Disorders of plasma calcium

Author(s):  
Aron Chakera ◽  
William G. Herrington ◽  
Christopher A. O’Callaghant

The extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) and vitamin D (1,25-dihydroxyvitamin D) on bone, kidney, and intestines. Abnormalities in these homeostatic mechanisms may lead to increased or decreased serum calcium concentrations, resulting in hypercalcaemia or hypocalcaemia, respectively. Hypercalcaemic disorders may be further divided into those associated with a high/high-normal serum PTH level, and those associated with a low serum PTH concentration. Hypocalcaemia occurs when abnormalities in the physiological regulation of PTH and vitamin D results in calcium levels lower than the desired normal range. Failure of release of calcium from bone, and increased binding of calcium in the circulation, are other factors causing hypocalcaemia. This chapter discusses hypercalcaemia and hypocalcaemia, exploring definitions of the diseases, their etiologies, typical and uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.

Author(s):  
Rajesh V. Thakker

Extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) on kidney and bone (Fig. 4.5.1). The intact peptide is secreted by the parathyroid glands at a rate that is appropriate to and dependent upon the prevailing extracellular calcium ion concentration. The causes of hypocalcaemia (Box 4.5.1) can be classified according to whether serum PTH concentrations are low (that is hypoparathyroid disorders) or high (that is disorders associated with secondary hyperparathyroidism) (1–6). The most common causes of hypocalcaemia are hypoparathyroidism, a deficiency or abnormal metabolism of vitamin D, acute or chronic renal failure, and hypomagnesaemia. This chapter will initially review the clinical features and management of hypocalcaemia, and then discuss the specific hypocalcaemic disorders.


Author(s):  
Zohreh Firouzi ◽  
Saeideh Mahdizadeh Sajjadieh ◽  
Saeideh Mahdizadeh Sajjadieh ◽  
Maryam Mousavi ◽  
Zahra Erfanian ◽  
...  

Background: Previous studies have indicated that parathyroid hormone (PTH) has been linked to post-myocardial infarction (MI) development. The aim of this cross-sectional study was to evaluate the relationship between PTH level and heart failure due to post infarction remodeling during the first 72 hours of hospitalization. Methods: Seventy patients with a diagnosis of acute MI (age ≥18 years, 22 females and 48 males) were enrolled. Patients were admitted to the Imam Raza Educational, Research and Treatment Center, Mashhad University of Medical Sciences, Iran between July 2014 to September 2015. We measured PTH and vitamin D level. Blood samples were taken after 24 hours and 72 hours. Results: During the first 72 hours, the PTH level significantly increased in patients with Post-MI heart failure. 68% of the subjects had an inappropriate vitamin D level at the time of admission. Mean levels of vitamin D and PTH increased compared with the baselines (95% CI, 0.15 to 10.03, P: 0.044), (95% CI, 6.5 to 24.8, P:0.001) respectively. Conclusion: Acute elevations of serum PTH levels increased early remodeling heart failure after MI. Serum vitamin D status was independent of high serum PTH level. Based on the current evidence, PTH excess may be a risk factor for heart failure, so early treatment and omitting risk factors are the most effective strategies for the patients with acute myocardial infarction. J Pharm Care 2020; 8(1): 11-15.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Maria Bucova ◽  
Magda Suchankova ◽  
Elena Tibenska ◽  
Eva Tedlova ◽  
Juraj Demian ◽  
...  

TREM-1 and TREM-2 molecules are members of the TREM transmembrane glycoproteins. In our previous study we identified increased expressions of TREM-1 and TREM-2 receptors in pulmonary sarcoidosis (PS). Only a few studies concerning the association between vitamin D and TREM receptor expression can be found. The aim of our current study was to determine the association between the levels of an inactive form of 25(OH)D vitamin and TREM-1 and TREM-2 receptor expressions. We have detected low levels of 25(OH)D vitamin in 79% of PS patients. Only 21% of patients had normal serum level of 25(OH)D vitamin with values clustered within the low-normal range. The most striking findings were the increased TREM-2 expressions on myeloid cells surfaces in BALF of PS patients with normal 25(OH)D vitamin serum levels compared with those with its decreased levels. The total number of TREM-2 positive cells was 5.7 times higher and the percentage of TREM-2 positive cells was also significantly increased in BALF of PS patients with normal compared to PS patients with low 25(OH)D vitamin serum levels. A significant correlation between total TREM-2 expression and vitamin D levels has been detected too. However, we have not detected similar differences in TREM-1expression and 25(OH)D vitamin serum levels.


PEDIATRICS ◽  
1981 ◽  
Vol 68 (1) ◽  
pp. 109-112
Author(s):  
Dagfinn Aarskog ◽  
Lage Aksnes ◽  
Trond Markestad

Indices of vitamin D metabolism were studied before and after infusion of bovine parathyroid hormone extract in three children with osteopetrosis. Basal serum concentrations of calcium, alkaline phosphatase, and 25-hydroxyvitamin D tended to be low. Serum immunoreactive parathyroid hormone levels were in the upper normal range in two patients. A marked increase in urinary cyclic adenosine 3': 5'-monophosphate(cAMP) in all patients was solely due to an increase in the nephrogenous cAMP. The basal concentration of 1,25-dihydroxyvitamin D was clearly more than the upper limit of normal range in all three patients and increased after parathyroid extract infusion in one patient. The basal serum levels of 24,25-dihydroxyvitamin D were within normal limits and tended to decrease after parathyroid extract infusion in two of the patients. Parathyroid hormone and 1,25-dihydroxyvitamin D act in concert to increase calcium resorption from bone, and the increased serum levels of both these factors may reflect lack, or unresponsiveness, of target cells in bone.


Author(s):  
Joana de Brito Chagas ◽  
Carolina Cordinhã ◽  
Carmen do Carmo ◽  
Cristina Alves ◽  
Karen E. Heath ◽  
...  

AbstractVitamin D-dependent type 1A rickets (VDDR-1A) is a rare autosomal recessive disease due to the inability to convert 25-hydroxyvitamin D [25(OH)D] to the active form 1.25-dihydroxyvitamin D [1.25(OH)2D] by the enzyme 25(OH)D-1α-hydroxylase leading to low or low-normal serum levels of [1.25(OH)2D].We report two sisters with rickets in whom the diagnosis of VDDR-1A was a challenge. They had normal 1.25(OH)2D levels, which are unusual with this condition but may be explained by the identified genotype. Both have compound heterozygous for two, most likely, hypomorphic CYP27B1 alleles: the novel p.(Arg117Gly) variant, and p.(Ala129Thr), which are present in 0.43% of the African population.This report illustrates the variability of clinical, laboratory, and radiological presentation between two sisters with the same genotype, during phases of faster or slower growth. Genetic testing was crucial for establishing the diagnosis that optimized the management and genetic counseling.


2009 ◽  
Vol 297 (5) ◽  
pp. F1192-F1198 ◽  
Author(s):  
Tomer Meir ◽  
Ronen Levi ◽  
Liesbet Lieben ◽  
Steven Libutti ◽  
Geert Carmeliet ◽  
...  

1,25(OH)2D3 decreases parathyroid hormone (PTH) gene transcription through the vitamin D receptor (VDR). Total body VDR−/− mice have high PTH levels, hypocalcemia, hypophosphatemia, and bone malformations. To investigate PTH regulation by the VDR specifically in the parathyroid, we generated parathyroid-specific VDR knockout mice ( PT-VDR−/−). In both strains, there was a decrease in parathyroid calcium receptor (CaR) levels. The number of proliferating parathyroid cells was increased in the VDR−/− mice but not in the PT-VDR−/− mice. Serum PTH levels were moderately but significantly increased in the PT-VDR−/− mice with normal serum calcium levels. The sensitivity of the parathyroid glands of the PT-VDR−/− mice to calcium was intact as measured by serum PTH levels after changes in serum calcium. This indicates that the reduced CaR in the PT-VDR−/− mice enables a physiologic response to serum calcium. Serum C-terminal collagen crosslinks, a marker of bone resorption, were increased in the PT-VDR−/− mice with no change in the bone formation marker, serum osteocalcin, consistent with a resorptive effect due to the increased serum PTH levels in the PT-VDR−/− mice. Therefore, deletion of the VDR specifically in the parathyroid decreases parathyroid CaR expression and only moderately increases basal PTH levels, suggesting that the VDR has a limited role in parathyroid physiology.


Author(s):  
Mohammed Khazaal Jumaahm ◽  
Ali Hussain Ali Alhamza ◽  
Abbas Ali Mansour

<b><i>Background:</i></b> Parathyroid hormone (PTH) has been reported to have a positive correlation with insulin resistance and the development of the metabolic syndrome. This study aims to evaluate if there is an association between obesity and serum PTH levels. <b><i>Methods:</i></b> This case-control study was conducted at the Faiha Specialized Diabetes Endocrine and Metabolism Center in Basrah (Southern Iraq) from September 2018 to July 2019. A total of 230 patients were recruited for this study (103 male and 127 female), divided into 2 groups according to the BMI: &#x3c;30 kg/m<sup>2</sup> were considered as the control group (83 persons) and ≥30 kg/m<sup>2</sup> were considered as obese persons (147 persons). The study groups were also subdivided into 3 groups according to the serum level of PTH: &#x3c;40 pg/mL, 40–65 pg/mL, and &#x3e;65 pg/mL. <b><i>Results:</i></b> The mean age of the obese and control groups was 44.39 ± 10.64 and 30.12 ± 8.95 years, respectively. About 46.25% of obese were men and 53.75% were women, while 42% of the control group were men and 58% were women. Serum PTH level was significantly higher (<i>p</i> &#x3c; 0.001) among obese persons with a mean level of 53.21 ± 19.58 pg/mL for obese and 37.63 ± 21.8 pg/mL for control. Vitamin D deficiency was seen in 84.4% of the obese group while in 71.1% of the control group (<i>p</i> value 0.04). Females turned to have higher PTH levels than males in both the obese and the control group (<i>p</i> value &#x3c;0.001). However, age and the presence of diabetes mellitus were not associated with higher PTH levels (<i>p</i> value 0.155 and 0.6, respectively). <b><i>Conclusion:</i></b> Obesity was associated with a higher serum PTH level related to the severity of vitamin D deficiency.


2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Andrea W. D. Stavenuiter ◽  
Maria Vittoria Arcidiacono ◽  
Evelina Ferrantelli ◽  
Eelco D. Keuning ◽  
Marc Vila Cuenca ◽  
...  

Vitamin D deficiency is associated with a range of clinical disorders. To study the mechanisms involved and improve treatments, animal models are tremendously useful. Current vitamin D deficient rat models have important practical limitations, including time requirements when using, exclusively, a vitamin D deficient diet. More importantly, induction of hypovitaminosis D causes significant fluctuations in parathyroid hormone (PTH) and mineral levels, complicating the interpretation of study results. To overcome these shortcomings, we report the successful induction of vitamin D deficiency within three weeks, with stable serum PTH and minerals levels, in Wistar rats. We incorporated two additional manoeuvres compared to a conventional diet. Firstly, the vitamin D depleted diet is calcium (Ca) enriched, to attenuate the development of secondary hyperparathyroidism. Secondly, six intraperitoneal injections of paricalcitol during the first two weeks are given to induce the rapid degradation of circulating vitamin D metabolites. After three weeks, serum 25-hydroxyvitamin D3(25D) and 1,25-dihydroxyvitamin D3(1,25D) levels had dropped below detection limits, with unchanged serum PTH, Ca, and phosphate (P) levels. Therefore, this model provides a useful tool to examine the sole effect of hypovitaminosis D, in a wide range of research settings, without confounding changes in PTH, Ca, and P.


Author(s):  
Aliya A Khan ◽  
Lars Rejnmark ◽  
Mishaela Rubin ◽  
Peter Schwarz ◽  
Tamara Vokes ◽  
...  

Abstract Context Hypoparathyroidism is characterized by insufficient levels of parathyroid hormone (PTH). TransCon PTH is an investigational long-acting prodrug of PTH(1-34) for the treatment of hypoparathyroidism. Objective Investigate the safety, tolerability, and efficacy of daily TransCon PTH in adults with hypoparathyroidism. Design Phase 2, randomized, double-blind, placebo-controlled 4-week trial with open-label extension. Patients Enrolled 59 subjects with hypoparathyroidism. Interventions TransCon PTH 15, 18, or 21 µg PTH(1-34)/day or placebo for 4 weeks, followed by a 26-week extension where TransCon PTH dose was titrated (6–60 µg PTH[1-34]/day). Results By Week 26, 91% of subjects treated with TransCon PTH achieved independence from standard of care (SoC, defined as active vitamin D = 0 mcg/day and calcium (Ca) ≤ 500 mg/day). Mean 24-hour urine Ca (uCa) decreased from a baseline mean of 415 mg/24h to 178 mg/24h by Week 26 (n=44) while normal serum Ca (sCa) was maintained and serum phosphate (sP) and Ca x P fell within the normal range. By Week 26, mean scores on SF-36 domains increased from below normal at baseline to within the normal range. The Hypoparathyroidism Patient Experience Scale Symptom and Impact scores improved through 26 weeks. TransCon PTH was well-tolerated with no treatment-related serious or severe adverse events. Conclusions TransCon PTH enabled independence from oral active vitamin D and reduced Ca supplements (≤ 500 mg/day) for most subjects, achieving normal sCa, sP, uCa, CaxP, and demonstrating improved health-related quality of life. These results support TransCon PTH as a potential hormone replacement therapy for adults with hypoparathyroidism.


1982 ◽  
Vol 42 (6) ◽  
pp. 487-491 ◽  
Author(s):  
Claus Christiansen ◽  
Merete Sanvig Christensen ◽  
Peter McNair ◽  
Britta Nielsen ◽  
Steen Madsbad

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