Foreword

The normal prostate excretes the vast majority of the PSA produced into the glandular duct, whereas only a small portion leaks out into the circulation. PSA levels are known to increase by physical changes to the prostatic architecture, caused not only by malignancy but by leakage (e.g. resulting from trauma, infection, inflammation, prostatic manipulation and BPH). Interpreting the data is further complicated by a lack of consensus on the optimum methods for measuring it and on the relative merits of the various forms and dynamics of the protein as the most appropriate variable. This timely workshop has been held to help develop further understanding of the value of PSA as an index of prostatic growth in both malignant and benign conditions. The conclusions from the group are based on examining the interrelationships between PSA and a variety of clinical endpoints relevant to prostatic disease. Of particular value has been the availability of data from the long-term NIH-sponsored cancer and BPH studies (PCPT and MTOPS, respectively) and access to the phase III clinical trials database for the new dual isozyme 5 α -reductase inhibitor, dutasteride.