Abstract
Purpose: This study analyzed the association between sex hormone concentrations and stage/condition in patients with prostate cancer. Materials and methods: The concentrations of sex hormones, including testosterone (total, free, and bioavailable), sex hormone-binding globulin (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH), were measured in 415 patients diagnosed with prostate cancer. Differences in serum hormone concentrations after receiving androgen deprivation therapy (ADT) and after withdrawal from ADT were evaluated. Pathologic characteristics were assessed in the 225 patients unexposed to ADT with a history of radical prostatectomy. Logistic regression analysis was performed to identify factors predictive of unfavorable pathology (Grade ≥3, ≥T3a, or N1). Results: Of the 415 prostate cancer patients, 130 (31.3%) were assessed before treatment, 171 (41.2%) after surgery, 35 (8.4%) after biochemical recurrence, and 59 (14.2%) during ADT, whereas 20 (4.8%) had castration-resistant prostate cancer. FSH was significantly lower after compared to before prostatectomy (3.229 ± 4.486 vs. 5.941 ± 7.044 mIU/mL, p < 0.001). LH, FSH, and testosterone decreased significantly 3 months after starting ADT, but increased 3 months after ADT withdrawal, whereas SHBG was unchanged. Multivariate analysis showed that high LH (odds ratio [OR]: 1.59, 95% confidence interval [CI]: 1.03–2.47, p = 0.0376) and prostate-specific antigen (PSA) (OR: 1.13, 95% CI: 1.03–1.24, p = 0.0133) concentrations were significantly associated with a high risk of unfavorable pathology. Conclusions: Sex hormones, including LH, FSH, and testosterone, were affected by ADT. The FSH level decreased after radical prostatectomy. High baseline LH concentration in patients unexposed to ADT was associated with an unfavorable pathology.
Highlights
The effect of castration, which eliminates androgen, has been proved to regulate prostate cancer development levels [1]
luteinizing hormone (LH) levels were significantly lower in patients with hormone-sensitive prostate cancer (HSPC) (1.970 ± 2.890 mIU/mL, p < 0.001) and castration-resistant prostate cancer (CRPC) (0.718 ± 0.854 mIU/mL, p < 0.001) than in androgen deprivation therapy (ADT)-unexposed patients (3.978 ± 2.206 mIU/mL)
Compared with prostate-specific antigen (PSA) levels in the pre-treatment cohort (12.709 ± 13.273 ng/mL), PSA levels were significantly lower in the post-operative (0.354 ± 1.335 ng/mL, p < 0.001) and biochemical recurrence (BCR) (1.823 ± 4.728 ng/mL, p < 0.001) groups and significantly higher in the HSPC (240.792 ± 620.381 ng/mL, p < 0.001) and CRPC (108.413 ± 163.057 ng/mL, p < 0.001) groups
Summary
The effect of castration, which eliminates androgen, has been proved to regulate prostate cancer development levels [1]. Luteinizing hormone releasing hormone (LHRH) agonists are frequently used to treat patients with metastatic disease or recurrence, and LHRH antagonists are used as androgen deprivation agents [2]. LHRH antagonists directly inhibit LHRH receptors in the pituitary gland and rapidly reduce the production of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) [3]. Three days after LHRH agonist administration, LH and FSH concentrations peak, with these hormones being about 10- and 5-fold higher, respectively, than their baseline levels [4]. Androgens initially regulate androgen receptor and androgen receptor activity and androgen receptor mutation/amplification leads to castration-resistant prostate cancer (CRPC) development. There are lots of studies about androgen receptor variants, but relatively less is known about the associations of sex hormones with the growth, proliferation, or progression of prostate cancer
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