Finasterideの意味・使い方・読み方 | Weblio英和辞書
The adverse effect profiles of finasteride are somewhat different for its indications of hair loss and BPH.[]
フィナステリド長期投薬後、ポストフィナステリド症候群(Post-Finasteride
The most common adverse effects of finasteride taken for hair loss are a decrease in sex drive, erectile dysfunction, and a decrease in the amount of semen.
In addition, finasteride has been reported in to cause sexual problems that persist after stopping the medication. A 2012 update to the FDA label noted reports of decreased sex drive, problems with ejaculation and difficulty achieving an erection which continued after stopping the medication. The update also referenced reports of testicular pain and "male infertility and/or poor quality of semen."
プロペシア（フィナステリド）は、AGAの治療薬の1つです。米国FDA（ ..
The most common adverse sexual effects of finasteride for BPH are: trouble getting or keeping an erection, decrease in sex drive, decreased volume of ejaculate, and ejaculation disorders.
A 2010 Cochrane review found that men taking finasteride for BPH (with a mean age of 62.4) are at increased risk for impotence, erectile dysfunction (ED), decreased libido, and ejaculation disorder for the first year of treatment. The rates became indistinguishable from placebo after 2–4 years and these side effects usually got better over time.
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Finasteride may cause persistent adverse sexual, neurological, and physical effects in a subset of men. A 2019 metastudy surveyed the literature on the reversibility of finasteride's side effects. It identified three studies that demonstrated full reversibility of side effects and eleven that described patients with irreversible adverse events. The findings were most convincing in a retrospective review of about 12,000 patients that 1.4% of the cohort developed persistent ED (ED lasting longer than 90 days post-withdrawal).
Reports of long-term, post-discontinuation adverse effects in some fraction of former finasteride users have led to a proposed post-finasteride syndrome (PFS), although some within the medical community question whether there is enough evidence to support a causal relationship between finasteride usage and PFS.
AGA治療薬「プロペシア（フィナステリド）」男性型脱毛症 飲み薬
Individuals claiming to experience PFS report sexual, neurological, hormonal, and psychological side effects that persist for an extended period after stopping the drug. Reported symptoms include penile and tissue changes, and quality, reduced libido, erectile dysfunction, loss of penile sensitivity, decreased orgasm sensation, dry skin, metabolic changes, muscle and strength loss, , depression, anxiety, panic attacks, insomnia, , concentration problems, memory impairment and . A meta-analysis found a significant association between finasteride use and post-discontinuation depression, suicidal ideation, and sexual dysfunction, but the quality of evidence was limited.
Use of finasteride is associated with an increased risk of including , and ejaculatory dysfunction. Sexual adverse effects of finasteride and dutasteride have been linked to lower and ability to maintain an intimate relationship, and can cause stress in relationships.
プロペシア（フィナステリド）とは · 治療から効果までの期間 · クリニック選び ..
As of 2016, Merck was a defendant in approximately 1,370 lawsuits which had been filed by customers alleging they have experienced persistent sexual side effects following cessation of treatment with finasteride. Most cases 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.
フィナステリド（Finasteride）は、男性型脱毛症（AGA）や前立腺肥大症 ..
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 for finasteride overdose.
AGA治療薬のフィナステリドってどんな薬？皮膚科医が解説します。
No significant have been observed between finasteride and a limited selection of medications.
海外で実施された、3,047 例（平均年齢：63 歳）の前⽴腺肥⼤症
Finasteride is a . It is specifically a of the and of the . By inhibiting these two isozymes of 5α-reductase, finasteride reduces the formation of the (DHT) from its in certain in the body such as the , , and . As such, finasteride is a type of , or more specifically, an . However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the .
フィナステリド 1mg｜海外のお薬薬局［H&Bストア公式サイト］
The FDA has added a warning to 5α-reductase inhibitors concerning an increased risk of high-grade , as the treatment of BPH lowers PSA (), which could mask the development of prostate cancer. Although overall incidence of male breast cancer in clinical trials for finasteride 5 mg was not increased, there are post-marketing reports of breast cancer in association with its use, though available evidence does not provide clarity as to whether there is a causative relationship between finasteride and these cancers. A 2018 found no higher risk of breast cancer with 5α-reductase inhibitors. Some men develop (breast development or enlargement) following finasteride usage. The risk of gynecomastia with 5α-reductase inhibitors is low at about 1.5%. Depressive symptoms and suicidality have been reported.
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Finasteride results in a decrease of circulating DHT levels by about 65–70% with an oral dosage of 5 mg/day and of DHT levels in the prostate gland by up to 80–90% 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 27–53%. 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). Finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II ( = 313 nM and 11 nM, respectively). This is in contrast to inhibitors of all three isoenzymes of 5α-reductase like , which can reduce DHT levels in the entire body by more than 99%. In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit (AKR1D1). However, its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than for 5α-reductase ) and hence is unlikely to be of clinical significance.
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By inhibiting 5α-reductase and thus preventing DHT production, finasteride reduces androgen signaling in tissues like the prostate gland and the scalp. In the prostate, this reduces prostate volume, which improves BPH and reduces the risk of prostate cancer. Finasteride reduces prostate volume by 20 to 30% in men with benign prostatic hyperplasia. Inhibition of 5α-reductase also reduces weight, and decreases motility and normal morphology of spermatozoa in the epididymis.
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like (derived from DHT) and (derived from ) activate the in the ; because finasteride prevents the formation of neurosteroids, it functions as a and may contribute to a reduction of GABAA activity. Reduction of GABAA receptor activation by these neurosteroids has been implicated in , , and .
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In accordance with finasteride being a potent 5α-reductase inhibitor but a weak inhibitor of 5β-reductase, the medication decreases circulating levels of 5α-reduced steroids like allopregnanolone but does not reduce concentrations of 5β-reduced steroids like . Pregnanolone acts as a potent GABAA receptor positive allosteric modulator similarly to allopregnanolone.