title: A switch from GnRH agonist to GnRH antagonist in castration-resistant prostate cancer patients leads to a low response rate on PSA.
abstract: OBJECTIVE
  At the time of castration resistance, it is recommended to realize hormonal manipulations before chemotherapy. We evaluated the impact of a switch from GnRH agonist to antagonist in patients with castration-resistant prostate cancer on PSA and testosterone levels at 3 months.
  
  
  METHODS
  Retrospectively, 17 patients from 5 different centers undergoing androgen deprivation therapy and presenting rising PSA confirmed on 3 blood samples 2 weeks apart and despite a castrate testosterone level (<0.5 ng/ml) were reviewed. Antiandrogen withdrawal syndrome had been tested before the switch. Degarelix was administered as followed: 240 mg for the first injection and then 80 mg every month, subcutaneously. We evaluated the PSA and testosterone level variation 3 months after the switch. Patients who experienced a variation in PSA of less than 10% compared to the baseline or who had a more than 10% PSA decrease were defined as responders.
  
  
  RESULTS
  Mean PSA level at the switch was 34.3 ± 50.3 ng/ml, with a mean testosterone level of 0.21 ± 0.13 ng/ml. Three months after the switch, mean PSA level was 59.9 ± 81.6 ng/ml (P = 0.061), with a mean testosterone level of 0.19 ± 0.08 ng/ml (P = 0.086). At 3 months, 4 patients (23%) responded to therapy. Thirteen patients (77%) experienced a rise in PSA of more than 10% compared to baseline; 41% of patients decreased their testosterone level. The limitations of this study are its retrospective nature and the limited number of patients.
  
  
  CONCLUSIONS
  Switch from an agonist to an antagonist of GnRH has a limited impact on PSA at 3 months in castration-resistant prostate cancer patients.
authors.affiliation: INSERM U955EQ07 - Department of Urology, CHU Henri Mondor, 51 av du Maréchal de Lattre de Tassigny, 94000, Créteil, France.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Masson-Lecomte
authors.forename: Laurent
authors.initials: L
authors.lastname: Guy
authors.forename: Philippe
authors.initials: P
authors.lastname: Pedron
authors.forename: Franck
authors.initials: F
authors.lastname: Bruyere
authors.forename: Morgan
authors.initials: M
authors.lastname: Rouprêt
authors.forename: Bonaventure
authors.initials: B
authors.lastname: Nsabimbona
authors.forename: Mickael
authors.initials: M
authors.lastname: Dahan
authors.forename: Patrice
authors.initials: P
authors.lastname: Hoffman
authors.forename: Laurent
authors.initials: L
authors.lastname: Salomon
authors.forename: Dimitri
authors.initials: D
authors.lastname: Vordos
authors.forename: Andras
authors.initials: A
authors.lastname: Hoznek
authors.forename: Philippe
authors.initials: P
authors.lastname: Le Corvoisier
authors.forename: Pierrick
authors.initials: P
authors.lastname: Morel
authors.forename: Claude
authors.initials: C
authors.lastname: Abbou
authors.forename: Alexandre
authors.initials: A
authors.lastname: de la Taille
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D018450:Disease Progression; D057915:Drug Substitution; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists / Q000037:antagonists & inhibitors*; D006801:Humans; D007610:Kallikreins / Q000097:blood; D008297:Male; D009842:Oligopeptides / Q000627:therapeutic use*; D017430:Prostate-Specific Antigen / Q000097:blood; D011471:Prostatic Neoplasms / Q000188:drug therapy*; D012189:Retrospective Studies; D013739:Testosterone / Q000097:blood; D016896:Treatment Outcome
chemical_list: D018931:Antineoplastic Agents, Hormonal; D009842:Oligopeptides; C431566:acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ILys-prolyl-alaninamide; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; C549870:KLK3 protein, human; D007610:Kallikreins; D017430:Prostate-Specific Antigen