Abstract
Treatment with Luteinizing Hormone-Releasing Hormone Antagonists: is Serum Testosterone Reduction the Only Mechanism?
Highlights
Androgen deprivation therapy (ADT) by either bilateral orchiectomy or medical castration (luteinizing hormonereleasing hormone (LHRH) agonists, luteinizing hormone receptor hormone (LHRH) antagonists or estrogens) is recommended for advanced or metastatic prostate cancer [1]
We describe the results of serum testosterone measurements in patients with advanced or metastatic prostate cancer on LHRH antagonist therapy using a highly sensitive and specific isotope dilutionliquid chromatography-tandem mass spectrometry (ID-LC-MS/MS) method [15]
Using a state-of-the-art method to assess levels of testosterone, we investigated whether a potential difference in clinical outcome between different forms of ADT might be related to differences in serum testosterone concentrations
Summary
Androgen deprivation therapy (ADT) by either bilateral orchiectomy (surgical castration) or medical castration (luteinizing hormonereleasing hormone (LHRH) agonists, LHRH antagonists or estrogens) is recommended for advanced or metastatic prostate cancer [1]. LHRH agonist therapy results in an initial increase in serum testosterone concentration, known as flare or flare-up. The authors concluded that degarelix was associated with prostate-specific antigen (PSA) progression-free and overall survival compared with LHRH agonists [6]. Androgen deprivation therapy (ADT) by surgical or medical castration is recommended for advanced or metastatic prostate cancer. Recent literature suggests that medical castration by luteinizing hormone receptor hormone (LHRH) antagonists might have advantages over treatment with LHRH agonists in patients with metastatic prostate cancer when prostate specific antigen (PSA) progression free survival and overall survival are concerned. We further searched for evidence in literature for other biochemical pathways explaining a potential benefit of LHRH antagonists over LHRH agonists
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