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

Serum beta-2-microglobulin levels were measured in patients with renal, vesical and prostatic cancer. Measurements were made only on samples with a serum creatinine less than or equal to 105 mumol./l. to eliminate the possibility of elevated beta-2-microglobulin being a result of impaired renal function. This criterion eliminated 28 to 50 per cent of the patients with bladder cancer and 73 per cent of those who had undergone nephrectomy for renal carcinoma, which, obviously, limits the value of beta-2-microglobulin measurement for the surveillance in these cancers. Beta-2-microglobulin values in patients with prostatic cancer were seldom increased to more than 3.0 mg./l. In bladder cancer patients with normal serum creatinine the frequency of an elevated serum beta-2-microglobulin increased with the increase in tumor stage.
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PMID:Serum beta-2-microglobulin levels in urological cancer. 8 16

In a series of 51 patients with prostate cancer and obstructive uropathy, unilateral or bilateral obstruction was identified in 22 (43%) and 29 (57%) respectively. This included a non-functioning kidney in 12 patients. In 86% of patients the T category was advanced. Bone metastases were present in 36 cases (71%); 19 patients (37%) had chronic retention. All patients with metastatic disease underwent hormonal manipulation and 43 underwent transurethral resection of the prostate. External beam radiotherapy, percutaneous nephrostomy and ureteric reimplantation were performed in 4, 5 and 1 patient respectively. Actuarial survival of all 51 patients was 57 and 25% at 2 and 5 years. Presentation with bilateral or non-function did not predict a worse prognosis in comparison with patients with unilateral hydroureteronephrosis. Raised alkaline phosphatase and prostatic acid phosphatase were of no prognostic value, while creatinine reached marginal significance. A positive bone scan and raised urea were strongly predictive of a poor outlook. It was concluded that prostate cancer and obstructive uropathy should not uniformly imply a terminal event, and interventional therapy is justified with a 25% 5-year survival rate.
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PMID:Outcome and prognostic factors in patients with advanced prostate cancer and obstructive uropathy. 145 Aug 51

In 224 consecutive patients with hormone-resistant prostatic cancer referred to 2 European Cancer Centres for palliation of painful bone metastases the one year survival for all patients was 24% (2-year survival: 7%). The median survival was 8 months. In univariate analyses the following prognostic factors were identified: performance status, serum creatinine, alkaline phosphatase, duration of response to primary hormone treatment, degree of bone scan involvement and hemoglobin. Multivariate analyses confirmed the four first parameters to be independent factors. A prognostic model was established (no or one risk factors vs 2 risk factors vs 3 or 4 risk factors) based on performance status, creatinine, alkaline phosphatase and hormone response duration. The median survival of these groups was 10 months, 6 months and 3 months, respectively. This model proved to be discriminative in an external data set of 214 patients with hormone-resistant prostatic cancer entered in two prospective trials. The above differences in outcome between readily and simply defined prognostic groups are greater than the differences one can realistically hope to produce using new treatment strategies. These prognostic factors should be taken into account both in the design and interpretation of clinical studies dealing with the treatment of hormone-resistant progressing prostatic cancer and painful bone metastases.
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PMID:Prognostic factors in hormone-resistant progressing cancer of the prostate. 161 86

In a controlled trial the effects of the osteoclast inhibitor disodium pamidronate were studied over a 6-month period in men with metastatic bone disease from prostate cancer. Using serial biochemical measurement of metabolic bone activity, and complementary subjective and quantitative bone histology, the effects of pamidronate were evaluated in tumour-free and metastatic regions of the skeleton, enabling analysis of the differential mechanisms of bone destruction in this disease. Following treatment, abnormally high markers of bone breakdown fell significantly (fasting urine hydroxyproline/creatinine (OHP): P less than 0.05; fasting urine calcium excretion (CaE): P less than 0.0001), confirming that activated osteoclasts play an integral role in the osteolytic process. Serial histomorphometry of bone from tumour-free areas showed that pamidronate restored abnormal levels of bone erosion to normal in 93% of cases. Suppression of bone destruction was also evident within metastases, although this was incomplete. The results confirm that osteoclast overactivity is responsible for a significant proportion of the accelerated osteolysis seen in both tumour-free and infiltrated bone in patients with prostate cancer. The differential effects in tumour-free and infiltrated bone suggest that the mechanisms of osteoclast activation may differ in metastatic and non-metastatic regions of the skeleton.
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PMID:Disodium pamidronate identifies differential osteoclastic bone resorption in metastatic prostate cancer. 173 55

Histomorphometric measurements of tumour-free bone have been undertaken in a closely matched group of patients with metastatic prostate cancer treated either by subcapsular orchidectomy (SCO) or luteinising hormone-releasing hormone (LHRH) agonists. Age, fasting morning urine hydroxyproline/creatinine ratios, alkaline and acid phosphatase levels and elapsed time after hormonal manipulation were similar in those receiving SCO (n = 8) as compared to LHRH therapy (n = 8). Results indicated that osteoid surface and mineralisation rate were significantly reduced in the SCO group (p less than 0.05); other indices were also lower in the SCO patients but failed to reach statistical significance. These changes, possibly due to increased adrenal cortical stimulation secondary to elevated gonadotrophin levels following orchidectomy suggest that medical castration by gonadotrophin inhibition may avoid unnecessary morbidity due to treatment-induced bone dysfunction.
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PMID:Preferential preservation of bone mineralisation by LHRH agonists in the treatment of metastatic prostate cancer. 182 70

We report our experience with 100 orchiectomies for advanced prostatic cancer in hospitalised patients. Approximately 60% of the patients required hospitalisation for additional treatment and investigation of complications due to their disease at the time of orchiectomy. In 51 cases the orchiectomy was combined with transurethral resection of the prostate (TURP); 37 patients had pathological levels of serum creatinine and 17 had pathological dilatation of the upper urinary tract, 6 of whom required a nephrostomy catheter. Because of anaemia on admission, 21 patients received a peri-operative blood transfusion. Two patients had significant post-operative bleeding, 2 developed a wound infection and 1 had a deep thrombophlebitis. The patients' mean age was 76.4 years and the period of hospitalisation ranged from 3 to 150 days with peaks at 3 and 8 days. The most important reason for prolonged hospitalisation was social problems. It was concluded that many patients who were hospitalised as a direct consequence of their prostatic carcinoma would have been in hospital for a similar period regardless of the method of hormonal manipulation used. Because so many patients have other reasons for hospitalisation, or require additional surgical procedures such as TURP, the true average cost of orchiectomy for advanced prostatic cancer is difficult to determine.
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PMID:Hospitalisation of prostatic cancer patients undergoing orchiectomy. 187 93

In a population-based randomized study comparing 150 patients with advanced prostatic cancer treated with orchiectomy or estrogen, some possible prognostic factors were analyzed. The observation period was 78 to 114 months. M category, T category, tumor grade, performance status, pain, prostatic acid phosphatase, sedimentation rate, hemoglobin and serum creatinine level were all statistically significantly related to the interval to progression and to disease-specific death on univariate analyses. Variables that were statistically significant on multivariate analyses were M category, T category, sedimentation rate and patient age. The sedimentation rate predicted the intervals to progression and to disease-specific death, with the relative hazard and 95% confidence interval for the latter end point being 1.018 (range 1.010 to 1.027) for each millimeter increase in sedimentation rate per hour. An analysis that was stratified according to the extent of the disease as measured on a bone scan showed that the sedimentation rate was the only prognostic factor of statistical significance with an estimate of relative hazard of 1.52 if the sedimentation rate was elevated 20 mm. per hour. Progression-free survival but not disease-specific survival was statistically significantly better in the estrogen group (relative hazard 0.47), as assessed by multivariate analysis in which all variables were taken into account.
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PMID:Prognostic factors in progression-free survival and corrected survival in patients with advanced prostatic cancer: results from a randomized study comprising 150 patients treated with orchiectomy or estrogens. 194 84

Twenty-nine patients with metastatic prostate cancer progressing after hormonal therapy (orchiectomy 19, diethylstilbestrol 10) and who had never received cytotoxic therapy were treated with carboplatin. Patients had good clinical performance status (66% PS 0,1) and adequate renal (creatinine less than 2.0 mg/dL) and bone marrow function. The standard dose of carboplatin administered was 400 mg/sq m. Seventeen patients received this dose and 12 either 320 mg/sq m or 250 mg/sq m based on reduced renal function or prior radiation. Five patients had bidimensionally measurable disease: one experienced a partial regression of cervical lymph node metastases of 97 days duration. Twenty-four patients had metastatic disease evaluable by clinical status, bone scan and acid phosphatase. In one patient greater than 50% reduction in number of abnormal areas of bone scan uptake occurred; 3 patients experienced improvement in clinical status; in no patient did an elevated prostate acid phosphatase return to normal. All patients entered on study have progressed and died: median time to progression was 94 days (6 to 625 days); median survival was 297 days (6-1152 days). The primary toxicity of carboplatin was myelosuppression. The median WBC and platelet nadirs after cycle one were 3150/cu mm and 93,000/cu mm, respectively. Dose escalations to grade 2 or greater myelosuppression were mandated. Twenty-six achieved at least grade 2 myelosuppression during carboplatin treatment. We conclude that carboplatin administered at this dose and schedule has no important activity in hormone refractory prostate cancer.
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PMID:A phase II trial of carboplatin (NSC 241240) in advanced prostate cancer, refractory to hormonal therapy. An Eastern Cooperative Oncology Group pilot study. 219 2

Patients with newly diagnosed prostatic cancer should be investigated with regard to the presence or absence of distant metastases by: (1) Clinical history especially of weight loss, recent pain, or analgesics intake. (2) Physical examination, looking especially for hepatic enlargement, peripheral lymph nodes, local bone tenderness. (3) Performance status. (4) Hemoglobin, creatinine, PSA and/or PAP, alkaline phosphatases, liver tests, testosterone. (5) Bone scan with X-ray of doubtful hot spots. (6) Chest X-ray. (7) Ultrasound scans (liver, kidney, lymph nodes) or CT scan may be indicated if abnormal blood parameters or in specific situations. (8) Other investigations are only indicated in special circumstances. Follow-up should include: (1), (2), (3), (4) every 3 months. For patients in clinical trials, depending on the end point, bone scan should be repeated every 6 months or possibly depending on the prognostic group (good: every 12 months; bad: 3 to 6 months). For routine clinical management, it could be repeated only when markers (PAP, PSA, alkaline phosphatase) show significant (25-50%) increase and provided the result will influence treatment. Other investigations should only be repeated or performed if abnormal at the start of if clinical data require them.
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PMID:The staging of M+ disease. 221 62

We retrospectively reviewed the outcome of 37 prostate cancer patients with ureteral obstruction treated by percutaneous nephrostomy. The over-all survival was 57% at 1 year and 29% at 2 years (median survival time 21 months). The 1 and 2-year survival rates of 15 patients with no prior hormonal therapy were 73 and 47%, respectively, while those of patients who had previously received hormonal therapy were 48 and 19%, respectively. Median survival times of these groups were 24 months and 12 months, respectively. Of 12 patients who had severe renal failure before percutaneous nephrostomy (serum creatinine greater than or equal to 6.9 mg. per dl.) 9 had an adequate return of renal function (serum creatinine less than 3 mg. per dl.) after drainage and 58% survived more than 1 year (median survival time 22 months). Percutaneous nephrostomy is safe and effective in relieving ureteral obstruction and reasonable survival can be achieved even in patients with renal failure. Percutaneous nephrostomy should be considered strongly in these patients.
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PMID:Ureteral obstruction associated with prostate cancer: the outcome after percutaneous nephrostomy. 232 11


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