Abstract
AbstractBackgroundAmongst its extragonadal effects, Follicle-Stimulating Hormone (FSH) has an impact on body composition and bone metabolism. Since androgen deprivation therapy (ADT) has a profound impact on circulating FSH concentrations, this hormone could potentially be implicated in the changes of fat body mass (FBM), lean body mass (LBM) and bone fragility induced by ADT. The objective of this study is to correlate FSH serum levels with body composition parameters, bone mineral density (BMD) and bone turnover markers at baseline conditions and after 12 months of ADT.Methods29 consecutive non-metastatic prostate cancer (PC) patients were enrolled from 2017 to 2019 in a phase IV study. All patients underwent administration of the Luteinizing Hormone-Releasing Hormone antagonist degarelix. FBM, LBM and BMD were evaluated by dual-energy x-ray absorptiometry at baseline and after 12 months of ADT. FSH, alkaline phosphatase (ALP) and C-terminal telopeptide of type I collagen (CTX) were assessed at baseline and after 6 and 12 months. For outcome measurements and statistical analysis, T-test or sign test and Pearson or Spearman tests for continuous variables were used when indicated.ResultsAt baseline conditions, a weak, non-significant, direct relationship was found between FSH serum levels and FBM at arms (r=0.36) and legs (r=0.33). Conversely, a stronger correlation was observed between FSH and total FBM (r=0.52, p=0.006), fat mass at arms (r=0.54, p=0.004) and fat mass at trunk (r=0.45, p=0.018) assessed after 12 months. On the other hand, an inverse relationship between serum FSH and appendicular lean mass index (ALMI)/FBM ratio was observed (r=0.64, p=0.001). This is an ancillary study of a prospective trial and this is the main limitation.ConclusionsFSH serum levels after ADT could have an impact on body composition, in particular on fat body mass. Therefore, FSH could be a promising marker to monitor the risk of sarcopenic obesity and cardiovascular complications in PC patients undergoing ADT.Fundingthis research was partially funded by Ferring Pharmaceuticals. The funder had no role in design and conduct of the study, collection, management, analysis, and interpretation of the data and in preparation, review, or approval of the manuscript.Clinical trial numberclinicalTrials.govNCT03202381, EudraCT Number 2016-004210-10.
Publisher
Cold Spring Harbor Laboratory