Correlations between Vitamin D Status and Biochemical/Clinical and Pathological Parameters in Primary Hyperparathyroidism

Özbey, Neşe; Erbil, Yeşim; Ademoğlu, Evin; Özarmağan, Selçuk; Barbaros, Umut; Bozbora, Alp

doi:10.1007/s00268-005-0239-y

Cited by 65 publications

(67 citation statements)

References 22 publications

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“…In that study, gland weight and serum levels of PTH, ALP and calcium were significantly higher in patients with serum 25(OH)D less than 15 ng/ml. Ozbey et al supported this finding [28]. In contrast, serum 25(OH)D was not significantly related to parathyroid gland size in other reports [20,17,19].…”

Section: Discussionsupporting

confidence: 34%

“…Bussey and Bruder also reported that 40 and 37% had vitamin D deficiency and insufficiency in pHPT patients, respectively [27]. Several studies suggested that vitamin D insufficiency is related with the severity of pHPT [16,28]. Serum levels of 25(OH)D were inversely related to parathyroid gland weight in the study of 148 pHPT patients [16].…”

Section: Discussionmentioning

confidence: 83%

“…In several studies, serum 25(OH)D levels were related with urinary calcium excretion in patients with pHPT [19,28]; however, the present study indicated that urinary calcium excretion and the prevalence of renal stones were not associated with serum levels of 25(OH)D in female patients with pHPT, compatible with a previous report [27]. Taken together, the vitamin D state does not seem to influence the severity of renal manifestation, compared with its effect on bone in female patients with pHPT.…”

Section: Discussionmentioning

confidence: 99%

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Vitamin D Status Affects Osteopenia in Postmenopausal Patients with Primary Hyperparathyroidism

et al. 2008

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Abstract. Controversy still exists about whether vitamin D status is related to the severity of primary hyperparathyroidism (pHPT), although vitamin D insufficiency is frequent in pHPT. The present study was therefore performed to examine the relationships between vitamin D status and various parameters in 30 postmenopausal pHPT patients. BMD values were measured by dual-energy x-ray absorptiometry at the lumbar spine (L 2-4 ), femoral neck (FN) and distal one third of the radius (Rad 1/3). Serum levels of 25 hydroxy-vitamn D 3 [25(OH)D] and 1,25-dihydroxy vitamin D 3 [1,25(OH) 2 D 3 ] were 15.8 ± 3.5 µg/l and 69.3 ± 33.3 ng/l in pHPT patients, respectively. Serum levels of calcium and PTH seemed to be negatively correlated to serum 25(OH)D levels, although the differences were not significant. However, when subjects with the highest serum PTH levels (PTH>1000 pg/ml) were excluded from the analysis, the correlation was significant between serum 25(OH)D levels and PTH, indicating that vitamin D status affects the severity of pHPT when severe cases were excluded. In addition, serum levels of 1,25(OH) 2 D 3 were significantly and negatively correlated to serum 25(OH)D levels. On the other hand, serum levels of 25(OH)D were significantly and positively correlated to BMD (Z-score) at the lumbar spine, but not at the radius and femoral neck; however, serum 25(OH)D levels were not correlated to the levels of any bone metabolic indices measured. Moreover, serum levels of 25(OH)D were not related to urinary calcium and the tubular reabsorption rate of phosphorus, and they were similar in groups with and without renal stones. In conclusion, vitamin D status seemed to be related to the severity of disease in postmenopausal patients with pHPT. In particular, the relationship between serum 25(OH)D level and BMD at the lumbar spine was predominant. Primary hyperparathyroidism (pHPT) is a relatively common endocrine disorder that causes secondary osteoporosis. Patients with pHPT have reduced BMD, especially at the cortical bone [6,7]. Several studies suggested that pHPT was associated with an increased risk of vertebral and forearm fractures, and a subsequent decrease of fracture risk after parathyroidectomy [8][9][10][11][12], although our recent cross-sectional study sug- gested that the threshold of BMD for vertebral fractures was lower, especially at radial bone in female pHPT patients [13]. As for bone geometry, our previous study using peripheral quantitative computed tomography in female pHPT patients suggested that an excess of endogenous PTH stimulated periosteal bone formation, which might partly compensate for a decrease in bone strength induced by low BMD [14].As for vitamin D insufficiency, several studies indicated that vitamin D insufficiency is related to the severity of pHPT [15][16][17][18]. Rao et al. [16] reported that suboptimal vitamin D nutrition stimulates parathyroid adenoma growth, although other reports did not confirm this [17,19,20]. Several reports suggested that vitamin D receptor polymorphisms a...

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Section: Discussionsupporting

confidence: 34%

Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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Vitamin D Status Affects Osteopenia in Postmenopausal Patients with Primary Hyperparathyroidism

et al. 2008

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“…The pathophysiological mechanisms responsible for the low serum 25(OH)D level in PHPT are not completely clarified. The data obtained from several studies suggest that vitamin D status might influence the clinical and biological expression of PHTP [1,2,[4][5][6][7][8][9][10][11][12][13][14][15] and even recovery after surgical treatment [11,16,17], although some authors have not found such an association [18,19].…”

Section: Introductionmentioning

confidence: 99%

Biochemical effects of calcifediol supplementation in mild, asymptomatic, hyperparathyroidism with concomitant vitamin D deficiency

Isidro

Ruano

2009

Endocr

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It has been proposed to cautiously supplement with vitamin D to any patient with asymptomatic primary hyperparathyroidism (PHTP) and a plasma 25-hydroxyvitamin D [25(OH)D] concentration <50 nmol/l. Evidence about the safeness of this intervention is limited to two studies. Our aim was to prospectively assess the biochemical effects of one-year 25(OH)D supplementation in this context. Twenty-seven patients were included in this study. Calcifediol was started at a dose of 480-960 IU/24 h (8-16 microg/24 h) and adjusted up to a maximum of 960 IU/24 h (16 microg/24 h). Basal calcium, phosphate, albumin, total alkaline phosphatase (ALP), creatinine, 24 h calcium urinary excretion, intact PTH (iPTH) and 25(OH)D were measured before and during vitamin D supplementation. The mean basal 25(OH)D was 28.7 +/- 8.0 nmol/l, and at 12 months was 71.5 +/- 32.5 nmol/l (P = 0.00 vs. baseline). After 3, 6 and 12 months iPTH levels were 141.7 +/- 108.4 ng/l (P = 0.00 vs. baseline), 131.1 +/- 95.7 ng/l (P = 0.03 vs. baseline) and 162.2 +/- 139.3 ng/l (P = ns vs. baseline). Mean calcium did not change. Mean urinary calcium excretion increased significantly (basal: 5.7 +/- 2.9 mmol/24 h, 12 months: 7.9 +/- 4.9 mmol/24 h, P = 0.02). Cautious calcifediol supplementation significantly increased mean 25(OH)D and temporarily reduced mean iPTH. It did not change mean serum calcium, but urinary calcium excretion increased significantly. We suggest that serum calcium and 24 h calciuria be measured at regular intervals in patients with PHTP, while on calcifediol supplementation.

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“…It has also been proposed that changes in dietary habits and the increasing use of vitamin D preparations could contribute to an increased proportion of clinically asymptomatic cases [6]. It has been estimated that 80% of PHPT cases are asymptomatic [7], familial forms representing about 5% [8].…”

Section: Introductionmentioning

confidence: 99%

Parathyroid hormone-dependent hypercalcemia

Tőke

Patócs

Balogh

et al. 2009

Wien Klin Wochenschr

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The past fifteen years have resulted in great progress in our understanding of the pathogenesis and pathophysiology of hypercalcemic disorders occurring either sporadically or in a familial setting. This paper briefly reviews the clinically most important new knowledge on sporadic and hereditary forms of parathyroid hormone-dependent hypercalcemic disorders, with special emphasis on familial syndromes such as multiple endocrine neoplasia type 1 and type 2A, hyperparathyroidism-jaw tumor syndrome, familial isolated hyperparathyroidism, familial hypocalciuric hypercalcemia and neonatal severe primary hyperparathyroidism. In addition, the authors briefly present the most important clinical characteristics of 141 patients with parathyroid hormone-dependent hypercalcemia, including index patients of 18 families with hereditary disorders, diagnosed in a Hungarian endocrine center between 1997 and 2007.

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Correlations between Vitamin D Status and Biochemical/Clinical and Pathological Parameters in Primary Hyperparathyroidism

Abstract: Vitamin D deficiency leads to more severe bone disease, increased parathyroid tumor growth, and delayed postoperative recovery of parathyroid function in patients with primary hyperparathyroidism.

Cited by 65 publications

References 22 publications

Vitamin D Status Affects Osteopenia in Postmenopausal Patients with Primary Hyperparathyroidism

Vitamin D Status Affects Osteopenia in Postmenopausal Patients with Primary Hyperparathyroidism

Biochemical effects of calcifediol supplementation in mild, asymptomatic, hyperparathyroidism with concomitant vitamin D deficiency

Parathyroid hormone-dependent hypercalcemia

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