Long-Term Treatment of 12 Children with Chronic Hypoparathyroidism: A Randomized Trial Comparing Synthetic Human Parathyroid Hormone 1-34 versus Calcitriol and Calcium
Open Access
- 1 June 2010
- journal article
- research article
- Published by The Endocrine Society in Journal of Clinical Endocrinology & Metabolism
- Vol. 95 (6), 2680-2688
- https://doi.org/10.1210/jc.2009-2464
Abstract
Context: Hypoparathyroidism is among the few hormonal insufficiency states not treated with replacement of the missing hormone. This is the first randomized controlled study in children comparing treatment with synthetic human PTH 1-34 and calcitriol. Objective: The primary objective was to assess the efficacy and safety of long-term PTH 1-34 vs. calcitriol treatment in the maintenance of normal serum calcium values and renal calcium excretion in children with hypoparathyroidism. Setting: The study was conducted at a clinical research center. Subjects: Subjects included 12 children aged 5–14 yr with chronic hypoparathyroidism and without severe renal or hepatic insufficiency. Study Design: The study was a 3-yr randomized parallel trial comparing twice-daily calcitriol (plus calcium and cholecalciferol in four daily doses) vs. sc PTH 1-34 treatment, with weekly or biweekly monitoring of serum and urine calcium. Results: Mean predose serum calcium levels were maintained at, or just below, the normal range, and urine calcium levels remained in the normal range throughout the 3-yr study, with no significant differences between treatment groups. Creatinine clearance, corrected for body surface area, did not differ between groups and remained normal throughout the study. Markers of bone turnover were mildly elevated during PTH 1-34 therapy and remained within the normal range during calcitriol therapy. Mean bone mineral density Z-scores at the anterior-posterior lumbar spine, femoral neck, distal radius, and whole body remained within the normal range and did not differ between groups throughout the study. Similarly, height and weight percentiles did not differ between treatment groups and remained normal throughout the 3-yr follow-up. Conclusion: We conclude that PTH 1-34 therapy is safe and effective in maintaining stable calcium homeostasis in children with hypoparathyroidism. Additionally, PTH 1-34 treatment allowed normal skeletal development because there were no differences in bone mineral accrual, linear growth, or weight gain between the two treatment arms over the 3-yr study period.Keywords
This publication has 15 references indexed in Scilit:
- Effects of OnceVersusTwice-Daily Parathyroid Hormone 1–34 Therapy in Children with HypoparathyroidismJournal of Clinical Endocrinology & Metabolism, 2008
- The Bone Mineral Density in Childhood Study: Bone Mineral Content and Density According to Age, Sex, and RaceJournal of Clinical Endocrinology & Metabolism, 2007
- Long-Term Treatment of Hypoparathyroidism: A Randomized Controlled Study Comparing Parathyroid Hormone-(1–34)VersusCalcitriol and CalciumJournal of Clinical Endocrinology & Metabolism, 2003
- Skeletal Changes in Rats Given Daily Subcutaneous Injections of Recombinant Human Parathyroid Hormone (1-34) for 2 Years and Relevance to Human SafetyToxicologic Pathology, 2002
- Effect of Parathyroid Hormone (1-34) on Fractures and Bone Mineral Density in Postmenopausal Women with OsteoporosisNew England Journal of Medicine, 2001
- Mutations in the Ca(2+)-sensing receptor gene cause autosomal dominant and sporadic hypoparathyroidismHuman Molecular Genetics, 1996
- Parathyroid Hormone for the Prevention of Bone Loss Induced by Estrogen DeficiencyNew England Journal of Medicine, 1994
- Restoration of spinal bone in osteoporotic men by treatment with human parathyroid hormone (1–34) and 1,25-dihydroxyvitamin DJournal of Bone and Mineral Research, 1986
- Hypercalciuria Associated With Long-term Administration of Calcitriol (1,25-Dihydroxyvitamin D3)American Journal of Diseases of Children, 1986
- Short-term effects of synthetic human parathyroid hormone-(1--34) administration on bone mineral metabolism in osteoporotic patients.JCI Insight, 1981