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.
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.
In patients with temporomandibular disorders, increased parathyroid hormone levels in response to vitamin D deficiency was significantly more prominent.
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).
However, more recently this pattern has further evolved into a presentation with normocalcaemia and raised parathyroid hormone (PTH) level without the presence of a recognised stimulus for its rise, in the form of vitamin D deficiency or renal impairment.
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.