糖皮質激素致股骨頭壞死?

看到了先輩的耐煩講授非常謝謝！我也是之前恰好有看到這塊內容～第一反響便是說的跟之前看的不一樣啊，大神錯了～之後有機遇遇好好相識一下的～底下的答案就改成表明為何糖皮質激素會導致骨質疏鬆的答案吧^_^

。。。。。。。。。

攔截樓上的答案，詳細緣故起因如下～測驗將近大家隨意看一下吧～

GLUCOCORTICOID-INDUCEDOSTEOPOROSIS

Themostcommonsecondarycauseofosteoporosisisglucocorticoid

induced.Thisisoftenaresultofpharmacologicdosesofsteroidsusedtotreat

inflammatoryorautoimmunedisorders.Generally,itisconsideredthatglu-

cocorticoids(Chapter34)haveadose-dependenteffectontheskeleton,

suchthatlongerdurationandhigherdosesofsteroidsaremostlikelytocause

bonelossandfractures.However,thereclearlyaresubsetsofindividualswho

aremoreorlesssensitivetotheskeletaleffectsofhighdosesofglucocorti-

coids.Asageneralclinicalrule,thoseindividualswithacushingoidappear-

anceandfatredistributionalmostalwayshavelowbonemassorfractures,or

both.

Theeffectsofglucocorticoidsontheskeletonaremultifacetedandare

particularlydevastatingbecausetheseagentscauseuncouplingintheremod-

elingunit.Besidestheindirectsuppressiveeffectsofglucocorticoidsonthe

hypothalamic-gonadalaxis,andinhibitionofcalciumabsorptioninthegut,

highdosesofsteroidscanstimulateosteoclastogenesis,increaseRANKL

production,anddecreaseOPG.Thissituationresultsinhigherratesofbone

resorption.Additionally,glucocorticoidsalsohaveastrongnegativeeffecton

boneformationbysuppressingexpressionofIGF-Iinbonecellsandbyshift-

ingmarrowstromalcellsintothefatlineageandawayfromtheosteoblast

differentiationpathway.Itispresumedthatjustasfatredistributionsyn-

dromeinthesupraclavicularandmediastinalareaisaclinicalhallmarkof

Cushing』ssyndrome,enhancedadiposityinthebonemarrowisacharacter-

isticfeature,almostcertainlyasafunctionofincreasedstromalcelldifferen-

tiationintoadipocytes.Bonestrengthismarkedlycompromisedbythe

uncouplinginremodeling,andbonelosscanberapidoverashorttime

period,particularlywithhighdosesofglucocorticoids.Althoughthereisno

truedose-dependenteffectonboneresorption,itisthoughtthatprednisone

dosesaslowas5mg/daymayincreasefracturerisk.Indeed,inthissyn-

drome,baselineBMDisnotpredictiveoffracturesandcanoftenbenormal

eveninthepresenceofongoingresorptionandrecurrentfractures.Trabecu-

larbonesuffersthemostinthissyndrome,andspineDXAisthemostsensi-

tiveindicatorofboneloss.Markersofboneturnoverarenothelpfulinthe

managementofthesepatients.

Therapyforsteroid-inducedbonelosscentersontreatingtheunderlying

diseaseorreducingthedoseofglucocorticoidstothelowestpossible

regimen,orboth.Barringthat,severalinterventionshavebeenshownto

retardbonelossandpreventfractures.AdequatecalciumandvitaminD

intakeiscriticalforeverypatientreceivingglucocorticoids.However,these

measuresalonearenotsufficient.Threebisphosphonateshavebeenshown

tohaveefficacyinglucocorticoid-inducedosteoporosis—etidronate,alen-

dronate,20andrisedronate—andtheyarenowconsideredthestandardof

careforthisdisease.Thesedrugsareadministeredeitherweeklyorcyclically

topreventbonelossandtoreducetheriskforfractures.Someanecdotaldata

supporttheuseofgonadalsteroidsinthiscondition,butclearlythebisphos-

phonatesaresuperior.Inarandomizedtrial,syntheticPTH(teriparatide,

20mgdailysubcutaneouslyfor18months)significantlyincreasedhipand

spinebonemassdensityandreducednewvertebralfractures(from7.2to

3.4%),butnototherfractures,comparedwithalendronate.21Morestudies

areneededtoestablishitslong-termefficacyinthisdisease,particularlybecausesecondaryhyperparathyroidismisafrequentaccompanimentofsteroid-inducedosteoporosis.

參考源頭[希氏內科學].(Goldman"s.Cecil.Medicine).LeeGoldman.筆墨版.pdf