Epidemiological studies related to androgens and prostate cancer (PC) have focused on serum determination of testosterone, androstenedione (A4), and DHEA, with inconsistent results. Herein, we hypothesized that differences in androgen biosynthetic and metabolic pathways, rather than differences in specific androgen concentrations, are associated with prostatic carcinogenesis. Therefore, spot urine samples from 111 incident PC cases with Gleason score at diagnosis and 227 healthy population controls, were analyzed. Urinary androgen concentrations (nanograms/milligrams of creatinine) were determined by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS). Using a factor analysis, we identified three androgen urinary excretion patterns. In a subsample, we evaluated a modification effect of the androgen receptor (AR) CAG polymorphism. Pattern I, characterized by A4 and testosterone hydroxylated metabolites (11β-OHT; 2β-OHT; 15β-OHT; 2α-OHT; 6β-OHT), was associated with high PC odds among carriers of AR gene (CAG)_>19 repeats (OR: 3.67 95% CI: 1.23–11.0; P for interaction= 0.009). Conversely, higher testosterone excretion (pattern III), was marginally associated with lower (OR: 0.35 95% CI: 0.12–1.00, P for trend= 0.08) poorly differentiated PC (Gleason ≥8). No clear association was observed with pattern II (DHEA; 16α and 16β-OHT). Our results were consistent with the previous evidence which suggests that the C11-oxy backdoor pathway is important for prostatic carcinogenesis. Androgen urine excretion analysis could be useful for PC diagnosis, treatment, and prognosis; however, further studies with a larger number of samples and the urinary determination of 11-ketoandrogens are necessary.

与雄激素和前列腺癌 (PC) 相关的流行病学研究集中在血清睾酮、雄烯二酮 (A4) 和 DHEA 的测定上，结果不一致。在这里，我们假设雄激素生物合成和代谢途径的差异，而不是特定雄激素浓度的差异，与前列腺癌发生有关。因此，分析了 111 例诊断时具有 Gleason 评分的 PC 病例和 227 例健康人群对照的尿液样本。通过超高效液相色谱-串联质谱 (UPLC-MS) 测定尿中雄激素浓度（纳克/毫克肌酐）。使用因子分析，我们确定了三种雄激素尿排泄模式。在子样本中，我们评估了雄激素受体 (AR) CAG 多态性的修饰作用。模式 I，以 A4 和睾酮羟基化代谢物（11β-OHT；2β-OHT；15β-OHT；2α-OHT；6β-OHT）为特征，与 AR 基因 (CAG) 携带者的高 PC 几率相关_{> 19}次重复（OR：3.67 95% CI：1.23–11.0；交互作用P = 0.009）。相反，较高的睾酮排泄（模式 III）与较低的（OR：0.35 95% CI：0.12-1.00，P趋势 = 0.08）低分化 PC（Gleason ≥8）略有相关。没有观察到与模式 II（DHEA；16α 和 16β-OHT）的明显关联。我们的结果与先前的证据一致，这表明 C11-oxy 后门途径对前列腺癌的发生很重要。雄激素尿排泄分析可用于 PC 诊断、治疗和预后；然而，需要更多样本的进一步研究和尿液中 11-酮雄激素的测定。