It has common features with other self-diagnosed "mystery syndromes" such as morgellons syndrome or multiple chemical sensitivity. There is no known underlying biological mechanism for the proposed syndrome, and its incidence is also unclear. A lack of clear diagnostic criteria and the variable reporting fraction in different health-care settings make the problem challenging to evaluate.Self-reported symptoms of post-finasteride syndrome include penile atrophy and tissue changes, decreased ejaculate volume and quality, libido loss, erectile dysfunction, loss of penile sensitivity, decreased orgasm sensation, dry skin, metabolic changes, muscle and strength loss, gynecomastia, depression, anxiety, panic attacks, insomnia, anhedonia, concentration problems, memory impairment and suicidal ideation. A meta-analysis found significant association between finasteride use and post-discontinuation depression, suicide ideation, and sexual dysfunction, but the quality of evidence was limited.Plaintiffs have filed over one thousand court cases against Merck over the effects of finasteride. Most were settled by 2018 when Merck paid a lump sum of US$4.3 million to be distributed. As of September 2019, 25 cases remained outstanding in the United States.In 2019 Reuters reported that faulty redactions in court documents revealed allegations from plaintiffs that Merck had known of persistent side effects in their original clinical trials but chose not to disclose them in warning labels. Overdose
Finasteride has been studied in humans at single doses of up to 400 mg and at continuous dosages of up to 80 mg/day for three months, without adverse effects observed. There is no specific recommended antidote for finasteride overdose.
Interactions
No significant drug interactions have been observed between finasteride and a limited selection of medications. Pharmacology
Pharmacodynamics
Finasteride is a 5α-reductase inhibitor. It is specifically a selective inhibitor of the type II and III isoforms of the enzyme. By inhibiting these two isozymes of 5α-reductase, finasteride reduces the formation of the potent androgen dihydrotestosterone (DHT) from its precursor testosterone in certain tissues in the body such as the prostate gland, skin, and hair follicles. As such, finasteride is a type of antiandrogen, or more specifically, an androgen synthesis inhibitor. However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the androgen receptor.Finasteride results in a decrease of circulating DHT levels by about 65 to 70% with an oral dosage of 5 mg/day and of DHT levels in the prostate gland by up to 80 to 90% with an oral dosage of 1 or 5 mg/day. In parallel, circulating levels of testosterone increase by approximately 10%, while local concentrations of testosterone in the prostate gland increase by about 7-fold and local testosterone levels in hair follicles increase by around 27 to 53%. An oral dosage of finasteride of only 0.2 mg/day has been found to achieve near-maximal suppression of DHT levels (68.6% for 0.2 mg/day relative to 72.2% for 5 mg/day).