Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Prostatism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,333 records · Page 74Linked to original sources
PubMed2006

Associations among benign prostate hypertrophy, atypical adenomatous hyperplasia and latent carcinoma of the prostate.

AIM: To investigate the frequency of atypical adenomatous hyperplasia (AAH) and its associations with benign prostate hypertrophy (BPH) and latent histological carcinoma of the prostate (LPC) in autopsy material. METHODS: Two hundred and twelve prostate specimens obtained from autopsy material were subjected to whole mount analysis in an attempt to investigate the associations among BPH, AAH and LPC. RESULTS: Most histological carcinomas and AAH lesions were found in enlarged prostates with intense hypertrophy. No statistically significant relation was found between BPH and the main characteristics of LPC, such as tumor volume, histological differentiation and biological behavior. Our data regarding multi-focal tumors showed a tendency for multi-focal carcinomas to develop in larger prostates, and a tendency of AAH lesions to develop in larger prostates. No statistically significant relation was found between AAH and LPC. CONCLUSION: There seems not any causative aetiopathogenetical or topographical relation between AAH lesions and prostate adenocarcinoma. AAH lesion seems to be a well-defined mimicker of prostatic adenocarcinoma, and the reported association of AAH with prostatic carcinoma could probably be an epiphenomenon.

Adenocarcinoma↗
PubMed1991

[A study of secretory IgA antibody titers for Chlamydia trachomatis in prostatic secretion of chronic prostatitis].

In order to study the correlation between chronic prostatitis and C. trachomatis, IgA and IgG antibody titers for C. trachomatis were measured in serum and prostatic secretion of cases of chronic prostatitis. IgA antibody titers have higher tendency in prostatic secretion than in serum. The other side, IgG antibody titers have higher tendency in serum than in prostatic secretion. This result suggested IgA antigen was reacted in local immunological response in prostatic gland. Subsequently, in order to confirm that IgA antibody in prostatic secretion is formed from secretory IgA antibody mainly, IgA antibody titers were compared with secretory IgA antibody titers. That results was considered that many cases with high IgA titers had high secretory IgA titers. The fact suggested in cases of C. trachomatis prostatitis, IgA antibody was mainly formed from secretory IgA antibody in prostatic secretion.

Chlamydia Infections↗
PubMed2004

Prostate pathology of genetically engineered mice: definitions and classification. The consensus report from the Bar Harbor meeting of the Mouse Models of Human Cancer Consortium Prostate Pathology Committee.

The Pathological Classification of Prostate Lesions in Genetically Engineered Mice (GEM) is the result of a directive from the National Cancer Institute Mouse Models of Human Cancer Consortium Prostate Steering Committee to provide a hierarchical taxonomy of disorders of the mouse prostate to facilitate classification of existing and newly created mouse models and the translation to human prostate pathology. The proposed Bar Harbor Classification system is the culmination of three meetings and workshops attended by various members of the Prostate Pathology Committee of the Mouse Models of Human Cancer Consortium. A 2-day Pathology Workshop was held at The Jackson Laboratory in Bar Harbor, Maine, in October 2001, in which study sets of 93 slides from 22 GEM models were provided to individual panel members. The comparison of mouse and human prostate anatomy and disease demonstrates significant differences and considerable similarities that bear on the interpretation of the origin and natural history of their diseases. The recommended classification of mouse prostate pathology is hierarchical, and includes developmental, inflammatory, benign proliferative, and neoplastic disorders. Among the neoplastic disorders, preinvasive, microinvasive, and poorly differentiated neoplasms received the most attention. Specific criteria were recommended and will be discussed. Transitions between neoplastic states were of particular concern. Preinvasive neoplasias of the mouse prostate were recognized as focal, atypical, and progressive lesions. These lesions were designated as mouse prostatic intraepithelial neoplasia (mPIN). Some atypical lesions were identified in mouse models without evidence of progression to malignancy. The panel recommended that mPIN lesions not be given histological grades, but that mPIN be further classified as to the absence or presence of documented associated progression to invasive carcinoma. Criteria for recognizing microinvasion, for classification of invasive gland-forming adenocarcinomas, and for characterizing poorly differentiated tumors, including neuroendocrine carcinomas, were developed and are discussed. The uniform application of defined terminology is essential for correlating results between different laboratories and models. It is recommended that investigators use the Bar Harbor Classification system when characterizing new GEM models or when conducting experimental interventions that may alter the phenotype or natural history of lesion progression in existing models.

Animals↗
PubMed2004

Protein profiling of microdissected prostate tissue links growth differentiation factor 15 to prostate carcinogenesis.

Identification of proteomic alterations associated with early stages in the development of prostate cancer may facilitate understanding of progression of this highly variable disease. Matched normal, high-grade prostatic intraepithelial neoplasia (hPIN) and prostate cancer cells of predominantly Gleason grade 3 were procured by laser capture microdissection from serial sections obtained from snap-frozen samples dissected from 22 radical prostatectomy specimens. From these cells, protein profiles were generated by surface-enhanced laser desorption/ionization-time of flight mass spectrometry. A 24-kDa peak was observed at low or high intensity in profiles of prostate cancer cells in 19 of 27 lesions and at low intensity in 3 of 8 hPIN lesions but was not detectable in matched normal cells. SDS-PAGE analysis of prostate cancer and matched normal epithelium confirmed expression of a prostate cancer-specific 24-kDa protein. Mass spectrometry and protein data-based analysis identified the protein as the dimeric form of mature growth differentiation factor 15 (GDF15). The increased expression of mature GDF15 protein in prostate cancer cells cannot be explained on the basis of up-regulation of GDF15 mRNA because reverse transcription-PCR analysis showed similar amounts of transcript in normal, hPIN, and prostate cancer cells that were obtained by laser capture microdissection in the same set of serial sections from which the protein profiles were obtained. Our findings suggest that early prostate carcinogenesis is associated with expression of mature GDF15 protein.

Adenocarcinoma↗
PubMed2005

p300 regulates androgen receptor-independent expression of prostate-specific antigen in prostate cancer cells treated chronically with interleukin-6.

Prostate cancer is the most frequent non-skin cancer in men. Although the mechanisms involved in the progression of prostate cancer are not entirely understood, androgen receptor has been shown to play an important role. Androgen receptor is expressed in both early and late-stage prostate cancer. Also, androgen-regulated pathways are thought to be active as evidenced by elevated levels of prostate-specific antigen (PSA). In addition, several androgen receptor coactivators and cytokines are involved in prostate cancer progression. In this regard, we have shown previously that the coactivator p300 plays a major role in the androgen-independent activation of PSA by interleukin 6 (IL-6), a cytokine involved in late-stage prostate cancer. In this study, we investigated the role of p300 and its homologue CREB-binding protein in prostate cancer cells treated chronically with IL-6. We found that p300 but not CREB-binding protein induced activation of PSA in these cells and that the histone acetyltransferase activity of p300 was critical. This effect was independent of the presence of androgens or antiandrogens. Moreover, we found markedly reduced levels of androgen receptor in these cells and p300 transfection did not affect those levels, suggesting that the p300 effect on PSA could be bypassing the androgen receptor. Transfection with exogenous androgen receptor showed minimal response of PSA to androgens but higher response to p300. We found similar effects of p300 on the androgen response element III, which mediates the androgen receptor-dependent activation of PSA. Finally, we showed that p300 alone regulates expression of the endogenous PSA gene in the IL-6-treated cells. These findings reveal a new insight in the progression of prostate cancer, suggesting that coactivators, such as p300, play more important roles in late-stage prostate cancer, and could regulate androgen-dependent genes in the absence or with very low levels of androgen receptor.

Androgens↗
PubMed2005

Targeted biallelic inactivation of Pten in the mouse prostate leads to prostate cancer accompanied by increased epithelial cell proliferation but not by reduced apoptosis.

The PTEN tumor suppressor gene is frequently inactivated in human tumors, including prostate cancer. Based on the Cre/loxP system, we generated a novel mouse prostate cancer model by targeted inactivation of the Pten gene. In this model, Cre recombinase was expressed under the control of the prostate-specific antigen (PSA) promoter. Conditional biallelic and monoallelic Pten knock-out mice were viable and Pten recombination was prostate-specific. Mouse cohorts were systematically characterized at 4 to 5, 7 to 9, and 10 to 14 months. A slightly increased proliferation rate of epithelial cells was observed in all prostate lobes of monoallelic Pten knock-out mice (PSA-Cre;Pten-loxP/+), but minimal pathologic changes were detected. All homozygous knock-out mice (PSA-Cre;Pten-loxP/loxP) showed an increased size of the luminal epithelial cells, large areas of hyperplasia, focal prostate intraepithelial neoplasia lesions and an increased prostate weight at 4 to 5 months. More extensive prostate intraepithelial neoplasia and focal microinvasion occurred at 7 to 9 months; invasive prostate carcinoma was detected in all male PSA-Cre;Pten-loxP/loxP mice at 10 to 14 months. At 15 to 16 months, a rare lymph node metastasis was found. In hyperplastic cells and in tumor cells, the expression of phospho-AKT was up-regulated. In hyperplastic and tumor cells, expression of luminal epithelial cell cytokeratins was up-regulated; tumor cells were negative for basal epithelial cell cytokeratins. Androgen receptor expression remained detectable at all stages of tumor development. The up-regulation of phospho-AKT correlated with an increased proliferation rate of the epithelial cells, but not with a reduced apoptosis.

Age Factors↗
PubMed2000

Prediction of prostate volume based on total and free serum prostate-specific antigen: is it reliable?

OBJECTIVE: To analyze the utility of total/free prostate-specific antigen (PSA) and age as predictors of the prostate volume in men with symptomatic benign prostatic hyperplasia (BPH) and no evidence of prostate cancer. PATIENTS AND METHODS: Total and free serum PSA were determined in 681 patients with normal digital rectal examination and symptomatic BPH using the Hybritech method. Prostate volume was measured by transrectal ultrasound (TRUS). TRUS-guided biopsy was performed in 459 (67.4%) of the patients with a serum PSA >4.0 ng/ml. RESULTS: The relationship with prostate volume was best described in a log linear fashion by free PSA (R(2) = 0.367), total PSA (R(2) = 0.264) and age (R(2) = 0.017). Multiple linear regression demonstrates no significant influence of age. Free PSA was able to predict the individual TRUS prostate volume +/-10% in 67% of the patients and +/-20% in 91.2% and total PSA in 63 and 90. 9%, respectively. CONCLUSION: Prostate volume is strongly related with free and total PSA. Both determinations would be able to predict the TRUS prostate volume +/-20% in more than 90% of the patients.

Adult↗
PubMed2001

Is there a relationship between the amount of tissue removed at transurethral resection of the prostate and clinical improvement in benign prostatic hyperplasia.

OBJECTIVE: To assess in a prospective trial the influence of the amount of tissue resected at transurethral resection of the prostate (TURP) for benign prostatic enlargement on the symptom improvement as assessed by symptom scores. METHODS: Between December 1996 and August 1998 a total of 138 men (mean age 68.2, range 53-89) with symptomatic benign prostatic enlargement who underwent TURP participated in this prospective study. Patients were assessed preoperatively with the International Prostate Symptom Score (IPSS), the American Urological Association Bother Score (AUA-BS) and the Benign Prostatic Hyperplasia Impact Index (BPH-II) as well as urinary flow rate measurements (Qmax) and prostate volume (PV) and residual urine determination by ultrasound. The amount of tissue resected was weighed. Patients were followed with reevaluation of Q(max), residual urine and the symptom and bother scores at 3 and 6 months. RESULTS: A close correlation between preoperative PV (mean 49.0 ml, SD 22.0, range 13-140) and the resected tissue weight (RTW, mean 24.7 g, SD 18.0, range 6-128) was seen (r = 0.75, p < 0.001). Age was correlated with preoperative PV (r = 0.23, p < 0.05). While significant mean improvements in Q(max), residual volume and IPSS, AUA-BS and BPH-II were found 3 and 6 months postoperatively, a negative correlation was seen between the RTW and the IPSS, the AUA-BS and the BPH-II 3 months after TURP (r = -0.23, p < 0.024; r = -0.23, p < 0.025; r = -0.20, p = 0.05). No statistically significant correlation was seen between symptom change and the percentage of PV removed or the residual prostatic weight. Classification of the patients into groups depending on preoperative PV (< 30, 31-50, 51-70 and >70 ml) showed a tendency for patients with larger PV to gain more symptom improvement postoperatively. CONCLUSIONS: Early symptom improvement after TURP will depend on the amount of tissue removed but the relationship is weak and affected by several other confounding factors. Apparently, the symptomatic improvement after TURP is not primarily dependent on the relative completeness of the resection. Patients with larger prostates and larger RTW tend to gain more symptomatic benefit from TURP than do patients with smaller prostates.

Aged↗
PubMed1996

Screening and early detection of prostate cancer will decrease morbidity and mortality from prostate cancer: the argument against.

The ability of prostate specific antigen, digital rectal examination and transurethral ultrasound, either individually or in combination, to detect unsuspected prostate cancer is beyond doubt. Early detection programmes have revealed prostate cancer in 6% of men over 50 years of age. Most are stage T1c, or confined to the prostate but, protagonists claim that, on the basis of size, they are 'clinically significant'. Mortality from this disease should be reduced by their treatment. Available statistics suggest that the lifetime incidence of 'screen-detected' cancers will far exceed the likelihood of dying from prostate cancer. Given the current operative mortality of total prostatectomy and the physical and psychological morbidity of screening, biopsy and treatment, it is far from certain that mortality or morbidity from prostate cancer will be decreased. Long-term outcome data for T1c prostate cancer do not exist. Is the likelihood of prostate cancer death the same for prostate-specific antigen thresholds of 2, 3 or 4 ng/ml, or from tumours found in 1 of 6, or 1 of 12 needle biopsies? None of this is known. European men deserve the benefit of scientifically based information before being exposed to another North American fashion. Prospective randomised trials investigating mortality, quality of life and cost benefit are the only solution.

Aged↗
PubMed1996

Prostate-specific antigen and prostatitis in men under fifty.

OBJECTIVE: To evaluate the occurrence of increased prostate-specific antigen (PSA) serum concentration in patients with prostatitis and low incidence of benign prostatic hyperplasia and prostatic cancer, PSA was measured in a selected population. METHODS: PSA levels were evaluated in 72 patients with prostatitis under 50 years of age. RESULTS: An increased PSA (> 4 ng/ml) was found in 5/7 (71%) patients with acute prostatitis, and in 2/13 (15%) and 2/32 (6%) patients with chronic bacterial and abacterial prostatitis, respectively. No patient with prostatodynia had an increased PSA. In patients with bacterial prostatitis PSA level decreased to normal value after effective antibiotic therapy in most cases. CONCLUSION: Prostatitis must be considered when using PSA as tumor marker.

Adult↗
PubMedDate not supplied

Prostate--specific G protein couple receptor genes and STAG1/PMEPA1 in peripheral blood from patients with prostatic cancer.

We investigated whether prostate - specific G protein couple receptor genes and STAG1/PMEPA1 gene expression in peripheral- blood could be useful as a diagnostic or prognostic marker of prostate cancer. Circulating cells were identified by reverse transcription-polymerase chain reaction (RT-PCR) to detect PSGR and STAG1/PMEPA1 mRNA in peripheral blood (PB) from 11 patients with treated prostate cancer (CaP), 11 with newly-diagnosed untreated CaP and 20 with benign prostatic hyperplasia (BPH) (controls). RT-PCR amplified PSGR in 8 of 11 untreated and in 9 of 11 treated patients with CaP and in 16 of 20 with BPH; whereas it amplified PMEPA1 in 1 of 11 untreated and in 7 of 11 treated patients with CaP and in 4 of 20 with BPH. In our control tissues and cell lines nearly all the prostatic and non- prostatic tissues and cell lines expressed PSGR mRNA, whereas only one prostatic neoplastic tissue and the androgen-responsive (LNCaP) and androgen non-responsive (PC3) prostatic cell lines expressed PMEPA1. These findings suggest that the investigated genes are poorly specific and probably of little use as diagnostic or prognostic markers in peripheral blood for monitoring prostate cancer progression and recurrence.

Base Sequence↗
PubMed2005

Java Web Start based software for automated quantitative nuclear analysis of prostate cancer and benign prostate hyperplasia.

BACKGROUND: Androgen acts via androgen receptor (AR) and accurate measurement of the levels of AR protein expression is critical for prostate research. The expression of AR in paired specimens of benign prostate and prostate cancer from 20 African and 20 Caucasian Americans was compared to demonstrate an application of this system. METHODS: A set of 200 immunopositive and 200 immunonegative nuclei were collected from the images using a macro developed in Image Pro Plus. Linear Discriminant and Logistic Regression analyses were performed on the data to generate classification coefficients. Classification coefficients render the automated image analysis software independent of the type of immunostaining or image acquisition system used. The image analysis software performs local segmentation and uses nuclear shape and size to detect prostatic epithelial nuclei. AR expression is described by (a) percentage of immunopositive nuclei; (b) percentage of immunopositive nuclear area; and (c) intensity of AR expression among immunopositive nuclei or areas. RESULTS: The percent positive nuclei and percent nuclear area were similar by race in both benign prostate hyperplasia and prostate cancer. In prostate cancer epithelial nuclei, African Americans exhibited 38% higher levels of AR immunostaining than Caucasian Americans (two sided Student's t-tests; P < 0.05). Intensity of AR immunostaining was similar between races in benign prostate. CONCLUSION: The differences measured in the intensity of AR expression in prostate cancer were consistent with previous studies. Classification coefficients are required due to non-standardized immunostaining and image collection methods across medical institutions and research laboratories and helps customize the software for the specimen under study. The availability of a free, automated system creates new opportunities for testing, evaluation and use of this image analysis system by many research groups who study nuclear protein expression.

Algorithms↗
PubMed2004

The use of real-time quantitative PCR to detect circulating prostate-specific membrane antigen mRNA in patients with prostate carcinoma.

Prostate-specific antigen (PSA) has long been criticized for its lack of specificity in screening for the occurrence of prostate cancer. In this study, we tried to measure levels of another biomarker, prostate-specific membrane antigen (PSM), in the peripheral circulation from subjects with either prostate cancer or benign prostatic hyperplasia (BPH). Total RNA was extracted from blood samples of 70 patients with prostate cancer and 19 with BPH. Reverse transcription was performed to convert mRNA to cDNA. The cDNA was analyzed with a novel real-time quantitative polymerase chain reaction (PCR) protocol to measure PSM mRNA levels in the circulation. Melting curve analysis was adapted to assure that correct amplification data were obtained. Results showed that 41 of 70 prostate cancer patients had positive results, whereas 9 of 19 BPH cases were negative. Therefore, the sensitivity and specificity were determined to be 58.6% and 47.4%, respectively. For comparison, traditional nested PCR was performed to investigate whether the new method was superior. The sensitivity and specificity of nested PCR were determined to be 27.1% and 57.9%, respectively. The detection limits of these two methods were 0.0005 ng (for the real-time quantitative PCR method) and 0.5 ng of PSM-cDNA (for the nested PCR method). In conclusion, we have successfully developed a novel, noninvasive real-time quantitative PCR method to detect the PSM mRNA levels in the peripheral circulation of prostate cancer subjects. This method may provide references for urologists diagnosing prostate cancer or monitoring the patient's condition after treatment.

Antigens, Surface↗
PubMed1997

Different expression patterns of somatostatin receptor subtypes in cultured epithelial cells from human normal prostate and prostate cancer.

The transcripts of five SRIH receptor subtypes (SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5) were investigated by RT-PCR in epithelial cells (EC) and stromal cells (SC) from primary cultures of five normal human prostates and six prostate cancers. Primary cultures of prostate EC were established in serum-free keratynocyte medium with 5% FCS, epidermal growth factor, and bovine pituitary extract; SC were cultured in MEM with 10% FCS. Total RNA was extracted from EC and SC using a modified guanidine thiocyanate method. RT-PCR was performed after deoxyribonuclease treatment, using SSTR1-, SSTR2-, SSTR3-, SSTR4-, and SSTR5-specific-primers and adding glyceraldehyde-3-phosphate dehydrogenase-specific primers as internal control. A PCR product of the expected size of 334 bp, corresponding to SSTR1, was expressed only in EC from prostate cancer, whereas the expected 461-bp product of SSTR2 was found only in EC from normal prostate. SSTR3 messenger RNA was undetectable in normal and cancer EC, whereas SSTR4 and SSTR5 were present in both cell types. SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5 messenger RNAs were not expressed in SC from both normal and cancer prostates. The RT-PCR method clearly demonstrated SSTRs' expression in the human prostate EC in vitro with differences between normal and tumoral samples. Our results may explain the ineffectiveness of some SSTR2 selective SRIH analogues in the treatment of prostate cancer and suggest that the absence of SSTR2 could represent a growth advantage in prostate cancer.

Aged↗
PubMed1991

Activation of cytotoxic cells by syngeneic prostate antigens in experimental autoimmune vesiculo-prostatitis.

In our experimental model of autoimmune vesiculo-prostatitis, obtained by immunization with syngeneic male accessory glands (MAG) and complete Freund's adjuvant, the presence of specific autoreactive cells with cytotoxic activity against prostate antigens was studied. The specific cytotoxicity generated in MAG immunized rats was tested using 51Cr labelled syngeneic prostate cells or labelled chicken erythrocytes coated with specific antigens (MAG homogenate or chromatographic fractions from prostate homogenate) which were used as target cells in a medium free of complement. The addition of spleen sensitized cells to prostate cells suspension produced a significant release of 51Cr in regard to normal effector cells (11.87 +/- SE 1.12 versus 1.5 +/- 0.75). Similar results were obtained when MAG-coated erythrocytes were used as target cells (10.87 +/- SE 0.62 versus 1.50 +/- 0.25). Depletion of T but no B or adherent-cells was shown to abolish the lytic effect indicating that MAG immunization provides determinants which are recognized by sensitized T-cells on cells of the prostate gland where the most severe tissue alterations were previously observed. Erythrocytes coated with chromatographic fractions obtained from prostate homogenate were used to identify the antigens triggering the lytic effect. It was demonstrated that two fractions (FI and FII) functioned as in vivo sensitizing antigens as well as in vitro activating antigens for themselves. The restimulation in vitro of sensitized cells with purified prostate fractions induces an additional lytic effect suggesting that an expansion of effector cells may take place after contacting the antigens at the prostate site.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Meta-analysis of prostate-specific antigen and digital rectal examination as screening tests for prostate carcinoma.

BACKGROUND: Physicians commonly screen for prostate cancer by using prostate-specific antigen (PSA) and digital rectal examination (DRE). The usefulness of these screening mechanisms is not well established, however. A meta-analysis of PSA and DRE to detect prostate carcinoma was conducted with a focus on sensitivity, specificity, and positive predictive value. METHODS: A literature search of OVID database (1966 to November 1999) using the medical subject headings "prostate-specific antigen" and "mass screening," as well as "prostate carcinoma," was performed. Thirteen articles were selected for the meta-analysis in this study. Most studies included asymptomatic men older than 50 years from various countries. Pooled results were calculated from the individual reports for sensitivity, specificity, and positive predictive value for PSA and DRE based on biopsy result as the reference standard. RESULTS: The overall detection rate of prostate carcinoma was 1.8% based on a positive biopsy. Of the prostate carcinoma detected, 83.4% was localized. The pooled sensitivity, specificity, and positive predictive value for PSA were 72.1%, 93.2% and 25.1%, respectively; and for DRE were 53.2%, 83.6% and 17.8%, respectively. CONCLUSIONS: There were two major outcomes of this meta-analysis. One was the potential for detecting early-stage prostate cancer with these screening tests, because 83.4% of total cancers detected were localized. The second important outcome was that the overall sensitivity, specificity, and positive predictive value for PSA were higher than those for DRE when used as a screening tool to detect prostate cancer. When a patient has abnormal findings using PSA and DRE, the chance of cancer is 1 in 4 or 5. Conversely, when findings from PSA and DRE are normal, the chance of missing a cancer is about 10%.

Adult↗
PubMed1992

[Significance of prostatic specific antigen in the mass screening for prostate cancer].

The significance of prostatic specific antigen (PSA) was investigated in the subjects examined by the mass screening for prostate cancer from 1985 to 1990. All subjects was examined by digital rectal examination (DRE) and with prostatic acid phosphatase (PAP) and the subjects in whom prostate cancer (Pca) was suspected from abnormal DRE and/or elevated PAP were recommended to receive the secondary screening to confirm the presence of Pca. PSA was measured by radioimmunoassay using Ball-Elsa-PSA-kit. 1,600 serum samples were obtained from our serum bank. The relationship among PSA, prostate size estimated by DRE and age was investigated. PSA was increased with age and the prostate size, PSA being more closely related with the latter. Therefore, we estimated that PSA has an ability to detect benign prostatic hypertrophy (BPH) in the mass screening. This estimation should be confirmed by using an ultrasound tomography because the prostate size obtained by DRE is inaccurate as compared with that obtained by ultrasound tomography. The cut off level of PSA was determined by control which was composed from the subjects with normal size prostate and one with BPH. When the cut off level was 8.6 ng/ml, the sensitivity, specificity and efficiency as Pca marker was 73.9%, 97.4% and 97.1%, respectively. PSA was more than 8.6 ng/ml in all of Pca with elevated PAP. PSA was expected to improve the Pca detection rate in our mass screening system.

Aged↗
PubMed1999

Screening for prostate cancer with the prostate-specific antigen test: are patients making informed decisions?

BACKGROUND: The benefits of early detection of prostate cancer are uncertain, and the American College of Physicians and the American Academy of Family Physicians recommend individual decision making in prostate cancer screening. This study reports the knowledge of male primary care patients about prostate cancer and prostate-specific antigen (PSA) testing and examines how that knowledge is related to PSA testing, preferences for testing in the future, and desire for involvement in physician-patient decision making. METHODS: The sample included 160 men aged 45 to 70 years with no history of prostate cancer who presented for care at a university-based family medicine clinic. Before scheduled office visits, patients completed a questionnaire developed for this study that included a 10-question measure of prostate cancer knowledge, the Deber-Kraestchmer Problem-Solving Decision-Making Scale, sociodemographic indicators, and questions on PSA testing. RESULTS: In general, patients who were college graduates were more knowledgeable about prostate cancer and early detection than those with a high school education or less. Aside from college graduates, most patients could not identify the principle advantages and disadvantages of PSA testing. Patients indicating previous or future plans for PSA testing demonstrated greater knowledge than other patients. Desire for involvement in decision making varied by patient education but was not related to past PSA testing. CONCLUSIONS: Patients lack knowledge about prostate cancer and early detection. This knowledge deficit may impede the early detection of prostate cancer and is a barrier to making an informed decision about undergoing PSA testing.

Adult↗