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PubMed1978

Demonstration of a progestin receptor in human benign prostatic hyperplasia and prostatic carcinoma.

Cytosol from human benign hyperplastic and carcinomatous prostatic tissue has been shown to contain a progestin receptor with a dissociation constant of approximately 10(-9) M. The receptor was measured using 3H-labeled R 5020 (17 alpha, 21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione) as ligand. Progesterone, cyproterone acetate, and R 1881 (methyltrienolone) were efficient competitors to R 5020 for binding sites on the receptor whereas testosterone, 5 alpha--dihydrotestosterone, estradiol, cortisol, and several hydroxylated and saturated derivatives of progesterone did not compete. The [3H]R 2020-receptor-complex had a sedimentation coefficient of approximately 4 S, an isoelectric point of approximately 5, was heat-labile, and was destroyed by treatment with trypsin but not with deoxyribonuclease or ribonuclease. Seventeen of 21 patients with benign prostatic hyperplasia and three patients with prostatic carcinoma had 1 to 40 fmoles of specific R 5020-binding sites per mg of cytosol protein. One sample of normal prostatic tissue did not contain significant amounts of progesting receptor. Tissue specimens removed by transvesical adenoma enucleation displayed a larger number of specific R 5020-binding sites than electroresected specimens. The progestin receptor in hyperplastic prostate may be involved in the mechanism of the action of progestins used in the medical treatment of benign prostatic hyperplasia. Quantitation of progestin receptor in cancer of the prostate may form part of the basis of a predictive test program for endocrine therapy of prostatic malignancy.

Aged↗
PubMed1999

Apoptosis and nuclear shapes in benign prostate hyperplasia and prostate adenocarcinoma: comparison with and relation to Gleason score.

PURPOSE: To compare differences in the number of apoptotic bodies and nuclear shapes (size and roundness) between untreated benign prostate hyperplasia (BPH) and untreated advanced prostate adenocarcinoma (PCA) and to elucidate differences in apoptosis number and nuclear shapes with increasing malignant potentiality, by Gleason score, in PCA. METHODS: A retrospective study was conducted on 40 patients with BPH and 12 patients with PCA I (Gleason score 2-4), 14 patients with PCA II (Gleason score 5-7) and 14 patients with PCA III (Gleason score 8-10). The frequency of apoptotic bodies (mean percentage calculated from 200 cells/high-power field over 10 fields) was examined on immunostain. Nuclear shapes were determined by an automatic image analyzer. Over 100 hyperplastic cells or cancer cells were detected by the image analyzer. RESULTS: The mean number of apoptotic bodies in BPH and PCA I were not significantly different, but patients with PCA II and PCA III showed significantly higher numbers of apoptotic bodies than patients with BPH. Patients with PCA III had significantly more apoptotic bodies than patients with PCA I. Benign prostate hyperplasia nuclei had the smallest mean nuclear area and the largest mean nuclear peripheral ellipse among the four groups. The study showed that PCA I, II, III nuclei had significantly larger areas and a less circular shape than nuclei from patients with BPH. Nuclei from patients with PCA I were smaller in size and rounder than nuclei from patients with PCA III. CONCLUSIONS: The present study clearly shows the presence of apoptosis in BPH and PCA and shows an increasing number of apoptotic bodies with higher cellular malignancy. The nuclear shapes in PCA were more irregular and larger in size with increasing cellular malignancy. As expected, nuclei in BPH were smaller in size and rounder than those of cancer nuclei.

Adenocarcinoma↗
PubMed2004

Deregulation of p73 isoform equilibrium in benign prostate hyperplasia and prostate cancer.

p73, a p53 homologue important for growth suppression, differentiation and induction of apoptosis, utilizes different promoters and undergoes alternative splicing to produce several isoforms differing in their ability to overlap p53 functions. Using reverse transcriptase-polymerase chain reaction (RT-PCR) to assess the mRNA levels of p53, p73 (total and isoforms specific for exons 2 and 13), MDM2, CDKN1A and beta2-microglobulin as internal control, we analyzed 35 prostate carcinomas and 44 benign prostate hyperplasias (BPH) compared to 14 normal prostates. Shift of p73 isoform mRNA levels from exon 13 lacking to exon 13 containing copies was observed in 80% of prostate cancer cases and in 52.3% of BPH specimens, and from exon 2 containing to exon 2 lacking (p73Deltaexon2) transcripts in 45.7% of cancer cases, but only in 9.1% of BPH samples. From these findings we deduce that p73 isoform balance is disrupted in prostate cancer and BPH, suggesting that this disequilibrium could play an important role in both prostate hyperplasia and malignancy.

Adult↗
PubMed1998

[Morphogenesis of benign prostatic hyperplasia and prostatic carcinoma].

Enlargement of the prostate is an age-related, physiological process that is unique in human tissue. The prostate gland is the most common site of neoplastic disorders in men. Despite the growing impact of the various prostate diseases in terms of morbidity and mortality, the pathogenesis of benign prostate hyperplasia (BPH) and prostate cancer remains poorly understood. This reflects the complex composition of the gland with different anatomic, cellular and functional compartments that are differentially involved in benign and malignant disease processes. The present review summarizes new concepts on the morphogenesis of normal and abnormal growth in the human prostate. There is increasing evidence that prostatic stem cells are located in the basal cell layer that is basically involved in normal growth and the development of glandular hyperplasia and prostate cancer. High-grade prostatic intraepithelial neoplasia is considered the most likely precursor of clinically important cancer of the peripheral zone. Severe differentiation and proliferation abnormalities occur during malignant transformation of the prostatic epithelium. These premalignant changes are associated with abnormal expression of growth factor receptors, oncogene and suppressor gene products and genetic instability. During the process of stromal invasion the transformed cells lose their basal cell phenotype and produce basement membrane-like matrices. Common prostate cancer is mainly composed of exocrine cell types that remain androgen-responsive even in hormone-independent disease. The frequent occurrence of neuroendocrine differentiation in common prostate cancer reflects the differentiation potency of its stem cells. The endocrine phenotype derives from exocrine tumor cells via intermediate (amphicrine) cell types. Neuroendocrine tumor cells consistently lack the nuclear androgen receptor and represent an androgen-insensitive cell population in prostate cancer.

Cell Transformation, Neoplastic↗
PubMed1993

Terazosin in the treatment of benign prostatic hyperplasia. Terazosin Benign Prostatic Hyperplasia Study Group.

OBJECTIVE: To evaluate the efficacy and tolerability of terazosin, a long-acting selective alpha 1-receptor antagonist, in patients with benign prostatic hyperplasia. DESIGN AND SETTING: Randomized, double-blind, multicenter (eight government and private facilities), placebo-controlled study. PATIENTS: Men aged 45 years or older, with qualifying signs and symptoms of benign prostatic hyperplasia (n = 160). INTERVENTIONS: Terazosin or placebo once daily, with terazosin dosage titrated to the patient's response. After a 4-week placebo lead-in, 1 to 10 mg of terazosin or placebo was administered for 24 weeks. OUTCOME MEASURES: Decreases in mean Boyarsky scores for obstructive and irritative symptoms and total scores and increases in peak urine flow rate. RESULTS: Terazosin-treated patients had decreases in Boyarsky obstructive, irritative, and total scores of 3.3 (52%), 1.3 (29%), and 4.6 (42%), respectively, compared with decreases of 0.7 (12%), 0.4 (9%), and 1.1 (11%), respectively, in the placebo group (P < .05). Peak urine flow increased by a mean of 2.6 mL/s (30%) in terazosin-treated patients and 1.2 mL/s (14%) in placebo-treated patients (P < or = .05). Adverse events that differed significantly in the two groups were dizziness (19% in the terazosin group vs 5% in the placebo group) and urinary tract infection (1% in the terazosin group vs 10% in the placebo group). CONCLUSIONS: These results suggest that terazosin given once daily in doses up to 10 mg alleviates symptoms and improves peak urine flow rate in men with benign prostatic hyperplasia and has an acceptable adverse event profile.

Adrenergic alpha-Antagonists↗
PubMed2001

[Diseases of the prostate in elderly patients. Benign prostate hyperplasia and prostate carcinoma].

The incidence of benign prostatic hyperplasia (BPH) increases constantly beyond the 3rd decade of life and is almost always present in men aged 80-90 years of age. Approximately half of the men with benign prostatic hyperplasia develop a clinically enlarged prostate (BPE), 50% of those with BPE lower urinary tract symptoms. The diagnostic work-up of men with lower urinary tract symptoms and BPH/BPE comprises subjective (symptom score) and objective (uroflowmetry, post void residual volume) parameters. The therapeutic armentarium has been substantially enlarged during the past decade and now comprises effective drugs, minimally invasive treatment options and surgical treatment. In industrialised countries, prostate cancer is currently the most frequently diagnosed malignancy and the second leading cause of cancer death. Prostate cancer diagnosis, treatment and follow-up was revolutionised by the introduction of the tumour marker prostate specific antigen. In cases of a localised prostate cancer and a life expectancy of at least 10 years, radical prostatectomy is the therapy of choice, in those with a life expectancy of less than 10 years radiotherapy leads to satisfactory results. In generalised cases antiandrogen therapy is still considered "Gold Standard".

Adult↗
PubMed1991

Is there a relationship between benign prostatic hyperplasia and prostatic cancer?

No definite relationship can be demonstrated between benign prostatic hyperplasia (BPH) and prostatic cancer on the basis of various anatomic and morphologic features. However, interesting recent observations suggest a link between BPH and prostate cancer. Clinically, the simultaneous presence of benign and malignant disease is observed quite often, and this coexistence is bound to increase with the age of patients. Possible intermediate forms between BPH and early cancer have been investigated. Two premalignant lesions have been identified: atypical adenomatous hyperplasia and prostatic intraepithelial neoplasia.

Humans↗
PubMed1996

Monocyte chemoattractant protein-1 gene expression in prostatic hyperplasia and prostate adenocarcinoma.

Human monocyte chemoattractant protein-1 (MCP-1) has been shown to act as a chemokine in the recruitment of monocyte/macrophages during inflammation states. Furthermore, there is increasing evidence that MCP-1 is involved in the recruitment of tumor-associated macrophages. In vivo, one of the major cellular sources of MCP-1 are the smooth muscle cells. As MCP-1 gene expression and/or protein production in these cells is not necessarily correlated with the accumulation of inflammatory cells, there might possibly be additional functions of this cytokine. In the present study, we investigated by use of 35S-labeled antisense RNA probes whether the MCP-1 gene is expressed in tissue specimens of benign prostatic hyperplasia (n = 13) and specimens of prostate carcinoma (n = 8), both of which are characterized by a prominent fibromuscular stroma and inconspicuous inflammatory infiltrates. MCP-1 transcripts were located in stromal smooth muscle cells and, additionally, in basal cells of benign prostatic glands. In prostate carcinoma, the number of MCP-1 mRNA-expressing cells was significantly less than in benign prostatic hyperplasia. MCP-1 transcripts were located in preserved fibromuscular stroma and in basal cells of entrapped non-neoplastic glands but not in carcinomatous cells. Immunohistochemical staining with polyclonal antibodies raised against MCP-1 revealed strong reactivity in the fibromuscular stroma surrounding both benign and malignant glands. MCP-1 gene expression or immunoreactivity for anti-MCP-1 antibodies was not related to the rare, lymphocytic interstitial infiltrates. The results show that 1) in the absence of significant leukocyte accumulation, it is unlikely that MCP-1 exerts chemotactic functions in the prostate and 2) that MCP-1, in contrast to previous findings in a wide variety of other human neoplasms, is not expressed in carcinomatous cells of the prostate.

Adenocarcinoma↗
PubMed2002

Expression of somatostatin receptor subtypes 2 and 4 in human benign prostatic hyperplasia and prostatic cancer.

BACKGROUND: The presence of receptor subtypes for the inhibitory peptide somatostatin in prostatic tissue has been a controversial issue with conflicting reports. To elucidate whether prostatic epithelial cells express mRNA for somatostatin receptor (SSTR) subtype 2 and 4, we have investigated the localization of SSTR2 and SSTR4 transcripts in prostatic tissues by in situ hybridization. METHODS: Nonradioactive in situ hybridization was performed with specific fluorescein-labeled SSTR2 and SSTR4 riboprobes on consecutive sections of benign prostatic hyperplasia (BPH) and prostate cancer tissues. RESULTS: We report, for the first time, tissue localization of SSTR2 and SSTR4 mRNA in BPH and malignant cells of human prostate. Hybridization signals for SSTR4 mRNA transcripts were confined to the prostatic epithelium (12 of 16 BPH cases, and in 12 of 13 carcinoma cases), whereas SSTR2 transcripts were predominantly localized in the stromal compartment but also were detectable in epithelial cells in a significant number of specimens (11 of 17 BPH cases, and in 12 of 14 carcinoma cases). Furthermore, the staining intensity for SSTR2 and SSTR4 transcripts is stronger in malignant cells compared with adjacent BPH epithelium. CONCLUSION: The data presented suggest that the expression of SSTR2 and SSTR4 transcripts is up-regulated in malignant cells and that not only SSTR2 agonists, but also compounds targeting the SSTR4 subtype may have a potential role in the treatment of prostate cancer.

Carcinoma↗
PubMed2004

Analysis of the inflammatory network in benign prostate hyperplasia and prostate cancer.

INTRODUCTION: The complexity of acute and chronic inflammatory processes may either lead to benign prostate hyperplasia (BPH) and/or prostate cancer. Obviously, various tissue cells are activated by chemokines via different chemotaxin receptors which then trigger subsequent processes in angiogenesis, cellular growth, and extravasation as well as neoplasia. METHODS: Using the surgically obtained tissue of patients (n = 36) with BPH or prostate carcinoma (PCA), we studied among others the expression of chemokines (Rantes, IL-8), chemotaxin receptors (CXCR-3 and -4, CCR-3, CCR-5), of matrixmetalloproteinases (MMP-2 and 9), of Toll-like (TL) receptors 1, 2, 3, 4, 5, 7, and 9 and of the inducible cyclooxygenase-2 (cox-2) by RT-PCR. Further support for the different properties of tissue from PCA was obtained using two different PCA cell lines (PC3 = androgen resistant cell) or LNCAP cells (androgen sensitive) with emphasis on IL-8, Il-6, and PGE(2) release. Cell lines were stimulated with either the tumor necrosis factor-alpha (TNF-alpha) and lipopolysacharide (LPS) over time. In addition to cytokine release, the quantification of mRNA by lightcycler for cox-2, IL-6, and IL-8 was performed on these cell lines. RESULTS: Remarkable differences in expression were obtained by RT-PCR when BPH tissue versus PCA was analyzed. Expression of CXCR-1 after incubation with LPS and TNF-alpha showed time-dependent differences for androgen-sensitive LNCAP as compared to androgen-resistant PC-3 cells. TNF-alpha incubation leads to a time-dependent induction of cox-2 expression unlike to activation with LPS. Differences with regard to cox-2, IL-6, and IL-8 expression were seen by quantitative lightcycler analysis. Significant differences were also observed when TL receptors 4, 5, 7, and 9 were analyzed which were significantly expressed in BPH- as compared to PCA-tissue. CONCLUSIONS: Our data clearly demonstrate that various inflammatory and cell biological cascades are involved which either lead to BPH or can be linked to the development of PCA. The exact cell biological mechanisms may provide novel therapeutic options in the treatment of both diseases.

Acute Disease↗
PubMed1983

Plasma estradiol, free testosterone, sex hormone binding globulin binding capacity, and prolactin in benign prostatic hyperplasia and prostatic cancer.

The nature of hormonal changes with age and the possible role of these changes in the development of benign prostatic hyperplasia (BPH) and prostatic cancer (PC) were studied by assaying the plasma levels of total and free testosterone (T), estradiol (E2), prolactin, and sex hormone binding globulin binding capacity (SHBG) in 20 normal healthy men aged 40-59 years, in 30 patients with BPH aged 63-79 years, and in 30 patients with PC of similar height, weight, and age as the BPH patients. The mean E2 was highly significantly (P less than 0.0005) lower in the PC patients and in the young controls than in the BPH patients. The mean free T was significantly higher in the young controls than in the BPH patients (P less than 0.025) and PC patients (P less than 0.0005). The PC patients had a slightly lower (P less than 0.05) mean free T and mean E2/free T ratio than the BPH patients. The mean E2/free T ratio was significantly higher in the BPH patients (P less than 0.0005) and in the PC patients (P less than 0.0025) than in the young controls. It seems possible that the observed age-dependent significant increase in plasma estrogen concentration in the BPH patients may act as a protective factor against prostatic cancer.

Adult↗
PubMed1994

Differential expression of transforming growth factor-beta 1 and beta 3 as well as c-fos mRNA in normal human prostate, benign prostatic hyperplasia and prostatic cancer.

The discrepancy between the incidence of latent prostate cancer and that of clinically overt carcinoma suggests that there can be different courses in the biological progression of prostate cancer. As this cancer is detected increasingly at an infraclinical stage, markers are needed to indicate which lesions will progress and lead to the patient's death. To investigate the possibility that specific growth factors and/or proto-oncogenes are expressed differentially, we measured mRNA levels of transforming growth factors beta 1 (TGF-beta 1), TGF-beta 2 and TGF-beta 3 and of the c-fos and c-jun oncogenes by Northern blotting in normal prostate, benign prostatic hyperplasia (BPH) and prostate cancer. Our data demonstrate that expression of TGF-beta 1 increased, whereas that of TGF-beta 3 fell to an almost undetectable level in carcinoma. Expression of c-fos followed the TGF-beta 1 pattern, whereas no difference could be seen in c-jun expression in cancer as compared with BPH and normal prostate. The differential expression of TGF-beta 1, TGF-beta 3 and c-fos could possibly be used to improve the characterisation of prostate cancer. Long-term follow-up of patients may indicate whether mRNA levels of these growth factors and oncogenes correlate clinically and whether they can be used as markers for progression in human prostate cancer.

Adult↗
PubMed2003

Increased discrimination between benign prostatic hyperplasia and prostate cancer with equimolar total prostate specific antigen measurement.

Although prostate specific antigen (PSA) is widely used in the discrimination of benign prostatic hyperplasia (BPH) and prostate cancer, its diagnostic value is controversial due to an appreciable false positive rate. In the present study, we compared a recently introduced assay method, equimolar PSA measurement, to non-equimolar PSA measurement and also determined the diagnostic value of percent free PSA with changing total PSA (tPSA) measurements. Between April 1999 and December 2001, the sera of 61 patients with BPH and 41 with prostate cancer were examined. Total PSA and free PSA was determined using the Immulite 2000 assay system, whereas equimolar tPSA measurement was performed using Bayer PSA Q for the Chiron ACS 180 system. Comparative analysis of the two different assays revealed better diagnostic sensitivity and specificity values for equimolar tPSA measurement, which in turn would have led to 10% of the patients avoiding an unnecessary biopsy. Additionally, percent free PSA with the changing denominator of tPSA assays showed that the free PSA/equimolar tPSA ratio was the best tumor marker among the studied forms of PSA. It was concluded that equimolar tPSA measurement using recombinant Fab fragments is superior to the classical measurements with monoclonal antibodies, and that the use of percent free PSA with the equimolarly measured tPSA has better sensitivity and specificity in the discrimination of benign and malignant diseases of the prostate.

Aged↗
PubMed1999

Antioxidant enzyme activities and lipid peroxides in the plasma of patients with benign prostatic hyperplasia or prostate cancer are not predictive.

In this study, lipid peroxide and total sulfhydryl contents and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were investigated in the plasma of patients with benign prostatic hyperplasia (BPH) and prostate cancer. No significant change was found in lipid peroxidation or antioxidant systems in the plasma of patients with BPH and prostate cancer. The results indicate that evaluation of the prooxidant-antioxidant balance in the plasma of BPH and prostate cancer patients cannot be used as a marker to discriminate between these diseases.

Aged↗
PubMed1994

Review of the role of androgenic hormones in the epidemiology of benign prostatic hyperplasia and prostate cancer.

OBJECTIVE: Examine current knowledge and concepts on the role of androgenic hormones in the epidemiology of benign prostatic hyperplasia (BPH) and prostate cancer (PCa). METHODS: Review of the clinical and scientific literature on normal androgen physiology, hormonal physiology of BPH and PCa tissue, serum hormone levels in patients with BPH or PCa, and the correlation between serum and tissue androgenic hormones. RESULTS: BPH and PCa are enormous clinical problems for our health care system; profound changes in the clinical aspects of these diseases are evident in recent years. Early identification or prevention are realistic goals; identification of higher risk groups would be extremely valuable. Androgen stimulation of the prostate is likely to be important in the promotion of BPH or PCa. Tissue hormone measurements have not identified substantial differences in hormone levels, but precise pathologic control of the tissue examined is suspect. Examinations of serum hormone levels in disease states have produced conflicting results, but the presence or absence of BPH or PCa was often based on imprecise clinical observations, making interpretation difficult. There are minimal data confirming that the serum hormones measured previously actually reflect intraprostatic tissue activity. CONCLUSIONS: The value of serum hormone measurements to identify higher risk groups for BPH or PCa is an area of continuing uncertainty because of substantial flaws in the design of many previous studies based on a failure both to define the presence or absence of BPH or PCa precisely in patients studied and measure the appropriate androgen metabolites. Similarly, it is not possible reliably to implicate differences in androgenic stimulation as a cause for racial differences in PCa. The ability of serum hormone levels to correlate with prostatic tissue androgenic stimulation has not been evaluated. Additional research in the relationships between androgenic stimulation and the development of clinically significant BPH or PCa is needed.

Androgens↗
PubMed2005

Studies on antibacterial, anti-inflammatory and antioxidant activity of herbal remedies used in the treatment of benign prostatic hyperplasia and prostatitis.

Crude water and ethanolic extracts of five herbal remedies reported in the literature for traditional treatment of benign prostatic hyperplasia (BPH) and/or prostatitis were investigated for their effect on hydroxyl scavenging activity, antibacterial activity and their ability to inhibit cyclooxygenase-1 and -2 (COX-1 and COX-2) catalysed prostaglandin biosynthesis. Both the water and ethanol extracts of Hypoxis hemerocallidea and Epilobium parviflorum inhibited the growth of Escherichia coli. All 10 extracts scavenged the hydroxyl radical but with various potencies (32-93%). Ethanolic extracts were the most active in inhibiting COX-1 catalysed prostaglandin biosynthesis. The ethanolic extract of Epilobium parviflorum showed inhibitory effects on both the COX-1 and -2 catalysed prostaglandin biosynthesis, inhibited growth of Escherichia coli and exerted antioxidant activity. Although these results support the traditional use of Epilobium parviflorum for treatment of prostatitis and BPH, further investigation is required, for this promising plant.

Anti-Bacterial Agents↗
PubMedDate not supplied

Associations between polymorphisms in the steroid 5-alpha reductase type II (SRD5A2) gene and benign prostatic hyperplasia and prostate cancer.

The prostate gland is an androgen-dependent, and polymorphisms in androgen synthesis gene steroid 5-alpha reductase type II (SRD5A2) may be associated with benign prostatic hyperplasia (BPH) and prostate cancer. We evaluated the association between 3 polymorphisms in the SRD5A2 gene (2 single nucleotide polymorphism: alanine-49 to threonine [A49T] and valine-89 to leucine [V89L], and a (TA)n dinucleotide repeat in the 3' untranslated region), and BPH and prostate cancer within a multiethnic population. Men between 60 and 86 years of age were recruited from annual prostate cancer screening programs and from a large urology clinic. Unconditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (95% CI). We genotyped 606 men (412 Hispanic, 98 Caucasian, 73 African-American, and 23 Asian), of whom 100 had prostate cancer, 393 had BPH (280 symptomatic and 113 asymptomatic), and 113 had normal prostates. Overall, the V89L variant was associated with prostate cancer; the OR for men with the leucine-leucine (LL) genotype compared to men with the valine-valine (VV) genotype was 4.47 (95% CI, 1.24-16.18). This association was stronger in Hispanics (OR=7.26; 95% CI: 1.49-35.47). Although V89L was nonsignificantly associated with BPH in overall population, BPH risk increased significantly with the number of L alleles in Hispanics (P for trend=0.03). Prostate cancer and BPH were not associated with the alanine-49 to threonine single nucleotide polymorphism and the (TA)n repeat. These results suggest that the SRD5A2 gene may play an important role in both BPH and prostate cancer.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1999

Determination of alpha1-antichymotrypsin-PSA complex in serum does not improve the differentiation between benign prostatic hyperplasia and prostate cancer compared with total PSA and percent free PSA.

OBJECTIVES: To evaluate the analytical performance and diagnostic utility of alpha1-antichymotrypsin (ACT)-prostate-specific antigen (PSA) complex in serum to improve the differentiation between benign prostatic hyperplasia (BPH) and prostate cancer (PCa). METHODS: Serum concentrations of total PSA (tPSA), free PSA (fPSA), and ACT-PSA were measured in 112 untreated patients with PCa (median age 65 years), 34 patients with BPH (median age 66 years) with histologic confirmation, and 33 men without prostate disease and with a normal digital rectal examination considered as controls (median age 54 years). Sera were frozen at -80 degrees C within 2 hours after collection and then analyzed during a 12-week period. Determinations were made with the Enzymun-Test for tPSA and fPSA and with a prototype assay for ACT-PSA on the ES system (Roche Diagnostics, Boehringer Mannheim). RESULTS: The new ACT-PSA assay showed reliable data of analytical performance. The lower detection limit amounted to 0.068 microg/L. The assay was linear to 50 microg/L. Spiking experiments showed a mean recovery rate of 98.2%. No interferences of the assay were observed in patients with acute inflammation and highly increased ACT concentrations. The values of intra- and interassay imprecision ranged from 1.51% to 3.48% and 2.1% to 6.3%, respectively. The median value of ACT-PSA concentrations were significantly different (P <0.001) between controls and patients with BPH and PCa (0.40, 3.86, 5.26 microg/L, respectively). The median fPSA/tPSA and fPSA/ACT-PSA ratios were significantly different between BPH and PCa (24.3% versus 12.2%, P <0.001 and 32.9% versus 15.0%, P <0.001, respectively), but no difference of the ACT-PSA/tPSA ratio was observed (78.2% versus 78.7%, P = 0.696). Receiver operating characteristics of ACT-PSA (area under the curve = 0.630) and all the derivative ratios of fPSA/ACT-PSA (area = 0.737) and ACT-PSA/tPSA (area = 0.528) were not different from that of tPSA (area = 0.619), but showed a lower discrimination power between BPH and PCa than the fPSA/tPSA ratio (area = 0.790). CONCLUSIONS: Using this prototype assay to quantify ACT-PSA in serum, we have demonstrated that ACT-PSA and the calculated derivatives are not superior in the differentiation between BPH and PCa compared with tPSA and the ratio of fPSA to tPSA.

Adult↗