PLASMA NEUROENDOCRINE MARKERS IN PATIENTS WITH BENIGN PROSTATIC HYPERPLASIA AND PROSTATIC-CARCINOMA

Citation
O. Cussenot et al., PLASMA NEUROENDOCRINE MARKERS IN PATIENTS WITH BENIGN PROSTATIC HYPERPLASIA AND PROSTATIC-CARCINOMA, The Journal of urology, 155(4), 1996, pp. 1340-1343
Citations number
20
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
155
Issue
4
Year of publication
1996
Pages
1340 - 1343
Database
ISI
SICI code
0022-5347(1996)155:4<1340:PNMIPW>2.0.ZU;2-O
Abstract
Purpose: Approximately 50% of all malignant prostatic tumors contain n euroendocrine cells, which cannot be attributed to small cell prostati c carcinoma or carcinoid-like tumors, and which represent only 1 to 2% of all prostatic malignancies. Only limited data are available concer ning the plasma levels of neuroendocrine markers in patients with pros tatic tumors. Therefore, we determined the incidence of high plasma le vels of neuroendocrine markers in patients with benign and malignant p rostatic disease. Materials and Methods: The presence of elevated plas ma neuropeptide levels was investigated in 135 patients with prostatic carcinoma and 28 with benign prostatic hyperplasia. Plasma chromogran in A, neurone-specific enolase, substance P, calcitonin, somatostatin, neurotensin and bombesin levels were analyzed by immunoassays, and we re compared to clinical and pathological stages of disease. Plasma pro static acid phosphatase and prostate specific antigen levels were also determined. All patients were followed for at least 2 years after inc lusion in the study. Results: Significantly elevated levels of chromog ranin A were detected in 15% of patients with prostatic carcinoma befo re any treatment. During hormone resistant prostate cancer progression plasma chromogranin A and neuron-specific enolase levels were elevate d in 55% and 30% of the patients, respectively. In patients with stage D3 disease survival curves were generated by the Kaplan-Meier method, and log rank analysis revealed a statistically significant difference between groups positive and negative for chromogranin A. Substance P and bombesin were also occasionally elevated in prostatic tumors. Dete rmination of neuroendocrine differentiation by neuron-specific enolase or chromogranin A immunoassays was not helpful in the prediction of p rogressive localized prostatic carcinoma. Conclusions: Future studies of plasma neuropeptide levels should confirm whether these parameters can be used as prognostic markers during late progression of prostatic carcinoma or for the selection of patients suitable for evaluation of new antineoplastic drugs known to be active against neuroendocrine tu mors.