In conclusion, our study indicated significant association between specific PTH gene promoter region variants and altered levels of 25(OH)D and vitamin D deficiency among specific nationals.
Herein we report two unrelated Turkish females who presented with brachydactyly type E and vitamin D deficiency in the absence of marked alterations in serum calcium, phosphate, and parathyroid hormone.
The mean forearm and spine BMD values in subjects with TT (VDR, TaqI) or bb (PTH, BstBI) genotypes were significantly higher than the values in subjects with Tt genotype and BB or Bb genotype, respectively.
Screening for Vitamin D Deficiency in Black Americans: Comparison of Total, Free, Bioavailable 25 Hydroxy Vitamin D Levels with Parathyroid Hormone Levels and Bone Mineral Density.
Disturbances in calcium, phosphate, fibroblast growth factor 23, parathyroid hormone concentrations and vitamin D deficiency are commonly encountered and contribute to the clinical syndromes of bone disorders in CKD, including hyperparathyroidism, osteomalacia, osteoporosis and adynamic bone disease.
This cross-sectional study was conducted in subjects with vitamin D deficiency (VDD) to observe associations between CaSR polymorphisms, plasma iPTH, and serum calcium levels.
Initial blood tests and history were thought possibly to suggest vitamin D deficiency rickets: calcium 5.1mg/dL, (8.8-10.8); phosphorus 4.1mg/dL, (4.5-5.5); alkaline phosphatase 1481 U/L (80-220); intact PTH 537.1 pg/mL (10-71).
Receiver operator characteristic curve (ROC) was created and the area under the ROC was used to evaluate the predictive accuracy of postoperative PTH and compared between patients with or without VDD.
Vitamin D deficiency is highly prevalent in patients with chronic kidney disease (CKD), and nutritional vitamin D supplementation decreases elevated parathyroid hormone concentrations in subgroups of these patients.
The CaSRQ459R mutation leads to mild functional inactivation in vitro, which explains the FHH-like phenotype in homozygous family members and the grossly exaggerated PTH response to vitamin D deficiency in the index case.
Cholecalciferol supplementation corrects vitamin D deficiency and is effective in lowering serum intact parathyroid hormone and bone turnover markers in early stages of CKD.
Cross sectional studies demonstrated that prevalence of HF is increased in patients with Vitamin D deficiency or parathyroid hormone (PTH) plasma level increase, whereas longitudinal studies showed enhanced risk of developing new HF in patients with Vitamin D deficiency.
The threshold for 25OHD at the point of maximal suppression of PTH estimated in this study was lower than the suggested threshold of vitamin D deficiency in the literature, perhaps due to race or assay differences, and the relationship between vitamin D and PTH changed with sex and age.
The management of hyperparathyroidism includes the correction of vitamin D deficiency and control of serum phosphorus and PTH without inducing hypercalcemia.
Multivariate regression analysis adjusted by other risk factors showed that among all clinical outcomes, admission hypovitaminosis D was associated with longer duration of ICU stay and a high admission of parathormone was associated with in ICU mortality.
Parathyroid hormone status is associated with impaired glucose homeostasis; hypovitaminosis D combined with high parathyroid hormone concentrations are associated with glycaemic dysregulation in elderly patients with prediabetes.
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.
Laboratory tests revealed hypocalcemia, hyperphosphatemia, hypomagnesemia, and hypovitaminosis D. Her parathyroid hormone concentration (PTH) was low at 14.2 pg/mL.
Its deficiency (vitamin D deficiency-VDD), being common in European population, combined with elevated concentration of parathyroid hormone (PTH), represents a vicious cycle of mechanisms leading to heart failure (HF).
Hyperparathyroidism-related histological changes were observed in fibrous dysplastic bone, but not in the unaffected bone, of patients with elevated serum PTH secondary to vitamin D deficiency.