BACKGROUND:ResearchesindicatethatpatientswithWilsondisease(WD)haveabnormalskeletalmetabolism,whichisinducedbyvariousfactors.OBJECTIVE:ToprobeintothechangingcharacteristicsofabnormalskeletalmetabolisminWDpatientsandobservetheeffectofdecoppertherapy.DESIGN:Case-contrastandself-controlstudy.SETTING:DepartmentofNeurology,AffiliatedHospitalofNeurologicalInstitute,AnhuiCollegeofTraditionalChineseMedicine.PARTICIPANTS:Atotalof35patientswithWDincluding21malesand14femalesagedfrom10to42yearswiththemeanageof(20±8)yearswereselectedfromDepartmentofNeurology,AffiliatedHospitalofNeurologicalInstitute,AnhuiCollegeofTraditionalChineseMedicinefromSeptember2000toFebruary2001.Allthepatientswereincompliancewiththediagnosticcriteria:historyoffamilyheredity;conesymptomsinvitro,physicalsignorliversymptoms;positiveKayser-Fleischerring;serumcopperprotein＜200mg/LorAcopperoxidase＜0.2;urinecopper＞1.6μmol/24hours;livercopper＞250μg/g(dryweight).Thecontrolgroupwasselectedfrom25casesofhealthinpidualsincluding13malesand12femalesagedfrom16to35yearswiththemeanageof(22±6)years.Allpatientswhoparticipatedinthestudywereinformedfirstandconsented.METHODS:Patientsintreatmentgroupweretreatedwithvenousinjectionof1.0gsodiumdimercaptosulfonate,onceadayfortotally6successivedays.Andthen,patientsrestedfor2days.Thisprocedurementionedabovewasregardedasacourse,andthetreatmentlastedfor4-8courses.Beforeandafterinjectionofsodiumdimercaptosulfonate,serumcalcitonin(CT),osteocalcin(BGP),parathyroidhormone(PTH)and1,25-(OH)2VitD3weremeasuredwithradio-immunitymethod:blood,urinecalcium,phosphorumandurinecreatinineweremeasuredwithbiochemicalanalyzer;urinedihydropyrimidinedehydrogenase(DPD)wasdetectedwithenzyme-immunitymethod;bonemineraldensity(BMD)wascheckedattheonethirdfromdistalendofulnaandradiuswithsingle
