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PD15-01 FSH IS UNRELATED TO MAJOR ADVERSE CARDIOVASCULAR EVENTS (MACE) AND MORTALITY AMONG MEN RECEIVING ANDROGEN DEPRIVATION THERAPY (ADT) FOR PROSTATE CANCER (PC)

INTRODUCTION AND OBJECTIVES: Previous studies found men starting a LHRH-agonist (LHRH-a) are at increased risk of MACE, however this conflicts with randomized trials where no links are seen. FSH is a pituitary hormone that regulates testosterone and is elevated with LHRH-a therapy. Some data suggest FSH may mediate the potential effects of ADT on MACE, though population-level data assessing this are lacking. We examined the effect of serum FSH on all-cause mortality (ACM) and MACE in men treated with ADT for PC. METHODS: All men (n=1,539) with PC receiving ADT who had a FSH within 2 years before starting ADT were identified in the Veterans Affairs (VA) Health System between 1999 and 2018. Men with MACE prior to ADT were excluded for the MACE outcome (n=477). FSH was dichotomized as low/normal (⩽8 IU/mL; n=878) and high (>8 IU/mL; n=661) and as continuous (secondary analysis). Differences in time from ADT to MACE and ADT to ACM by FSH were tested via the log-rank test and Cox proportional hazards. Multivariable models were adjusted for age, year, race, BMI, Charlson Comorbidity Index, primary treatment, biopsy grade group, PSA, time from FSH to ADT, and chemotherapy (yes/no). The MACE model was further adjusted for testosterone level (lowest, middle and highest tertile vs. missing). RESULTS: Patients with high FSH were older (median 76 vs 73 yrs, p<0.001), started ADT earlier (median 2007 vs 2009, p=0.027), and had a lower BMI (median 29.1 vs 30.1 kg/m2, p=0.004) vs. those with low/normal FSH. There were 337 (51%) men with high FSH and 381 (43%) with low/normal FSH who died over a median 86 mos (IQR 42-136). Men with low/normal FSH had longer survival (127 months, IQR 114-146) vs. men with high FSH (113 months, IQR 99-124) (p=0.008). High FSH predicted worse ACM on univariable analysis (HR 1.22, 95%CI 1.05-1.41), but not after multivariable adjustment (HR 1.03, 95%CI 0.88-1.20). There were 120 (27%) men with high FSH and 162 (26%) with low/normal FSH who had a MACE over a median 87 mos (IQR 44-141). There was no difference in time from ADT to MACE between FSH groups (p=0.43). Additionally, FSH did not predict MACE on multivariable analysis (high vs. low/normal HR 1.04, 95%CI 0.81-1.34). When treated as a continuous variable, similar null multivariable results were seen for MACE and survival. CONCLUSIONS: In this large study of men receiving ADT for PC, on multivariable analysis, FSH was unrelated to MACE and ACM. These data do not support pre-ADT FSH levels as being related to adverse cardiovascular outcomes of ADT. Source of Funding: Ferring Pharmaceuticals