Metabolic inactivation of vitamin D is enhanced in primary hyperparathyroidism

1987 ◽  
Vol 73 (6) ◽  
pp. 659-664 ◽  
Author(s):  
M. R. Clements ◽  
M. Davies ◽  
D. R. Fraser ◽  
G. A. Lumb ◽  
E. Barbara Mawer ◽  
...  

1. The elimination half-time of 25-hydroxyvitamin D in plasma was estimated after intravenous injection of the radioactively labelled metabolite in seven patients with primary hyperparathyroidism before and after excision of a parathyroid adenoma. 2. The elimination half-time of 25-hydroxyvitamin D was significantly shortened in primary hyperparathyroidism and reverted towards normal after parathyroidectomy. 3. The increased metabolic clearance of 25-hydroxyvitamin D in primary hyperparathyroidism was accounted for by an increased excretion of vitamin D-derived inactivation products in the faeces. 4. Enhanced hepatic inactivation of 25-hydroxyvitamin D may be important in the development of vitamin D deficiency in primary hyperparathyroidism.

2015 ◽  
Vol 18 (02) ◽  
pp. 1550008 ◽  
Author(s):  
Negin Masoudi Alavi ◽  
Mahla Madani ◽  
Mohsen Taghizadeh ◽  
Mohammad Reza Sharif

Purpose: To investigate the effect of weekly single high dose vitamin D supplementation on serum 25-hydroxyvitamin D [25(OH)D], and non-specific musculoskeletal pain in female nurses. Methods: In this prospective study in Kashan/Iran, from April 1, 2014, through September 30, 2014, the 150 nurses with vitamin D deficiency received the weekly pearls of 50,000 units of vitamin D3 for 10 weeks. The serum level of 25(OH)D was measured before and after supplement therapy. The subjects were also asked to complete the Extended Nordic Musculoskeletal Questionnaire. All analyses were conducted with SPSS version 16. Results: After 10 weeks of intervention there was [Formula: see text][Formula: see text]ng/mL increase in 25(OH)D. The 82 nurses (54.7%) had 25(OH)D in normal range, while the 68 nurses (45.3%) were still vitamin D deficient. Weight could explain 15.4% increase in 25(OH)D. Before intervention 135 (90%), of nurses reported musculoskeletal pain in at least one region, after intervention this number decreased to 72.7%. There was a statistically significant improvement in musculoskeletal pain in neck, shoulders, upper back, lower back, hips/tights, knees, and ankles/feet after intervention. Conclusions: The weekly single high dose of vitamin D for 10 weeks could resolve vitamin D deficiency in about half of the patients. Patients with non-specific musculoskeletal pain might benefit from vitamin D supplementation.


2020 ◽  
pp. 145749692096260
Author(s):  
M. A. Salman ◽  
A. Rabiee ◽  
A. Salman ◽  
A. Youssef ◽  
H. E.-D. Shaaban ◽  
...  

Background: We postulated that the preoperative correction of vitamin D levels can significantly reduce the incidence of hunger bone syndrome among patients undergoing parathyroidectomy for primary hyperparathyroidism. Methods: We performed a prospective, randomized, open-label study on 102 patients with primary hyperparathyroidism and coexisting vitamin D deficiency who were scheduled to undergo parathyroidectomy. Patients were divided into the following two groups: group I which included 52 patients who did not receive preoperative vitamin D supplementation; and group II which included 50 patients who received cholecalciferol 1000–2000 IU daily or 50000 IU weekly until they achieve vitamin D levels >20 ng/mL (group IIa = 25 patients) or vitamin D levels >30 ng/mL (group IIb = 25 patients). Results: The incidence of hunger bone syndrome in group IIb was lower than group I and group IIa (8% versus 16% versus 23%, respectively); however, this difference did not reach the level of statistical significance (p = 0.22). Patients with hunger bone syndrome were significantly younger and had higher serum phosphorus, alkaline phosphatase, magnesium, and bone mineral density at baseline than patients without hunger bone syndrome. On the other hand, patients with hunger bone syndrome had significantly lower 25-hydroxyvitamin D at baseline than patients without hunger bone syndrome (p = 0.001). The ROC curve showed that the baseline level of serum 25-hydroxyvitamin D was not an independent discriminator of hunger bone syndrome (area under curve = 0.21 (95% CI: 0.06–0.34); p = 0.011). Conclusion: Preoperative course of vitamin D supplements has no preventive role on the postoperative incidence of hunger bone syndrome among patients with primary hyperparathyroidism and coexisting vitamin D deficiency undergoing parathyroidectomy.


2012 ◽  
Vol 1 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Ranganathan R Rao ◽  
Harpal S Randeva ◽  
Sailesh Sankaranarayanan ◽  
Murthy Narashima ◽  
Matthias Möhlig ◽  
...  

Introduction/backgroundVitamin D deficiency further increases circulating parathyroid hormone (PTH) levels in patients with primary hyperparathyroidism (pHPT), with potential detrimental effects on bone mass.MethodsThis was an observational clinical study in consecutive conservatively treated postmenopausal women (n=40) with pHPT and coexistent 25-hydroxyvitamin D deficiency (25OHD ≤50 nmol/l (≤20 ng/ml)). Patients who showed an increase in serum 25OHD above the threshold of vitamin D deficiency (>50 nmol/l; n=28) using treatment with various commonly prescribed vitamin D preparations were, for the purposes of statistical analyses, allocated to the treatment group. Patients who were retrospectively identified as having received no treatment with vitamin D and/or remained vitamin D deficient were considered as non-responders/controls (n=12). Adjusted calcium (adjCa), PTH and 25OHD concentrations were monitored in all subjects up to 54 months (mean observation period of 18±2 months).ResultsProlonged increased vitamin D intake, regardless of the source (serum 25OHD, increase from 32.2±1.7 nmol/l at baseline to 136.4±11.6 nmol/l, P<0.0001), significantly reduced serum PTH (13.3±1.1 vs 10.5±1.0 pmol/l, P=0.0001), with no adverse effects on adjCa levels (2.60±0.03 vs 2.60±0.02 mmol/l, P=0.77) and renal function tests (P>0.73). In contrast, serum PTH remained unchanged (15.8±2.6 vs 16.3±1.9 pmol/l, P=0.64) in patients who remained vitamin D deficient, with a significant difference between groups in changes of PTH (P=0.0003). Intrapartial correlation analyses showed an independent negative correlation of changes in 25OHD with PTH levels (ric=−0.41, P=0.014).ConclusionsProlonged treatment with vitamin D in various commonly prescribed preparations appeared to be safe and significantly reduced PTH levels by 21%.


1987 ◽  
Vol 115 (3) ◽  
pp. 345-352 ◽  
Author(s):  
Reinhard Kaune ◽  
Johein Harmeyer

Abstract. Vitamin D metabolism was studied in the 'Hannover Pig', a strain which suffers from pseudo vitamin D-deficiency rickets, type I. Animals of this strain are known to be devoid of renal 25-hydroxyvitamin D3-1α-hydroxylase and -24-hydroxylase activities. Pigs with florid rickets and hypocalcaemia were treated with single im injections of 0.25 to 1.25 mg of vitamin D3, doses that have been shown in previous studies to be effective in producing transient healing of rachitic symptoms. The levels of vitamin D3 and its most relevant physiological metabolites in plasma were estimated at intervals before and after this vitamin D3 treatment. Vitamin D3 rose from 14.8 ± 8.1 to 364 ± 190 nmol/l (mean ± sd) 2 to 3 days post injectionem, 25-hydroxyvitamin D3 from 131.0 ± 46.2 to 1068 ± 160 nmol/l within 7 days post injectionem. The 1α,25-dihydroxyvitamin D3 concentration in plasma was elevated from 73.9 ± 25.0 to 281 ± 168 pmol/l 2 to 3 days post injectionem and declined continually from that time. 24R,25-dihydroxyvitamin D3 and 25S,26-dihydroxyvitamin D3 levels after treatment showed different responses in different animals being either elevated or unchanged. Clinical healing of the pigs with these doses of vitamin D3 was attributed to the transient rise of 1α,25-dihydroxyvitamin D3 in plasma. It was assumed that 1α,25-dihydroxyvitamin D3 synthesis takes place under these circumstances in extrarenal tissues.


2006 ◽  
Vol 155 (2) ◽  
pp. 237-244 ◽  
Author(s):  
B Moosgaard ◽  
P Vestergaard ◽  
L Heickendorff ◽  
F Melsen ◽  
P Christiansen ◽  
...  

Background: Primary hyperparathyroidism (PHPT) is associated with reduced plasma 25-hydroxyvitamin D (P-25OHD) and usually increased plasma 1α,25-dihydroxyvitamin D (P-1,25(OH)2D). Parathyroid tissue expresses the vitamin D receptor and it is thought that circulating 1,25(OH)2D participate in the regulation of parathyroid cell proliferation, differentiation and secretion. Aim: To investigate the relations between circulating levels of 1,25(OH)2D and 25OHD respectively and parathyroid adenoma weight (AW), plasma-parathyroid hormone (P-PTH) and PTH secretion expressed as P-PTH/AW. Design: Cross-sectional study. Material: One hundred and seventy-one consecutive hypercalcaemic caucasian patients aged 19–87 years (median 63, 84% females) with surgically proven parathyroid adenoma. Results: A weak positive correlation was found between P-25OHD and P-1,25(OH)2D (r = 0.24, P < 0.005). AW depended on sex and body mass index. Following adjustment, it was correlated positively to P-PTH, calcium (Ca) and alkaline phosphatase (AP) and inversely to plasma phosphate in a multiple regression model. AW was not associated with vitamin D metabolites. Preoperative P-PTH correlated positively to plasma levels of Ca and AP, but inversely to phosphate and 25OHD (P < 0.001) levels. P-PTH was not associated with P-1,25(OH)2D (P = 0.65). The P-PTH:AW ratio correlated inversely to P-25OHD (P < 0.05), but showed no relations to plasma levels of Ca, phosphate or 1,25(OH)2D (P = 0.22). Conclusion: In this material, low levels of 25OHD were related to higher levels of P-PTH and higher PTH:AW ratios in patients with PHPT suggesting that vitamin D deficiency increase PTH secretion activity. Neither PTH secretion nor AW was associated with circulating levels of 1,25(OH)2D.


2019 ◽  
Vol 16 (4) ◽  
pp. 340-347
Author(s):  
Yuge Wang ◽  
Yanqiang Wang ◽  
Bingjun Zhang ◽  
Yinyao Lin ◽  
Sha Tan ◽  
...  

Background and Objective: Vitamin D deficiency is internationally recognized among the potentially modifiable risk factors for ischemic cardio-cerebrovascular diseases. However, the association between vitamin D deficiency and stroke morbidity or mortality remains insufficiently known. Our aim is to investigate their relevance to 25-hydroxyvitamin D [25(OH) D] levels and clinical severity and outcome after 3 months in first-ever ischemic stroke. Methods: Retrospective analysis of 356 consecutive patients in first-ever ischemic stroke between 2013 and 2015. Serum 25(OH) D levels were measured at baseline. Stroke severity was assessed at admission using the National Institutes of Health Stroke Scale (NIHSS) score. Functional outcome after 3 months of onset was evaluated using the modified Rankin scale (mRS). Results: Among the 356 enrolled patients, HbA1c was higher in insufficiency/deficiency group than that in the sufficiency group (6.3 ± 1.7 vs. 5.9 ± 1.1, p =0.015). The hospital stay was longer in insufficiency/deficiency group than that in the sufficiency group (11 (8-17) vs. 9.5 (7-13), p = 0.035). There was a significant inversed trend between serum 25(OH) D levels and hospital stay (OR 0.960, P = 0.031), using logistic regression. Conclusions: 25(OH)D levels are associated with glucose homeostasis, 25(OH) D contributes to increase the length of hospital stay. Low serum 25-OHD level is an independent predictor for hospital stay in first-ever ischemic stroke. Vitamin D deficiency did not predict functional outcome in the span of 3 months.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Xiao ◽  
Jingyi Lv ◽  
Shiyu Wang ◽  
Yang Zhou ◽  
Lunwen Chen ◽  
...  

Abstract Background Vitamin D deficiency has been associated with type 2 diabetes (T2D) and metabolic syndrome (MS) and its components. However, it is unclear whether a low concentration of vitamin D is the cause or consequence of these health conditions. Thus, this study aimed to evaluate the association of vitamin D concentrations and its genetic risk scores (GRSs) with MS and its component diseases, such as T2D, in middle-aged and elderly participants from rural eastern China. Methods A subset of 2393 middle-aged and elderly individuals were selected from 70,458 participants of the Nantong Chronic Diseases Study of 2017–2018 in China. We used two 25-hydroxyvitamin D (25[OH]D) synthesis single-nucleotide polymorphisms (SNPs) (DHCR7-rs12785878 and CYP2R1-rs10741657) and two 25(OH) D metabolism SNPs (GC-rs2282679 and CYP24A1-rs6013897) for creating GRSs, which were used as instrumental variables to assess the effect of genetically lowered 25(OH) D concentrations on MS and T2D based on the Wald ratio. F statistics were used to validate that the four SNPs genetically determined 25(OH) D concentrations. Results Compared to vitamin D sufficient individuals, individuals with vitamin D insufficiency had an odds ratio (OR [95% confidence interval {CI}]) of MS of 1.30 (1.06–1.61) and of T2D of 1.32 (1.08–1.64), individuals with vitamin D deficiency had an ORs (95% CI) of MS of 1.50 (1.24–1.79) and of T2D of 1.47 (1.12–1.80), and those with vitamin D severe deficiency had an ORs (95% CI) of MS of 1.52 (1.29–1.85) and of T2D of 1.54 (1.27–1.85). Mendelian randomization analysis showed a 25-nmol/L decrease in genetically instrumented serum 25(OH) D concentrations using the two synthesis SNPs (DHCR7 and CYP2R1 genes) associated with the risk of T2D and abnormal diastolic blood pressure (DBP) with ORs of 1.10 (95%CI: 1.02–1.45) for T2D and 1.14 (95%CI: 1.03–1.43) for DBP. Conclusions This one sample Mendelian randomization analysis shows genetic evidence for a causal role of lower 25(OH) D concentrations in promoting of T2D and abnormal DBP in middle-aged and elderly participants from rural China.


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