An observational retrospective evaluation of 79 young men with long‐term adverse effects after use of finasteride against androgenetic alopecia
Chiriacò et al., 2016
“Symptoms reported by our PFS patients are suggestive of androgens deficiency in several different tissues...thus, this phenomenon seems to indicate that some permanent changes occurred and spread in [the] human body.”
79 symptomatic PFS patients suffering for a minimum of six months post-cessation were retrospectively evaluated via 100 ad-hoc questions, a pre and post-finasteride ASEX questionnaire, and the Aging Male Symptom Scale (AMS) questionnaire.
Mean age of participants was 33. Finasteride had been taken for an average of 2 years. 89.9% of participants noticed some symptoms during finasteride use, and the trend of symptoms after discontinuation was worsening in 62% of patients, with a trend of improvement reported in only 13.9%.
Sexual symptoms included loss of penile sensitivity (87.3%), decreased ejaculatory force (82.3%), decreased penile temperature (78.5%), reduced ejaculate volume (73.4%), reduction in penile dimension (65.8%), perineal tightness (45.6%).
Other symptoms included anhedonia (75.9%), concentration problems (72.2%), loss of muscle tone and mass (51.9%), and increased body weight (48.1%).
Post-finasteride ASEX score ranged from 13–30 (21.0 ± 2.67), with 78.5% having ASEX ≥19 points indicating sexual dysfunction. This included 44.3% of patients indicating severe difficulty or incapability of getting/keeping an erection. Pre-finasteride ASEX score was far lower (p < 0.001) ranging 5–15 (7.7 ± 2.52), indicating no overt sexual dysfunction.
Of 78 patients with available data, all had some signs of androgen deficiency, with 60.3% having an AMS score of ≥50 points indicating severe deficiency.
The authors note the reports by their PFS patients suggest androgen deficiency across different tissues where 5alpha reductase is expressed at an average of four years after finasteride discontinuation, indicating that permanent changes occurred in the human body.
They conclude further studies are necessary to investigate the pathophysiological and biochemical pathways leading to the post‐finasteride syndrome.
