This case-control study aimed to examine the effect of high serum parathyroid hormone (PTH) level, especially the effect of secondary hyperparathyroidism (SHPT) related to hypovitaminosis D, on bone metabolism and bone phenotypes.
Multivariate logistic regression analyses showed that being female, urban residency, lower body mass index, higher serum parathyroid hormone levels, no fish consumption, and less sun exposure time were all significant and independent determinants of vitamin D deficiency.
Moreover, parathyroid hormone and serum calcium levels of patients were obtained to assess for severe vitamin D deficiency and secondary hyperparathyroidism.
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.
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.
Age and PTH levels were potential confounding variables, but in the multiple linear regressions only BMI (95% CI: 0.11-4.16; P < 0.01), 25(OH)D (95% CI: -0.007 to 1.70; P = 0.05) and CTX (95% CI: -149.04 to 21.80; P < 0.01) predicted Dcomp, while BMI (95% CI: 1.13-4.18; P < 0.01) and 25(OH)D (95% CI: 0.24-1.52; P < 0.01) predicted D100.
We hypothesize that vitamin D deficiency in these patients may create a subclinical secondary hyperparathyroidism that leads to intraoperative parathyroid hormone elevation when the glands are manipulated.
In patients with temporomandibular disorders, increased parathyroid hormone levels in response to vitamin D deficiency was significantly more prominent.
Vitamin D deficiency (<20 ng/mL) and secondary hyperparathyroidism (plasma intact parathyroid hormone >65 ng/mL) were present in 68.8% and 45.4%, respectively.
Cholecalciferol supplementation corrects vitamin D deficiency and is effective in lowering serum intact parathyroid hormone and bone turnover markers in early stages of CKD.
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.
Treatment with ergocalciferol could significantly improve vitamin D deficiency with no significant effects of serum calcium or parathyroid hormone levels.
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.
Five of the nine tested family members had vitamin D deficiency (25OHD < 30 nmol/L), three had insufficiency (< 50 nmol/L) and 6/9 members had elevated PTH and ALP levels.
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).
The purpose of this paper is to report the study design of a prospective eight week prospective double-blind randomized, placebo-controlled trial (n = 330 allocated 2:1 to intervention vs. control) to assess the effect of placebo vs. high-dose oral cholecalciferol (100,000 IU vitamin D3 at baseline and week 2) on 6-week change of select biologic cardiometabolic risk factors (including parathyroid hormone to assess biologic activity, pro-inflammatory/pro-thrombotic/fibrotic markers, insulin sensitivity and vitamin D metabolites) and their relationship to vitamin D administration and modification by vitamin D receptor polymorphisms in overweight, hypertensive African Americans with hypovitaminosis D. Findings from this trial will present insights into potential causal links between vitamin D repletion and mechanistic pathways of CV disease, including established and novel genomic markers.
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.
There was no correlation between serum 25(OH)D level and levels of calcium (Ca) (r = -0.16), alkaline phosphatase (ALP) (r = -0.12), P (r = 0.13), and parathyroid hormone (PTH) (r = -0.15,) in children with VDD.
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.
A few cut- offs have correlated vitamin D deficiency to physiological markers such as parathyroid hormone (PTH), calcium and phosphate with varying results.
As the rate of vitamin D deficiency decreases in the early years due to vitamin D supplementation, the recommendation should be set due to a clinical threshold level of 30 ng/ml for 25-OHD based on PTH levels in children of our population.