Post-Finasteride Syndrome And Post-Ssri Sexual Dysfunction: Two Clinical Conditions Apparently Distant, But Very Close

• Published in: Frontiers in neuroendocrinology Vol. 72; p. 101114
• Main Authors: Giatti, Silvia, Diviccaro, Silvia, Cioffi, Lucia, Cosimo Melcangi, Roberto
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.01.2024
• Subjects: 5-alpha Reductase Inhibitors - adverse effects; Alopecia - chemically induced; Alopecia - drug therapy; Antidepressive Agents; Dysbiosis; Finasteride - adverse effects; Gut; Humans; Male; Microbiome; Neuroactive steroids; Neurotransmitters; Persistent effects; Sexual Dysfunction, Physiological - chemically induced; Sexual Dysfunction, Physiological - diagnosis; Sexual Dysfunction, Physiological - drug therapy; Neurotransmitters; Neuroactive steroids; Dysbiosis; Persistent effects; Gut; Microbiome
• ISSN: 0091-3022; 1095-6808
• DOI: 10.1016/j.yfrne.2023.101114

[Display omitted] •Side effects associated with finasteride treatment may persist after drug suspension.•Side effects induced by SSRI treatment may persist after stopping the drug.•Steroids, neurotransmitters, and gut microbiota, have a crucial role in PFS and PSSD. Post-finasteride syndrome and post-SSRI sexual dysfunction, are two poorly explored clinical conditions in which men treated for androgenetic alopecia with finasteride or for depression with SSRI antidepressants show persistent side effects despite drug suspension (e.g., sexual dysfunction, psychological complaints, sleep disorders). Because of some similarities in the symptoms, common pathological mechanisms are proposed here. Indeed, as discussed, clinical studies and preclinical data obtained so far suggest an important role for brain modulators (i.e., neuroactive steroids), neurotransmitters (i.e., serotonin, and cathecolamines), and gut microbiota in the context of the gut-brain axis. In particular, the observed interconnections of these signals in these two clinical conditions may suggest similar etiopathogenetic mechanisms, such as the involvement of the enzyme converting norepinephrine into epinephrine (i.e., phenylethanolamine N-methyltransferase). However, despite the current efforts, more work is still needed to advance the understanding of these clinical conditions in terms of diagnostic markers and therapeutic strategies.