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Bone mineral density decreases during the first 24 months of androgen suppression with the most relevant effect occurring in the first year. Ward's triangle is the axial skeletal site that reflects the major bone mass loss. Because the deleterious impact of long-term androgen suppression on bone mineral density is inversely related to fracture risk and indirectly related to survival in patients with prostate cancer, early diagnosis and prevention of bone mass loss are warranted in these patients.

The objective of our study was to analyze the value of prostate-specific antigen (PSA) levels before and after androgen suppression to predict the time to androgen-independent progression (AIP) in patients with advanced and metastatic prostate cancer. A series of 283 prostate cancer patients under androgen suppression as a single treatment was studied. The disease was locally advanced in 98 patients and metastatic in the remainder 185. AIP was defined after 2 consecutive increases of serum PSA after the nadir value. The mean follow-up before AIP was 29.2 months (3-198). AIP was detected in 205 patients (72.4%). In 152 patients (74.1%), the event was detected within 24 months, while in 53 patients (25.9%), it was observed beyond 24 months. The multivariate analysis showed that the nadir PSA and the time to reach the nadir PSA were the most significant predictors of the time to AIP. The odds ratio of having a biochemical response greater than 24 months was 20 times higher in patients that achieved an undetectable PSA level of 0.2 ng/mL or less. Moreover in those patients whose nadir PSA reached beyond 12 months after androgen suppression the odds ratio was 18 times higher. These results show that the ability to achieve an undetectable nadir PSA and the time to reach it are the most significant predictors of the time to AIP in patients with locally advanced and metastatic prostate cancer under androgen suppression as a single therapy. Key words: nadir prostatic specific antigen; androgen suppressionAndrogen suppression therapy remains an important treatment and the primary therapy for patients with metastatic prostate cancer. Early androgen suppression may contribute to increase survival and clearly to decrease major complications of prostate cancer. 1 Prostatic specific antigen (PSA) has proved to be an excellent serum marker for the detection of recurrent prostate cancer after potentially curative treatments for localized disease and for the detection of tumor progression after palliative treatments for metastatic disease. 2 Clinical experiences reported that PSA almost always declines after androgen suppression and then stabilizes for varying intervals. 3 Subsequent elevation invariably predicts tumor progression and precedes objective evidence of the event by about 6 to 12 months. 4,5 There is conflicting information about the prognostic significance of the pre-treatment PSA serum level; however PSA serum levels after androgen suppression provide useful information for the prediction of the clinical response and survival. 6 -8 The magnitude and pattern of decline in PSA serum levels have been used to predict the duration of response to androgen deprivation therapy. In metastatic prostate cancer patients, a nadir PSA of less than 10 ng/mL 9,10 and 4 ng/mL 11,12 after androgen suppression has been related with longer progressionfree survival and overall survival.A rising PSA after androgen deprivation is used as a surrogate of androgen-independent progression (AIP) of prostate cancer. Recently, some studies hav...

Objectives: It was the aim of this study to analyze the failure rates in achieving or maintaining castrate levels of serum testosterone in patients with advanced prostate cancer treated with the 3-month luteinizing hormone-releasing hormone agonist (LH-RH) therapy. Methods:Total serum testosterone was determined in 234 patients with prostate cancer in a cross-sectional study. A subset of 90 patients submitted to radical prostatectomy was used as the control group (group 1), and 144 patients with advanced prostate cancer under androgen suppression therapy were included in the study group (groups 2 and 3). The study group was divided into 93 patients (group 2) treated with 50 mg daily bicalutamide and LH-RH agonist (maximal androgen blockade, MAB) and 51 patients treated with the LH-RH agonist alone (group 3). Median follow-up after androgen suppression was 42 months. The castrate testosterone level was defined below 50 ng/dl. Results: The mean serum testosterone level was 29.1 ng/dl in patients undergoing MAB (group 2) and 29.5 ng/dl in patients treated with the LH-RH agonist (group 3; p > 0.05). In group 1, the mean serum testosterone was 445.2 ng/dl (p < 0.0001). The rate of patients with a serum testosterone level higher than 50 ng/dl was 10.9% in patients undergoing androgen suppression, 10% in patients with MAB treatment and 12.5% in those with LH-RH agonist therapy (p > 0.05). In group 1, 98.9% of the patients had a serum testosterone level higher than 50 ng/dl. Conclusions: A small but clinically significant rate of patients under 3-month LH-RH agonist therapy fail to achieve or maintain castrate testosterone serum levels. This finding supports the need of monitoring testicular response during LH-RH agonist therapy.

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