Reduced Parathyroid Hormone-Stimulated 1,25-Dihydroxyvitamin D Production in Vitamin D Sufficient Postmenoposual Women with Low Bone Mass and Idiopathic Secondary Hyperparathyroidism |
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| Institution: | 1. University of Maryland School of Medicine, Baltimore, Maryland;2. Baltimore Washington Medical Center Baltimore, Maryland;3. University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;4. Boston University Medical Center, Boston, Massachusetts;1. Endocrinology and Metabolism Institute, Cleveland Clinic Foundation, Cleveland, Ohio;2. Education Institute, Cleveland Clinic Lerner College of Medicine, Cleveland, Ohio;3. Yale Pediatric Endocrinology Department, Yale University School of Medicine, New Haven, Connecticut;4. Yale Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, Connecticut;5. Pathology and Laboratory Medicine Institute, Cleveland Clinic Foundation, Cleveland, Ohio;1. Sapienza University of Rome Experimental Medicine Department Medical Physiopathology, Food Science and Endocrinology Section Food Science and Human Nutrition Research Unit;1. Department of Orthopedic Surgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel;2. Maccabi Healthcare Services, Israel;3. Center for Clinical Quality and Safety, Jerusalem, Israel;4. Endocrinology and Metabolism Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel;1. Barbara Davis Center for Diabetes, University of Colorado Anschutz Medical Center Aurora, Colorado;2. Diabetes Technology and Therapeutics;3. University of Colorado Anschutz Medical Campus, Aurora, Colorado;4. School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado;5. Atlanta Diabetes Associates, Atlanta, Georgia;6. Rainier Clinical Research Center, Renton, Washington;7. CPC Clinical Research and Department of Medicine/Cardiology, University of Colorado School of Medicine, Aurora, Colorado |
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| Abstract: | ObjectiveDistinguishing secondary hyperparathyroidism (sHPT) from eucalcemic primary hyperparathyroidism (EC-pHPT) is important. The objective of this study was to measure parathyroid hormone (PTH)-stimulated production of 1α,25-dihydroxyvitamin D (1,25OH]2D) in early postmenopausal patients with idiopathic sHPT, who also fit the criteria for EC-pHPT, compared to age-matched controls.MethodsIn this pilot case-control study, postmenopausal women aged 44 to 55 years with normal serum calcium (Ca), glomerular filtration rate (GFR) ≥65 mL/min, and 25-hydroxyvitamin D (25OH]D) ≥75 nmol/L (30 ng/mL) were given an 8 hour infusion of PTH(1-34), 12 pmol/kg/h. Patients (n = 5) had elevated PTH, normal 1,25(OH)2D, and no hypercalciuria. Controls (n = 5) had normal PTH. At baseline, 4, and 8 hours, serum Ca, creatinine (Cr), phosphorus (P), 1,25(OH)2D, fibroblast growth factor (FGF23), and 24,25(OH)2D as well as urine Ca, P, Cr, and cAMP/GFR were measured. The fractional excretion of calcium (FeCa) and tubular reabsorption of phosphorus (TMP)/GFR were calculated.ResultsPatients had lower 1,25(OH)2D levels (± SD) than controls at 4 (39.8 ± 6.9 versus 58.8 ± 6.7; P = .002) and 8 hours (56.4 ± 9.2 versus 105 ± 2.3; P = .003) of PTH infusion, attenuated after adjusting for higher body mass index (BMI) in patients (P = .05, .04), respectively. The 24,25(OH)2D levels were lower in patients than controls (1.9 ± 0.6 versus 3.4 ± 0.6, respectively; P = .007). No differences were seen in serum Ca or P, urine cAMP/GFR, TRP/GFR, FeCa, or PTH suppression at 8 hours (patients 50%, controls 64%).ConclusionVitamin D sufficient patients who fit the criteria for EC-pHPT had reduced PTH-stimulated 1,25(OH)2D compared to controls, partially attributable to their higher BMI. Other causes of reduced 1,25(OH)2D production ruled out were excessive catabolism of vitamin D metabolites, elevated FGF23, and CYP27B1 mutation. Elevated BMI and idiopathic reduced PTH-stimulated 1,25(OH)2D production should be considered in the differential of sHPT. (Endocr Pract. 2013;19:91-99) |
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