According to an article recently published, the failure to suppress testosterone to levels below 0.7 nM in men with castrated sensitive prostate cancer is associated with poor clinical outcomes. Therefore, it is standard practice or should be, to evaluate testosterone levels in men on hormone therapy (ADT), especially if it looks as if they are becoming castrate resistant.
Mass spectrometry is considered the gold standard used to measure levels of testosterone; however, many hospitals use an immunoassay method.
In this study, researchers evaluated the accuracy of an immunoassay method to measure castrate testosterone levels, against mass spectrometry, which is the reference standard. In a retrospective evaluation of a cohort of 435 serum samples retrieved from castrated prostate cancer patients from April to September 2017 serum testosterone levels were measured using the same sample using liquid chromatography coupled with tandem mass spectrometry and electrochemiluminescent immunoassay methods.
The findings were that the mean testosterone levels were significantly higher with immunoassay than with mass spectrometry. Half of the samples with testosterone greater than 0.7 nM assessed by immunoassay were measured <0.7 nM when using mass spectrometry. However, the researchers observed that only 2.95% of the samples with testosterone <0.7 nM measured by immunoassay were quantified ≥less than 0.7 nM using mass spectrometry.
What this means that in this research sample, the percentage of serum samples experiencing testosterone breakthrough at >0.7 nM was significantly higher using immunoassay (22.1%) than with mass spectrometry (13.1%; P < 0.0001).
This glaring difference may mean that the standard use of the immunoassay method can result in an inaccurately identified castration status. In other words, it is highly probable that men who have their testosterone levels measured by the immunoassay system, commonly used in hospitals, are at a high risk of being inaccurately diagnosed as being castrate resistant instead of having suboptimal testosterone control.
This error can lead to men moving on to the more advanced drugs like Xtandi or Zytiga before they need these drugs. Since these drugs all have a limited effective life, come with an increased economic cost, and lead to a negative quality of life impact, we need to be sure that a man is castrate resistant and not adequately controlled.
Given the significance of this finding and the ultimate additional costs of too early use of these secondary drugs, we need to be sure that we know our actual levels of testosterone.
The only way to make these significant clinical decisions with confidence is to be sure that before assuming that you are castrate resistant your testosterone levels must be confirmed by either mass spectrometry or an immunoassay method that has been validated at low testosterone levels and interpreted with caution before any changes are made to treatment management.
https://pdfs.semanticscholar.org/b8a2/0b3c7e32e4bcf4ed344d69dd849d2cfcbe7f.pdf?_ga=2.50762537.1096794760.1570400977-315406302.1570400977
