title: Variation in chromogranin A serum levels during intermittent versus continuous androgen deprivation therapy for prostate adenocarcinoma.
abstract: OBJECTIVE
  It has been hypothesized that continuous androgen-suppression therapy produces hyperactivation of neuroendocrine (NE) cells and an increase in chromogranin A (CgA) in prostate carcinoma (PC). The aim of this study was to verify whether the intermittent administration of androgen deprivation (IAD) reduces the risk of CgA increase in PC cases treated with complete androgen deprivation (CAD).
  
  
  METHODS
  We analyzed changes in serum CgA levels in patients with PC who successfully responded to the first 24 months of IAD versus continuous CAD therapy. Two different populations were analyzed: Type 1 = pT3pN0M0 prostate cancers with biochemical (PSA) progression after RRP; Type 2 = metastatic PC directly submitted to CAD. Cases in Type 1 and Type 2 population were randomly assigned to IAD versus continuous CAD therapy. Forty cases each in Type 1 and Type 2 population were included in the analysis. At 1, 3, 6, 12, 18, 24 months of IAD versus continuous therapy, serum levels of CgA compared to PSA levels were analyzed.
  
  
  RESULTS
  In population Type 1 and Type 2, in the group of cases continuously treated with CAD (Group 2), there was a significant trend to increase for CgA levels from baseline to 24 months of therapy. On the contrary, no significant variations were found in cases treated with IAD (Group 1). Either in population Type 1 or Type 2, at 12- and 24-month follow-up, mean and median serum levels of CgA were significantly (P < 0.005) lower in Group 1 than in Group 2.
  
  
  CONCLUSIONS
  The present study represents the first evidence in the literature that the intermittent administration of CAD therapy significantly reduces the increase in serum CgA levels during CAD therapy.
authors.affiliation: Department of Urology U Bracci, University La Sapienza, Rome, Italy. sciarrajr@hotmail.com
authors.forename: Alessandro
authors.initials: A
authors.lastname: Sciarra
authors.forename: Salvatore
authors.initials: S
authors.lastname: Monti
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Gentile
authors.forename: Gianna
authors.initials: G
authors.lastname: Mariotti
authors.forename: Antonio
authors.initials: A
authors.lastname: Cardi
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Voria
authors.forename: Rossana
authors.initials: R
authors.lastname: Lucera
authors.forename: Franco
authors.initials: F
authors.lastname: Di Silverio
mesh_terms: D000230:Adenocarcinoma / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology; D000368:Aged; D000726:Androgen Antagonists / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D018931:Antineoplastic Agents, Hormonal / Q000008:administration & dosage; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000097:blood*; D053379:Chromogranin A; D002864:Chromogranins / Q000097:blood*; D005485:Flutamide / Q000008:administration & dosage; D006801:Humans; D008297:Male; D008875:Middle Aged; D009376:Neoplasms, Hormone-Dependent / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D011446:Prospective Studies; D017430:Prostate-Specific Antigen / Q000097:blood; D011471:Prostatic Neoplasms / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology; D016032:Randomized Controlled Trials as Topic; D017329:Triptorelin Pamoate / Q000008:administration & dosage
chemical_list: D000726:Androgen Antagonists; D018931:Antineoplastic Agents, Hormonal; D014408:Biomarkers, Tumor; C506150:CHGA protein, human; D053379:Chromogranin A; D002864:Chromogranins; D017329:Triptorelin Pamoate; D005485:Flutamide; D017430:Prostate-Specific Antigen