John P Bilezikian

Columbia University, New York, New York, United States

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Publications (504)3215.79 Total impact

  • 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 · 4.24 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 · 4.23 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 · 6.59 Impact Factor
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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; 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 · 1.41 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 · 6.31 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 · 3.69 Impact Factor
  • Natalie E Cusano, John P Bilezikian
    JAMA The Journal of the American Medical Association 12/2014; 312(24):2680-1. DOI:10.1001/jama.2014.9195 · 30.39 Impact Factor
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    ABSTRACT: Daily 20-mg and once-weekly 56.5-mg teriparatide (parathyroid hormone 1–34) treatment regimens increase bone mineral density (BMD) and prevent fractures, but changes in bone turnover markers differ between the two regimens. The aim of the present study was to explain changes in bone turnover markers using once-weekly teriparatide with a simulation model. Temporary increases in bone formation markers and subsequent decreases were observed during once-weekly teriparatide treatment for 72 weeks. These observations support the hypothesis that repeated weekly teriparatide administration stimulates bone remodeling, replacing old bone with new bone and leading to a reduction in the active remodeling surface. A simulation model was developed based on the iterative remodeling cycle that occurs on residual old bone. An increase in bone formation and a subsequent decrease were observed in the preliminary simulation. For each fitted time point, the predicted value was compared to the absolute values of the bone formation and resorption markers and lumbar BMD. The simulation model strongly matched actual changes in bone turnover markers and BMD. This simulation model indicates increased bone formation marker levels in the early stage and a subsequent decrease. It is therefore concluded that remodeling-based bone formation persisted during the entire treatment period with once-weekly teriparatide.
    12/2014; DOI:10.1038/boneres.2014.43
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    Natalie E Cusano, Mishaela R Rubin, John P Bilezikian
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    ABSTRACT: Hypoparathyroidism is a rare disease characterized by hypocalcemia and insufficient circulating levels of parathyroid hormone (PTH). Conventional therapy includes calcium and active vitamin D supplementation, often in large doses. Therapy with calcium and vitamin D, however, does not address certain problematic aspects of the disease, including abnormal bone metabolism and reduced quality of life. Hypoparathyroidism is the only classic endocrine deficiency disease for which the missing hormone, PTH, is not yet an approved treatment. PTH(1-84) may soon become a therapeutic option for patients with hypoparathyroidism. PTH(1-84) has been demonstrated to maintain serum calcium while reducing or eliminating requirements for calcium and active vitamin D supplementation. Data from bone densitometry, bone turnover markers and histomorphometry of bone biopsy specimens show positive structural and dynamic effects on the skeleton. PTH replacement therapy may also be associated with improved quality of life. PTH(1-84) replacement therapy for hypoparathyroidism is promising, although further acquisition of long-term data is needed.
    Expert Review of Endocrinology &amp Metabolism 10/2014; 10(1). DOI:10.1586/17446651.2015.971755
  • Cristiana Cipriani, John P Bilezikian
    Endocrine Practice 10/2014; 1(-1):1-8. DOI:10.4158/EP14313.CO · 2.59 Impact Factor
  • Neil Binkley, Robert Adler, John P Bilezikian
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    ABSTRACT: Osteoporosis becomes common with aging in both sexes, but is often ignored in men. The 2013 International Society for Clinical Densitometry consensus conference endorsed a Caucasian female referent database for T-score calculation in men. This recommendation has generated controversy and concern. Accumulating data indicate that at the same DXA-measured body mineral density (BMD) (g/cm(2)), men and women are at approximately the same fracture risk. With this point in mind, using the same database to derive the T-score in men and women is reasonable. As a result, a greater proportion of men who sustain a fragility fracture will have T-scores that are higher than they would if a male database were used; in fact, many men will fracture at T-scores that are "normal." This highlights the importance of diagnosing osteoporosis not just by T-score, but also by the presence of fragility fracture and/or by estimations of fracture risk as generated by tools such as the FRAX calculator. The practical consequences of this change in densitometric definition of osteoporosis in men should be monitored, including the proportion of men at risk identified and treated as well as defining the response to treatment in those assessed by this more comprehensive approach.
    Current Osteoporosis Reports 09/2014; DOI:10.1007/s11914-014-0242-z
  • Natalie E. Cusano, Mishaela R. Rubin, John P. Bilezikian
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    ABSTRACT: Hypoparathyroidism is a disease characterized by hypocalcemia and insufficient parathyroid hormone (PTH). It is a rare disorder that has been given an orphan disease designation in the United States and European Union. Hypoparathyroidism is the only endocrine deficiency disease for which the missing hormone, PTH, is not yet an approved therapy. Conventional therapy includes calcium and active vitamin D supplementation, often in large doses. Although serum calcium can be controlled with conventional therapy, it can be a challenge and, moreover, does not address other aspects of the disease, such as abnormal skeletal features and reduced quality of life. This review focuses on PTH replacement therapy in hypoparathyroidism, utilizing the full-length molecule PTH(1-84) as well as the fully active but truncated form PTH(1-34). PTH therapy addresses some aspects of the disease not ameliorated with conventional therapy.
    Best Practice & Research: Clinical Endocrinology & Metabolism 09/2014; 29(1). DOI:10.1016/j.beem.2014.09.001 · 4.91 Impact Factor
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    ABSTRACT: Objective: Asymptomatic primary hyperparathyroidism (PHPT) is routinely encountered in clinical practices of endocrinology throughout the world. This report distills an update of current information about diagnostics, clinical features, and management of this disease into a set of revised guidelines. Participants: Participants, representing an international constituency, with interest and expertise in various facets of asymptomatic PHPT constituted four Workshop Panels that developed key questions to be addressed. They then convened in an open 3-day conference September 19-21, 2013, in Florence, Italy, when a series of presentations and discussions addressed these questions. A smaller subcommittee, the Expert Panel, then met in closed session to reach an evidence-based consensus on how to address the questions and data that were aired in the open forum. Evidence: Preceding the conference, each question was addressed by a relevant, extensive literature search. All presentations and deliberations of the Workshop Panels and the Expert Panel were based upon the latest information gleaned from this literature search. Consensus Process: The expert panel considered all the evidence provided by the individual Workshop Panels and then came to consensus. Conclusion: In view of new findings since the last International Workshop on the Management of Asymptomatic PHPT, guidelines for management have been revised. The revised guidelines include: 1) recommendations for more extensive evaluation of the skeletal and renal systems; 2) skeletal and/or renal involvement as determined by further evaluation to become part of the guidelines for surgery; and 3) more specific guidelines for monitoring those who do not meet guidelines for parathyroid surgery. These guidelines should help endocrinologists and surgeons caring for patients with PHPT. A blueprint for future research is proposed to foster additional investigation into issues that remain uncertain or controversial.
    Journal of Clinical Endocrinology &amp Metabolism 08/2014; 99(10):jc20141413. DOI:10.1210/jc.2014-1413 · 6.31 Impact Factor
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    ABSTRACT: Objective: This report summarizes data on traditional and nontraditional manifestations of primary hyperparathyroidism (PHPT) that have been published since the last International Workshop on PHPT. Participants: This subgroup was constituted by the Steering Committee to address key questions related to the presentation of PHPT. Consensus was established at a closed meeting of the Expert Panel that followed. Evidence: Data from the 5-year period between 2008 and 2013 were presented and discussed to determine whether they support changes in recommendations for surgery or nonsurgical follow-up. Consensus Process: Questions were developed by the International Task Force on PHPT. A comprehensive literature search for relevant studies was undertaken. After extensive review and discussion, the subgroup came to agreement on what changes in the recommendations for surgery or nonsurgical follow-up of asymptomatic PHPT should be made to the Expert Panel. Conclusions: 1) There are limited new data available on the natural history of asymptomatic PHPT. Although recognition of normocalcemic PHPT (normal serum calcium with elevated PTH concentrations; no secondary cause for hyperparathyroidism)is increasing,data on the clinical presentation and natural history of this phenotypeare limited. 2) Although there are geographic differences in the predominant phenotypes of PHPT (symptomatic, asymptomatic, normocalcemic), they do not justify geography-specific management guidelines. 3) Recent data using newer, higher resolution imaging and analytic methods have revealed that in asymptomatic PHPT, both trabecular bone and cortical bone are affected. 4) Clinically silent nephrolithiasis and nephrocalcinosis can be detected by renal imaging and should be listed as a new criterion for surgery. 5) Current datadonot support a cardiovascular evaluation or surgery for the purpose of improving cardiovascular markers, anatomicalor functional abnormalities. 6) Some patients with mildPHPT have neuropsychological complaints and cognitive abnormalities, and some of these patients may benefit from surgical intervention. However, it is not possible at this time to predict which patients with neuropsychological complaints or cognitive issues will improve after successful parathyroid surgery.
    Journal of Clinical Endocrinology &amp Metabolism 08/2014; 99(10):jc20141415. DOI:10.1210/jc.2014-1415 · 6.31 Impact Factor
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    ABSTRACT: Bone mineralization density distribution (BMDD) is an important determinant of bone mechanical properties. The most available skeletal site for access to the BMDD is the iliac crest. Compared to cancellous bone much less information on BMDD is available for cortical bone. Hence, we analyzed complete transiliac crest bone biopsy samples from premenopausal women (n = 73) aged 25-48 years, clinically classified as healthy, by quantitative backscattered electron imaging for cortical (Ct.) and cancellous (Cn.) BMDD. The Ct.BMDD was characterized by the arithmetic mean of the BMDD of the cortical plates. We found correlations between Ct. and Cn. BMDD variables with correlation coefficients r between 0.42 and 0.73 (all p < 0.001). Additionally to this synchronous behavior of cortical and cancellous compartments, we found that the heterogeneity of mineralization densities (Ct.CaWidth), as well as the cortical porosity (Ct.Po) was larger for a lower average degree of mineralization (Ct.CaMean). Moreover, Ct.Po correlated negatively with the percentage of highly mineralized bone areas (Ct.CaHigh) and positively with the percentage of lowly mineralized bone areas (Ct.CaLow). In conclusion, the correlation of cortical with cancellous BMDD in the iliac crest of the study cohort suggests coordinated regulation of bone turnover between both bone compartments. Only in a few cases, there was a difference in the degree of mineralization of >1wt % between both cortices suggesting a possible modeling situation. This normative dataset of healthy premenopausal women will provide a reference standard by which disease- and treatment-specific effects can be assessed at the level of cortical bone BMDD.
    Calcified Tissue International 08/2014; 95(4). DOI:10.1007/s00223-014-9901-4 · 2.75 Impact Factor
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    ABSTRACT: Context: We previously reported on four patients treated with PTH(1-84) who recovered from postoperative hypoparathyroidism many years after onset. Because vascular endothelial growth factor (VEGF) has been shown to be necessary for the induction of PTH-mediated angiogenesis, we postulated a possible role for VEGF in the recovery of parathyroid function in these subjects. Objective: Our objective was to measure VEGF levels in subjects with hypoparathyroidism who regained parathyroid gland function and matched controls. Setting and Design: Subjects with hypoparathyroidism who regained parathyroid gland function were each matched to two hypoparathyroid controls by postoperative etiology, age (within 5 y), menopausal status, and duration of hypoparathyroidism. We measured serum VEGF levels at baseline and through 48 months of PTH(1-84) therapy. Results: VEGF levels increased after the initiation of PTH(1-84) therapy for the entire cohort, from 309.7 ± 162 pg/ml at baseline to 380.2 ± 178 pg/ml at 12 months (P = .03). Levels trended downward thereafter. There were no significant differences in VEGF levels between the subjects with recovery of parathyroid function and the matched controls. Conclusions: PTH(1-84) alters serum VEGF levels in subjects with hypoparathyroidism. Additional investigation is necessary to understand the mechanisms by which some subjects with postoperative hypoparathyroidism recover parathyroid gland function.
    Journal of Clinical Endocrinology &amp Metabolism 08/2014; 99(10):jc20141500. DOI:10.1210/jc.2014-1500 · 6.31 Impact Factor

Publication Stats

19k Citations
3,215.79 Total Impact Points

Institutions

  • 1978–2015
    • Columbia University
      • • College of Physicians and Surgeons
      • • Division of Endocrinology
      • • Department of Medicine
      • • Department of Pharmacology
      New York, New York, United States
  • 1978–2014
    • CUNY Graduate Center
      New York City, New York, United States
  • 2013
    • Universidade Católica de Brasília
      Brasília, Federal District, Brazil
  • 2009
    • CARDIO MD
      Newark, New Jersey, 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
  • 2006
    • University of Vermont
      Burlington, Vermont, United States
  • 2005
    • Università degli Studi di Siena
      • Department of Medicine, Surgery and Neuroscience
      Siena, Tuscany, Italy
    • Indiana University-Purdue University Indianapolis
      • Department of Medicine
      Indianapolis, IN, United States
  • 2003–2005
    • University of California, San Francisco
      • Department of Epidemiology and Biostatistics
      San Francisco, CA, United States
    • Duke University
      • Department of Surgery
      Durham, North Carolina, United States
  • 1990–2004
    • Gracie Square Hospital, New York, NY
      New York, New York, United States
  • 2002
    • Kaiser Permanente
      Oakland, California, United States
  • 2001
    • University of Maine
      Orono, Minnesota, United States
  • 2000
    • McMaster University
      • Department of Medicine
      Hamilton, Ontario, Canada
  • 1990–2000
    • Helen Hayes Hospital
      West Haverstraw, New York, United States
  • 1999
    • Universidade Federal do Paraná
      Curityba, Paraná, Brazil
  • 1998
    • The Jackson Laboratory
      Bar Harbor, Maine, United States
  • 1984–1998
    • 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
      베서스다, Maryland, United States