2005
Continuous PTH and PTHrP Infusion Causes Suppression of Bone Formation and Discordant Effects on 1,25(OH)2Vitamin D
Horwitz MJ, Tedesco MB, Sereika SM, Syed MA, Garcia‐Ocaña A, Bisello A, Hollis BW, Rosen CJ, Wysolmerski JJ, Dann P, Gundberg C, Stewart AF. Continuous PTH and PTHrP Infusion Causes Suppression of Bone Formation and Discordant Effects on 1,25(OH)2Vitamin D. Journal Of Bone And Mineral Research 2005, 20: 1792-1803. PMID: 16160737, DOI: 10.1359/jbmr.050602.Peer-Reviewed Original ResearchConceptsContinuous infusionVitamin DBone formationPhosphorus handlingRenal calciumIGF-1Anabolic skeletal responseDoses of PTHVitamin D homeostasisVitamin D metabolismPlasma IGF-1Vitamin D productionVitamin D synthesisOsteoblastic bone formationHealthy young adultsRenal PTH receptorsContinuous PTHCalcemic responseD homeostasisPrimary hyperparathyroidismHumoral hypercalcemiaSerum calciumD metabolismBone turnoverBone resorption
2003
A Syndrome of Hypocalciuric Hypercalcemia Caused by Autoantibodies Directed at the Calcium-Sensing Receptor
Kifor O, Moore FD, Delaney M, Garber J, Hendy GN, Butters R, Gao P, Cantor TL, Kifor I, Brown EM, Wysolmerski J. A Syndrome of Hypocalciuric Hypercalcemia Caused by Autoantibodies Directed at the Calcium-Sensing Receptor. The Journal Of Clinical Endocrinology & Metabolism 2003, 88: 60-72. PMID: 12519831, DOI: 10.1210/jc.2002-020249.Peer-Reviewed Original ResearchMeSH KeywordsAdultAutoantibodiesBlood Physiological PhenomenaBlotting, WesternCalciumCell LineEnzyme ActivationExtracellular SpaceFemaleHumansHypercalcemiaImmunoglobulinsInositol PhosphatesMiddle AgedMitogen-Activated Protein KinasesParathyroid GlandsParathyroid HormonePedigreePeptide FragmentsReceptors, Calcium-SensingReceptors, Cell SurfaceSyndromeConceptsPTH-dependent hypercalcemiaFamilial hypocalciuric hypercalcemiaHeterozygous inactivating mutationsHypocalciuric hypercalcemiaPTH releaseParathyroid cellsCaR's extracellular domainPatient seraExtracellular amino terminusAnti-CaR antiserumNormocalcemic control subjectsHuman parathyroid cellsBovine parathyroid cellsCalcium-sensing receptorAnti-CAR antibodyCaR-transfected HEK293 cellsInactivating mutationEffect of serumExtracellular domainAntithyroid antibodiesAutoimmune manifestationsEndocrine dysfunctionControl subjectsBlood calciumCaR gene
2000
POSTTRANSPLANT BONE DISEASE: EVIDENCE FOR A HIGH BONE RESORPTION STATE
Cayco A, Wysolmerski J, Simpson C, Mitnick M, Gundberg C, Kliger A, Lorber M, Silver D, Basadonna G, Friedman A, Insogna K, Cruz D, Bia M. POSTTRANSPLANT BONE DISEASE: EVIDENCE FOR A HIGH BONE RESORPTION STATE. Transplantation 2000, 70: 1722-1728. PMID: 11152104, DOI: 10.1097/00007890-200012270-00011.Peer-Reviewed Original ResearchConceptsLong-term renal transplant recipientsRenal transplant recipientsBone mineral densityTransplant recipientsBone lossBone resorptionFirst post-transplant yearCumulative prednisone doseElevated urinary levelsIntact parathyroid hormonePercent of patientsDuration of dialysisPost-transplant yearPrevalence of osteoporosisCross-sectional studyLoss of boneBone resorption statePrednisone doseYear posttransplantIntact PTHRenal transplantLevels of calciumRenal functionSerum levelsTransplant year