Vitamin D Status Affects Osteopenia in Postmenopausal Patients with Primary Hyperparathyroidism

Abstract

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...

Vitamin D in Primary Hyperparathyroidism: Effects on Clinical, Biochemical, and Densitometric Presentation

“…Vitamin D-deficient PHPT patients have been reported to have higher PTH levels, greater adenoma weight, lower aBMD particularly at cortical sites, higher bone turnover, and increased fracture risk (1,2,(12)(13)(14)(15)(16)(17)(18)(19). Our disparate findings may be explained by the fact that these earlier studies were performed in settings (geographic or temporal) where long-standing, severe vitamin D deficiency and perhaps low calcium intake were commonplace.…”

Vitamin D Status in Patients with Recurrent Kidney Stones

“…The reason for the low levels of 25(OH)D and the correlation with PTH in the stone formers of our study is not clear; the complexity of PTH and vitamin D interactions, resulting in muscle and bone abnormalities in the general population [10,] have been related recently with the role of fibroblast growth factor 23 (FGF-23) and KLOTHO -regulators of phosphate excretion, PTH and calcitriol synthesis [11]. Reduced bone mass and high risk for osteoporotic fractures as a consequence of PTH and vitamin D abnormalities have also been documented in calcium stone formers [12,13,14,15], as well as a contributing role of FGF-23 and KLOTHO gene polymorphism in the pathogenesis of calcium nephrolithiasis [16,17].…”

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

“…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].…”