Locker F G, Silverberg S J, Bilezikian J P
Department of Medicine, College of Physicians & Surgeons, Columbia University, New York, New York 10032, USA.
Am J Med. 1997 Jun;102(6):543-50. doi: 10.1016/s0002-9343(97)00053-3.
The purpose of this study was to investigate whether dietary calcium intake in primary hyperparathyroidism is associated with differences in bone mineral density and biochemical parameters, and to determine whether these observations are related to 1,25-dihydroxyvitamin D.
Dietary calcium intake was determined from diet records in 71 unselected patients enrolled in an ongoing longitudinal study on the natural history of primary hyperparathyroidism. Subjects were placed into one of three dietary calcium groups based on their mean dietary calcium intake: very low (< 300 mg/day; mean = 199 +/- 14), low (300 to 800 mg/day; mean = 529 +/- 21), and US RDA (> 800 mg/day; mean = 1023 +/- 73). Biochemical indices were indicative of patients with modern day primary hyperparathyroidism, showing mild hypercalcemia (2.79 +/- 0.02 mmol/L), low normal serum phosphorus (0.90 +/- 0.03 mmol/L), elevated parathyroid hormone levels by midmolecule (764 +/- 69 pg/mL) and immunoradiometric (118 +/- 8 pg/mL) assays, and high normal 1,25-dihydroxyvitamin D (60 +/- 3 pg/mL) and urinary calcium excretion (6.3 +/- 0.4 mmol/day). Bone mineral density was measured by dual energy x-ray absorptiometry at the lumbar spine, right femoral neck and distal third of the nondominant radius for each subject.
Over the entire range, there was no significant effect of dietary calcium on serum parathyroid hormone levels, calcium, phosphorus, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, urinary calcium excretion, or bone mineral density of the lumbar spine, femoral neck or distal one-third radius. Serum 1,25-dihydroxyvitamin D was elevated in 37 patients (52%). Despite similarly low dietary calcium intake among patients with normal and elevated levels of 1,25-dihydroxyvitamin D (477 +/- 50 mg/day vs. 533 +/- 40 mg/day), patients with elevated levels of 1,25-dihydroxyvitamin D had higher parathyroid hormone levels by immunoradiometric assay (136 +/- 11 pg/mL vs. 97 +/- 10 pg/mL; P < .05), and urinary calcium (7.4 +/- 0.05 mmol/day vs. 5.1 +/- 0.05 mmol/day; P < .05 or 0.82 +/- 0.04 mmol/mmol creatinine vs. 0.56 +/- 0.04 mmol/mmol creatinine; P < .01).
The data suggest that patients with normal levels of 1,25-dihydroxyvitamin D can liberalize their calcium intake without adverse consequences. However those with elevated levels of 1,25-dihydroxyvitamin D are advised to be more restrictive in order to prevent hypercalciuria.
本研究旨在调查原发性甲状旁腺功能亢进症患者的膳食钙摄入量是否与骨矿物质密度及生化指标的差异相关,并确定这些观察结果是否与1,25 - 二羟维生素D有关。
在一项正在进行的关于原发性甲状旁腺功能亢进症自然病史的纵向研究中,通过饮食记录确定了71例未经挑选患者的膳食钙摄入量。根据平均膳食钙摄入量,受试者被分为三个膳食钙组之一:极低(<300毫克/天;平均 = 199±14)、低(300至800毫克/天;平均 = 529±21)和美国推荐膳食摄入量(>800毫克/天;平均 = 1023±73)。生化指标表明这些患者患有现代原发性甲状旁腺功能亢进症,表现为轻度高钙血症(2.79±0.02毫摩尔/升)、血清磷略低于正常(0.9±0.03毫摩尔/升)、通过中分子(764±69皮克/毫升)和免疫放射分析(118±8皮克/毫升)测定甲状旁腺激素水平升高,以及1,25 - 二羟维生素D和尿钙排泄略高于正常(分别为60±3皮克/毫升和6.3±0.4毫摩尔/天)。通过双能X线吸收法测量了每位受试者腰椎、右股骨颈和非优势侧桡骨远端三分之一处的骨矿物质密度。
在整个范围内,膳食钙对血清甲状旁腺激素水平、钙、磷、25 - 羟维生素D、1,25 - 二羟维生素D、尿钙排泄或腰椎、股骨颈或桡骨远端三分之一处的骨矿物质密度均无显著影响。37例患者(52%)的血清1,25 - 二羟维生素D升高。尽管1,25 - 二羟维生素D水平正常和升高的患者膳食钙摄入量同样较低(分别为477±50毫克/天和533±40毫克/天),但1,25 - 二羟维生素D水平升高的患者通过免疫放射分析测定的甲状旁腺激素水平更高(分别为136±11皮克/毫升和97±10皮克/毫升;P<.05),尿钙水平也更高(分别为7.4±0.05毫摩尔/天和5.1±0.05毫摩尔/天;P<.05或分别为0.82±0.04毫摩尔/毫摩尔肌酐和0.56±0.04毫摩尔/毫摩尔肌酐;P<.01)。
数据表明,1,25 - 二羟维生素D水平正常的患者可以放宽钙摄入量而无不良后果。然而,建议1,25 - 二羟维生素D水平升高的患者更严格限制钙摄入,以预防高钙尿症。