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Influence of anthropometric measurements, age, and prostate volume on prostate-specific antigen levels in men with a low risk of prostate cancer.

OBJECTIVES: To assess the correlation between age, height, body weight, body mass index, body surface area (BSA), prostate volume, and prostate-specific antigen (PSA) level, and to determine the significant factors for predicting the PSA level in men with a low risk of having prostate cancer. METHODS: Men who had undergone at least one ultrasound-guided extended prostate biopsy at the M.D. Anderson Cancer Center from 1998 to 2003 and were proven, on pathologic examination, to be without cancer were included in this study. All patients underwent clinical evaluations, including digital rectal examination, serum PSA determination, transrectal ultrasound examination, and anthropometric measurements. The relationship between the clinical parameters and PSA level was examined by the Mann-Whitney U test and determination of the Pearson correlation coefficient. RESULTS: A total of 653 men were eligible for analysis in our study. The median age was 62.0 years; the median prostate volume was 48.3 cm3; and the median PSA level was 5.5 ng/mL. The PSA level correlated with age (P < 0.001) and prostate volume (P < 0.001), but not with height, body weight, body mass index, or BSA. The prostate volume correlated with age (P < 0.001), body weight (P < 0.001), body mass index (P < 0.01), and BSA (P < 0.01), but not with height. Multivariate analysis revealed that prostate volume and BSA were significant factors for predicting the PSA level. CONCLUSIONS: Of the variables tested, prostate volume was most significantly related to the PSA level. The anthropometric parameters were not directly associated with the PSA level, but were associated with the prostate volume. Our findings suggest that differences in the PSA level may be influenced by body size, if the prostate volume is held constant in men with a low risk of having prostate cancer.

Age Factors↗

Prostate-specific antigen adjusted for the transition zone volume versus free-to-total prostate-specific antigen ratio in predicting prostate cancer.

BACKGROUND: We performed this study to assess the efficacy of prostate-specific antigen adjusted for the transition zone volume (PSATZ) and free-to-total prostate-specific antigen (PSA) ratio (F/T ratio) in predicting prostate cancer in men with intermediate PSA levels of 4.1-10.0 ng/mL. METHODS: Between March 1997 and September 1998, PSATZ was obtained from 67 patients who underwent ultrasonography guided systemic sextant biopsies and had a PSA of 4.1-10.0 ng/mL. PSATZ was compared with F/T ratio via receiver operating characteristic (ROC) curves. RESULTS: Of 67 patients, 22 (32.8%) had prostate cancer and 45 (67.2%) had benign prostatic hyperplasia (BPH) on pathologic examination. Mean PSA, PSA density, F/T ratio and PSATZ were 7.96+/-2.01ng/mL, 0.28+/-0.14 ng/mL/cc, 0.10+/-0.06 and 0.70+/-0.28 ng/mL/cc in patients with prostate cancer and 6.39+/-1.68 ng/mL, 0.16+/-0.06 ng/mL/cc, 0.15+/-0.05 and 0.29+/-0.10 ng/mL/cc in patients with BPH, respectively. The ROC curve analysis demonstrated that PSATZ predicted the biopsy outcome significantly better than F/T ratio in all 67 patients (P<0.01) and in a subset of 53 men with normal digital rectal examination (P<0.01). With a cut-off value of 0.35 ng/mL/cc, PSATZ had a sensitivity of 86% and a specificity of 89% for predicting prostate cancer. CONCLUSIONS: These results suggest that PSATZ and F/T ratio may be useful in diagnosing prostate cancer with intermediate levels of PSA. Prostate-specific antigen adjusted for the transition zone volume is more accurate than F/T ratio in distinguishing benign prostatic disease from prostate cancer. But large prospective studies are required to assess the precise role of PSATZ and F/T ratio in early prostate cancer detection.

Age Factors↗

Transforming growth factor beta 1 and its receptor types I and II. Comparison in human normal prostate, benign prostatic hyperplasia, and prostatic carcinoma.

An immunohistochemical and semiquantitative comparative study of transforming growth factor beta 1 (TGF-beta 1) and its receptor types I (TGF-beta RI) and II (TGF-beta RII) was carried out in normal prostates and in the prostates from men with benign prostatic hyperplasia (BPH), and men with prostatic adenocarcinoma. Immunoreaction to TGF-beta 1 was limited to the basal epithelial cells in the normal prostates. Some cells in the connective tissue stroma were also stained. In BPH immunolabelling was also observed in columnar (secretory) cells of the epithelium. In prostatic adenocarcinoma, all epithelial cell types were intensely immunostained. Some stromal cells were also stained. Immunostaining to TGF-beta RI was only present in the basal cells in normal prostates. In BPH, this immunoreaction was found in the whole epithelium and in some stromal cells. In prostatic cancer, the immunostaining pattern for this receptor was similar to that of BPH but more intense in the epithelial cells. Immunoreactivity to TGF-beta RII appeared in some basal cells and some scattered columnar cells of the normal prostate epithelium. In the BPH sections, this pattern was maintained, and a weak immunolabelling was also observed in the stroma. In prostate cancer, all epithelial cells appeared intensely labelled. In the stroma, immunolabelling was similar to that of the BPH specimens. The results of the present study suggest that, in normal prostates, only the basal cells of the epithelium possess both receptor types, and hence can transduce TGF-beta 1 signal intracellularly. The basal cells can also secrete this growth factor which would act as an autocrine inhibitory growth factor for them. In addition, TGF-beta 1 is secreted in some zones by stromal cells, acting then as a paracrine growth factor for basal cells in those areas. In BPH, in addition to the basal cells, some secretory columnar cells also secrete TGF-beta 1 and possess both types of TGF-beta 1 receptors, and thus, both epithelial cell types are susceptible to TGF-beta 1 action. Since both receptor types are also present in some stromal cells, these cells also perform an autocrine secretion, in addition to their paracrine secretion to the epithelial cells. TGF-beta RIIs seem to be more numerous than TGF-beta RIs and this lead us to hypothesize that these incomplete receptors might be a protection against the inhibition caused by TGF-beta 1 action. In prostatic carcinoma all cell types display the same characteristics as in BPH, although both receptor types are found in similar numbers, and thus, the above mentioned protection would not occur.

Adenocarcinoma↗

Correlation of prostate-specific antigen and prostate-specific antigen density with outcome of prostate biopsy.

OBJECTIVE: We attempt to correlate prebiopsy serum prostate-specific antigen (PSA) concentration and prostate-specific antigen density (PSAD) with histologic results of prostate biopsy. METHOD: Sixty-two consecutive patients underwent prostate biopsy because of elevated PSA greater than 4 ng/mL and/or abnormal findings on digital rectal examination (DRE). PSAD was calculated from dividing the serum PSA concentration by the prostate volume as determined by transrectal ultrasound (TRUS). PSA and PSAD were compared to biopsy outcome. RESULTS: The mean PSAD values of the cancer versus noncancer (benign prostatic tissue, benign prostatic hyperplasia, and prostatitis) groups were significantly different (p < 0.019). However, there was great overlap in individual values. The mean PSA levels of the cancer versus noncancer groups also were significantly different (p < 0.0079). In patients with PSA levels between 4 and 10 ng/mL, 11 of 32 (34%) had positive biopsy findings for cancer. Eleven of 29 patients (38%) with normal DRE findings and elevated PSA levels (> 4 ng/mL) had positive biopsy findings for cancer. Seven of 19 patients (37%) with normal DRE findings and elevated PSA levels between 4 and 10 ng/mL had positive biopsy specimens for cancer. CONCLUSIONS: PSAD, though suggestive, is not definitive for cancer or noncancer. Patients with inflammation (prostatitis) present in their biopsy specimens have serum PSA levels and PSAD values intermediate between those with benign tissue (without inflammation) and cancer. We think that prostate biopsy is important in patients with PSA levels between 4 and 10 ng/mL even if their DRE result is normal, as our data indicate that over one third of these patients harbor detectable prostate cancer.

Aged↗

Prostate targeting: PSP94 gene promoter/enhancer region directed prostate tissue-specific expression in a transgenic mouse prostate cancer model.

To date, only a few prostate-specific vector genes have been tested for prostate targeting in gene therapy of prostate cancer (CaP). Current clinical trials of gene therapy of CaP utilize the only two available vector genes with a combination of a rat probasin promoter and a human PSA promoter sequence in an adenovirus vector to target CaP. There is an urgent need to establish additional vector gene systems to sustain and propagate the current research. Since PSP94 (prostate secretory protein of 94 amino acids) is one of the three most abundant proteins secreted from the human prostate and is generally considered to be prostate tissue-specific in both human and rodents, we performed a transgenic experiment to assess the promoter/enhancer region of PSP94 gene-directed prostate targeting. Firstly, a series of progressive deletion mutants of a 3.84 kb PSP94 gene promoter/enhancer region (including parts of the intron 1 sequence) linked with a reporter LacZ gene was constructed and assessed in vitro in cell culture. Next, transgenic mice were generated with two transgene constructs using the SV40 early region (Tag oncogene) as a selection marker. PSP94 gene promoter/enhancer region-directed SV40 Tag expression specifically in the mouse was demonstrated in three breeding lines (A, B, C, n = 374) by immunohistochemistry staining of Tag expression. Specific targeting to the prostate in the PSP94 gene-directed transgenic CaP model was characterized histologically by correlation of SV40 Tag-induced tumorigenesis (tumor grading) with puberty and age (10-32 weeks). Prostatic hyperplasia was observed as early as 10 weeks of age, with subsequent emergence of prostatic intraepithelial neoplasia (PIN) and eventually high grade carcinoma in the prostate. The PSP94 transgenic mouse CaP model was further characterized by its tumor progression and metastatic tendency at 20 weeks of age and also by its responsiveness and refractoriness to androgen manipulation. This study indicates that the PSP94 gene promoter/enhancer has the potential for prostate specific targeting and may ultimately be of use in gene therapy of CaP.

Animals↗

Relationship between serum prostate specific antigen and histological prostatitis in patients with benign prostatic hyperplasia.

The relationship between the serum values of prostate specific antigen (PSA) and the extent of histological prostatitis was investigated in 42 patients undergoing transurethral resection of the prostate for benign hyperplasia (BPH) without clinical evidence of prostatitis. Histological prostatitis was divided into three groups: acute, chronic-active, and chronic-inactive inflammation. The extent of histological prostatitis was expressed as the number of prostatic acinar and ductal glands with inflammatory infiltrate per total number of glands (%). The serum PSA values significantly correlated with the extent of acute and chronic-active prostatitis (correlation coefficient r = 0.765 and 0.656, P < 0.01). A relationship between PSA values and the extent of chronic-inactive prostatitis was not found. In the immunohistochemical study, prostatic epithelial cells with acute and chronic-active inflammation showed negative staining for PSA antigen. These results indicate that histological acute and chronic-active prostatitis is considered an important factor for inducing the high increase in serum PSA values via the leak phenomenon.

Aged↗

Total and Gleason grade 4/5 cancer volumes are major contributors of human kallikrein 2, whereas free prostate specific antigen is largely contributed by benign gland volume in serum from patients with prostate cancer or benign prostatic biopsies.

PURPOSE: We measured concentrations of human glandular kallikrein 2 (hK2), total prostate specific antigen (tPSA), free PSA (fPSA) and percent fPSA to evaluate their relationship to total prostate gland volume, benign prostatic hyperplasia (BPH) volume, total prostate cancer (PCa) volume (CaVol) and the volume of Gleason grades 4/5 cancer (CaVolGl4) in the serum of 256 patients with PCa undergoing radical retropubic prostatectomy and 185 with negative systematic sextant biopsies. MATERIALS AND METHODS: Free and total PSA was measured using the Delfia Prostatus (Perkin-Elmer, Turku, Finland) total/free PSA assay and hK2 was measured using a research immunofluorometric assay. Transrectal ultrasound was used to determine total prostate and BPH volume. Total CaVol and CaVolGl4/5 were calculated using a volumetric program in specimens from 158 men with pT2a/b and 98 with pT3a or greater PCa. The Pearson correlation was performed after logarithmic conversion of PSA and hK2 levels. Benign gland, and pT2a/b and pT3a or greater PCa cases were subdivided into small vs large prostate gland volumes (42 cc or less vs greater than 42 cc). RESULTS: Total prostate and BPH volumes correlated closely with free PSA (r = 0.64 to 0.65, p <0.0001) in 143 patients with negative biopsy and a prostate of greater than 42 cc. Correlations of hK2 and tPSA with total prostate and BPH volumes were weaker (r = 0.35 to 0.36 and 0.45 to 0.46, respectively). In pT2a/b and pT3a or greater PCa cases hK2 most closely correlated with CaVol (range 0.31 to 0.62, p = 0.0072 and <0.0001) and with CaVolGl4/5 (range 0.26 to 0.56, p = 0.021 and <0.0001, respectively). The tPSA level correlated significantly with CaVol and CaVolGl4/5 except in glands 42 cc or greater harboring pT2a/b PCa (p = 0.08). Free PSA correlated significantly with CaVolGl4/5 only in pT3a or greater PCa (p <0.05), and with CaVol in pT3a or greater PCa and in small prostates harboring pT2a/b PCa. CONCLUSIONS: Large benign prostate gland volume affects fPSA more than tPSA in serum. In PCa hK2 more closely correlates with total cancer volume and high grade PCa volume compared with tPSA or fPSA.

Fluoroimmunoassay↗

Active principle of swine prostate extract: II. Effect of a peptide isolated from swine prostate extract on rat prostate.

Previously, we purified a substance from swine prostate extract (PE) that had been reported to have therapeutic effect on benign prostatic hypertrophy. The purified substance (PPE) suppressed 3H-testosterone uptake into the prostate in castrated rats. The present study was carried out to examine the effect of PPE on the weight of accessory sexual organs including the prostate and biochemical parameters in the prostate of normal and/or castrated and testosterone-treated rats. 1) In normal rats, the p.o. administration of PPE daily for a total of 30 days did not affect the prostate weight, but reduced the citric acid content in the prostate. The treatment had little or no influence tissue O2 uptake, aconitase activity or isocitrate dehydrogenase activity in the prostate. 2) In castrated and testosterone-treated rats, the p.o. treatment with PPE for 15 or 30 days reduced the weight of the prostate as well as the total citric acid, DNA and RNA contents in prostatic tissue. However, these biochemical parameters per tissue weight were not obviously affected except for the citric acid content. These findings suggest that PPE is one of the active principals of PE for the therapeutic efficiency on benign prostatic hypertrophy, probably due to its suppressive effect on excessive uptake of androgen by the prostate.

Aconitate Hydratase↗

Prostate-specific antigen levels in 1695 men without evidence of prostate cancer. Findings of the American Cancer Society National Prostate Cancer Detection Project.

The American Cancer Society National Prostate Cancer Detection Project is a prospective, multidisciplinary, and multicenter trial to assess the potential for early detection of prostate cancer by transrectal ultrasonography (TRUS), digital rectal examination (DRE), and serum prostate-specific antigen assay (PSA). By November 1990, 2805 men between the ages of 55 and 70 years with no known signs or symptoms of prostate cancer were enrolled in the study, which is planned to run for 5 years. Annual TRUS, DRE, and PSA tests were done on these subjects, and biopsies were recommended for suspicious lesions when detected. To study the performance of PSA testing in presumed normal subjects, all men were eliminated who had (1) prostate cancer detected on their initial examinations and proven by biopsy or (2) cancer detected during the year or subsequent examinations. Additionally, all men with TRUS or DRE findings that were interpreted as suspicious for cancer but who are being followed and have not yet had biopsies done were removed from this series. This left a unique, extensively screened group of 1695 men who were free of prostate cancer, as far as could be determined. Analyses of the PSA levels in this large population in the appropriate age range for increasing risk of prostate cancer revealed several important findings. First, there was a direct relationship between serum PSA levels and estimated prostate volume for both the currently available monoclonal and polyclonal PSA assays. Individuals with benign prostatic hyperplasia and larger gland volume have a higher normal limit of PSA than men with normal gland volume. Second, analyses showed no relationship between age and PSA levels or between symptoms of prostatism and PSA levels independent of gland enlargement. It was concluded that volume-adjusted upper limits of normal PSA can be determined for different levels of specificity desired. This information may be applicable to the use of PSA in men not already suspected of having prostate cancer and may increase its effectiveness as a tool for early detection.

Age Factors↗

Obesity, serum prostate specific antigen and prostate size: implications for prostate cancer detection.

PURPOSE: Obesity has been associated with lower serum testosterone, theoretically resulting in decreased PSA production. Obesity has also been associated with prostatic enlargement, making the detection of existent cancer more difficult. Together these findings would result in an apparent protective effect of obesity on prostate cancer risk due to technical detection issues unrelated to cancer biology. We examined the association between BMI, and PSA and prostate weight in a cohort of men undergoing RP. MATERIALS AND METHODS: We evaluated the association of BMI with prostate weight and PSA using linear regression, adjusting for patient age at RP, year of RP, race, and pathological stage and grade in 1,414 men treated with RP between 1988 and 2004 at the 5 equal access medical centers that comprise the Shared Equal Access Regional Cancer Hospital Database. RESULTS: On multivariate analysis increasing BMI was associated with increasing prostate weight but only in men younger than 63 years and not in men 63 years or older (p-trend <0.001 and 0.44, respectively). In men younger than 63 years mean multivariate adjusted prostate weight +/- SE in those with a BMI of less than 25 vs 30 to 34.9 kg/m was 33.8 +/- 1.4 vs 41.4 +/- 1.6 gm. There was no significant association between BMI and preoperative PSA (p-trend = 0.70). CONCLUSIONS: In a cohort of men undergoing RP obesity was associated with larger prostate size but only in younger men. There was no association between BMI and PSA. Assuming equal PSA, the degree of prostatic enlargement observed in younger obese men in this study would be expected to result in a modest decrease in the odds of detecting prostate cancer in a contemporary series of PSA screened men due to the decreased sensitivity of cancer detection related to larger prostate size. Obesity may appear protective for prostate cancer in younger men due to technical issues unrelated to cancer biology.

Humans↗

Prostate and bone fibroblasts induce human prostate cancer growth in vivo: implications for bidirectional tumor-stromal cell interaction in prostate carcinoma growth and metastasis.

Prostate cancer selectively metastasizes to the axial skeleton to produce osteoblastic lesions, which suggests that bidirectional paracrine interactions exist between prostate cancer and bone cells. To evaluate the role of tumor-stromal cell interaction and stromal-specific growth factors in prostate cancer growth and dissemination, we coinoculated nontumorigenic human prostate cancer cells (LNCaP) and various tissue-specific fibroblasts subcutaneously in athymic mice. LNCaP tumors were induced most consistently by human bone fibroblasts (62%), followed by two prostate fibroblast cell lines (31% and 17%), but not by lung, kidney, or embryonic 3T3 fibroblasts. Carcinomas formed preferentially in male hosts, demonstrating in vivo androgen sensitivity. Immunohistochemical and biochemical techniques confirmed the human prostate component of these tumors and were paralleled by elevations in serum prostate specific antigen. In vitro mitogenic assays revealed a two-to three-fold bidirectional stimulation between LNCaP and bone or prostate fibroblast conditioned media, but not lung, kidney, or 3T3 fibroblast conditioned media. A novel method developed to deliver concentrated bone or prostate fibroblast conditioned media in vivo using a slowly absorbed matrix (gelfoam) also induced tumor formation, emphasizing the importance of fibroblast growth factors in LNCaP tumor formation. Northern analysis identified the stromal compartment as the primary source of extracellular matrix (collagen, fibronectin), while only LNCaP cells expressed transforming growth factor alpha. Although LNCaP and stromal cells express basic fibroblast growth factor (bFGF), the bidirectional paracrine-mediated mitogenic activity between these cells is not inhibited by anti-bFGF antibodies, suggesting that other undefined growth factors may be involved in stimulating LNCaP growth. These observations illustrate the importance of stromal-epithelial interaction in prostate tumor growth and suggest that extracellular matrix and paracrine-mediated growth factors play a role in prostate cancer growth and metastasis.

Androgens↗

Relationships between prostate-specific antigen and prostate volume in black and white men with benign prostate biopsies.

OBJECTIVES: To determine whether the higher age-adjusted serum prostate-specific antigen (PSA) levels in black compared with white men with no clinical evidence of prostate cancer reflect racial differences in relationships between PSA and prostate volume. METHODS: The age, PSA, findings on digital rectal examination (DRE), prostate volume, and PSA density were assessed prospectively in 810 consecutive, evaluable men who underwent prostate biopsy for suspected cancer but who had benign histologic findings. RESULTS: Among the black and white patients, there were significant differences in age (mean 67.2 +/- 8.1 and 65.9 +/- 7.7 years, respectively, P = 0.02), PSA (median 4.7 and 3.9 ng/mL, respectively, P <0.0001), prostate volume (median 41 and 36 mL, respectively, P = 0.004), and PSA density (median 0.11 and 0.08 ng/mL/mL, respectively, P = 0.005). Multiple linear regression analyses showed that black race was significantly associated with increased prostate volume when controlled for age (P = 0.02), with increased PSA when controlled for prostate volume and age (P = 0.002), and with increased PSA density when controlled for age (P = 0.007). When controlled for prostate volume, PSA was not significantly different in black and white men 50 to 59 years old but was significantly greater in black men 60 to 69 and 70 to 79 years old (P = 0.02 and 0.002, respectively). CONCLUSIONS: On a volume/volume basis, the benign prostatic tissue of black men appears to contribute more PSA to the circulating blood than does the benign prostatic tissue of white men, and the difference increases with advancing age. These phenomena provide a reasonable explanation for the age-adjusted racial differences in the PSA of men with no clinical evidence of cancer.

Adult↗

Is chronic inflammatory change in the prostate the major cause of rising serum prostate-specific antigen in patients with clinical suspicion of prostate cancer?

AIM: To evaluate the cause of elevated prostate-specific antigen (PSA) in patients with transrectal needle biopsy negative for prostate cancer. METHODS: Serum PSA concentration, prostate volume, and pathologic findings were examined in 223 patients with negative biopsy for prostate cancer. The degree of prostate inflammation was determined by the extent and degree of inflammation shown by biopsy specimens and is expressed as an inflammation score (range: 0-36). RESULTS: A significant correlation was found between PSA concentration and prostate total volume (P=0.0001). Prostate chronic inflammation showed no correlation with PSA concentration (P=0.485, F=0.488). After allocating patients to normal PSA ( 4 ng/mL) groups, we found that serum PSA concentrations in both groups were predominantly affected by prostate total volume. CONCLUSIONS: An increase in prostate volume appears to be the major contributor to a high serum PSA concentration in patients with negative biopsy for prostate cancer. However, in contrast to previous reports, there was no correlation between the degree of prostate chronic inflammation and serum PSA concentrations.

Adult↗

Prognostic significance of changes in short-term prostate volume and serum prostate-specific antigen after androgen withdrawal in men with metastatic prostate cancer.

OBJECTIVE: Endocrine therapy is the standard treatment for metastatic prostate cancer although progression to androgen independence is inevitable. To evaluate prognostic factors in metastatic prostate cancer, patients who had been treated with endocrine therapy were investigated especially for the change in prostate volume. METHODS: Fifty-nine patients with untreated metastatic prostate cancer who received endocrine therapy were included in the present study. Blood chemistry, histological grade, extent of bony metastasis, clinical response to hormone therapy including the short-term change in prostate volume and serum prostate-specific antigen (PSA), and prognosis of the patients were evaluated. RESULTS: With univariate analysis, hemoglobin concentration, serum alkaline phosphatase, lactate dehydrogenase (LDH), histological grade, extent of bony disease, the short-term change of prostate volume and response of PSA at 3 months were shown to be significant prognostic factors. Response of PSA, LDH and the change in prostate volume were significant for predicting prognosis with multivariate analyses. Five-year survival rate in patients whose prostate had regressed 20% or more at 1 month and whose PSA had been normalized at 3 months was 67%, whereas that in patients whose prostate had regressed less than 20% and whose PSA had not been normalized was 0%. CONCLUSIONS: The patients in whom PSA had not been normalized at 3 months and the prostate volume had regressed less than 20% at 1 month were in the high-risk group. New or more aggressive treatment should be considered.

Aged↗

Rationale for using serum prostate-specific antigen (PSA) level and PSA density (PSAD) to detect prostatic malignancy in a country with low prostate cancer incidence.

Prostate-specific antigen (PSA) and PSA density (PSAD) values in Indonesia had been found uniquely much higher than the normal accepted values in western countries. However, PSA more than 10 ng/ml and PSAD above 0.15 in intermediate PSA of 4-10 ng/ml are still indicative of a prostate biopsy. This condition had led to unnecessary biopsies in view of the low incidence of prostatic carcinoma in our country. Our objective is to find alternative serum PSA levels and PSAD cutoff points that enhance the specificity and sensitivity of prostate cancer detection. This retrospective cross-sectional study included 805 consecutive patients from 40 to 95 years old in Sumber Waras Hospital (SWH) and Cipto Mangunkusumo Hospital (CMH) from 1994 to 1997. All patients underwent digital rectal examination (DRE) and transrectal ultrasonography (TRUS) to measure prostate volume. After the serum PSA level was determined and PSAD was calculated, prostate biopsies were performed if the PSA level was greater than 10 ng/ml or PSAD more than 0.15 at intermediate PSA levels of 4-10 ng/ml. The ability of PSA, intermediate PSA level, and PSAD to improve the accuracy of prostate cancer detection was evaluated using univariate analysis. Among 805 patients, 240 patients had PSA level < 4 ng/ml, 230 patients had PSA level 4-10 ng/ml, and 335 had PSA level > 10 ng/ml. Of the 230 patients with intermediate PSA level, 108 had PSAD > 0.15. Thirty-five patients had histologically confirmed prostatic carcinoma, i.e., 3 of 108 patients with PSA 4-10 ng/ml and PSAD > 0.15, and 32 of 335 patients with PSA > 10 ng/ml. There were 105 and 303 unnecessary biopsies in those groups. With a PSA cutoff level of > or = 8 ng/ml, we found 100% sensitivity to prostate cancer. PSAD > or = 0.20 within a PSA level of 8-30 ng/ml gave 100% sensitivity to prostate cancer. Using these new cutoffs there would be 148 biopsies (33.4%) saved. We concluded from this study that the commonly accepted values of serum PSA level and PSAD resulted in many unnecessary biopsies in our patients. Instead, the most sensitive cutoff points to perform prostate biopsy are serum PSA level greater than 8.0 ng/ml, and PSAD of more than 0.20 at an intermediate serum PSA level of 8-30 ng/ml.

Aged↗

Relationship between prostate size and percent free prostate-specific antigen in patients with operable prostate cancer.

BACKGROUND: The free-to-total prostate-specific antigen ratio is the best marker for optimizing prostate cancer detection. The main problem with studies of percent free PSA is the variability of reported cutoff values. OBJECTIVES: To evaluate the influence of prostate size on the ratio of free to total PSA. METHODS: The study group included 58 patients (mean age 66.4 years) with clinically localized prostate cancer treated surgically at our institution. Total PSA and free PSA levels were measured by a solid phase enzyme immunoassay test (Hoffman-La Roche, Basel, Switzerland). The percent free PSA was compared with prostate size as determined from the surgical specimen. RESULTS: A direct relation was noted between prostate size and the percent free PSA value (r = 0.49, P = 0.0001). Mean percentage free PSA was 9% +/- 0.004 in men with normal-sized gland while in men with large prostate (> 60 g) the average percent free PSA was 15.9 +/- 0.09 (P = 0.001). CONCLUSIONS: In patients with prostate cancer the percent free PSA level is influenced by the gland size. The larger the prostate the higher the proportion of the free PSA. Such information may have influence on the recommendation for prostate biopsy in screening programs for early detection of prostate cancer.

Aged↗

[Expression and significance of clusterin in normal prostate, benign prostate hyperplasia and prostate cancer].

OBJECTIVE: To investigate the expression and significance of Clusterin in normal prostate, benign prostate hyperplasia (BPH) and prostate cancer. METHODS: Clusterin expression in samples of 12 normal prostate, 15 BPH, and 56 prostate cancer were studied by immunohistochemical stain. RESULTS: Of 83 cases, 67 are positive or weak positive (81%). The rate of positive or weak positive for normal prostate, BPH and prostate cancer was 17% (2/12), 73% (11/15), and 96% (54/56) respectively. The expression level of Clusterin in prostate cancer was much higher than in normal prostate (t = 8.82, P < 0.01). BPH (t = 7.63, P < 0.01) was related positively with pathological grade (r = 0.649, P < 0.01) and stage (r = 0.609, P < 0.01) of prostate cancer. CONCLUSION: Clusterin may play an important role in the biological characteristics of prostate cancer by the anti-apoptosis pathway.

Apoptosis↗

[The significance of serum prostate-specific antigen, gamma-seminoprotein and prostatic acid phosphatase as prostate cancer markers].

Prostate-specific antigen (PA), gamma-seminoprotein (gamma-Sm) and prostatic acid phosphatase (PAP) have been evaluated in patients with prostate cancer, benign prostatic hyperplasia (BPH), chronic prostatitis and acute prostatitis. PA has proved to be diagnostically more sensitive than PAP and gamma-Sm for the detection of prostatic cancer. Although PA may be elevated more frequently than PAP and gamma-Sm in patients with BPH, there are possibilities that these patients with elevated PA and normal PAP and gamma-Sm may have prostatic cancer or precancerous conditions not detectable in our routine diagnostic procedures. We report two cases of prostatic cancer with persistently elevated PA and diagnosed after repeated biopsies. Our data suggest that PA is a sensitive and useful tumor marker for the diagnosis of prostatic cancer. PAP and gamma-Sm in combination with PA may serve as more useful for differential diagnosis and confirmation of prostatic cancer.

Acid Phosphatase↗