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.
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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
In patients with temporomandibular disorders, increased parathyroid hormone levels in response to vitamin D deficiency was significantly more prominent.
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).
A statistically significant difference was observed between the pre-treatment and post-treatment values in 25(OH)D levels (p:0.001, 10.27±4.62 ng/ml and 51.40±14.62 ng/ml, respectively), PTH levels (p:0.001, 50.32±19.05 pg/ml and 33.97±13.12 pg/ml, respectively) and sclerostin levels (p:0.002, 858.98±351.63 pg/ml and 689.52±197.92 pg/ml, respectively).