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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

64% of all patients with newly diagnosed prostatic carcinoma present with metastases. Hormone application with or without orchiectomy appears to be the adequate form of primary treatment. The most common therapeutic modality is estrogen administration, which has, however distinct disadvantages: The patient is protected up to 5 years only, there is a 27% cardiovascular mortality, it induces a prolactin surge, and is immunosuppressive. Phase III-studies of the EORTC and VACURG have demonstrated that medroxyprogesterone acetate and cyproterone acetate parallel the effectiveness of estrogens. In a phase II-trial adjunctive bromocriptine was found to be necessary to suppress estrogen or antiandrogen induced hyperprolactinemia. The following concept is derived: In disseminated untreated prostatic cancer estrogens or antiandrogens in combination with bromocriptine or high dose injectable gestagens are effective means of primary treatment. Distinct clinical parameters determine the "hormone of first choice". Orchiectomy is reserved for patients with ureteral compression or progressing disease.
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PMID:[Hormone therapy of prostatic cancer (author's transl)]. 719 68

The following endocrine treatment modalities have been used in advanced prostatic carcinoma: 1. orchiectomy plus estrogens; 2. primary orchiectomy with delayed estrogen employment; 3. initial estrogen therapy with delayed orchiectomy; 4. initial cyproterone acetate or medroxyprogesterone acetate; 5. a combination treatment: estramustine phosphate, cyproterone acetate or estrogens plus bromocriptine. The application of phase-III studies permits the subsequent conclusions: Simultaneous orchiectomy is to no advantage (exception: urinary stasis). Cyproterone acetate does neither yield better nor worse results regarding survival than estrogen alone, but has fewer side effects. Estrogens and cyproterone acetate produce a rise of serum prolactin justifying the use of bromocriptine (or lisuride). Estramustine phosphate should be reserved for relapsing prostatic cancer.
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PMID:[Current aspects of hormonal therapy in prostate cancer]. 728 76

In 32 subjects with histologically and/or cytologically verified prostatic cancer the hormonal pattern was studied by assaying 18 plasma and urinary hormones or groups of hormones. The tumours were classified according to the UICC classification system and the hormone values were correlated to the local extent of the tumour (T classification), the presence of metastases (M classification) and the differentiation of grade (G classification). It was found that patients with metastases had significantly higher plasma oestradiol and lower testosterone/oestradiol and testosterone/oestrone plus oestradiol ratios as compared to those subjects without metastases. In subjects with moderately or poorly differentiated tumours plasma oestrone + oestradiol was significantly higher and the testosterone/oestrone + oestradiol ratio was significantly lower than in the subjects with well differentiated tumours. In the various TNM classification groups no obvious trends were found with regard to urinary hormones and no significant differences between the groups for plasma FSH, LH, prolactin, progesterone and cortisol were observed. It is concluded that in more advanced cases with metastatic cancer and when tumours are less well differentiated the androgen/oestrogen ratio may be decreased. These alterations have no diagnostic significance because of greater overlapping of individual results between the various groups of patients.
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PMID:Hormonal pattern in prostatic cancer. I. Correlation with local extent of tumour, presence of metastases and grade of differentiation. 730 85

In 32 subjects with histologically and/or cytologically verified prostatic cancer the hormonal pattern was studied by assaying 18 plasma and urinary hormones or groups of hormones and relating the values to the response to endocrine treatment. Total orchidectomy (orchiepididymectomy) was performed on 9 patients, subcapsular orchidectomy on 13 patients and oestrogen therapy with Estradurin was given in 4 patients. Six patients had total orchidectomy followed by estrogen therapy. With few exceptions all values were within the normal range. The only significant exceptions were the high urinary oestrogen values and the low urinary oestrone + oestradiol/oestriol ratio observed as compared to healthy males working in a factory. No urinary hormone values or ratios of hormone values could be used for the prediction of prognosis in prostatic carcinoma patients. However, the ratios of plasma testosterone/oestradiol (T/Oe2) and testosterone/prolactin (T/Prl) were found to give good information with regard to the response to endocrine treatment. High values for one or both of these ratios meant a good response to treatment in all subjects without exception in this material. Subjects with both ratios low had a good response to endocrine treatment in 50% of the cases. No other plasma hormones measured were of any help prognostically. It is concluded that by measuring the T/Oe2 and T/Prl ratios it seems possible to select a group of patients with favourable primary response to endocrine treatment.
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PMID:Hormonal pattern in prostatic cancer. II. Correlation with primary response to endocrine treatment. 730 86

Cyproterone acetate was given to patients with stages C and D prostatic cancer and its effect on endocrine parameters was studied. At a daily oral dose of 100 mg. cyproterone acetate induced marked reduction in the size and consistency of tumor, while it caused moderate suppression of serum luteinizing hormone, follicle-stimulating hormone and testosterone levels. Elevation of serum prolactin levels was observed after treatment with cyproterone acetate but was to a lesser degree than that caused by estrogens.
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PMID:Endocrine effects of cyproterone acetate in patients with prostatic cancer. 735 12

Thanks to our preoccupation with androgen ablative therapy, no significant progress has been made in combating prostate cancer (PCa) in 50 years. Also, there have been only limited advances in medical treatment of benign prostatic hyperplasia (BPH). The intent of this essay is to explore the mode of participation of prolactin (Prl) in prostatic physiology in the hope that such knowledge will reveal new avenues through which both BPH and PCa can be opposed-even prevented. An especially novel aspect of this study is the recognition of the presence and androgen- and prolactin-dependent concentration of the tripeptide, thyrotropin-releasing hormone (TRH) in prostatic tissue. It is hypothesized that, whereas TRH is the hypothalamic stimulus of hypophyseal Prl secretion, it may, in the prostate, serve as the mediator of Prl's independent and androgen-dependent controls of the gland's growth and function. Through an overview of these relationships, methods are suggested both for their study and for their adaptation to early detection and prevention of imminent pathogenesis.
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PMID:TRH: mediator of prolactin in the prostate? 751 76

The present study was undertaken mainly to investigate whether prolactin manipulation combined with maximal androgen blockage improves the effectiveness of treatment in advanced prostatic cancer. The efficacy of oral hydrocortisone as an alternative to commercial anti-androgens in reducing the adrenal androgens, and of bromocriptine in reducing the prolactin level were also examined. A consecutive series of 30 patients with untreated and advanced prostatic cancer were entered into a three-arm prospective randomised trial. 10 patients received subcapsular orchiectomy alone (arm 1), another 10 had subcapsular orchiectomy plus flutamide (arm 2), and the remaining 10 had subcapsular orchiectomy plus oral hydrocortisone and bromocriptine (arm 3). Clinical and biochemical parameters, including trans-rectal ultrasound-determined prostatic volumes, hormonal profiles and radionuclide bone scan were evaluated at regular intervals. At 12 months, serum testosterone was reduced by more than 90% in all arms, however, maximum suppression of androstenedione, prolactin, and reduction of prostatic volumes were only observed in arm 3; this was reflected by the significant improvement in clinical response in arm 3 compared with other arms. This study suggests that a combined maximal suppression of androgens and prolactin offers a significant improvement in response over conventional treatments without prolactin suppression in the treatment of advanced prostatic cancer. Importantly, a better clinical outcome in arm 3 was still apparent at the end of 36 months.
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PMID:A case for synchronous reduction of testicular androgen, adrenal androgen and prolactin for the treatment of advanced carcinoma of the prostate. 764 10

NK cell activity was measured in 24 patients with untreated prostate cancer (11 subjects with localized disease, D0, and 13 patients with stage D tumor) and 10 healthy controls. In these same subjects serum prostate-specific antigen (PSA), prostatic acid phosphatase (PAP), testosterone, prolactin and cortisol concentrations were assessed. The data obtained were correlated with both tumor spread (localized vs disseminated disease) and grade (well-differentiated cancer, G1, vs moderately and poorly differentiated carcinoma, G2 and G3). In patients with stage D0 cancer mean NK activity (33.0 +/- 10.6) was virtually identical with the mean value recorded in healthy men (34.5 +/- 7.1), while in subjects with stage D1-D2 disease NK activity was significantly reduced (11.9 +/- 7.1). These findings correspond with our data on treated subjects, in whom NK activity level was found to correlate well with the presence of tumor cells in the circulation. In subjects free of malignant tumors but with a chronic disease (diabetes, arthritis, severe rheumatic disorders) mean NK activity was clearly reduced (5.7 +/- 1.5). The use of NK activity data as a probe for tumor metastases was found to be statistically as reliable as was the application of the PSA serotest (but not serum PAP concentrations). None of the measured hormonal parameters correlated well with tumor stage. Both testosterone and prolactin serum concentrations were found to be lower in the G2 and G3 cancer group than in well-differentiated (G1) tumors, in accordance with the published literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison between NK cell activity and prostate cancer stage and grade in untreated patients: correlation with tumor markers and hormonal serotest data. 768 Dec 42

We have conducted a double-blind comparative study of flutamide and chlormadinone acetate (CMA) on patients with stage C or D prostatic cancer and with no prior experience of hormone therapy. This is believed to be the first such trial entered in the medical literature, fifty-four patients were randomly selected to undergo flutamide (p.o.) monotherapy at a daily dose of 375 mg, which was determined as the optimal dose in Japan in our previous phase II study. Forty-nine others were randomly selected to undergo CMA (p.o.) monotherapy at a daily dose of 100 mg, which is the most commonly used dosage in Japan for patients with prostatic cancer. Ultimately, 47 patients from the flutamide group and 40 patients from the CMA group were judged eligible, with efficacy being evaluated after 12 weeks of treatment. Similar objective responses were seen in both groups: 48.9% (95% confidence limits 34.1-63.9%) in the flutamide group, 45% (95% confidence limits 29.3-61.5%) in the CMA group. The response at each organ site was also similar between the groups. Serum prostatic specific antigen decreased by more than 50% of the abnormal pretreatment level in 87.5% of the flutamide group and in 85.7% of the CMA group. Serum luteinizing hormone, follicle-stimulating hormone, testosterone and 5 alpha-dihydrotestosterone decreased significantly in the CMA group, but increased significantly in the flutamide group. The serum testosterone level after 12 weeks of treatment was 0.955 +/- 0.13 ng/ml in the CMA group and 6.64 +/- 0.38 ng/ml in the flutamide group. The serum estradiol level also increased significantly in patients in the flutamide group. The serum prolactin level decreased significantly in the flutamide group, but increased significantly in the CMA group. Eight patients on flutamide manifested gynecomastia. Diarrhea and hepatic toxicity were observed in both groups, but only rarely, and were well tolerated. We have thus concluded that flutamide is as effective as CMA in maintaining libido and potency without decreasing testosterone levels.
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PMID:A randomized phase II trial of flutamide vs chlormadinone acetate in previously untreated advanced prostatic cancer. The Japan Flutamide Study Group. 768 29

The nonsteroidal androgen-receptor antagonist nilutamide has previously been shown to inhibit adrenal androgen steroidogenesis in patients with prostatic carcinoma treated in combination with an LHRH agonist. In order to understand better the mechanisms subserving this observation, we have studied the effects of nilutamide alone on the serum concentrations of androstenedione (A), dehydroepiandrosterone (DHEA), and DHEA-sulphate (DHEA-S) in 12 patients with prostatic cancer and compared them with those achieved in 21 patients treated with the agonist D-Trp-6-LHRH. In addition, the adrenocorticotropic hormone (ACTH)-stimulated adrenal response and the thyrotropin releasing hormone (TRH)-stimulated prolactin (PRL) response observed in the patients treated with nilutamide were compared with a control group of healthy age-matched controls. No significant variation in the basal concentrations of adrenal androgens occurred either within or between both treatment groups. In response to ACTH, a decreased 17-alpha hydroxyprogesterone (17-OHP) accumulation and an augmented A/17-OHP ratio were observed in the antiandrogen group (P < 0.05 for both), suggesting the partial removal of the 17,20 lyase block which was distinctive of the untreated controls, while no significant difference was found for other steroids. Basal PRL levels were not affected by the antiandrogen, but the response to TRH was increased. We conclude that no significant inhibition of adrenal androgen secretion occurs after nilutamide or LHRH agonist treatment. Rather, administration of the antiandrogen alone may partially remove the physiological decrease in adrenal androgen secretion observed in the elderly.
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PMID:Effect of the nonsteroidal antiandrogen nilutamide on adrenal androgen secretion. 829 Mar 86


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