Browse
Submit Data
Databases
API
Help

Dataset Information

23 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Parathyroid Hormone in Pregnancy: Vitamin D and Other Determinants.

ABSTRACT: We aimed to assess the parathyroid hormone (PTH) concentration in pregnant women at the beginning of pregnancy (1st trimester) and within days before delivery (3rd trimester) and evaluate its determinants. From September 2014 through December 2015 in a cross-sectional study, 204 women in the 1st trimester of pregnancy and 203 women in the 3rd trimester of pregnancy were recruited. Blood samples were collected to measure PTH and circulating 25-hydroxy-vitamin D (25(OH)D) concentrations. Lifestyle and demographic data were collected using a questionnaire. Serum 25(OH)D and PTH were inversely correlated in both early and late pregnancy. Our analyses suggest that in the 3rd trimester of pregnancy, a 25(OH)D level of 18.9 ng/mL (47.3 nmol/L) could serve as an inflection point for the maximal suppression of PTH. Statistically significant determinants of PTH concentrations in multiple regression were 25(OH)D concentrations, season, multiparity and education of the partner (all p < 0.05) in early pregnancy. In late pregnancy, 25(OH)D concentrations and country of origin were statistically significant determinants of PTH concentrations (all p < 0.05). These factors and their effect on PTH appear to be vastly determined by 25(OH)D; however, they might also affect PTH through other mechanisms besides 25(OH)D.

SUBMITTER: Hysaj O

PROVIDER: S-EPMC7911996 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Parathyroid hormone in Sri Lankan pregnant women: Vitamin D and other determinants.

Project description:IntroductionDeterminants of parathyroid hormone level during pregnancy have been less frequently studied. We aimed to describe the serum parathyroid hormone (PTH) and its determinants in Sri Lankan pregnant women in a community setting.Materials and methodsIn this cross-sectional analysis, 390 pregnant mothers in their third trimester were enrolled from primary care centers of 15 health divisions in the Colombo District in Sri Lanka. Venous blood was analyzed for a total 25-hydroxyvitamin-D [25(OH)D], serum parathyroid hormone (PTH), serum calcium, and alkaline phosphatase. The bone quality was assessed in terms of speed of sound (SOS) using the quantitative ultrasound scan (QUS). Univariate and multivariate regression analysis was used to examine the determinants of PTH concentration in blood.ResultsMedian serum 25(OH)D was 17.5ng/mL. Most (61.6%) were vitamin D deficient (<20ng/mL). Median PTH was 23.7pg/mL. Only 0.8% had hyperparathyroidism (PTH >65pg/mL). The correlation between 25(OH)D and PTH was weak but significant (r = -0.197; p<0.001). SOS Z-score was below the cut-off (≤-2) in fifty-six women (14.7%), and SOS did not relate significantly to PTH. In regression analysis, serum 25(OH)D, serum calcium, body mass index, educational level, and weeks of pregnancy were significant independent variables when adjusted. The model explained 16% of the variation in the PTH level.ConclusionsA high prevalence of vitamin D deficiency was observed among Sri Lankan pregnant women in the present study. Serum 25(OH)D, calcium, weeks of pregnancy, and educational level were determinants of serum PTH.

| S-EPMC8500411 | biostudies-literature

Association of Vitamin D and Parathyroid Hormone With Barrett's Esophagus.

Project description:BACKGROUND:Esophageal adenocarcinoma has been inversely associated with exposure to ultraviolet radiation. This could be because of vitamin D deficiency or hyperparathyroidism promoting gastroesophageal reflux disease (GERD) and Barrett's esophagus. AIM:The aim of this study is to determine the association between parathyroid hormone (PTH) and vitamin D deficiency with GERD symptoms, erosive esophagitis, and Barrett's esophagus. METHODS:We assayed banked serum for PTH and total 25-hydroxy vitamin D from a cross-sectional cohort. Logistic regression was performed to estimate the associations of vitamin D deficiency and hyperparathyroidism with GERD symptoms, erosive esophagitis, and Barrett's esophagus. RESULTS:Sera from 605 men were assayed, including 150 with GERD, 216 with erosive esophagitis, 145 with Barrett's esophagus, and 174 normal subjects. Contrary to our hypothesis, we found a strong inverse association between Barrett's esophagus and hyperparathyroidism (odds ratio=0.516; 95% confidence interval=0.265, 1.01), and a trend toward an inverse association with vitamin D deficiency. We found no association between vitamin D deficiency or hyperparathyroidism with GERD symptoms or erosive esophagitis. CONCLUSIONS:Contrary to our hypothesis, we found an inverse association between serum PTH and Barrett's esophagus. Validation of the finding and the mechanism of that association deserves further study.

| S-EPMC6395569 | biostudies-literature

Parathyroid hormone decreases renal vitamin D receptor expression in vivo.

Project description:The vitamin D receptor (VDR) is a nuclear transcription factor responsible for mediating the biological activities of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]. Renal and parathyroid gland VDR content is an important factor in calcium homeostasis, vitamin D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy. In these tissues, VDR expression is highly regulated by the calcium and vitamin D status. Although 1,25(OH)(2)D(3) up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastically reduced expression of the receptor. The generation of 25-hydroxyvitamin D(3)-1alpha-hydroxylase-null mice, which are incapable of endogenously producing 1,25(OH)(2)D(3), has allowed us to investigate the influence of parathyroid hormone (PTH) on VDR expression independent of PTH-mediated increases in 1,25(OH)(2)D(3). Administration of human PTH (1-34) (110 microg/kg per day) for 48 h reduced renal VDR levels from 515 to 435 fmol/mg protein (15%, P < 0.03) in wild-type mice. In the 25-hydroxyvitamin D(3)-1alpha-hydroxylase-null mice, PTH administration strongly reduced renal VDR levels, from 555 to 394 fmol/mg protein (29%, P < 0.001). These results demonstrate that PTH is a potent down-regulator of VDR expression in vivo.

| S-EPMC555704 | biostudies-other

Parathyroid hormone reference ranges in healthy individuals classified by vitamin D status.

Project description:PURPOSE:Parathyroid hormone (PTH) concentrations are routinely measured in the diagnosis and management of bone and kidney diseases, but reference ranges can be overestimated if determined in otherwise healthy individuals for whom vitamin D deficiency was not evaluated. We establish PTH reference ranges in apparently healthy, normocalcemic, normophosphatemic individuals categorized by 25-hydroxyvitamin D (25(OH)D) status using the Elecsys® PTH (cobas e 601) and Elecsys® Vitamin D total II electrochemiluminescence immunoassays (cobas e 411). METHODS:This prospective, non-interventional study measured PTH in serum from 653 apparently healthy adults [56.7% female; 68.2% white/Caucasian; 28.6% African American; median age 44 years (range 21-83)] from three diverse geographic sites across the USA during summer and winter months. Subjects were classified by concomitant vitamin D sufficiency (??30 ng/mL), insufficiency (>?20 to <?30 ng/mL) or deficiency (??20 ng/mL). RESULTS:In vitamin D sufficiency, median PTH was 31.9 pg/mL [range (2.5th-97.5th percentile) 17.9-58.6] compared with 35.5 pg/mL (17.0-60.4) for insufficiency, and 39.8 pg/mL (19.5-86.4) for deficiency. A significant inverse relationship was found between PTH and 25(OH)D (P?<?0.001). After accounting for vitamin D, potential effects of race or season as covariates were relatively small or absent. CONCLUSIONS:Upper reference limits (URL) for PTH in vitamin D sufficiency/insufficiency were similar and lower than current values. Clinically important PTH elevations were observed in vitamin D deficiency, where revised reference ranges with a higher URL may be appropriate. These data may help to distinguish vitamin D-related PTH elevations from other causes [e.g., primary (normocalcemic) or secondary hyperparathyroidism].

| S-EPMC6790182 | biostudies-literature

Physiological regulation of phosphate by vitamin D, parathyroid hormone (PTH) and phosphate (Pi).

Project description:Inorganic phosphate (Pi) is an abundant element in the body and is essential for a wide variety of key biological processes. It plays an essential role in cellular energy metabolism and cell signalling, e.g. adenosine and guanosine triphosphates (ATP, GTP), and in the composition of phospholipid membranes and bone, and is an integral part of DNA and RNA. It is an important buffer in blood and urine and contributes to normal acid-base balance. Given its widespread role in almost every molecular and cellular function, changes in serum Pi levels and balance can have important and untoward effects. Pi homoeostasis is maintained by a counterbalance between dietary Pi absorption by the gut, mobilisation from bone and renal excretion. Approximately 85% of total body Pi is present in bone and only 1% is present as free Pi in extracellular fluids. In humans, extracellular concentrations of inorganic Pi vary between 0.8 and 1.2 mM, and in plasma or serum Pi exists in both its monovalent and divalent forms (H2PO4- and HPO42-). In the intestine, approximately 30% of Pi absorption is vitamin D regulated and dependent. To help maintain Pi balance, reabsorption of filtered Pi along the renal proximal tubule (PT) is via the NaPi-IIa and NaPi-IIc Na+-coupled Pi cotransporters, with a smaller contribution from the PiT-2 transporters. Endocrine factors, including, vitamin D and parathyroid hormone (PTH), as well as newer factors such as fibroblast growth factor (FGF)-23 and its coreceptor ?-klotho, are intimately involved in the control of Pi homeostasis. A tight regulation of Pi is critical, since hyperphosphataemia is associated with increased cardiovascular morbidity in chronic kidney disease (CKD) and hypophosphataemia with rickets and growth retardation. This short review considers the control of Pi balance by vitamin D, PTH and Pi itself, with an emphasis on the insights gained from human genetic disorders and genetically modified mouse models.

| S-EPMC6326012 | biostudies-literature

Parathyroid hormone and parathyroid hormone type-1 receptor accelerate myocyte differentiation.

Project description:The ZHTc6-MyoD embryonic stem cell line expresses the myogenic transcriptional factor MyoD under the control of a tetracycline-inducible promoter. Following induction, most of the ZHTc6-MyoD cells differentiate to myotubes. However, a small fraction does not differentiate, instead forming colonies that retain the potential for myocyte differentiation. In our current study, we found that parathyroid hormone type 1 receptor (PTH1R) expression in colony-forming cells at 13 days after differentiation was higher than that in the undifferentiated ZHTc6-MyoD cells. We also found that PTH1R expression was required for myocyte differentiation, and that parathyroid hormone accelerated the differentiation. Our analysis of human and mouse skeletal muscle tissues showed that most cells expressing PTH1R also expressed Pax7 and CD34, which are biomarkers of satellite cells. Furthermore, we found that parathyroid hormone treatment significantly improved muscle weakness in dystrophin-deficient mdx mice. This is the first report indicating that PTH1R and PTH accelerate myocyte differentiation.

| S-EPMC4052750 | biostudies-literature

Placental uptake and metabolism as determinants of pregnancy vitamin D status

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-25 | GSE167431 | GEO

Vitamin D, parathyroid hormone and cardiovascular risk: the good, the bad and the ugly.

Project description:: 25-Hydroxyvitamin D insufficiency and increased cardiovascular risk (CVR) association is still debated. The vitamin D (VitD)-dependent parathyroid hormone (PTH) is considered as the possible actuator of VitD effects on CVR. To investigate the association of CVR, PTH and VitD, we carried out blood pressure measurements and blood samples and collected information on dietary habits, anamnestic, clinical and metabolic data of 451 participants in the Salerno area (Southern Italy) during the World Hypertension Day (17 May). CVR was calculated according to the Framingham CVR charts. The overall population mean age was 51.6?±?0.7 years, and female sex was slightly prevalent (55%). VitD deficiency (<20?ng/ml) was most frequent (59.7%). In this population, VitD and CVR did not correlate. VitD and PTH inversely correlated (r?=?-0.265, P?<?0.001) as expected. PTH was in direct correlation (r?=?0.225, P?<?0.001) with CVR. Elevated PTH (75 percentile; ?49.5?pg/ml) levels identify a population with higher CVR (11.8?±?0.5 vs. 8.5?±?0.3, P?<?0.001). In a multivariate analysis, both age and PTH correlate to CVR, but not VitD. In conclusion, VitD does not directly affect CVR in the overall population. Rather, increased PTH might be a better predictor of CVR.

| S-EPMC5757656 | biostudies-literature

Reduction of Parathyroid Hormone with Vitamin D Supplementation in Blacks: A Randomized Controlled Trial.

Project description:BACKGROUND:Response of parathyroid hormone (PTH) to vitamin D supplementation is determined by the baseline PTH level and change in vitamin D status. Conflicting reports in Blacks exist on the PTH response to vitamin D to supplementation. METHODS:During 3 winters from 2007-2010, 328 healthy Blacks (median age, 51 years) living in Boston, MA were randomized into a 4-arm, double-blind trial for 3 months of placebo, 1000, 2000, or 4000 IU of vitamin D3. PTH was measured in 254 participants at baseline and at the end of vitamin D supplementation period. RESULTS:The differences in PTH between baseline and 3 months were 3.93 pg/mL for those receiving placebo, -3.37 pg/mL for those receiving 1000 IU/d, -6.76 pg/mL for those receiving 2000 IU/d, and -8.99 pg/mL for those receiving 4000 IU/d ( -2.98 pg/mL for each additional 1000 IU/d of vitamin D3; p<0.001). CONCLUSION:We found a significant decrease in PTH with increasing doses of vitamin D supplementation up to intakes of 4000 IU/d in Blacks. Clinical Trials.gov: NCT00585637.

| S-EPMC4743037 | biostudies-literature

Parathyroid hormone exacerbates pulmonary hypertension through hypoxia-induced parathyroid hormone receptor upregulation.

Project description:Pulmonary hypertension (PH) is an incurable right heart failure disease. Parathyroid hormone (PTH) is secreted from the parathyroid gland and plays a crucial role in calcium homeostasis. PTH also acts on the cardiovascular system and affects cardiovascular prognosis. We assessed whether the regulation of PTH affected PH in a hypoxia (Hx)-induced PH mouse model. PTH treatment exacerbated right ventricular hypertrophy and right ventricular systolic pressure in Hx mice. Our data showed how is PTH effected for PH model murine lung.

2023-10-11 | GSE244861 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data