In the majority of cases inflammation was present in the transiti

In the majority of cases inflammation was present in the transitional zone. A total of 93 glands (56%) were involved with benign prostatic hyperplasia and 49 (29%) with cancer. Of the glands

harboring benign prostatic hyperplasia 75% were also involved with chronic inflammation compared to only 50% of those without benign prostatic hyperplasia (p <0.01). Comparatively the glands with or without any evidence of cancer learn more were similarly involved with chronic inflammation (55% vs 58%, p >0.1). Of the 27 glands involved with cancer and benign prostatic hyperplasia, chronic inflammation was more associated with benign prostatic hyperplasia than cancer (p = 0.006). Acute inflammation was not significantly associated with either benign prostatic hyperplasia or cancer.

Conclusions: Chronic inflammation was a common finding in autopsied prostates. It appeared to be directly associated with the presence of benign prostatic hyperplasia but not with

“Purpose: We determined whether the ratio of serum testosterone to prostate specific antigen might provide diagnostic value regarding the risk of prostate Selleckchem CHIR 99021 cancer in a population of hypogonadal men undergoing prostate biopsy.

Materials and Methods: The study population consisted of 184 consecutive men with symptomatic hypogonadism and prostate specific antigen 4.0 ng/ml or less who under-went prostate biopsy before the anticipated initiation of testosterone therapy. All men had testosterone 300 ng/dl or less. Testosterone concentrations were converted to ng/ml, eg 270 ng/dl equals 2.7 ng/ml, to calculate the testosterone-to-prostate specific antigen ratio.

Results: Mean patient age was 58.5 years. There were 154 men with benign biopsies and 30 with cancer. Testosterone concentrations were similar in the prostate cancer and noncancer groups, although mean prostate specific antigen was higher in the prostate cancer group. The testosterone-to-prostate specific

antigen ratio was inversely related to prostate cancer risk (OR 0.49, 95% CI 0.33-0.74). On multivariate analysis performed by logistic regression neither age nor prostate specific antigen was be predictive of prostate cancer. However, the testosterone-to-prostate specific antigen ratio remained strongly Givinostat associated with prostate cancer risk. An ROC for the testosterone-to-prostate specific antigen ratio suggested that a ratio of below 1.8 was diagnostic for prostate cancer, while values below this threshold were associated with an OR of 3.17 (95% CI 1.17-8.59) for prostate cancer.

Conclusions: A low ratio of testosterone to prostate specific antigen is an independent predictor of prostate cancer in hypogonadal men with prostate specific antigen 4.0 ng/ml or less. Ratios less than 1.8 were associated with a greater than 3-fold increase in prostate cancer risk.

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