Abstrakt
Endogenny zespół Cushinga (CS) prowadzący do zwiększonego wydzielania kortyzolu jest główną przyczyną wtórnej osteoporozy. Powikłania kostne w CS, mimo że nie tylko obniżają jakość życia, ale także zwiększają śmiertelność, są wciąż niedostatecznie diagnozowane. Hiperkortyzolemia skutkuje się m.in. zmniejszeniem gęstości mineralnej kości (BMD). Jednakże zwiększone ryzyko złamań może wystąpić nawet w kościach z niewielkim zmniejszeniem lub nawet prawidłowym BMD. Choroba ma zwykle podstępny przebieg, co wydłuża okres trwania hiperkortyzolemii przed postawieniem rozpoznania. Dlatego też powikłania szkieletowe takie jak obniżone BMD, osteoporoza czy złamania kostne są częste w CS. Częstość występowania osteoporozy wynosi 40-70%, osteopenii 80-85% i złamań 30-70% u pacjentów z CS (1, 2). Złamania dotyczą najczęściej kręgów lędźwiowych i piersiowych, bioder, żeber i miednicy, ponieważ uszkodzeniu ulega głównie kość trabekularna. Najczęstsza patogeneza CS prowadząca do zmian kostnych pozostaje tematem badań. Przewlekła hiperkortyzolemia prowadzi nie tylko do zmniejszenia BMD, ale również do zmian w mikroarchitekturze kości. Zwiększona resorpcja i zahamowanie tworzenia kości to główne mechanizmy opisywane w CS. Po wyzdrowieniu z CS obserwowane jest odwrócenie zmian gęstości mineralnej kości. Leczenie chirurgiczne guzów przysadki lub nadnerczy powinno być pierwszą linią leczenia. Istotna wydaję się również suplementacja witaminą D i wapniem, jak również leczenie lekami antyresorpcyjnymi. W niniejszej pracy przedstawiono przegląd aktualnej literatury dotyczącej powikłań kostnych w CS.
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