Our retrospective study based on large data set supports the suitability of the currently accepted clinical cut-off of 75 nmol/L for sufficient 25(OH)D. However, the issue of assessing Vitamin D deficiency remains difficult due to seasonal variations in serum 25(OH)D. Therefore, PTH measurements should complement 25(OH)D results for diagnosing Vitamin D deficiency.
Vitamin D deficiency (HR 1.62, 95% CI 1.01 to 2.58) and elevated PTH (HR 1.42, 95% CI 1.09 to 1.84) were independently associated with all-cause mortality.
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.
A few cut- offs have correlated vitamin D deficiency to physiological markers such as parathyroid hormone (PTH), calcium and phosphate with varying results.
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.
Humans with CKD experience decreased Klotho expression as early as stage 1 CKD; Klotho continues to decline as CKD progresses, causing FGF-23 resistance and provoking large FGF-23 and parathyroid hormone increases, and hypovitaminosis D. Secreted Klotho protein, formed by extracellular clipping, exerts FGF-23-independent phosphaturic and calcium-conserving effects through its paracrine action on the proximal and distal tubules, respectively.
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.
PTH decreased by 34% (VIDD with HPT, <i>P</i> < 0.01 for decrease), 32% (all VIDD, <i>P</i> < 0.01) and increased by 8% in the controls (<i>P</i>-values: <0.01 for relative changes between VIDD with HPT or all VIDD patients vs controls).
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.
Treatment with ergocalciferol could significantly improve vitamin D deficiency with no significant effects of serum calcium or parathyroid hormone levels.
Supplementation may improve some biochemical parameters, such as reducing PTH levels in patients to CKD-stage 4 who have vitamin D deficiency; but it remains to be established whether the role of nutritional vitamin D in maintaining bone health in the general population can be extrapolated to the CKD population.
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.
The goal of our study was to evaluate the prevalence of hypovitaminosis D and its determinants as well as PTH serum level determinants and associations of the 25-hydroxyvitamin D and PTH serum levels with MetS and its individual components in a sample of the Portuguese mainland population.
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.
To demonstrate the relationship between hyperglycemia and PTH level, subjects with type 2 diabetes and vitamin D deficiency (124 adults) were divided into 4 groups based on their FPG and HbA1c levels.
In the multivariate analysis, ethnic Malays (adjusted OR (aOR)=14·72; 95 % CI 2·12, 102·21) and Indians (aOR=14·02; 95 % CI 2·27, 86·59), those at risk for depression (aOR=1·88, 95 % CI 1·27, 2·79) and those with higher parathyroid hormone level (aOR=1·13; 95 % CI 1·01, 1·26) were associated with vitamin D deficiency, while vitamin D deficiency was negatively associated with mental health-related quality of life (Mental Component Summary) scores (aOR=0·98; 95 % CI 0·97, 0·99).
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.
In women with chronic autoimmune thyroiditis and vitamin D deficiency we have found reference levels of relevant metabolic-hormonal parameters except for parathormone and total calcium.