Abstract

Abstract Introduction It has been known in the literature that Black men are disproportionately affected by prostate cancer in the United States. Various mechanistic pathways have been evaluated including PSA and/or testosterone levels (T) in this at-risk population. Based on prior studies, low PSA is suggested to be predictive of low testosterone independent of prostate cancer pathology. In this study, we aim to evaluate the correlation between race and PSA/T levels in men diagnosed with prostate cancer. Objective To further study the relationship between testosterone, PSA, and race in men with prostate cancer. Methods An IRB approved database was utilized to obtain values for prostate cancer patients. Prostate cancer patients who had testosterone, PSA, and Gleason scores (GS) were included in our cohort with demographic information. Patients were stratified by PSA category. Low testosterone was defined as T<300 ng/dL, and very low T as 0–200 ng/dL. Results In our cohort of 653 prostate cancer patients, the mean age was 66 years. The cohort included 34% African American (AA), 62% White, and 4% other. AA men had a median PSA of 8.0 ng/mL, compared to 0.8 ng/mL in white men (p<0.001). For AA men with GS (8–10) and PSA>4, proportions were: very low T (27%), low T (24%) and normal T (49%). For GS (8–10) and PSA<2, very low T (35%), low T (22%) and normal T (43 %) (p<0.05). For White men with GS (8–10) and PSA>4, very low T (33%), low T (17%) and normal T (50%). For GS (8–10) and PSA<2, very low T (37%), low T (20%) and normal (43%) (p<0.05). In GS (8–10), logistic regression demonstrated neither race nor PSA category were statistically significant predictors of low T. Conclusions Our results show that despite significantly higher PSA among AA men with prostate cancer, there was no statistically significant difference in T and GS 8–10 prostate cancer. This finding highlights that racial variation may influence PSA but not GS prostate cancer or T level. Further studies are warranted to elucidate the correlation between PSA and T in higher-risk populations. Disclosure No.

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