Elevated Prostatic Acid Phosphatase Research Articles

Effects of combined ethanol extract of Funtumia africana and Abutilon mauritianum leaves on prostate biomarkers and serum mineral levels in prostatic hyperplasia induced male rats

Introduction: Benign prostatic hyperplasia (BPH) is a prostate disorder in ageing males that negatively affects the quality of life and requires multidimensional approaches to ameliorate its adverse health effects. Objectives: This study evaluated the effects of combined ethanol extract of Funtumia africana and Abutilon mauritianum leaves on the prostate biomarkers, serum mineral levels and prostate histomorphology of BPH induced rats. Materials and Methods: Thirty-six male Wistar albino rats randomly distributed into 5 groups containing 6 rats each was used for this study. Group 1 served as the normal control rats without BPH induction while groups 2–5 were BPH induced rats that served as BPH control (untreated), finasteride control, and BPH induced treated with 200 and 600 mg/kg/d of the combined ethanol extract of F. africana and A. mauritianum leaves respectively. BPH was induced in the rats by subcutaneous injection of 5 mg/kg/d of testosterone propionate injection and treatment followed 1h after the induction for 28 consecutive days. All the biochemical analyses and prostate histological examinations were carried out using standard methods. Results: BPH induction significantly elevated serum prostatic acid phosphatase activities and serum prostate-specific antigen (PSA) concentrations in the BPH control rats relative to the normal control. The BPH induction caused significant (P<0.05) reductions in the serum levels of calcium and selenium levels and significantly increased the serum inorganic phosphate concentration in the BPH control when compared with the normal control. Treatment with the combined extract significantly (P<0.05) increased the serum zinc, calcium, copper, iron and inorganic phosphate and significantly reduced serum selenium level when compared with the BPH control. The combined extract further significant (P<0.0) reduced the serum prostatic acid phosphatase activities and PSA level relative to the BPH control. The BPH control showed severe prostate histomorphological alterations consistent with BPH which were largely reduced to mild alterations in combined extract-treated BPH induced rats. Conclusion: This study revealed that the combined ethanol extract of F. africana and A. mauritianum leaves positively regulate the serum mineral levels, serum prostatic acid phosphatase activities, PSA levels and improves prostate histomorphology BPH induced rats.

Long-Term Prostate Cancer Control Using Palladium-103 Brachytherapy and External Beam Radiotherapy in Patients with a High Likelihood of Extracapsular Cancer Extension

To report the long-term biochemical control rates with brachytherapy-based treatment for patients with prostate cancer at high risk of extracapsular cancer extension. A total of 243 consecutive patients with at least one higher risk factor (Gleason score of 7 or worse, prostate-specific antigen [PSA] level greater than 10 ng/mL, or elevated prostatic acid phosphatase level greater than 2.5 U) who were treated with palladium-103 plus supplemental external beam radiotherapy from 1992 through 1996 were included in this study. Patients received 41 Gy external beam radiotherapy to a limited pelvic field, followed 4 weeks later by a palladium-103 boost. The prescribed minimal palladium-103 dose to the prostate was 80 to 90 Gy. Freedom from biochemical failure was defined as a serum PSA level of 0.2 ng/mL or less at the last follow-up visit. Of the 243 patients, 41 developed biochemical failure. The overall actuarial freedom from biochemical progression rate at 13 years was 81%, with 198 patients followed up for longer than 5 years. The overall actuarial freedom from failure rate for the 93 patients with a PSA level of 10 ng/mL or greater and Gleason score of 7 or greater was 74% at 5 years and 72% at 10 years. The overall actuarial freedom from failure rate for the 66 patients with elevated prostatic acid phosphatase was 65% at 10 years. The absolute risk of failure decreased progressively with time, falling to 1% by 6 years after treatment. On Cox proportional hazard multivariate analysis, considering each factor as a continuous variable, the strongest predictor of failure was the acid phosphatase level (P <0.0001), followed by Gleason score (P = 0.42) and PSA level (P = 0.15). The evidence from this patient group at high risk of extracapsular cancer extension suggests that the relatively high tumor control rates with brachytherapy-based therapy are durable.

Persistence of spermatozoa and prostatic acid phosphatase in specimens from deceased individuals during varied postmortem intervals.

The survival of spermatozoa and the persistence of prostatic acid phosphatase has been an area of interest for investigators of sexual assault. However, not much documentation exists concerning the examination of a deceased individual with regard to the postmortem interval and presence of such evidence. The authors reviewed cases referred to the medical examiner's office during a 10-year period. During this time, 199 cases were both autopsied and examined for sexual assault. In particular, these examinations included procurement of swabs for Papanicolaou staining of smears and for quantitation of prostatic acid phosphatase. Most of the victims were female, although a few were male. In the majority of cases, the swabs for smears and prostatic acid phosphatase were taken from oral, vaginal, and anorectal areas in females and oral and anorectal areas in males. The smears all were stained with the routine Papanicolaou stain, and intact spermatozoa and spermatozoan heads were sought. The prostatic acid phosphatase was analyzed by the microparticle enzyme immunoassay method and reported as ng/ml. A level of greater than 100 ng/ml was considered positive. The cases were analyzed with respect to postmortem interval; presence or absence of intact spermatozoa or spermatozoan heads; presence of an elevated prostatic acid phosphatase; body location of the specimen; the time of year; location of the victim; and physical injury (anogenital) of sexual assault. The authors hope that by examining the laboratory evidence of sexual assault, a correlation can be drawn between the presence or absence of such evidence and the aforementioned variables.

Prognostic role of serum prostatic acid phosphatase for 103Pd-based radiation for prostatic carcinoma

Purpose: To establish the prognostic role of serum enzymatic prostatic acid phosphatase (PAP) in patients treated with palladium ( 103Pd) and supplemental external beam irradiation (EBRT) for clinically localized, high-risk prostate carcinoma. Methods and Materials: One hundred twenty-four consecutive patients with Stage T2a–T3 prostatic carcinoma were treated from 1992 through 1995. Each patient had at least one of the following risk factors for extracapsular disease extension: Stage T2b or greater (100 patients), Gleason score 7–10 (40 patients), pretreatment prostate specific antigen (PSA) > 15 ng/ml (32 patients), or elevated serum PAP (25 patients). Patients received 41 Gy conformal EBRT to a limited pelvic field, followed 4 weeks later by a 103Pd boost (prescription dose 80 Gy). Biochemical failure was defined as a PSA greater than 1 ng/ml (normal < 4 ng/ml). Results: The overall, actuarial freedom from biochemical failure at 4 years after treatment was 79%. In Cox-proportional hazard multivariate analysis, the strongest predictor of failure was elevated pretreatment acid phosphatase ( p = 0.02), followed by Gleason score ( p = 0.1), and PSA ( p = 0.14). Conclusion: PAP was the strongest predictor of long-term biochemical failure. It may be a more accurate indicator of micrometastatic disease than PSA, and as such, we suggest that it be reconsidered for general use in radiation-treated patients.

103P d brachytherapy and external beam irradiation for clinically localized, high-risk prostatic carcinoma

Purpose : To summarize biochemical failure rates and morbidity of external irradiation (EBRT) combined with palladium ( 103Pd) boost for clinically localized high-risk prostate carcinoma. Methods and Materials : Sevently-three consecutive patients with stage T2a-T3 prostatic carcinoma were treated from 1991 through 1994. Each patient had at least one of the following wisk factors for extracapsular disease extension: Stage T2b or greater (71 patients), Gleason score 7–10 (40 patients), prostate specific antigen (PSA) >15 (32 patients), or elevated prostatic acid phosphatase (PAP) (17 patients). Patients received 41 Gy EBRT to a limited pelvic field, followed 4 weeks later by a 103Pd boost (prescription dose: 80 Gy). Biochemical failure was defined as a PSA greater than 1.0 ng/ml (normal < 4.0 ng/ml). Patients whose PSA was still decreasing at the last follow-up were censored at that time. Patients whose PSA plateaued at a value greater than 1.0 were scored as failures at the time the PSA first plateaued. Results : The overall, actuarial freedom from biochemical failure at 3 years after treatment was 79%. In Cox proportional hazard multivariate analysis, the strongest predictor of failure was elevated acid phosphatase ( p = 0.04), followed by PSA ( p = 0.17), stage ( p = 0.17), Stage ( p = 0.23). Treatment-related morbidity was usually limited to temporary, RTOG Grade 1–2 urinary symptoms. One patient, who had both a transurethral incision of the prostate (TUIP) and a transurethral resection of the prostate (TURP), developed low-volume urinary incontinence. The actuarial potency rate at 3 years after implantation was 77% for 46 patients who were sexually potent prior to implant. Conclusion : Biochemical freedom from failure rates following combined EBRT and 103Pd brachytherapy for clinically localized,, high-risk prostate cancer compare favorably with that reported conventional dose EBRT alone. Morbidity has been acceptable.

Conservative management with symptomatic treatment and delayed hormonal manipulation is justified in men with locally advanced carcinoma of the prostate.

To examine the clinical course following surveillance and symptomatic treatment, and compare the outcomes of immediate and delayed hormonal treatment in men with locally advanced prostatic cancer. Of a consecutive series of 199 men (mean age 74 years) with T2-T4 Nx M0 prostatic cancer, 110 (55%) were followed until death and the rest had a mean follow-up of 4.2 years. Fifty-one men received immediate orchidectomy, 88 had this treatment delayed until metastatic progression, and 60 had the treatment in the intervening period. The actuarial survival was compared with the expected survival for an age-matched healthy population in Scotland. The adjusted effect of the timing for hormonal manipulation was assessed by including it with age, Gleason score and clinical stage in a multiple Cox regression. The actuarial survival for the whole group was 17% less at 5 years and 15% less at 10 years when compared with the expected survival for an age-matched population in Scotland. This was despite the fact that their nodal status was unknown and also those with occult metastasis (elevated serum prostatic acid phosphatase, M1a) at presentation were not excluded. In terms of metastatic progression, overall survival and cause-specific survival, there was no significant difference between immediate and delayed hormonal treatment. A conservative approach with surveillance and symptomatic treatment for locally advanced prostatic cancer is justified by the present evidence on disease progression and survival, which do not differ from alternative methods of treatment as reported in contemporary literature. This study has the limitations relative to the ideal of a prospective randomized trial on immediate versus delayed hormonal treatment, but the lack of significant differences in outcome even after adjustment for other established prognostic factors does suggest that there may be little to be gained from an immediate orchidectomy.

Conditions associated with normal levels of prostate-specific antigen and elevation of prostatic acid phosphatase.

Thirteen cases are reported with normal levels of prostate-specific antigen and elevated prostatic acid phosphatase (PAP). Conditions that were associated with an elevated PAP were myeloproliferative syndromes (four cases), metastatic nonprostatic carcinoma (six cases), prostatic carcinoma (one case), tuberculosis with a concurrent lupus-like syndrome (one case), and osteomyelitis (one case). The inclusion of PAP in the initial investigation of cases with suspected prostatic disease results in a decreased specificity.

Chemotherapy for Small Cell Carcinoma of Prostatic Origin

A total of 21 patients with metastatic small cell carcinoma of the prostate was treated with combination chemotherapy, either following initial hormonal therapy (15) or as initial therapy (6). Of the patients 13 (62%) had pure small cell carcinoma, whereas 8 (38%) had mixed histology of small cell carcinoma and adenocarcinoma. Patients presented with a characteristic clinical picture of a large primary mass (16 cases) with a high frequency of visceral metastases to the liver (9), lungs (7) and brain (2). The majority of the patients did not have an elevated serum prostate specific antigen (1 of 14, 7%) or prostatic acid phosphatase (2 of 21, 10%). Serum carcinoembryonic antigen was elevated in 13 patients (62%).Of the 21 patients 13 (62%) responded to chemotherapy. Survival after the diagnosis of small cell carcinoma of the prostate resulted in a median of 9.4 months with a range of 1 to 25 months. The regimens used were those considered active in the treatment of small cell carcinoma of the lung (vincristine, doxorubicin and cyclophosphamide, or etoposide and cisplatin with or without doxorubicin). Small cell carcinoma of the prostate has a characteristic clinical picture and a high response rate to cytotoxic therapy. Early introduction of chemotherapy in the treatment of small cell carcinoma of the prostate may increase the survival rate.

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.

Clinical course of bone metastasis from prostatic cancer following endocrine therapy: examination with bone x-ray.

X-ray findings of bone metastatic lesions from 81 cases of stage D2 prostatic cancer were examined before and following endocrine therapy. Untreated lesions were classified into five types; osteoblastic (15%), mixed, but mainly osteoblastic (31%), mixed, but mainly osteolytic (17%), osteolytic (10%), and undetermined with a positive bone scan (27%). Patients with two mixed types had a tendency of widely speeded areas of metastasis and elevated serum prostatic acid phosphatase. Temporal enlargement of sclerotic lesion immediately after the start of therapy did not indicate disease progression. In many cases, changes from osteolytic to osteoblastic patterns were noticed in the same lesion regardless of the effects of endocrine therapy. Remodeling to the sclerotic pattern appeared as curative changes. From these findings, it was concluded that the natural course of bone lesions showed a tendency to change from the osteolytic to osteoblastic type and relapse was often accompanied by an increase of the osteolytic type lesion. Evaluation of therapeutic effects based on remodeling, changes in number and areas of lesions, and the appearance of new lesion correlated well with prognosis.

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The clinical courses of bone metastases in 81 cases of prostatic cancer were examined using conventional X-ray. All patients received endocrine therapy as the initial treatment; castration and estrogen were given to 46 cases, castration and antiandrogen to 19, LH-RH analog to 11, flutamide to 5. The response to endocrine therapy was evaluated every 6 months after the start of the treatment according to National Prostatic Cancer Project criteria. The prognosis was calculated by cause-specific survival. The types of untreated bone metastases on X-ray were classified into five: sclerotic in 12 cases (15%), mixed but mainly sclerotic in 25 (31%), mixed but mainly lytic in 14 (17%), lytic in 8 (10%) and undetermined with positive scintigraphy in 22 (27%). Two mixed types showed more spread metastases and tendency of elevated prostatic acid phosphatase when compared with other types. Temporary enlargement of sclerotic area within 6 months after start of the treatment did not correlate with deterioration of disease. Remodeling of metastatic areas occurred 6-36 months after start of the treatment showed curative course and the prognosis of these groups were favorable. Most of lytic areas tended to sclerotic finding following endocrine therapy regardless of effects by endocrine therapy. Sclerotic and two mixed types showed better and worse tendencies, respectively. On viewpoint of remodeling, change of metastatic area and newly appearance of metastases, an evaluation criteria of response to the therapy was proposed, which showed good correlation with prognosis. From these observations, it was concluded that bone metastases tended from lytic to sclerotic changes and that lytic-sclerotic cycles occurred repeatedly along with disease progression regardless of effect to therapy. Remodeling seemed to be curative signs of metastatic area.

Grossly elevated serum prostatic acid phosphatase in a patient with carcinoid

We report a case of carcinoid, diagnosed histochemically and biochemically, which was associated with grossly elevated serum prostatic acid phosphatase and normal serum prostate specific antigen.

The role of prostatic acid phosphatase in the radiotherapeutic management of adenocarcinoma of the prostate

Between 1965 and 1984, 472 patients treated with external beam radiation therapy (EBRT) for adenocarcinoma of the prostate had pretreatment and follow-up serum prostatic acid phosphatase (PAP) measurements performed by the Roy method. All patients were clinically staged (46 A2, 67 B, and 359 C), and none had hormonal manipulation prior to relapse. Four hundred and twenty-five had pretreatment PAP values in the normal range (0.00 0.80 mIU/ml) and had an actuarial 5-year disease-free survival (DFS) of 67% (A 89%, B 93%, and C 59%). Forty-seven patients had elevated pretreatment PAP values. Three of these patients ha have remained disease free. ?l A3 or B disease, and all The remaining 44 patients were in Stage C and had a 5-year D S of 38%. This was significantly worse than the 59% DFS observed in the normal-PAP Stage C group (p 0.4 but <0.8 (P <O.Ol). In Stage C, tumor grade was found to be correlated with initial PAP values so that the higher the grade, the higher the PAP value and the greater was the incidence of elevated PAP values. Of patients with M. D. Anderson grade 4 lesions 8/33 (24%) had elevated PAP values as compared with only 6/89 (7%) elevated PAP values in patients with M. D. Anderson grade 1 tumors (p <O.OZ). Similarly a PAP <0.4 was found in 55/89 (62%) patients with grade 1 lesions while only lo/33 (30%) patients with grade 4 lesions had such low PAP values (p <O.Ol). When corrected for grade, the prognostic significance of low-normal PAP versus high-normal PAP was lost. However, an elevated PAP value was an independent adverse prognostic factor for patients with intermediate (grades 2-3) or high grade (grade 4) tumors. In grades 2 and 3, patients with elevated PAP values had a 5-year DFS of 29% compared with 57% for those with normal values (p <0.05). Patients with grade 4 tumors and elevated PAP values had a 5-year DFS of 13% versus 28% for patients with normal range PAP (p = N.S. due to small patient numbers). The role of post-treatment follow-up PAP measurements was also investigated. Following EBRT mean PAP values decreased significantly within 1 to 3 months. This was true for patients with normal pretreatment values as well as for patients with elevated initial values. For patients with initially normal PAP, the fall in PAP after treatment was of no prognostic significance. For the group of 47 patients with elevated pretreatment PAP, the initial mean PAP was 2.34 and the mean at 1 to 3 months was 0.64 (p <O.Ol). Of these 47 patients, 35 (74%) achieved normal values within 1 to 9 months after treatment and 9 (19%) did not. Of the 35 patients whose PAP normalized, 18 (51%) subsequently relapsed; of the 9 patients whose PAP did not decrease to normal range, 8 (89%) relapsed (p = 0.04). However, the 51% relapse rate of the group whose values normalized was significantly higher than the 33% relapse rate of patients who started with normal PAP (p = 0.04). We conclude that (1) the incidence of elevated PAP correlates with stage; (2) PAP has no prognostic significance in Stage A2 and B; (3) Stage C patients with higher grade tumors are more likely to have high-normal or elevated PAP; (4) even when corrected for grade elevated PAP in Stage C is an adverse factor; and (5) PAP values tend to fall after EBRT and persistent elevation post-EBRT is an especially adverse factor.

Bone Scintigraphy, Radiographic Survey and Prostatic Acid Phosphatase in Patients With Prostatic Carcinoma. A Comparison of Sensitivity

In 62 patients with histologically confirmed carcinoma of the prostate bone scintigraphy, radiographic survey and serum prostatic acid phosphatase determinations were carried out to evaluate the progression of the disease and to compare the relative sensitivity of the diagnostic tools. Thirty-five patients had scintigraphic evidence of skeletal metastases, whereas abnormal X-ray survey and elevated prostatic acid phosphatase levels were found in only 4 and 19 patients, respectively, all of whom had positive scintigraphic findings. Radiographic evidence of metastases was not found in any of the patients with normal scintigraphy, while elevated prostatic acid phosphatase was found in two patients. It is concluded that bone scintigraphy is far more sensitive than either radiographic survey or determination of prostatic acid phosphatases in the diagnosis of skeletal involvement in prostatic carcinoma, and should be the method of choice for this purpose.

The value of acid phosphatase measurements in predicting extraprostatic cancer growth before radical prostatectomy.

Acid phosphatase levels were determined using both an enzymatic method (32 cases) and radioimmunoassay (35 cases) in 35 patients with clinically localised prostatic cancer. All patients underwent total prostatectomy and pelvic lymphadenectomy. In cases of intracapsular prostatic cancer the level of prostatic acid phosphatase (PAP) measured by radioimmunoassay was 1.4 +/- 0.8 micrograms/l. In patients with either local extraprostatic disease or pelvic lymph node metastases the mean level of PAP was 3.5 +/- 2.8 micrograms/l. The difference was statistically significant. The specificity, sensitivity and accuracy of an elevated PAP (greater than 3.0 micrograms/l) in revealing extraprostatic extension of clinically localised prostatic cancer were 100, 37 and 66% respectively. When the enzymatic method was used, the level of acid phosphatase was elevated (greater than 13 u/l) in only 1 case. The specificity, sensitivity and accuracy of the enzymatic method were 100, 6 and 47% respectively. Elevation of PAP predicts, with a high degree of probability, either local extension outside the prostate or lymph node metastases. A normal PAP does not exclude extraprostatic extension of prostatic cancer.

Is Prostate-Specific Antigen the Most Useful Marker for Screening in Prostate Cancer?

Prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) levels were determined in 241 patients attending the Department of Urology. The population consisted of 140 prostate cancer patients (34 newly diagnosed and 106 under treatment) and 101 patients with benign prostatic hypertrophy (BPH). The diagnostic values of PAP measured by enzymatic assay (EA) and by immunoenzymetric assay (IEMA) appeared to be similar. Elevated PAP (IEMA) levels were found in 10% of the patients with BPH and in 38% of the cancer patients. PSA was measured by immunoradiometric assay (IRMA) and receiver operating characteristic curves were constructed to compare the diagnostic benefits of different cutoff values. PSA (10 micrograms/L) reached a specificity of 88% and a sensitivity of 46%. With a cutoff value of 2.7 micrograms/L, the sensitivity increased to 64%, whereas the specificity fell to 58%. It is concluded that PSA is the most useful marker as a screening test.

Comparison of Prostate-Specific Antigen and Prostatic Acid Phosphatase in the Management of Prostatic Cancer

Prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) have been evaluated in patients with prostatic cancer. All patients, who participated in a phase III trial (n = 110), had disseminated disease and received first line endocrine treatment of either orchidectomy or a monthly injection of a depot luteinizing hormone-releasing hormone analogue (Zoladex). Serum samples were analyzed for PSA and PAP at 0, 3, 6, and 12 months and patients were clinically assessed at 6 and 12 months. At diagnosis, 72 and 97% of all patients had elevated PAP and PSA concentrations (greater than 4 ng/ml), respectively. Patients with progressive disease had significantly higher PSA and PAP levels at both assessments. A small number of patients in the "complete remission" group had both PSA and PAP levels within the normal range after 3 months of treatment. Similarly, both PSA and PAP levels steadily declined in the group of patients who had partial regression of the disease. The patients with stable disease, however, had a significant rise only in their PSA levels at the 12-month assessment. This data suggest that PSA is more sensitive than PAP in those patients who have a "slow progression" of the disease.

Elevated Prostatic Acid Phosphatase: A Prognostic Factor for Stage C Adenocarcinoma of the Prostate

The clinical course of 25 patients with clinical stage C adenocarcinoma of the prostate who had pre-treatment elevations of the prostatic acid phosphatase (Roy test) was analyzed retrospectively. All patients were treated with definitive external beam radiation therapy at our hospital between 1974 and 1980. Of the 25 patients 17 (68 per cent) have had disease progression. The median time to treatment failure for this group was 27 months (range 10 to 101 months), and the over-all median survival for these patients has not been reached (range 16 to 120 months). Local control of disease was achieved in 84 per cent (21 of 25) of the patients. The control group consisted of 75 consecutive age-matched patients with normal pre-treatment prostatic acid phosphatase levels whose disease was identically staged and treated at our hospital from July 1977 to January 1979. The median time to disease progression in this group has not yet been reached. Of these 75 patients 24 (32 per cent) have had disease progression within a median time of 38 months. Therefore, an elevated pretreatment prostatic acid phosphatase value is a harbinger of systemic disease and indicates that radiotherapy will be significantly (p equals 0.002) less effective as a definitive local therapeutic modality.

Pre-Treatment Testosterone Levels: Significance in Androgen Deprivation Therapy

From June 1982 to February 1985, 53 patients with stage D2 carcinoma of the prostate confirmed by tissue biopsy, elevated prostatic acid phosphatase and a positive bone scan were initiated on androgen deprivation therapy. Before commencement of treatment all patients underwent determination of serum testosterone levels at 8 a.m. Of the patients 23 received 200mcg. buserelin per day, 17 received 1mg. diethylstilbestrol 3 times daily, 6 received 40mg. megestrol acetate 4 times daily, 2 received 1mg. leuprolide per day and 5 underwent bilateral orchiectomy.Evaluation of the best response in each patient revealed 3 (6 per cent) complete and 17 (32 per cent) partial responses, while 22 patients (41 per cent) remained stable and 11 (21 per cent) had progression. Pre-treatment serum testosterone levels ranged from 150 to 879ng. per dl. The mean serum testosterone level in patients having a complete response was 524 ± 18.04ng. per dl. The mean in the progression group was 279.4 ± 110.1ng. per dl. This difference was not statistically significant owing to the large standard deviation in the progression group. However, of the 15 patients who had a pre-treatment serum testosterone level of more than 500ng. per dl. only 1 (7 per cent) had progression. None of the patients whose pre-treatment testosterone level was less than 200ng. per dl. had objective tumor regression.Our study suggests that pre-treatment serum testosterone levels may predict the probability of a satisfactory response to androgen deprivation therapy.

Comparison of radioimmunoassay and immunoradiometric assay for serum prostatic acid phosphatase

We have compared the laboratory performance of immunoradiometric (IRMA) and radioimmunoassay (RIA) methods developed in this laboratory for measurement of serum prostatic acid phosphatase (PAP). The IRMA utilizes a radiolabelled mouse monoclonal anti-PAP and a solid phased rabbit polyclonal anti-PAP. The same rabbit antibody is used in the RIA. The IRMA shows excellent precision over a much wider working range (0.25–1000 μg/l) than the RIA (0.73–14.0 /gmg/l), and can be completed in 5 h, while the RIA requires 3 days. Levels in healthy males and in patients with benign prostatic hypertrophy are similar in both assays, upper limits of normal being 1.8 μg/l (IRMA) and 4.7 μg/l (RIA). The two assay methods correlate very well ( r = 0.97) when PAP is measured in serum from prostatic cancer patients, although IRMA results are generally lower than those obtained by RIA. About 20% of patients with non-metastatic prostatic carcinoma had elevated serum PAP, whereas about 80% of those with metastatic disease had raised levels. The diagnostic efficiencies of the RIA and IRMA appeared similar. The value of the IRMA in follow-up and staging remains to be determined.