Post-finasteride syndrome: a surmountable challenge for clinicians
Traish, 2020
In a further review, Traish draws upon significant and relatively recent understanding of the physiological role of 5alpha reductase and androgens as well as the evidence of PFS. He suggests the irreversible nature of the inhibition by this class of drugs may lead to epigenetic changes, such as DNA methylation of the androgen receptor or 5a-reductases. He suggests the endocrine disruptive effect of the drug class may contribute to several potential mechanisms by which these drugs elicit the serious and undesirable sexual and psychological adverse effects.
Traish suggests the rarity, variability and dose independence of the syndrome depends upon epigenetic phenotype.
Traish reviews many studies that demonstrate increased onset of sexual dysfunction and psychiatric dysfunction. He challenges a frequent dismissal of studies as low-quality evidence, noting that considerable bias is introduced in many of these studies since a large number of the clinical trials were funded and administered by the drug manufacturers. The fundamental shortcomings in the vast majority of the trials that underpin the drug’s perceived safety for hair loss is highlighted, and he implores clinicians to do their due diligence and not fall for the slogan, ‘‘these drugs are well tolerated and safe.’’
He mentions that rejection of new ideas in science and medicine is very common in both scientific and clinical literature. However the unusual resistance to acceptance of PFS, and the motives underlying this, are strongly questioned in line with mounting evidence and the severity of the harm. As some patients are presenting with very severe, peculiar and classical symptoms, he argues it should be unacceptable to outright dismiss PFS even with limited evidence.
Traish concludes it is time that PFS patients no longer have these serious and debilitating drug-induced symptoms misattributed as being psychosomatic. He calls for action towards pathophysiological understanding of the disease mechanism so as to develop novel therapeutic options.