Serhat SEKMEK, Bülent ÖZKURT, Mirmehdi MEHTİYEV, Öznur BAL, Efnan ALGIN
Journal of Oncological Sciences - 2026;12(1):94-97
Abiraterone acetate (AA) is an inhibitor of cytochrome P450c17 that suppresses androgen synthesis from steroid precursors. Prednisone (P) is coadministered with AA to correct the glucocorticoid deficiency resulting from AA-induced alterations in steroid synthesis and to suppress excessive mineralocorticoid effects. We report bilateral avascular necrosis of the femoral head in a patient treated with AA+P; this condition is usually seen with long-term, high-dose glucocorticoid use. A 54-year-old male patient was diagnosed with castration-resistant metastatic prostatic adenocarcinoma (Gleason score 4+5). Following progression on androgen deprivation therapy+docetaxel, AA+P treatment was initiated. During this treatment period, the patient was in remission for thirty months; later, he developed bilateral avascular necrosis of the femoral heads and was referred to orthopaedics. Core decompression surgery was performed on both femoral necks due to avascular necrosis. Management and outcome: AA+P treatment was not discontinued because of the highly successful results in treating prostate cancer, and the patient remains in remission while continuing this treatment. AA+P is a treatment for prostate cancer that inhibits androgen synthesis. Although P is administered in low doses to prevent abiraterone-induced reductions in glucocorticoid levels, serious glucocorticoid side effects may, in rare cases, develop in these patients. To our knowledge, this is the first report of such a side effect in the literature.
