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Rapid elimination kinetics of free PSA or human kallikrein-related peptidase 2 after initiation of gonadotropin-releasing hormone-antagonist treatment of prostate cancer: potential for rapid monitoring of treatment responses
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David Ulmert
Published/Copyright:
July 5, 2012
Abstract
Background: The utility of conventional prostate-specific antigen (PSA) measurements in blood for monitoring rapid responses to treatment for prostate cancer is limited because of its slow elimination rate. Prior studies have shown that free PSA (fPSA), intact PSA (iPSA) and human kallikrein-related peptidase 2 (hK2) are eliminated more rapidly after radical prostatectomy. In contrast, all three markers have similarly slow elimination rates after castration induced by gonadotropin-releasing hormone (GnRH) agonists, possibly due to the slow onset of castration. Therefore, we assessed elimination rates of tPSA, fPSA, iPSA and hK2 after rapid induction of castration with degarelix (Firmagon®), a novel GnRH antagonist.
Methods: This study included 24 patients treated with degarelix. Blood was taken at 1, 3, 7, 14, 21 and 28 days after injection of degarelix. Free and total PSA were measured with a commercial dual-label assay, and with inhouse research assays of intact PSA and hK2.
Results: Median (interquartile range, IQR) tPSA at baseline was 23.4 (15.8, 59.8). Twenty-two patients (92%) reached castrate levels of testosterone within 24 h of degarelix initiation, and all patients did so within 72 h. All kallikrein forms declined in an exponential fashion after degarelix administration. The median time to 50% reduction in biomarker level was 8–9 days for tPSA or complexed PSA vs. 2–4 days for hK2, iPSA and fPSA. The percentage eliminated at day 3 and day 7 was significantly higher for hK2, iPSA and fPSA than for tPSA (all p<0.02), while tPSA and complexed PSA were similar.
Conclusions: The rapid decline of fPSA, iPSA and hK2 after fast induction of castration with degarelix is similar to that reported after prostatectomy and offers a novel, informative method to monitor rapid onset of therapeutic action targeting signaling of the androgen receptor.
Keywords: androgen deprivation therapy; human kallikrein-related peptidase 2; prostate cancer; prostate-specific antigen; tumor markers
Received: 2011-12-30
Accepted: 2012-05-07
Published Online: 2012-07-05
Published in Print: 2012-11-01
©2012 by Walter de Gruyter Berlin Boston
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Keywords for this article
androgen deprivation therapy;
human kallikrein-related peptidase 2;
prostate cancer;
prostate-specific antigen;
tumor markers
Articles in the same Issue
- Congress Abstracts
- 44th National Congress of the Italian Society of Clinical Biochemistry and Clinical Molecular Biology
- Masthead
- Masthead
- Editorials
- Tumor biomarkers: PSA and beyond
- Error reporting in transfusion medicine: an important tool to improve patient safety
- The measurement of 25-hydroxy vitamin D – an analytical challenge
- Reviews
- Kallikrein-related peptidases (KLKs): a gene family of novel cancer biomarkers
- Exhaled breath analysis for early cancer detection: principle and progress in direct mass spectrometry techniques
- γ′ Fibrinogen as a novel marker of thrombotic disease
- Mini Review
- Revaluating serum ferritin as a marker of body iron stores in the traceability era
- Genetics and Molecular Diagnostics
- Association of PBEF gene polymorphisms with acute lung injury, sepsis, and pneumonia in a northeastern Chinese population
- General Clinical Chemistry and Laboratory Medicine
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