背景：原发性甲状旁腺功能亢进（PHPT），以各种临床形式表现的病症，是一个重大的健康问题。尽管甲状旁腺激素（PTH）水平升高，但正常血钙的原发性甲状旁腺功能亢进（NPHPT）的特征是正常的钙血症。维生素D缺乏可导致NPHPT的临床谱和复杂性。低维生素D水平可以提高PTH，很难区分NPHPT和继发性甲状旁腺功能亢进。此外,它可能会掩盖高钙血症，导致对疾病严重程度的低估。我们的研究旨在揭示这些复杂性通过调查正常血钙和高血钙PHPT患者的临床，荷尔蒙，和生化模式，包括他们的维生素D状态。材料：在这项回顾性研究中，我们招募了60例PHPT患者，这些患者使用联合超声检查证实了自主性甲状旁腺功能，放射性核素扫描,和甲状旁腺功能指数计算。我们评估了白蛋白校正的血钙,钙尿症,PTH,25(OH)D级,血清磷酸盐，骨矿物质密度，和主要临床症状(骨折，肾结石）。在正常和高钙血症，维生素D缺乏和维生素D不缺乏组之间进行了比较分析和相关性研究。
结果：中位年龄为62岁，51.66％（31/60）的血钙正常，46.66％（29/60）的25（OH）D水平不足。在25（OH）D低于20ng/mL的组中，我们观察到白蛋白校正的钙血症水平降低，与适当的25（OH）D水平组相比，PTH没有显着增加。25（OH）D缺乏组（20/60，33.33％和8/60，13.33％）的NPHPT频率和骨折风险明显高于适当组（11/60，18.33％和1/60，1.66％），OR=4.7（p<0.004）和OR=9.7（p<0.027），分别。我们还发现PTH与腺瘤大小呈正相关，甲状旁腺功能指数和腺瘤大小，以及PTH和磷酸盐水平。然而,25（OH）D和磷酸盐水平之间的相关性为负和中等（rho=-0.504，p<0.001），为我们对这些关系的理解增加了一层新的复杂性。
结论：我们的研究提供了对维生素D状态与正常血钙PHPT之间联系的重要见解。我们发现，缺乏维生素D的正常血钙的PHPT患者骨折风险增加，这需要细致的监测和可能的补充维生素D。这应该小心地进行，以避免加剧高钙血症或高钙尿症。需要进一步的研究来完善这些管理策略，并加深我们对所分析参数之间复杂关系的理解。
BACKGROUND: Primary hyperparathyroidism (PHPT), a condition that manifests in various clinical forms, is a significant health concern. Normocalcemic primary hyperparathyroidism (NPHPT) is characterized by normal calcemia despite elevated parathyroid hormone (PTH) levels. Vitamin D deficiency can contribute to the clinical spectrum and complexity of NPHPT. Low vitamin D levels can elevate PTH, making it difficult to distinguish between NPHPT and secondary hyperparathyroidism. Additionally, it might mask hypercalcemia, leading to an underestimation of the disease severity. Our
study aims to shed light on these complexities by investigating normocalcemic and hypercalcemic PHPT patient\'s clinical, hormonal, and biochemical patterns, including their vitamin D status. Materials: In this retrospective
study, we enrolled 60 PHPT patients with autonomous parathyroid function confirmed using a combination of ultrasonography, radionuclide scan, and parathyroid function index calculation. We evaluated the albumin-corrected calcemia, calciuria, PTH, 25(OH)D level, serum phosphate, bone mineral density, and major clinical symptoms (fracture, nephrolithiasis). A comparative analysis and a correlation
study were performed between normo- and hypercalcemic and vitamin D-deficient and vitamin D-non-deficient groups.
RESULTS: The median age was 62 years, 51.66% (31/60) being normocalcemic and 46.66% (29/60) presenting a deficient 25(OH)D level. In the group with 25(OH)D below 20 ng/mL, we observed a reduced level of albumin-corrected calcemia, without a significant increase of PTH compared to the adequate 25(OH)D level group. The frequency of the NPHPT and the risk of fracture were significantly higher in the deficient 25(OH)D group (20/60, 33.33% and 8/60, 13.33%) than in the adequate one (11/60, 18.33% and 1/60, 1.66%) with OR=4.7 (p<0.004) and OR=9.7 (p<0.027), respectively. We also found a positive correlation between PTH and adenoma size, the parathyroid function index and adenoma size, as well as PTH and phosphate levels. However, the correlation between 25(OH)D and phosphate levels was negative and moderate (rho=-0.504, p<0.001), adding a new layer of complexity to our understanding of these relationships.
CONCLUSIONS: Our
study provided significant insight into the link between vitamin D status and normocalcemic PHPT. We found that vitamin D-deficient patients with normocalcemic PHPT have an increased fracture risk, which requires meticulous monitoring and possible supplementation with vitamin D. This should be done carefully to avoid exacerbating hypercalcemia or hypercalciuria. Further research is needed to refine these management strategies and deepen our understanding of the complex relationships between the analyzed parameters.
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