John P Bilezikian

CUNY Graduate Center, New York, New York, United States

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Publications (550)3419.82 Total impact

  • Mishaela R. Rubin · Claudio Marcocci · John P. Bilezikian ·
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    ABSTRACT: The effects of chronic parathyroid hormone (PTH) deficiency on the human skeleton are profound. In normal adults, bone mass is regulated by a precise balance between bone resorption and formation in the tightly regulated process of bone remodeling. PTH is a key regulator of the rate and extent of this process, which characteristically decreases with a reduction or absence of circulating PTH with a consequent increase in bone mass. Numerous lines of evidence employing biochemical, imaging, and histomorphometric methodologies have all demonstrated major abnormalities in a skeleton that is deprived of PTH. More recent studies have demonstrated that many of these abnormalities are reversible with PTH treatment.
    The Parathyroids, 12/2015: pages 771-779; , ISBN: 9780123971661
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    ABSTRACT: Primary hyperparathyroidism is a common endocrine disease that has undergone a series of changes in its clinical presentation over the past 60 years. The form of primary hyperparathyroidism (PHPT) that is seen most often in countries where biochemical screening is routine is described as “asymptomatic” because these individuals do not have classical signs and symptoms that are typically associated with hypercalcemia or high levels of parathyroid hormone. Four international workshops on the management of this form of PHPT have been held: 1991, 2002, 2008, and 2013. In this chapter, we present the results of the 2013 conference that led to a revision of the 2008 guidelines. It constitutes an update of evidence-based information about diagnostics, clinical features, and management of this disease. The conference also highlighted areas for which research is needed to clarify issues that remain uncertain or controversial.
    The Parathyroids, 12/2015: pages 489-497; , ISBN: 9780123971661
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    John P. Bilezikian · Robert Marcus · Michael A. Levine ·

    The Parathyroids, 12/2015: pages xxiii-xxv; , ISBN: 9780123971661
  • David W. Dempster · Shonni J. Silverberg · Elizabeth Shane · John P. Bilezikian ·
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    ABSTRACT: Primary hyperparathyroidism (PHPT) is a relatively common disorder that is often asymptomatic in the western world. Reports of the devastating effects of excess parathyroid hormone (PTH) secretion on the skeleton are both part of the history of the disease and seen now in settings where routine biochemical screening tests are not widespread and vitamin D deficiency is prevalent. Severe bone involvement is now distinctly uncommon. However, the question of bone involvement and fracture risk in PHPT, as part of the current phenotypic presentation of the disease, is an important issue. The introduction of bone densitometry helped to focus attention on the extent and sites of bone loss in mild, asymptomatic PHPT, especially with regard to involvement of the two major skeletal compartments, cortical and cancellous bone. Application of the technique of bone histomorphometry to the percutaneous bone biopsy has also provided much new insight into the effects of mild PHPT on the skeleton. Furthermore, the biopsy sample can be used to investigate the material properties of both the mineral and organic components of the bone matrix. This chapter reviews the histomorphometric characteristics of bone involvement in PHPT and the effects of the disease on the material properties of bone matrix.
    The Parathyroids, 12/2015: pages 429-445; , ISBN: 9780123971661
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    ABSTRACT: Primary hyperparathyroidism (PHPT) was originally described as a symptomatic disease with overt radiological skeletal manifestations. When the multichannel biochemical screening test became widely used in the early 1970s in the Western world, the predominant presentation of PHPT became an asymptomatic one. Radiological signs were relegated to a vanishingly small percentage of patients. In the late 1980s, when dual-energy X-ray absorptiometry (DXA) became widely used, skeletal manifestations could be readily demonstrated with this more sensitive imaging technology. With the application of even more sensitive imaging technologies, such as high resolution peripheral quantitative computed technology (HRpQCT), applications such as the trabecular bone score (TBS) to DXA, individual trabecula segmentation (ITS), and finite element analysis (FEA) modeling to HRpQCT, a more complete profile of skeletal involvement in PHPT has emerged. This chapter reviews this skeletal profile in asymptomatic PHPT, as assessed by these imaging approaches.
    The Parathyroids, 12/2015: pages 447-454; , ISBN: 9780123971661
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    ABSTRACT: Context: Canagliflozin is a sodium glucose co-transporter 2 inhibitor developed to treat type 2 diabetes mellitus (T2DM). Objective: To describe the effects of canagliflozin on bone mineral density (BMD) and bone biomarkers in patients with T2DM. Design: Randomized study, consisting of a 26-week, double-blind, placebo-controlled period and a 78-week, double-blind, placebo-controlled extension. Setting: 90 centers in 17 countries. Patients: Aged 55-80 years (N = 716) with T2DM inadequately controlled on a stable antihyperglycemic regimen. Interventions: Canagliflozin 100 or 300 mg or placebo once daily. Outcome: measures: BMD was assessed using dual-energy x-ray absorptiometry at weeks 26, 52, and 104. Bone strength was assessed using quantitative computed tomography and finite element analysis at week 52. Serum collagen type-1 beta-carboxy-telopeptide (beta-CTX), osteocalcin, and estradiol were assessed at weeks 26 and 52. Results: Canagliflozin doses of 100 and 300 mg were associated with a decrease in total hip BMD over 104 weeks, (placebo-subtracted changes: -0.9% and -1.2%, respectively), but not at other sites measured (femoral neck, lumbar spine, or distal forearm). No meaningful changes in bone strength were observed. At week 52, canagliflozin was associated with an increase in beta-CTX that was significantly correlated with a reduction in body weight, an increase in osteocalcin, and, in women, a decrease in estradiol. Conclusions: In older patients with T2DM, canagliflozin showed small but significant reductions in total hip BMD and increases in bone formation and resorption biomarkers, due at least in part to weight loss.
    The Journal of Clinical Endocrinology and Metabolism 11/2015; DOI:10.1210/jc.2015-1860 · 6.21 Impact Factor
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    ABSTRACT: Context: Canagliflozin is a sodium glucose co-transporter 2 inhibitor developed to treat type 2 diabetes mellitus (T2DM). Objective: To describe the effects of canagliflozin on bone fracture risk. Design and setting: Randomized phase 3 studies in patients with T2DM. Patients and interventions: Canagliflozin 100 and 300 mg were evaluated in the overall population of patients from 9 placebo- and active-controlled studies (N=10194), as well as in separate analyses of a single trial enriched with patients with a prior history/risk of cardiovascular disease (ie, CANagliflozin cardioVascular Assessment Study [CANVAS]; N=4327) and a pooled population of 8 non-CANVAS studies (N=5867). Outcome: Measures: Incidence of adjudicated fracture adverse events (AEs), fall-related AEs, and volume depletion-related AEs were assessed. Results: The incidence of fractures was similar with canagliflozin (1.7%) and non- canagliflozin (1.5%) in the pooled non-CANVAS studies. In CANVAS, a significant increase in fractures was seen with canagliflozin (4.0%) versus placebo (2.6%) that was balanced between upper and lower limbs. The incidence of fractures was higher with canagliflozin (2.7%) versus non-canagliflozin (1.9%) in the overall population that was driven by the increase of fractures in CANVAS. The incidence of reported fall-related AEs was low, but significantly higher with canagliflozin in CANVAS, potentially related to volume depletion-related AEs, but not significantly different in the pooled non-CANVAS studies and the overall population. Conclusions: Fracture risk was increased with canagliflozin treatment, driven by CANVAS patients, who were older, with prior history/risk of cardiovascular disease, and with lower baseline eGFR and higher baseline diuretic use. The increase in fractures may be mediated by falls; however, the cause of increased fracture risk with canagliflozin is unknown.
    The Journal of Clinical Endocrinology and Metabolism 11/2015; DOI:10.1210/jc.2015-3167 · 6.21 Impact Factor
  • Aline G Costa · John P Bilezikian ·
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    ABSTRACT: Chronic diseases typically require long-term treatment. Osteoporosis is a chronic disease in which fracture risk is high, and treatment is required to prevent fragility fractures. Denosumab is a fully human monoclonal antibody that inhibits RANK ligand, a powerful bone-resorbing cytokine. It is approved for individuals with osteoporosis who are at high risk for fracture. Clinical trial results confirm that denosumab is effective over the long term and has an excellent safety profile. In patients at high risk for osteoporotic fracture, therefore, long-term treatment with denosumab appears to present an attractive benefit profile.
    Current Osteoporosis Reports 10/2015; 13(6). DOI:10.1007/s11914-015-0295-7

  • 09/2015; 1(4):e255-e259. DOI:10.4158/EP14353.CR
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    ABSTRACT: In hypoparathyroidism, areal bone mineral density (BMD) by dual energy X-ray absorptiometry (DXA) is above average and skeletal indices by bone biopsy are abnormal. We used high resolution peripheral quantitative computed tomography (HRpQCT) and finite element analysis (FEA) to further investigate skeletal microstructure and estimated bone strength. We studied 60 hypoparathyroid subjects on conventional therapy using DXA, HRpQCT and FEA of the distal radius and tibia compared to normative controls from the Canadian Multicentre Osteoporosis Study. In hypoparathyroid women and men, areal BMD was above average at the lumbar spine and hip sites by DXA; radial BMD was also above average in hypoparathyroid women. Using HRpQCT, cortical volumetric BMD was increased in the hypoparathyroid cohort compared to controls at both the radius and tibia. Cortical porosity was reduced at both sites in pre- and postmenopausal women and at the tibia in young men with a downward trend at the radius in men. At the tibia, trabecular number was increased in premenopausal women and men and trabecular thickness was lower in women. Ultimate stress and failure load at both sites for the hypoparathyroid subjects were similar to controls. Using a linear regression model, at both radius and tibia, each increment in age decreased ultimate stress and failure load while each increment in duration of hypoparathyroidism increased these same indices. These results provide additional evidence for the critical role of parathyroid hormone in regulating skeletal microstructure. Longer disease duration may mitigate the adverse effects of age on estimated bone strength in hypoparathyroidism. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 08/2015; DOI:10.1002/jbmr.2609 · 6.83 Impact Factor
  • Aline G Costa · John P Bilezikian · E Michael Lewiecki ·
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    ABSTRACT: Sclerostin is a regulator of the osteoanabolic canonical Wnt signaling pathway, and thus helps to govern rates of bone formation. The Wnt pathway is also recognized as playing an important role in the pathophysiology of the chronic kidney disease - mineral and bone disorder (CKD-MBD). It also may serve as an interface between bone and the vascular system. Pharmacological inhibition of sclerostin has shown promise as an osteoanabolic approach to the treatment of osteoporosis. Inhibition of sclerostin is a potentially useful but unproven strategy in the management of CKD-MBD. Clinical trials with humanized monoclonal sclerostin antibodies (Scl-Ab) have shown a rapid initial increase in bone formation and a marked increase in bone mineral density. Although clinical data, to this point, in CKD are not available, animal models of low bone turnover CKD show that Scl-Ab improves trabecular bone volume and mineralization without affecting biochemical indices. Targeted clinical trials are needed to evaluate the potential effectiveness of Scl-Ab in CKD. Based upon the available data, there is potential not only for this new therapeutic class to improve skeletal health but perhaps also to have substantial cardiovascular benefits in CKD.
    Current Opinion in Nephrology and Hypertension 07/2015; 24(4):324-329. DOI:10.1097/MNH.0000000000000133 · 3.86 Impact Factor
  • Barbara C Silva · John P Bilezikian ·
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    ABSTRACT: Parathyroid hormone (PTH) is essential for the maintenance of calcium homeostasis through, in part, its actions to regulate bone remodeling. While PTH stimulates both bone formation and bone resorption, the duration and periodicity of exposure to PTH governs the net effect on bone mass, that is whether it is catabolic or anabolic. PTH receptor signaling in osteoblasts and osteocytes can increase the RANKL/OPG ratio, increasing both osteoclast recruitment and osteoclast activity, and thereby stimulating bone resorption. In contrast, PTH-induced bone formation is explained, at least in part, by its ability to downregulate SOST/sclerostin expression in osteocytes, permitting the anabolic Wnt signaling pathway to proceed. The two modes of administration of PTH, that is, continuous vs. intermittent, can regulate, in bone cells, different sets of genes; alternatively, the same sets of genes exposed to PTH in sustained vs. transient way, will favor bone resorption or bone formation, respectively. This article reviews the effects of PTH on bone cells that lead to these dual catabolic and anabolic actions on the skeleton. Copyright © 2015. Published by Elsevier Ltd.
    Current Opinion in Pharmacology 06/2015; 22. DOI:10.1016/j.coph.2015.03.005 · 4.60 Impact Factor
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    ABSTRACT: Patients with hypoparathyroidism have low circulating parathyroid (PTH) levels and higher cancellous bone volume and trabecular thickness. Treatment with PTH(1-84) was shown to increase abnormally low bone remodeling dynamics. In this work, we studied the effect of 1yr or 2yr PTH(1-84) treatment on cancellous and cortical bone mineralization density distribution (Cn. and Ct.BMDD) based on quantitative backscattered electron imaging (qBEI) in paired transiliac bone biopsy samples. The study cohort comprised 30 adult hypoparathyroid patients (14 treated for 1yr/16 treated for 2yr). At baseline, Cn.BMDD was shifted to higher mineralization densities in both treatment groups (average degree of mineralization Cn.CaMean +3.9% and +2.7%, p < 0.001) compared to reference BMDD. After 1yr PTH(1-84), Cn.CaMean was significantly lower than that at baseline (-6.3%, p < 0.001), while in the 2yr PTH(1-84) group Cn.CaMean did not differ from baseline. Significant changes of Ct.BMDD were observed in the 1yr treatment group only. The change in histomorphometric bone formation (mineralizing surface) was predictive for Cn.BMDD outcomes in the 1yr PTH(1-84) group, but not in the 2yr PTH(1-84) group. Our findings suggest higher baseline bone matrix mineralization consistent with the decreased bone turnover in hypoparathyroidism. PTH(1-84) treatment caused differential effects dependent on treatment duration which were consistent with the histomorphometric bone formation outcomes. The greater increase in bone formation during the first yr of treatment was associated with a decrease in bone matrix mineralization, suggesting that PTH(1-84) exposure to the hypoparathyroid skeleton has the greatest effects on BMDD early in treatment. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 06/2015; DOI:10.1002/jbmr.2588 · 6.83 Impact Factor
  • M D Walker · E Cong · J A Lee · A Kepley · C Zhang · D J McMahon · J P Bilezikian · S J Silverberg ·
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    ABSTRACT: We compared temporal trends in serum 25-hydroxyvitamin D and parathyroid hormone (PTH) in two primary hyperparathyroidism (PHPT) cohorts recruited 20 years apart. The prevalence of 25-hydroxyvitamin D levels <20 and <30 ng/mL declined by 30-50 %, respectively, and was accompanied by lower PTH. In the older cohort, higher PTH may be due to lower 25-hydroxyvitamin D. Vitamin D deficiency may exacerbate PHPT. Whether there have been temporal trends in 25-hydroxyvitamin D (25OHD) levels in PHPT is unclear. The prevalence of low vitamin D levels (25OHD <20 and <30 ng/mL) and associated biochemical and bone mineral density (BMD) profiles were assessed in two PHPT cohorts recruited over 20 years apart. This is a cross-sectional comparison of serum 25OHD levels, calciotropic hormones, and BMD between two PHPT cohorts recruited at the same hospital: the "old" (N = 103) and "new" (N = 100) cohorts were enrolled between 1984 and 1991 and between 2010 and 2014, respectively. Mean 25OHD levels were 26 % higher in the new cohort (23 ± 10 vs. 29 ± 10 ng/mL, p < 0.0001). Levels of 25OHD <20 and <30 ng/mL declined from 46 and 82 %, respectively, to 19 and 54 % (both p < 0.0001). Supplemental vitamin D use was common in the new (64 %) but not the old cohort (0 %). The new cohort demonstrated 33 % lower serum PTH levels (p < 0.0001). Neither serum nor urine calcium differed. BMD was higher in the new cohort at all skeletal sites (all p < 0.001). With the rise in vitamin D supplementation over the last two decades, low 25OHD levels are no longer common in PHPT patients in the New York area. Those with 25OHD <20 and <30 ng/mL have declined by over 50 and 30 %, respectively. The lower mean PTH levels in the new cohort are most likely accounted for by higher vitamin D intake. Whether improved vitamin D status also underlies the relatively higher BMD in the more vitamin D replete cohort of PHPT patients is unknown.
    Osteoporosis International 06/2015; DOI:10.1007/s00198-015-3199-6 · 4.17 Impact Factor
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    ABSTRACT: This article reports a taxonomic classification of rare skeletal diseases based on metabolic phenotypes. It was prepared by The Skeletal Rare Diseases Working Group of the International Osteoporosis Foundation (IOF) and includes 116 OMIM phenotypes with 86 affected genes. Rare skeletal metabolic diseases comprise a group of diseases commonly associated with severe clinical consequences. In recent years, the description of the clinical phenotypes and radiographic features of several genetic bone disorders was paralleled by the discovery of key molecular pathways involved in the regulation of bone and mineral metabolism. Including this information in the description and classification of rare skeletal diseases may improve the recognition and management of affected patients. IOF recognized this need and formed a Skeletal Rare Diseases Working Group (SRD-WG) of basic and clinical scientists who developed a taxonomy of rare skeletal diseases based on their metabolic pathogenesis. This taxonomy of rare genetic metabolic bone disorders (RGMBDs) comprises 116 OMIM phenotypes, with 86 affected genes related to bone and mineral homeostasis. The diseases were divided into four major groups, namely, disorders due to altered osteoclast, osteoblast, or osteocyte activity; disorders due to altered bone matrix proteins; disorders due to altered bone microenvironmental regulators; and disorders due to deranged calciotropic hormonal activity. This article provides the first comprehensive taxonomy of rare metabolic skeletal diseases based on deranged metabolic activity. This classification will help in the development of common and shared diagnostic and therapeutic pathways for these patients and also in the creation of international registries of rare skeletal diseases, the first step for the development of genetic tests based on next generation sequencing and for performing large intervention trials to assess efficacy of orphan drugs.
    Osteoporosis International 06/2015; 26(10). DOI:10.1007/s00198-015-3188-9 · 4.17 Impact Factor

  • 05/2015; DOI:10.1530/endoabs.37.OC3.5
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    ABSTRACT: Trabecular plate and rod microstructure plays a dominant role in the apparent mechanical properties of trabecular bone. With high-resolution computed tomography (CT) images, digital topological analysis (DTA) including skeletonization and topological classification was applied to transform the trabecular three-dimensional (3D) network into surface and curve skeletons. Using the DTA-based topological analysis and a new reconstruction/recovery scheme, individual trabecula segmentation (ITS) was developed to segment individual trabecular plates and rods and quantify the trabecular plate- and rod-related morphological parameters. High-resolution peripheral quantitative computed tomography (HR-pQCT) is an emerging in vivo imaging technique to visualize 3D bone microstructure. Based on HR-pQCT images, ITS was applied to various HR-pQCT datasets to examine trabecular plate- and rod-related microstructure and has demonstrated great potential in cross-sectional and longitudinal clinical applications. However, the reproducibility of ITS has not been fully determined. The aim of the current study is to quantify the precision errors of ITS plate-rod microstructural parameters. In addition, we utilized three different frequently used contour techniques to separate trabecular and cortical bone and to evaluate their effect on ITS measurements.
    Pattern Recognition Letters 04/2015; DOI:10.1016/j.patrec.2015.03.012 · 1.55 Impact Factor
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    ABSTRACT: The 2014 Santa Fe Bone Symposium provided a setting for the presentation and discussion of the clinical relevance of recent advances in the fields of osteoporosis and metabolic bone disease. The format included oral presentations of abstracts by endocrinology fellows, plenary lectures, panel discussions and breakout sessions, with ample opportunities for informal discussions before and after scheduled events. Topics addressed in these proceedings included a review of the important scientific publications in the past year, fracture prevention in patients with dysmobility and immobility, fracture liaison services for secondary fracture prevention, management of pre-menopausal osteoporosis, the role of bone microarchitecture in determining bone strength, measurement of microarchitecture in clinical practice and methods to improve the quality of bone density testing. This is a report of the proceedings of the 2014 Santa Fe Bone Symposium.
    Endocrine Research 03/2015; 40(2). DOI:10.3109/07435800.2015.1005746 · 1.28 Impact Factor
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    ABSTRACT: Context: The fourth International Workshop on the Management of Asymptomatic Primary Hyperparathyroidism (PHPT) has recently suggested that skeletal and renal imaging be routinely conducted. So far, no study has systematically assessed this issue. Objective: To evaluate the prevalence of kidney stones (KS), and vertebral fractures (VFs) in a cohort of patients with PHPT utilizing non-invasive imaging technology. Design: Prospective study evaluating patients consecutively diagnosed with PHPT in a single center over a five-year period (2009-2013). Setting: Referral Center. Patients: One-hundred-forty patients with PHPT [127 women (18 pre- and 109 postmenopausal) and 13 men; mean age 63.2±11 yrs] Main Outcomes Measures: The prevalence of KS by abdominal ultrasound, osteoporosis by DXA (Lumbar spine, femoral neck, total hip and distal 1/3 radius) and VFs by vertebral spine X-ray with attention to those categorized as symptomatic or asymptomatic. Results: Fifty-five percent of all subjects had KS by ultrasound, 62.9% had osteoporosis by T-score at any site and 35.1% had VFs by X-ray. There was no difference in the incidence of VFs and densitometric osteoporosis between symptomatic and asymptomatic patients (VFs: 34.4% vs 34.7%; osteoporosis by DXA: 59.4% vs 65.8%), while more KS were detected in symptomatic (78%) than asymptomatic (35.5%). Twenty-two percent of patients classified as asymptomatic at baseline without osteoporosis by DXA were found to have KS and/or VFs. Conclusions: Nephrolithiasis and VFs are common in asymptomatic subjects with PHPT. The results provide evidence in support of recent recommendations that a more proactive approach be taken to detect silent bone and stone disease in asymptomatic PHPT.
    Journal of Clinical Endocrinology &amp Metabolism 02/2015; 100(4):jc20143708. DOI:10.1210/jc.2014-3708 · 6.21 Impact Factor
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    ABSTRACT: Objective: Primary hyperparathyroidism (PHPT) is diagnosed by the presence of hypercalcemia and elevated or non-suppressed parathyroid hormone (PTH) levels. Although surgery is usually curative, some individuals fail or are unable or unwilling to undergo parathyroidectomy. In such individuals, targeted medical therapy may be of value. Cinacalcet normalized calcium and lowered PTH in patients with PHPT in several phase 2 and open-label studies. We compared cinacalcet and placebo in subjects with PHPT unable to undergo parathyroidectomy. Design: Phase 3, double-blind, multi-centred, randomized, placebo-controlled study. Methods: Sixty-seven subjects (78% women) with moderate PHPT were randomized (1:1) to cinacalcet or placebo for ≤28 weeks. Main outcome measure: Achievement of a normal mean corrected total serum calcium concentration of ≤10.3 mg dl-1 (2.575 mmol l-1). Results: Baseline median (Q1, Q3) serum PTH was 164.0 (131.0, 211.0) pg ml-1 and mean (SD) serum Ca was 11.77 (0.46) mg dl-1. Serum Ca normalized (≤10.3 mg dl-1) in 75.8% of cinacalcet- vs. 0% placebo-treated subjects (p<0.001). Corrected serum Ca decreased by ≥1.0 mg dl-1 from baseline in 84.8% of cinacalcet- vs. 5.9% of placebo-treated subjects (p<0.001). Least squares mean (SEM) plasma PTH change from baseline was 23.80% (4.18%) (cinacalcet) vs. 1.01% (4.05%) (placebo) (p<0.001). Similar numbers of subjects in the cinacalcet and placebo groups reported adverse events (27 vs. 20) and serious adverse events (3 vs. 4). Most commonly reported AEs were nausea and muscle spasms. Conclusions: These results demonstrate that cinacalcet normalizes serum calcium in this PHPT population and appears to be well tolerated.
    European Journal of Endocrinology 01/2015; 172(5). DOI:10.1530/EJE-14-0877 · 4.07 Impact Factor

Publication Stats

22k Citations
3,419.82 Total Impact Points


  • 1978-2015
    • CUNY Graduate Center
      New York, New York, United States
    • Columbia University
      • • College of Physicians and Surgeons
      • • Division of Endocrinology
      • • Department of Medicine
      • • Department of Pharmacology
      New York, New York, United States
  • 1984-2009
    • New York Medical College
      • Department of Medicine
      New York City, NY, United States
  • 2008
    • New Mexico Clinical Research and Osteoporosis Center
      Albuquerque, New Mexico, United States
  • 2007
    • University of Pittsburgh
      Pittsburgh, Pennsylvania, United States
  • 2005
    • Indiana University-Purdue University Indianapolis
      • Department of Medicine
      Indianapolis, IN, United States
    • Università degli Studi di Siena
      • Department of Medicine, Surgery and Neuroscience
      Siena, Tuscany, Italy
  • 2003-2005
    • University of California, San Francisco
      • Department of Epidemiology and Biostatistics
      San Francisco, CA, United States
  • 1990-2004
    • Gracie Square Hospital, New York, NY
      New York, New York, United States
  • 2002
    • Kaiser Permanente
      Oakland, California, United States
  • 1990-2001
    • Helen Hayes Hospital
      West Haverstraw, New York, United States
  • 1992-1997
    • Albert Einstein College of Medicine
      • • Department of Pathology
      • • Department of Medicine
      New York City, NY, United States
  • 1995
    • Temple University
      Philadelphia, Pennsylvania, United States
  • 1987
    • National Institutes of Health
      • Branch of Metabolic Diseases Branch (MDB)
      베서스다, Maryland, United States