectomy, performed at intervals during the first 2-h period, resulted in significantly increased serum calcium concentrations by 4 h relative to animals with kidneys during the first 2-h period. The magnitude of this increase was directly related to the length of time kidneys were absent during the first 2 h after injection of hormone. These findings indicate that, in the hamster, the effects of PTH on the addition of calcium to blood and conservation of calcium by the kidney occur simultaneously and are both of very short duration (2 to 3 h). These short-lived effects of PTH in this species seem to be due, at least in part, to the participation of a renal influence.

scholarly journals Interactions between calcium and phosphorus in the regulation of the production of fibroblast growth factor 23 in vivo

2013 ◽  
Vol 304 (3) ◽  
pp. E310-E320 ◽  
Author(s):  
Stephen J. Quinn ◽  
Alex R. B. Thomsen ◽  
Jian L. Pang ◽  
Lakshmi Kantham ◽  
Hans Bräuner-Osborne ◽  
...  
Keyword(s):  
Serum Calcium ◽  
Fibroblast Growth Factor 23 ◽  
Threshold Level ◽  
Serum Levels ◽  
Serum Phosphorus ◽  
Dihydroxyvitamin D ◽  
Dietary Phosphorus ◽  
Calcium Phosphorus ◽  
Calcium And Phosphorus

Calcium and phosphorus homeostasis are highly interrelated and share common regulatory hormones, including FGF23. However, little is known about calcium's role in the regulation of FGF23. We sought to investigate the regulatory roles of calcium and phosphorus in FGF23 production using genetic mouse models with targeted inactivation of PTH (PTH KO) or both PTH and the calcium-sensing receptor (CaSR; PTH-CaSR DKO). In wild-type, PTH KO, and PTH-CaSR DKO mice, elevation of either serum calcium or phosphorus by intraperitoneal injection increased serum FGF23 levels. In PTH KO and PTH-CaSR DKO mice, however, increases in serum phosphorus by dietary manipulation were accompanied by severe hypocalcemia, which appeared to blunt stimulation of FGF23 release. Increases in dietary phosphorus in PTH-CaSR DKO mice markedly decreased serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] despite no change in FGF23, suggesting direct regulation of 1,25(OH)2D3 synthesis by serum phosphorus. Calcium-mediated increases in serum FGF23 required a threshold level of serum phosphorus of about 5 mg/dl. Analogously, phosphorus-elicited increases in FGF23 were markedly blunted if serum calcium was less than 8 mg/dl. The best correlation between calcium and phosphorus and serum FGF23 was found between FGF23 and the calcium × phosphorus product. Since calcium stimulated FGF23 production in the PTH-CaSR DKO mice, this effect cannot be mediated by the full-length CaSR. Thus the regulation of FGF23 by both calcium and phosphorus appears to be fundamentally important in coordinating the serum levels of both mineral ions and ensuring that the calcium × phosphorus product remains within a physiological range.

The Effect of Long-Term Mestranol Administration on Calcium and Phosphorus Homeostasis in Oophorectomized Women

1971 ◽  
Vol 41 (3) ◽  
pp. 233-236 ◽  
Author(s):  
J. M. Aitken ◽  
D. McKay Hart ◽  
D. A. Smith
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Hormone Activity ◽  
Phosphorus Excretion ◽  
Calcium And Phosphorus ◽  
Urinary Phosphorus Excretion ◽  
Parathyroid Hormone Activity

1. A group of women who had undergone hysterectomy and bilateral salpingooophorectomy were studied and subsequently given either 20–40 μg of mestranol per day or a placebo for 1 year. 2. The administration of mestranol to these oophorectomized women for 1 year was associated with significant falls in serum calcium and phosphorus concentrations, a fall in urinary calcium excretion and a rise in relative urinary phosphorus excretion. 3. It is suggested that these results are consistent with an increase in sensitivity to calcitonin and that the relative hyperphosphaturia reflects a compensatory rise in parathyroid hormone activity.

Metabolism of 1,25-dihydroxyvitamin D3

1984 ◽  
Vol 64 (2) ◽  
pp. 478-504 ◽  
Author(s):  
R. Kumar
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Biliary Excretion ◽  
Extracellular Fluid ◽  
Serum Phosphorus ◽  
General Terms ◽  
Wide Range ◽  
Calcium Phosphorus ◽  
Calcium And Phosphorus ◽  
Low Serum

Synthesis of 1,25(OH)2D3 is controlled by numerous factors. The major ones, however, are the circulating amounts of parathyroid hormone (the secretion of which is stimulated by low serum calcium), serum or extracellular fluid phosphorus concentrations, circulating levels of 1,25(OH)2D3 itself, and perhaps serum calcium directly. Many of the other factors noted have effects in vitro only or effects that are observed inconsistently or in one species only. Thus, in low-calcium states, 1,25(OH)2D3 synthesis increases because of increased parathyroid hormone activity. Parathyroid hormone may stimulate 1,25(OH)2D3 synthesis directly or via alterations (a decrease) in serum phosphorus or both. Low serum phosphorus will stimulate 1,25(OH)2D3 synthesis independent of parathyroid hormone levels. Low serum calcium may directly stimulate 25(OH)D3 1 alpha-hydroxylase activity independently of parathyroid hormone. In general terms the vitamin D-endocrine system tends to correct abnormalities in calcium and phosphorus homeostasis. The further metabolism of 1,25(OH)2D3 to other metabolites appears to be mainly a degradative or excretory process. Currently there is no evidence that 1,25(OH)2D3 must itself be altered to other metabolites prior to inducing intestinal calcium transport or bone mobilization. The processes involved in the excretion of 1,25(OH)2D3, such as side-chain oxidation and biliary excretion, are not regulated by serum calcium, phosphorus, or 1,25(OH)2D3 levels. The biliary excretion pathway is also unsaturable over a very wide range and not regulated by calcium, phosphorus, or vitamin D3. Therefore these processes, which account for a large part of the metabolism of 1,25(OH)2D3, are largely unregulated by factors that control the synthesis of 1,25(OH)2D3 and regulate the formation of other calcium-controlling hormones. Other processes involved in the metabolism of 1,25(OH)2D3, such as 24-hydroxylation and 26-hydroxylation, occur in normocalcemic and normophosphatemic states. 24-Hydroxylation is also induced by 1,25(OH)2D3, which benefits the organism, because excessive 1,25(OH)2D3 in various tissues can be altered to a less active metabolite, 1,24,25(OH)3D3. Although there is still no evidence concerning the regulation of C-24 oxidation by dietary calcium and phosphorus levels, the fact that this process is induced by 1,25(OH)2D3 suggests that the metabolic pathway functions in much the same manner as the 24-hydroxylation pathway. The formation of 1,25(OH)2D3-26,23-lactone occurs in normocalcemic states and in situations in which 1,25(OH)2D3 has been administered.

scholarly journals Serum Sulphate Levels in Hemodialysis Patients

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Ibrahim Yildirim ◽  
Ender Hur ◽  
Kemal Magden ◽  
Sevil İlikhan ◽  
Hüseyin Engin ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Serum Levels ◽  
Hemodialysis Patients ◽  
Free Form ◽  
Control Group ◽  
Dialysis Patients ◽  
Sulphur Compounds ◽  
Adequate Knowledge ◽  
Inorganic Sulphate ◽  
Calcium Phosphorus

Objective. Sulphur, similar to phosphorus, is easily attached to organic compounds. The inadequate elimination of sulphate may cause high sulphate concentrations in hemodialysis (HD) patients because sulphate is low in free form in plasma. Although we are well aware of the accumulation of phosphorus in chronic dialysis patients, we do not have an adequate knowledge database about the sulphur compounds. This study was designed to determine the level of sulphate in hemodialysis patients. Materials and Methods. Ninety-four prevalent HD patients and 33 patients without renal failure were included in the study. The serum inorganic sulphate levels were measured by turbidimetric technique. Moreover, the serum level of urea, creatinine, albumin, calcium, phosphorus, and parathyroid hormone concentrations was simultaneously recorded. Results. Mean levels of plasma sulphate were significantly higher (0.56 ± 0.17 mM vs 0.31 ± 0.13 mM, p<0.001) in HD patients. Serum sulphate level correlated with patient’s age, serum albumin, serum BUN and creatinine, and serum phosphorus level in HD patients. Serum sulphate levels were not associated with serum parathyroid hormone levels. Conclusion. Serum sulphate levels were approximately twofold higher in HD patients than in the normal control group. Inorganic sulphate does not seem to accumulate in long-term dialysis patients, and mild increased serum levels of sulphate has no poor clinical outcome in these patients.

scholarly journals Safety and Efficacy of 5 Years of Treatment With Recombinant Human Parathyroid Hormone in Adults With Hypoparathyroidism

2019 ◽  
Vol 104 (11) ◽  
pp. 5136-5147 ◽  
Author(s):  
Michael Mannstadt ◽  
Bart L Clarke ◽  
John P Bilezikian ◽  
Henry Bone ◽  
Douglas Denham ◽  
...  
Keyword(s):  
Serum Calcium ◽  
Urinary Calcium ◽  
Open Label ◽  
Oral Calcium ◽  
Efficacy Outcome ◽  
Open Label Extension ◽  
Calcium Phosphorus ◽  
Safety Parameters ◽  
Turnover Markers

Abstract Context Conventional hypoparathyroidism treatment with oral calcium and active vitamin D is aimed at correcting hypocalcemia but does not address other physiologic defects caused by PTH deficiency. Objective To evaluate long-term safety and tolerability of recombinant human PTH (1-84) [rhPTH(1-84)]. Design Open-label extension study; 5-year interim analysis. Setting 12 US centers. Patients Adults (N = 49) with chronic hypoparathyroidism. Intervention(s) rhPTH(1-84) 25 or 50 µg/d initially, with 25-µg adjustments permitted to a 100 µg/d maximum. Main Outcome Measure(s) Safety parameters; composite efficacy outcome was the proportion of patients with ≥50% reduction in oral calcium (or ≤500 mg/d) and calcitriol (or ≤0.25 µg/d) doses, and albumin-corrected serum calcium normalized or maintained compared with baseline, not exceeding upper limit of normal. Results Forty patients completed 60 months of treatment. Mean albumin-corrected serum calcium levels remained between 8.2 and 8.7 mg/dL. Between baseline and month 60, levels ± SD of urinary calcium, serum phosphorus, and calcium-phosphorus product decreased by 101.2 ± 236.24 mg/24 hours, 1.0 ± 0.78 mg/dL, and 8.5 ± 8.29 mg2/dL2, respectively. Serum creatinine level and estimated glomerular filtration rate were unchanged. Treatment-emergent adverse events (AEs) were reported in 48 patients (98.0%; hypocalcemia, 36.7%; muscle spasms, 32.7%; paresthesia, 30.6%; sinusitis, 30.6%; nausea, 30.6%) and serious AEs in 13 (26.5%). At month 60, 28 patients (70.0%) achieved the composite efficacy outcome. Bone turnover markers increased, peaked at ∼12 months, and then declined to values that remained above baseline. Conclusion Treatment with rhPTH(1-84) for 5 years demonstrated a safety profile consistent with previous studies and improved key biochemical parameters.

scholarly journals Hipocalcemia Crónica por Anticorpos Anti-Recetor do Cálcio

2014 ◽  
Vol 27 (3) ◽  
pp. 399
Author(s):  
Pedro Marques ◽  
Rita Santos ◽  
Branca Cavaco ◽  
Valeriano Leite
Keyword(s):  
Parathyroid Hormone ◽  
Genetic Disorder ◽  
Neck Surgery ◽  
Urinary Calcium ◽  
Clinical Report ◽  
Calcium Sensing Receptor ◽  
Casr Gene ◽  
Calcium Sensing ◽  
Calcium Phosphorus ◽  
Receptor Antibodies

<strong>Introduction:</strong> Hypoparathyroidism is an entity associated with hypocalcemia, more frequently a consequence of neck surgery. An autoimmune etiology is rare and its diagnosis difficult to establish.<br /><strong>Clinical report:</strong> 52 year-old woman, with irrelevant past medical history and no significant familial conditions, referred because of hypocalcemia and basal ganglia calcifications, detected in the course of investigation of myalgias. Besides hypocalcemia (4.6 mg/ dL), hyperphosphatemia (8.7 mg/dL), undetectable parathyroid hormone and low urinary calcium, phosphorus and magnesium were present. Molecular analysis of CaSR gene excluded germinal mutations. Anti-calcium sensing receptor antibodies (anti-CaSR) were present. The patient is asymptomatic and normocalcemic under treatment with calcium and vitamin D.<br /><strong>Discussion:</strong> Although rare, hypocalcemia due to anti-CaSR hypoparathyroidism must be considered in the absence of previous neck surgery, hypocalcemic drugs, familial history or phenotype suggesting a genetic disorder. Low or undetectable parathyroid hormone excludes pseudohypoparathyroidism and anti-CaSR positivity establishes the diagnosis.<br /><strong>Keywords:</strong> Hypocalcemia; Hypoparathyroidism; Autoantibodies; Receptors, Calcium-Sensing.

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