Bone density in men receiving androgen deprivation therapy for prostate cancer: A randomized comparison between transdermal estrogen and luteinising hormone-releasing hormone agonists.

Le résumé fourni par la source

5067 Background: Androgen deprivation therapy (ADT) for prostate cancer with luteinising hormone-releasing hormone agonists (LHRH) reduces bone mineral density (BMD), as testosterone suppression also causes estrogen deficiency in men. Transdermal estrogen is a compelling alternative to LHRH as it achieves similar castrate levels of testosterone but mitigates the cardiovascular toxicity associated with oral estrogen (Langley et al. Lancet Oncology 2013;14:306-16) and may avoid estrogen depletion related toxicities including osteoporosis. Methods: PATCH (Prostate Adenocarcinoma: TransCutaneous Hormones,PR09) is a randomised trial (n=686) comparing estrogen patches (EP; FemSeven 100 µg/24 hr, 4 patches changed twice-weekly reducing to 3 after 4 weeks) versus LHRH for locally advanced or metastatic prostate cancer (allocation ratio 2:1 before 21/2/2011, 1:1 after). In a bone-sub-study, dual-energy x-ray absorptiometry (DXA) scans were performed at baseline, 1 and 2 years. Primary outcome was change in lumbar spine (LS) BMD (mean L1-L4) at 1 year, compared between arms based on intention-to-treat using analysis of covariance, adjusting for baseline values. Results: 85 patients were enrolled from October 2007 to September 2012 from 7 centres (31 LHRH, 54 EP), of whom 8 were excluded (2 withdrew, 6 not eligible as they had osteoporosis on baseline scan). LS BMD data were available for 60 patients (21 LHRH, 39 EP). Median age was 77 years (IQR 73-80), 24 (40%) had bone metastases. At 1 year, mean LS BMD change was -0.03 g/cm3 (95% CI -0.06, -0.003) in LHRH vs 0.08 g/cm3(0.04, 0.11) EP arm (p<0.001); corresponding mean percentage change was -2.11% vs +6.43%, respectively. In patients without bone metastases, the difference was -3.74% LHRH vs +5.04% EP (p=0.001). At 2 years, LS BMD decreased further in LHRH patients (-6.09% from baseline, n=10) while the increase was maintained in those on EP (+4.58%, n=20); p<0.001 comparing arms. Conclusions: Transdermal estrogen, used for achieving androgen deprivation in prostate cancer, protects against bone mineral density loss, confirming the need to continue evaluation of its clinical efficacy. Clinical trial information: ISRCTN70406718.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.