Rubin M R, Sliney J, McMahon D J, Silverberg S J, Bilezikian J P
Department of Medicine, Division of Endocrinology, Metabolic Bone Diseases Unit, College of Physicians and Surgeons, Columbia University, 630 W. 168th St., New York, NY 10032, USA.
Osteoporos Int. 2010 Nov;21(11):1927-34. doi: 10.1007/s00198-009-1149-x. Epub 2010 Jan 22.
Hypoparathyroidism, a disorder characterized by low parathyroid hormone (PTH), is generally treated with oral calcium and vitamin D supplementation. We investigated the effects of PTH(1-84) treatment in 30 hypoparathyroid subjects for 24 months. PTH(1-84) treatment in hypoparathyroidism significantly reduced supplemental calcium and 1,25-dihydroxyvitamin D requirements without generally altering serum and urinary calcium levels.
Hypoparathyroidism, a disorder characterized by low PTH, is associated with hypocalcemia, hypercalciuria, and increased bone mineral density (BMD). Conventional therapy with calcium and 1,25-dihydroxyvitamin D can maintain the serum calcium concentration, but doses are high, and control is variable. We investigated the effects of human PTH(1-84) treatment in hypoparathyroidism.
Thirty subjects with hypoparathyroidism were treated in an open-label study of PTH(1-84) 100 µg every other day by subcutaneous injection for 24 months, with monitoring of calcium and vitamin D supplementation requirements, serum and 24 h urinary calcium excretion, and BMD by dual energy X-ray absorptiometry.
Requirements for supplemental calcium decreased significantly (3,030±2,325 to 1,661±1,267 mg/day (mean±SD); p<0.05), as did requirements for supplemental 1,25-dihydroxyvitamin D (0.68±0.5 to 0.40±0.5 µg/day; p<0.05). Serum calcium levels and 24 h urinary calcium excretion were mostly unchanged at 24 months. BMD increased at the lumbar spine by 2.9±4% from baseline (p<0.05), while femoral neck BMD remained unchanged and distal one third radial BMD decreased by 2.4±4% (p<0.05).
PTH(1-84) treatment in hypoparathyroidism significantly reduces supplemental calcium and 1,25-dihydroxyvitamin D requirements without generally altering serum and urinary calcium levels.
甲状旁腺功能减退症是一种以甲状旁腺激素(PTH)水平低为特征的疾病,通常采用口服补充钙和维生素D进行治疗。我们对30名甲状旁腺功能减退症患者进行了为期24个月的PTH(1-84)治疗效果研究。甲状旁腺功能减退症患者接受PTH(1-84)治疗可显著降低钙和1,25-二羟维生素D补充需求,且一般不会改变血清和尿钙水平。
甲状旁腺功能减退症是一种以PTH水平低为特征的疾病,与低钙血症、高钙尿症及骨密度(BMD)增加有关。传统的钙和1,25-二羟维生素D治疗可维持血清钙浓度,但剂量高且控制效果不一。我们研究了人PTH(1-84)治疗甲状旁腺功能减退症的效果。
30名甲状旁腺功能减退症患者参与一项开放标签研究,每隔一天皮下注射100μg PTH(1-84),持续24个月,同时监测钙和维生素D补充需求、血清和24小时尿钙排泄量,并用双能X线吸收法测量骨密度。
补充钙的需求显著降低(从3,030±2,325降至1,661±1,267毫克/天(均值±标准差);p<0.05),补充1,25-二羟维生素D的需求也显著降低(从0.68±0.5降至0.40±0.5微克/天;p<0.05)。24个月时血清钙水平和24小时尿钙排泄量大多未变。腰椎骨密度较基线增加了2.9±4%(p<0.05),而股骨颈骨密度未变,桡骨远端三分之一处骨密度下降了2.4±4%(p<0.05)。
甲状旁腺功能减退症患者接受PTH(1-84)治疗可显著降低钙和1,25-二羟维生素D补充需求,且一般不会改变血清和尿钙水平。