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 Table of Contents  
Year : 2020  |  Volume : 4  |  Issue : 1  |  Page : 1-11

A bird's eye view of common antiandrogens used by dermatologists

Department of Dermatology, IQ City Medical College, Durgapur, West Bengal, India

Date of Submission01-Feb-2019
Date of Decision23-Sep-2019
Date of Acceptance18-Nov-2019
Date of Web Publication06-Jan-2020

Correspondence Address:
Aditya Kumar Bubna
Department of Dermatology, IQ City Medical College, Sovapur, Bijra Road, Jemua, Durgapur - 713 206, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CDR.CDR_5_19

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The use of antiandrogens is gaining significance in dermatology practice these days. Though once considered a domain of endocrinologists and gynecologists, these drugs now constitute an important category while treating a number of dermatologic conditions. A thorough knowledge of these drugs, as well as their applications in dermatology would therefore be of immense value for the practicing dermatologist. This review will throw a bird's eye view on the salient aspects of these drugs and their importance in those conditions, where their usage in applicable.

Keywords: Cyproterone acetate, dutasteride, finasteride, flutamide, spironolactone

How to cite this article:
Bubna AK. A bird's eye view of common antiandrogens used by dermatologists. Clin Dermatol Rev 2020;4:1-11

How to cite this URL:
Bubna AK. A bird's eye view of common antiandrogens used by dermatologists. Clin Dermatol Rev [serial online] 2020 [cited 2023 Jan 31];4:1-11. Available from: https://www.cdriadvlkn.org/text.asp?2020/4/1/1/275247

  Introduction Top

Antiandrogens are a class of drugs that have found to be useful in treating a number of dermatologic conditions. They are broadly classified into three categories.

  • Androgen receptor antagonists: These include spironolactone (SPL), flutamide (FD), cyproterone acetate (CA), and cimetidine. These drugs act on androgen receptors and block effects of circulating androgens
  • Androgen synthesis inhibitors: These include drugs such as finasteride (FT) and dutasteride (DT). They act by lowering androgen levels by other mechanisms
  • Antigonadotrophins: These include gonadotropin-releasing hormone (GnRH) modulators, estrogens, and progestogens.[1]

There are a number of dermatologic conditions where these drugs have been utilized and include hirsutism, acne (particularly the hormonal variant), androgenetic alopecia, hidradenitis suppurativa, and frontal fibrosing alopecia (FFA).

  Hirsutism Top

Hirsutism presents as excessive terminal hair growth in women at locations where hair is normally minimal or absent. Hirsutism can be androgenic or non-androgenic. Polycystic ovarian syndrome (PCOS) is a major contributor of androgenic hirsutism. Other causes include androgen-secreting tumors, non-classic adrenal hyperplasia, and syndromes of severe insulin resistance. However, in some patients, no etiology is identifiable, and these patients are labeled to have idiopathic hirsutism.[1]

Various drugs have been utilized by dermatologists to treat this condition and include SPL, FD, cyproterone acetate, FT, and GnRH analogs.


SPL in hirsutism acts as a competitive antagonist for cytosolic androgenic receptors and causes reduction in the concentration of cytochrome P450 in the gonads. Further, at higher doses, it also inhibits 17-β hydroxylase and 17, 20 desmolase adrenal activities.[2]

Prior to starting SPL, the cause of hirsutism needs to be ascertained. In those cases of hirsutism secondary to PCOS, congenital adrenal hyperplasia (CAH) or idiopathic hirsutism; SPL can be considered.

SPL can be given either at low dosing or high dosing for this indication and the decision is best left to the treating dermatologist.

For the high dosing schedule, a daily dose of 100–200 mg of SPL is administered. In most cases, the duration of treatment generally extends for 9-12 months. Combining SPL with oral contraceptives (OCs) or with dexamethasone may also prove beneficial here.[3]

In low-dose therapy, SPL given at a dose of 50 mg from day 4 to day 22 of the menstrual cycle, over 12 consecutive cycles, has demonstrated to reduce the concentration of total and free levels of testosterone.[4]

On comparing FT with SPL in treating hirsutism, SPL proved superior. However, FD was more efficacious than SPL for treating hirsutism.[5],[6]


FD is a pure anti-androgen, with little or no measurable interaction with any of the other steroid hormone receptors. Although not commonly employed in the dermatological set up for treating hirsutism owing to its toxicity profile, it is indeed a very valuable drug for this indication. Various guidelines have been proposed for the use of FD in hirsutism and have been tabulated in [Table 1].
Table 1: Guidelines for flutamide in hirsutism

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Though the standard recommended dose of FD in hirsutism ranges from 62.5 to 500 mg/day,[7],[8],[9] de Zegher and Ibáñez [10] have suggested that FD dosed at 1 mg/kg/day could be a better alternative because this dosing could help balance between its antiandrogenic efficacy and hepatic safety for women and adolescent girls with hirsutism or other androgen-related symptoms. Therapy is generally long term ranging from 6 months to 1 year, and therefore, careful monitoring of the drug is mandated.[11]

Although other antiandrogens are considered a safer alternative than FD, Cusan et al.[6] in their study demonstrated that FD is more effective than SPL in hirsute women treated with OC pills (OCPs) plus antiandrogens.

Cyproterone acetate

CA is a strong progestin, resulting in a decrease in circulating testosterone and androstenedione levels through a decrease in circulating luteinizing hormone levels. It further antagonizes the effect of androgens at the peripheral level and is an effective agent for treating hirsutism. CA has been utilized in various dosing schedules for treating hirsutism, the details of which have been elaborated in [Table 2].
Table 2: Studies demonstrating the efficacy of cyproterone acetate in hirsutism

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In some cases of hirsutism, FT has also been of benefit. It has been suggested that increase in 5α reductase activity in hair follicles of hirsute women may be responsible for this clinical outcome, and thus the role of FT.[15] It has been clearly demonstrated that FT at a dose of 5 mg/day taken for 6 months is equally effective as SPL (100 mg/day) and FD (250 mg/day).[15]

The efficacy of 5 mg/day of FT in idiopathic hirsutism and hirsutism secondary to PCOS has further been elaborated by Faloia et al.[16] and Lakrye et al.[17]

Gonadotropin-releasing hormone agonists

GnRH agonists like leuprolide given parenterally as a depot (3.75 mg/month), has been of value in those severe hirsute patients not responding to OCs and antiandrogens.[18] Two to three months of treatment may be required for the full suppressive effect of the agonist to occur. Long-acting GnRH analogs decrease gonadotropin secretion and therefore reduce ovarian stimulation and hence testosterone. However, estrogen production is also reduced with this therapy and therefore concomitant usage of OCPs containing estrogen and progestin is recommended.[19]

  Acne Top

Antiandrogens are of particular value in treating acne when faced with the following presentations:[20]

  • In females with late-onset or persistent acne with or without signs of hyperandrogenism
  • In females not responding to conventional therapy and unwilling to take or cannot take oral isotretinoin (ISO)
  • In females where acne flares coincide with menses
  • In females where OCs cannot be used but require antiandrogens as part of their acne regimen
  • Women with acne tarda or sudden onset acne vulgaris after 25 years of age
  • Women also presenting with clinical signs like hirsutism, androgenic alopecia and seborrhea with acne vulgaris (SAHA syndrome)
  • The predominance of inflammatory papules concentrated along the lower half of the cheeks, jawline, chin, and lateral neck.

In most patients presenting with the above quality of acne, other associations like menstrual irregularities, hirsutism, and androgenetic alopecia may also be observed. Though these features correlate with a high androgenic state in many patients, the circulating levels of androgens may be normal. Nevertheless, it is mandatory to evaluate the hormonal profile in all such patients to rule out the two most important disorders associated with excess levels of circulating androgens, namely PCOS and CAH.[20]


SPL, in this setting, decreases 5α reductase activity via increased clearance of testosterone secondary to augmented liver hydroxylase activity. Furthermore, SPL increases the level of sex hormone-binding globulin (SHBG), thereby providing a sink that reduces free testosterone as more of it gets bound to SHBG. This facilitates in reducing free testosterone in the circulation and an increased estrogenic state thus. In addition, SPL also competes with dihydrotestosterone (DHT) for cutaneous androgen receptors thereby antagonizing the binding of testosterone and DHT to these receptors.[21],[22],[23]

For hormonal acne (HA), SPL can be used as monotherapy or in combination with OCs, oral antibiotics, and ISO.[24]

SPL is preferred as monotherapy in those women who are intolerant to OCs and are at an increased risk of developing thromboembolism or stroke following intake of OCs, or in those women who do not want OC induced melasma to occur.[24]

The dose of SPL employed ranges from 25 to 200 mg/day. The author feels, it is best to start at a lower dosing, generally 50–100 mg/day, and if mandated, the dose could be escalated depending upon the clinical requirement. Even at lower doses, SPL is effective in reducing seborrhea, which in turn heralds reduction in the number and size of acne lesions. The response to therapy with SPL is usually evident after 3 months of initiation of treatment with SPL.[25],[26],[27]

Apart from its beneficial role in facial acne SPL has also shown to be effective in truncal acne.[28]

Once the desired endpoint of control of acne lesions has been obtained, maintenance dosing of SPL ranging from 25 to 50 mg/day maybe particularly beneficial in those women who tend to have sporadic outbreaks of inflammatory or isolated nodulocystic lesions.[29]

When SPL is used with OCs there usually is an added benefit in improving acne lesions along with alleviating concerns about unwanted pregnancy while taking SPL. Use of OCs along with SPL also reduces menstrual-related side effects like irregular menses and breast tenderness both of which is commonly seen with SPL monotherapy, especially in high doses. Further, combining OCs with SPL enables lower doses of SPL to be dispensed without compromising its efficacy.[30]

OCs containing EE (20 mcg or 30 mcg) with drosiperone 3 mg or EE (35 mcg) with CA 2 mg can be used along with SPL. A 3 mg dose of drosiperone has been reported to be equivalent to 25 mg of SPL, and therefore, regular monitoring of serum potassium maybe required when administering SPL along with drosiperone containing OCs. However, no significant adverse effects have ever occurred with this combination, and this combination has a good safety profile.

SPL can also be combined with most antibiotics for acne, namely minocycline, tetracycline, and erythromycin.[29] The combination definitely is associated with better overall clinical outcome. It must be however be remembered that topical benzoyl peroxide is of value in these combinations to reduce the risk of emergence of antibiotic-resistant strain of Propionibacterium acnes. Other antibiotics combined with SPL include amoxicillin and co-trimoxazole.[31] However, co-trimoxazole has been associated with hyperkalemia, and therefore, its combination with SPL should be used with caution and only as a last resort if at all necessary.[32],[33]

In severe cases of nodulocystic acne, not responding to oral ISO alone, addition of SPL at an initial dose of 100 mg/day and gradually escalating the dose to 200 mg/day if needed has demonstrated beneficial effects in bringing about regression of acne lesions. Once the desired benefit is obtained, the dose of SPL is generally reduced to 50 mg/day as a maintenance dosing.[24]

Also, topical 5% SPL has been used in Europe for grade II acne with a similar efficacy compared to topical therapy with antibiotic agents.[34] Further, topical SPL gel when used along with topical corticosteroids has been found effective in limiting glucocorticoid-induced epidermal activity by blocking mineralocorticoid receptors.[35] However, this concept needs further exploration.


FD has been purported as a potential therapy for HA owing to its antiandrogenic effects. Few studies have indicated the beneficial properties of FD in HA. Carmina and Lobo [36] in 2002 demonstrated that FD has similar efficacy to ethinyl estradiol and CA in 48 hyperandrogenic women.

Similarly, in 2011, Paradisi et al.[37] demonstrated the clinical efficacy of low dose FD over a 6-years period. However, FD needs to be cautiously used given its potential for hepatotoxicity.[37]

Cyproterone acetate

CA 2 mg along with EE 35 mcg has been used in the management of HA. In adult females, when acne is resistant to conventional therapy, a possible existing hormonal etiology requires evaluation. Treatment needs to be continued for at least 1 year with periodicc assessments.[38] Improvement of acne is noticeable within 3 months of initiation of therapy.

It can also be combined with ISO in some cases.

If CA is being used alone in acne without being combined with EE, it should begin on the 1st or 5th day of the menstrual cycle and should be stopped on day 14 just before ovulation.[39] When used alone, the recommended dose of CA is 50–100 mg/day. Studies have shown that overall improvement of acne can be witnessed in 75%–90% cases.[40],[41]

CA inhibits conversion of DHEA to androstenedione by 3 β-hydroxysteroid dehydrogenase, decreasing the production of adrenal androgens. CA also inhibits the production of follicle stimulating hormone and luteinizing hormone which blocks ovarian function and reduces serum levels of androgens. Further, CA also reduces comedones indirectly by an increase in the sebaceous linolenic acid concentration.[42]

Gruber et al.[43] have utilized topical CA in a liposomal lotion consisting of soyabean oil, lecithin, glycerol, and oleic acid containing 20 mg of CA in 10 ml of the liposomal lotion used. They found that after 3 months of topical usage, the lesion counts had decreased from a mean of 35.9 to 9.1, thereby suggesting this to be a valuable modality of treating HA. Whether topical CA acts directly on the skin or whether serum levels of CA (though low with topical therapy), are responsible for the effect needs to be determined in future studies.


In some women with hormonal acne having normal levels of free serum testosterone, no clinical improvements can be reached with classical antiandrogens and ISO. In some of these women, there could be an underlying excessive activity of the enzyme 5α reductase making the use of FT, a valuable option in these cases. The dose of FT here is 5 mg/day.[44]

  Androgenetic Alopecia Top

AGA is a common genetically determined disorder affecting both men and women and is characterized by the gradual conversion of terminal hairs into indeterminate and finally into vellus hairs. There are a number of drugs used in its treatment and have been described below.


Oral FT (1 mg/day) has been approved by the US FDA since December 1997 for the treatment of AGA in males. Regarding the use of FT in women for AGA, its efficacy has not been established and is used as an off label treatment with doses ranging from 2.5 to 5 mg/day.[45],[46],[47]

In AGA in males, it has been concluded that:

  • The daily use of oral FT increases hair count and improves patient and investigator assessment of hair appearance [48]
  • Long term use of FT for up to 5 years has shown to decrease the likelihood of developing further invisible hair loss [49]
  • If FT is started at a younger age, responses obtained are superior [50]
  • In cases where adequate responses are not observed even after 1 year of FT therapy, long term continuation of the drug is associated with a positive trend in bringing about hair growth [51]
  • Combination therapy of oral FT with minoxidil and ketoconazole shows a better response than either drugs being used as monotherapy.[52]

The efficacy of topical FT has also been documented in AGA. Tanglertsampan [53] has compared the efficacy of 3% minoxidil versus 3% minoxidil and 0.1% FT in AGA. A significant improvement was demonstrable in the group obtaining both topical drugs.

Hajheydari et al.[54] have also demonstrated the beneficial properties of topical 1% FT gel applied twice daily.

Topical FT therefore could be considered a valuable maintenance option once initial improvement with oral FT occurs, because of its property of maintaining hair density. This would also prevent in the indefinite use of oral FT.[55]

Evidence, however, for topical formulations of FT is scanty, requiring more systematic documentation in further studies.

In patients who are apprehensive about the side effects of FT, it could be worthwhile considering administration of lower/staggered doses of FT to enhance patient compliance. As the t1/2 of FT is 6–8 h and its tissue binding remains for 4–5 days,[56] a dose of 0.2 mg is adequate enough to suppress DHT levels. It has been seen that while 0.2 mg caused 55% suppression of DHT, 5 mg achieved 69% suppression.[57],[58] Therefore, in such patients, the drug maybe started at 0.5 mg/day for a short term period. This would enable gaining patient confidence, following which 1 mg/day of FT can be started once the patient is comfortable. However, this suggestion of stepping up the dose of FT is only an opinion of experts.[59]

In female pattern hair loss (FPHL) the mechanism of FT is still unclear. In those patients who fail minoxidil therapy or cannot tolerate minoxidil therapy, FT can be tried. Although data is sparse, menopausal status, circulating androgen concentrations, and concomitant symptoms of hyperandrogenism do not appear to predict a response to FT.

FT is generally well-tolerated in women. However, in women with childbearing potential, owing to the teratogenic effects of FT, adherence to a reliable method of contraception is mandatory.[60] Price et al.[61] in 2000, demonstrated that FT given at 1 mg/day for FPHL was ineffective in increasing hair growth or improving the appearance of hair. Given the lack of clinical efficacy with this dosing, higher dosing of FT ranging from 2.5 to 5 mg/day have been advocated. This dosing has demonstrated clinical efficacy in postmenopausal women in the absence of clinical or laboratory signs of hyperandrogenism.[62],[63] However, there is limited evidence for the use of FT at higher dosages for treating FPHL in postmenopausal women. FT is usually a useful option in those cases of FPHL which have failed other therapies.


There have been no randomized trials in evaluating the efficacy of SPL in FPHL, but case reports and series have been described.

Adamopoulos et al.[64] demonstrated that SPL at a daily dose of 200 mg reduced hair loss by 60% and also increased the number of anagen hairs.

Sinclair et al.[65] in an open-label comparative study of 80 women with biopsy-proven FPHL using either SPL 200 mg/day or CA 50mg/day depicted both therapies to be equally effective.

Further, when SPL 200 mg once daily is combined with 5% topical minoxidil twice daily application, for FPHL, it acts as an effective adjunct to stimulate hair growth if a plateau has been reached with topical minoxidil monotherapy.[66]


DT (0.5 mg/day) though not approved by the FDA for AGA, has shown to be more superior than FT (1 mg/day) in men. In various studies, the positive effects of DT have been demonstrated. Some of them have been summarized in [Table 3].
Table 3: Various studies demonstrating the beneficial effects of systemic dutasteride in androgenic alopecia

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Further, DT has also been utilized as mesotherapy in AGA. Mesotherapy schedules require frequent treatment sessions and that could be a limiting factor in patient adherence. Various studies utilizing DT mesotherpay for AGA has been summarized in [Table 4].
Table 4: Various studies utilizing dutasteride mesotherapy for androgenetic alopecia

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The reason why DT mesotherapy has been considered to be as efficacious as oral therapy is because systemic absorption after mesotherapy is almost similar to oral DT because of the highly vascular scalp.


FD has been shown to be effective in treating FPHL in women who have associated hyperandrogenism. The dose of FD for this indication is 250 mg/day. Carmina and Lobo [73] demonstrated that FD led to greater improvements in stemming hair loss after 1 year of treatment when compared to FT and CA.

Similarly, Sinclair et al.[65] found a significant treatment advantage for FD over SPL with regard to slowing or halting hair loss, reduction of total acne and seborrhea and also in treating hirsutism.

Further, Paradisi et al.[37] noticed in 80% of their study patients with FPHL after 2 years of therapy with FD that most of them were satisfied or highly satisfied regardless of whether they were consuming OCPs or not.

Cyproterone acetate

A number of studies have suggested the role of CA in AGA with some suggesting that this role is greater in patients with evidence of hyperandrogenism.

Brzezińska-Wcisło [74] in a study of 25 subjects aged between 31 and 35 years where CA 2 mg and EE 35 mcg was administered for FPHL, clearly demonstrated reduction in hair loss, hair thinning and seborrhea.

Lucky et al.[75] in 20 patients with FPHL, administered 50 mcg of EE and 2 mg of CA along with an additional 20 mg of CA on days 5–20 of the menstrual cycle. The authors concluded that though reduction in hair shedding was noticed, actual increased hair growth was not appreciated.

Vexiau et al.[76] in a 12-month randomized comparative trial of 2% minoxidil and combined OCPs in 33 patients; and 52 mg of CA along with 35 mcg of EE for 20 days of every 28 days in another 33 patients, found that CA was more effective in those patients who demonstrated features of hyperandrogenism along with an elevated body mass index, whereas 2% minoxidil was effective in those patients without evidence of clinical and biochemical hyperandrogenism.

Futterweit et al.[77] compared SPL with CA in 80 women with biopsy-confirmed FPHL. It was found that in 88% of individuals, there was improvement with no progression of hair loss and no significant difference in the efficacy of both medications.

However, in a randomized study by Carmina and Lobo,[36] CA failed to demonstrate therapeutic benefit in FPHL.

However, given the balance of evidence, CA does have a role in FPHL associated with hyperandrogenism.

Though doses utilized vary, it appears that CA 100 mg/day on days 5–15 of the menstrual cycle supplemented with EE 50 mcg/day on days 5–25 of the cycle appears to be the most effective dosing schedule of CA for AGA.[78]

  Hidradenitis Suppurativa Top

HS is an inflammatory disease of the skin occurring as a reaction pattern of the skin dependant on the patients inherent and specific risk factors in a setting of predisposing genetic factors and inflammation.[79] It is commonly seen in postpubertal young adults and has a diverse spectrum of presentation including comedones, folliculitis, abscesses, scars and disfiguring tracts and fistulas. Currently, HS is considered to be a disease of follicular pathology rather than apocrinitis.


In HS, FT is employed owing to its ability to reduce local concentrations of DHT at the level of hair follicles by altering end-organ sensitivity rather than a systemic effect on circulating androgens.[80]

As HS is now identified to be a disorder secondary to inflammation of the terminal follicular epithelium, inhibition of 5α reductase brings about reduction of local concentrations of DHT at the level of the hair follicles and thereby reducing target tissue concentrations of androgens.[81] The precise mechanism of FT in HS, however is speculative, since it has not been confirmed conclusively in any study, and confounded by the difficulty of measuring tissue and intercellular levels DHT, as circulating levels may not be an accurate assessment.[82]

FT has been employed at a dose of 5 mg/day with dramatic improvement in HS. Some of the published reports have been elucidated in [Table 5].
Table 5: Some reports demonstrating the valuable effects of finasteride in hidradenitis suppurativa

Click here to view

It has been clearly seen that FT in HS has been effective both as monotherapy and as adjunctive therapy. In most cases, however, FT was advocated in more advanced disease where multiple regimens were unsuccessful. No documented cases have been found where FT was introduced early in disease management in adults. However, in a 7-year-old girl FT was employed within a year of disease onset with excellent outcomes. It has been postulated that if an effective drug is used early in HS, presumably during puberty, the disease-modifying effect would be superior, and could be a potential avenue for further evaluation.[81]

Both finite and continuous regimens of FT for HS have been reported. Joseph et al.[80] used a finite regimen discontinuing the drug within a month of healing. Recurrences did occur following a month of drug cessation. This could be explained on the grounds of the chronic nature of HS.

Continuous therapy exceeding 6 years have also been utilized. Both finite and continuous regimens with FT have demonstrated benefits. Finite regimens have been associated with prolonged remissions whereas the continuous regimens demonstrate reduced intensity and frequency of recurrences.[80],[81] Owing to the limited data available for the use of FT, the exact regimen and duration of treatment still cannot be completely ascertained.


SPL has been effective at a dose of 100–125 mg daily after 3–6 months of therapy in patients with mild to moderate HS.[85]

  Frontal-Fibrosing Alopecia Top

Georgala et al.[86] have reported a positive response with oral DT (0.5 mg/day) on a daily basis for a year in 13 patients with FFA. FFA is considered to be an anatamoclinical form of lichen planopilaris with selective topography.[87],[88] FFA has been treated earlier with FT (2.5 mg/day) combined with 2% minoxidil, and there was a halt in disease progression as demonstrated by Tosti et al.[88]

Further, Katoulis et al.[89] have also demonstrated significant re-growth of eyebrows and axillary hair in postmenopausal patients with FFA and a moderate improvement in frontotemporal scalp hair in postmenopausal women following treatment with DT (0.5 mg/day) and topical 1% pimecrolimus cream for 3 months.

Given the tendency of FFA for spontaneous stabilization some of the apparent responses may be considered to be the natural course of the disease process. Therefore DT needs to be further evaluated with more randomized controlled trials for the same.

  Conclusion Top

Through this review we do observe the utility of antiandrogens in a variety of dermatologic conditions. Certain side effects like hepatotoxicity and hyperkalemia associated with FD and SPL respectively should be carefully monitored to ensure patient safety while on these drugs. Other drugs like FT, DT, and CA are relatively safer. With a change in the profile of a number of disorders, for example, acne, it would be prudent for any dermatologist to have a fairly good knowledge regarding these drugs.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Agrawal NK. Management of hirsutism. Indian J Endocrinol Metab 2013;17:S77-82.  Back to cited text no. 1
Tremblay RR. Treatment of hirsutism with spironolactone. Clin Endocrinol Metab 1986;15:363-71.  Back to cited text no. 2
Cumming DC. Use of spironolactone in treatment of hirsutism. Cleve Clin J Med 1990;57:285-7.  Back to cited text no. 3
Ylöstalo P, Heikkinen J, Kauppila A, Pakarinen A, Järvinen PA. Low-dose spironolactone in the treatment of female hirsutism. Int J Fertil 1987;32:41-5.  Back to cited text no. 4
Erenus M, Yücelten D, Durmuşoǧlu F, Gürbüz O. Comparison of finasteride versus spironolactone in the treatment of idiopathic hirsutism. Fertil Steril 1997;68:1000-3.  Back to cited text no. 5
Cusan L, Dupont A, Gomez JL, Tremblay RR, Labrie F. Comparison of flutamide and spironolactone in the treatment of hirsutism: A randomized controlled trial. Fertil Steril 1994;61:281-7.  Back to cited text no. 6
Martin KA, Anderson RR, Chang RJ, Ehrmann DA, Lobo RA, Murad MH, et al. Evaluation and treatment of hirsutism in premenopausal women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2018;103:1233-57.  Back to cited text no. 7
ACOG Committee on Practice Bulletins--Gynecology. ACOG practice bulletin No. 108: polycystic ovary syndrome. Obstet Gynecol 2009;114:936-49.  Back to cited text no. 8
Escobar-Morreale HF, Carmina E, Dewailly D, Gambineri A, Kelestimur F, Moghetti P, et al. Epidemiology, diagnosis and management of hirsutism: A consensus statement by the androgen excess and polycystic ovary syndrome society. Hum Reprod Update 2012;18:146-70.  Back to cited text no. 9
de Zegher F, Ibáñez L. Therapy: Low-dose flutamide for hirsutism: Into the limelight, at last. Nat Rev Endocrinol 2010;6:421-2.  Back to cited text no. 10
Moghetti P, Castello R, Negri C, Tosi F, Magnani CM, Fontanarosa MC, et al. Flutamide in the treatment of hirsutism: long-term clinical effects, endocrine changes, and androgen receptor behavior. Fertil Steril 1995;64:511-7.  Back to cited text no. 11
Ylöstalo P, Laakso L, Viinikka L, Ylikorkala O, Vihko R. Cyproterone acetate in the treatment of hirsutism. Acta Obstet Gynecol Scand 1981;60:399-401.  Back to cited text no. 12
Barth JH, Cherry CA, Wojnarowska F, Dawber RP. Cyproterone acetate for severe hirsutism: Results of a double-blind dose-ranging study. Clin Endocrinol (Oxf) 1991;35:5-10.  Back to cited text no. 13
Holdaway IM, Croxson MS, Ibbertson HK, Sheehan A, Knox B, France J. Cyproterone acetate as initial treatment and maintenance therapy for hirsutism. Acta Endocrinol (Copenh) 1985;109:522-9.  Back to cited text no. 14
Moghetti P, Tosi F, Tosti A, Negri C, Misciali C, Perrone F, et al. Comparison of spironolactone, flutamide, and finasteride efficacy in the treatment of hirsutism: A randomized, double blind, placebo-controlled trial. J Clin Endocrinol Metab 2000;85:89-94.  Back to cited text no. 15
Faloia E, Filipponi S, Mancini V, Di Marco S, Mantero F. Effect of finasteride in idiopathic hirsutism. J Endocrinol Invest 1998;21:694-8.  Back to cited text no. 16
Lakryc EM, Motta EL, Soares JM Jr., Haidar MA, de Lima GR, Baracat EC. The benefits of finasteride for hirsute women with polycystic ovary syndrome or idiopathic hirsutism. Gynecol Endocrinol 2003;17:57-63.  Back to cited text no. 17
Pazos F, Escobar-Morreale HF, Balsa J, Sancho JM, Varela C. Prospective randomized study comparing the long-acting gonadotropin-releasing hormone agonist triptorelin, flutamide, and cyproterone acetate, used in combination with an oral contraceptive, in the treatment of hirsutism. Fertil Steril 1999;71:122-8.  Back to cited text no. 18
Sachdeva S. Hirsutism: Evaluation and treatment. Indian J Dermatol 2010;55:3-7.  Back to cited text no. 19
[PUBMED]  [Full text]  
Elsaie ML. Hormonal treatment of acne vulgaris: An update. Clin Cosmet Investig Dermatol 2016;9:241-8.  Back to cited text no. 20
Thiboutot D, Harris G, Iles V, Cimis G, Gilliland K, Hagari S. Activity of the type 1 5 alpha-reductase exhibits regional differences in isolated sebaceous glands and whole skin. J Invest Dermatol 1995;105:209-14.  Back to cited text no. 21
Burke BM, Cunliffe WJ. Oral spironolactone therapy for female patients with acne, hirsutism or androgenic alopecia. Br J Dermatol 1985;112:124-5.  Back to cited text no. 22
Goulden V, Clark SM, Cunliffe WJ. Post-adolescent acne: A review of clinical features. Br J Dermatol 1997;136:66-70.  Back to cited text no. 23
Kim GK, Del Rosso JQ. Oral spironolactone in post-teenage female patients with acne vulgaris: Practical considerations for the clinician based on current data and clinical experience. J Clin Aesthet Dermatol 2012;5:37-50.  Back to cited text no. 24
Thiboutot D. Acne: Hormonal concepts and therapy. Clin Dermatol 2004;22:419-28.  Back to cited text no. 25
Akamatsu H, Zouboulis CC, Orfanos CE. Spironolactone directly inhibits proliferation of cultured human facial sebocytes and acts antagonistically to testosterone and 5 alpha-dihydrotestosterone in vitro. J Invest Dermatol 1993;100:660-2.  Back to cited text no. 26
Thiboutot D, Chen W. Update and future of hormonal therapy in acne. Dermatology 2003;206:57-67.  Back to cited text no. 27
Goodfellow A, Alaghband-Zadeh J, Carter G, Cream JJ, Holland S, Scully J, et al. Oral spironolactone improves acne vulgaris and reduces sebum excretion. Br J Dermatol 1984;111:209-14.  Back to cited text no. 28
Shaw JC. Low-dose adjunctive spironolactone in the treatment of acne in women: a retrospective analysis of 85 consecutively treated patients. J Am Acad Dermatol 2000;43:498-502.  Back to cited text no. 29
Shaw JC. Spironolactone in dermatologic therapy. J Am Acad Dermatol 1991;24:236-43.  Back to cited text no. 30
Turowski CB, James WD. The efficacy and safety of amoxicillin, trimethoprim-sulfamethoxazole, and spironolactone for treatment-resistant acne vulgaris. Adv Dermatol 2007;23:155-63.  Back to cited text no. 31
Velázquez H, Perazella MA, Wright FS, Ellison DH. Renal mechanism of trimethoprim-induced hyperkalemia. Ann Intern Med 1993;119:296-301.  Back to cited text no. 32
Antoniou T, Gomes T, Juurlink DN, Loutfy MR, Glazier RH, Mamdani MM. Trimethoprim-sulfamethoxazole-induced hyperkalemia in patients receiving inhibitors of the renin-angiotensin system: A population-based study. Arch Intern Med 2010;170:1045-9.  Back to cited text no. 33
Califano L, Cannavò S, Siragusa M, Girardi R. Experience in the therapy of acne with topical administration of spironolactone as an antiandrogen. Clin Ter 1990;135:193-9.  Back to cited text no. 34
Maubec E, Laouénan C, Deschamps L, Nguyen VT, Scheer-Senyarich I, Wackenheim-Jacobs AC, et al. Topical mineralocorticoid receptor blockade limits glucocorticoid-induced epidermal atrophy in human skin. J Invest Dermatol 2015;135:1781-9.  Back to cited text no. 35
Carmina E, Lobo RA. Treatment of hyperandrogenic alopecia in women. Fertil Steril 2003;79:91-5.  Back to cited text no. 36
Paradisi R, Porcu E, Fabbri R, Seracchioli R, Battaglia C, Venturoli S. Prospective cohort study on the effects and tolerability of flutamide in patients with female pattern hair loss. Ann Pharmacother 2011;45:469-75.  Back to cited text no. 37
Hammerstein J, Meckies J, Leo-Rossberg I, Moltz L, Zielske F. Use of cyproterone acetate (CPA) in the treatment of acne, hirsutism and virilism. J Steroid Biochem 1975;6:827-36.  Back to cited text no. 38
Thiboutot DM. Endocrinological evaluation and hormonal therapy for women with difficult acne. J Eur Acad Dermatol Venereol 2001;15 Suppl 3:57-61.  Back to cited text no. 39
van Wayjen RG, van den Ende A. Experience in the long-term treatment of patients with hirsutism and/or acne with cyproterone acetate-containing preparations: efficacy, metabolic and endocrine effects. Exp Clin Endocrinol Diabetes 1995;103:241-51.  Back to cited text no. 40
Gollnick H, Albring M, Brill K. The effectiveness of oral cyproterone acetate in combination with ethinylestradiol in acne tarda of the facial type. Ann Endocrinol (Paris) 1999;60:157-66.  Back to cited text no. 41
Stewart ME, Greenwood R, Cunliffe WJ, Strauss JS, Downing DT. Effect of cyproterone acetate-ethinyl estradiol treatment on the proportions of linoleic and sebaleic acids in various skin surface lipid classes. Arch Dermatol Res 1986;278:481-5.  Back to cited text no. 42
Gruber DM, Sator MO, Joura EA, Kokoschka EM, Heinze G, Huber JC. Topical cyproterone acetate treatment in women with acne: A placebo-controlled trial. Arch Dermatol 1998;134:459-63.  Back to cited text no. 43
Kohler C, Tschumi K, Bodmer C, Schneiter M, Birkhaeuser M. Effect of finasteride 5 mg (Proscar) on acne and alopecia in female patients with normal serum levels of free testosterone. Gynecol Endocrinol 2007;23:142-5.  Back to cited text no. 44
Thai KE, Sinclair RD. Finasteride for female androgenetic alopecia. Br J Dermatol 2002;147:812-3.  Back to cited text no. 45
Trüeb RM; Swiss Trichology Study Group. Finasteride treatment of patterned hair loss in normoandrogenic postmenopausal women. Dermatology 2004;209:202-7.  Back to cited text no. 46
Iorizzo M, Vincenzi C, Voudouris S, Piraccini BM, Tosti A. Finasteride treatment of female pattern hair loss. Arch Dermatol 2006;142:298-302.  Back to cited text no. 47
Mella JM, Perret MC, Manzotti M, Catalano HN, Guyatt G. Efficacy and safety of finasteride therapy for androgenetic alopecia: A systematic review. Arch Dermatol 2010;146:1141-50.  Back to cited text no. 48
Kaufman KD, Rotonda J, Shah AK, Meehan AG. Long-term treatment with finasteride 1 mg decreases the likelihood of developing further visible hair loss in men with androgenetic alopecia (male pattern hair loss). Eur J Dermatol 2008;18:400-6.  Back to cited text no. 49
Camacho FM, García-Hernández MJ, Fernández-Crehuet JL. Value of hormonal levels in patients with male androgenetic alopecia treated with finasteride: better response in patients under 26 years old. Br J Dermatol 2008;158:1121-4.  Back to cited text no. 50
Rossi A, Cantisani C, Scarno M, Trucchia A, Fortuna MC, Calvieri S. Finasteride 1mg daily administration on male androgenetic alopecia in different age groups: 10 year follow up. Dermatol Ther 2011;24:455-61.  Back to cited text no. 51
Khandpur S, Suman M, Reddy BS. Comparative efficacy of various treatment regimens for androgenetic alopecia in men. J Dermatol 2002;29:489-98.  Back to cited text no. 52
Tanglertsampan C. Efficacy and safety of 3% minoxidil versus combined 3% minoxidil/0.1% finasteride in male pattern hair loss: A randomized, double-blind, comparative study. J Med Assoc Thai 2012;95:1312-6.  Back to cited text no. 53
Hajheydari Z, Akbari J, Saeedi M, Shokoohi L. Comparing the therapeutic effects of finasteride gel and tablet in treatment of the androgenetic alopecia. Indian J Dermatol Venereol Leprol 2009;75:47-51.  Back to cited text no. 54
[PUBMED]  [Full text]  
Chandrashekar BS, Nandhini T, Vasanth V, Sriram R, Navale S. Topical minoxidil fortified with finasteride: An account of maintenance of hair density after replacing oral finasteride. Indian Dermatol Online J 2015;6:17-20.  Back to cited text no. 55
[PUBMED]  [Full text]  
Leyden J, Dunlap F, Miller B, Winters P, Lebwohl M, Hecker D, et al. Finasteride in the treatment of men with frontal male pattern hair loss. J Am Acad Dermatol 1999;40:930-7.  Back to cited text no. 56
Anitha B, Inamadar AC, Ragunatha S. Finasteride-its impact on sexual function and prostate cancer. J Cutan Aesthet Surg 2009;2:12-6.  Back to cited text no. 57
[PUBMED]  [Full text]  
Drake L, Hordinsky M, Fiedler V, Swinehart J, Unger WP, Cotterill PC, et al. The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia. J Am Acad Dermatol 1999;41:550-4.  Back to cited text no. 58
Mysore V, Shashikumar BM. Guidelines on the use of finasteride in androgenic alopecia. Indian J Dermatol Venereol Leprol 2016;82:128-34.  Back to cited text no. 59
[PUBMED]  [Full text]  
Stout SM, Stumpf JL. Finasteride treatment of hair loss in women. Ann Pharmacother 2010;44:1090-7.  Back to cited text no. 60
Price VH, Roberts JL, Hordinsky M, Olsen EA, Savin R, Bergfeld W, et al. Lack of efficacy of finasteride in postmenopausal women with androgenetic alopecia. J Am Acad Dermatol 2000;43:768-76.  Back to cited text no. 61
Yeon JH, Jung JY, Choi JW, Kim BJ, Youn SW, Park KC, et al. 5 mg/day finasteride treatment for normoandrogenic Asian women with female pattern hair loss. J Eur Acad Dermatol Venereol 2011;25:211-4.  Back to cited text no. 62
Trüeb RM, Swiss Trichology Study Group. Finasteride treatment of patterned hair loss in normoandrogenic postmenopausal women. Dermatology 2004;209:202-7.  Back to cited text no. 63
Adamopoulos DA, Karamertzanis M, Nicopoulou S, Gregoriou A. Beneficial effect of spironolactone on androgenic alopecia. Clin Endocrinol (Oxf) 1997;47:759-60.  Back to cited text no. 64
Sinclair R, Wewerinke M, Jolley D. Treatment of female pattern hair loss with oral antiandrogens. Br J Dermatol 2005;152:466-73.  Back to cited text no. 65
Hoedemaker C, van Egmond S, Sinclair R. Treatment of female pattern hair loss with a combination of spironolactone and minoxidil. Australas J Dermatol 2007;48:43-5.  Back to cited text no. 66
Shanshanwal SJ, Dhurat RS. Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia: A randomized controlled open-label, evaluator-blinded study. Indian J Dermatol Venereol Leprol 2017;83:47-54.  Back to cited text no. 67
[PUBMED]  [Full text]  
Olsen EA, Hordinsky M, Whiting D, Stough D, Hobbs S, Ellis ML, et al. The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. J Am Acad Dermatol 2006;55:1014-23.  Back to cited text no. 68
Jung JY, Yeon JH, Choi JW, Kwon SH, Kim BJ, Youn SW, et al. Effect of dutasteride 0.5 mg/d in men with androgenetic alopecia recalcitrant to finasteride. Int J Dermatol 2014;53:1351-7.  Back to cited text no. 69
Abdallah MA, El-Zawahry KA, Besar H. Mesotherapy using dutasteride containing solution in male pattern hair loss: A controlled pilot study. J Pan Arab Leag Dermatol 2009;20:137-45.  Back to cited text no. 70
Moftah N, Moftah N, Abd-Elaziz G, Ahmed N, Hamed Y, Ghannam B, et al. Mesotherapy using dutasteride-containing preparation in treatment of female pattern hair loss: Photographic, morphometric and ultrustructural evaluation. J Eur Acad Dermatol Venereol 2013;27:686-93.  Back to cited text no. 71
Sobhy N, Aly H, El Shafee A, El Deeb M. Evaluation of the effect of injection of dutasteride as a mesotherapeutic tool in treatment of androgenic alopecia in males. Our Dermatol Online 2013;4:40-5.  Back to cited text no. 72
Carmina E, Lobo RA. A comparison of the relative efficacy of antiandrogens for the treatment of acne in hyperandrogenic women. Clin Endocrinol (Oxf) 2002;57:231-4.  Back to cited text no. 73
Brzezińska-Wcisło L. Assessment of efficacy of Diane-35 in androgenetic feminine alopecia. Wiad Lek 2003;56:202-5.  Back to cited text no. 74
Lucky AW, Piacquadio DJ, Ditre CM, Dunlap F, Kantor I, Pandya AG, et al. A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss. J Am Acad Dermatol 2004;50:541-53.  Back to cited text no. 75
Vexiau P, Chaspoux C, Boudou P, Fiet J, Jouanique C, Hardy N, et al. Effects of minoxidil 2% vs. cyproterone acetate treatment on female androgenetic alopecia: A controlled, 12-month randomized trial. Br J Dermatol 2002;146:992-9.  Back to cited text no. 76
Futterweit W, Dunaif A, Yeh HC, Kingsley P. The prevalence of hyperandrogenism in 109 consecutive female patients with diffuse alopecia. J Am Acad Dermatol 1988;19:831-6.  Back to cited text no. 77
Dawber RP, Sonnex T, Ralfs I. Oral antiandrogen treatment of common baldness in women. Br J Dermatol 1982;107:20-1.  Back to cited text no. 78
Scheinfeld N. Hidradenitis suppurativa: A practical review of possible medical treatments based on over 350 hidradenitis patients. Dermatol Online J 2013;19:1.  Back to cited text no. 79
Joseph MA, Jayaseelan E, Ganapathi B, Stephen J. Hidradenitis suppurativa treated with finasteride. J Dermatolog Treat 2005;16:75-8.  Back to cited text no. 80
Randhawa HK, Hamilton J, Pope E. Finasteride for the treatment of hidradenitis suppurativa in children and adolescents. JAMA Dermatol 2013;149:732-5.  Back to cited text no. 81
Berck JS. Endocrine disorders. In: Berck and Novak's Gynecology. 15th ed. Philadelphia: Wolter Kluwer Lippincott Williams and Wilkins; 2011. p. 1066.  Back to cited text no. 82
Farrell AM, Randall VA, Vafaee T, Dawber RP. Finasteride as a therapy for hidradenitis suppurativa. Br J Dermatol 1999;141:1138-9.  Back to cited text no. 83
Doménech C, Matarredona J, Escribano-Stablé JC, Devesa JP, Vicente J, Jaén A. Facial hidradenitis suppurativa in a 28-year-old male responding to finasteride. Dermatology 2012;224:307-8.  Back to cited text no. 84
Lee A, Fischer G. A case series of 20 women with hidradenitis suppurativa treated with spironolactone. Australas J Dermatol 2015;56:192-6.  Back to cited text no. 85
Georgala S, Katoulis AC, Befon A, Danopoulou I, Georgala C. Treatment of postmenopausal frontal fibrosing alopecia with oral dutasteride. J Am Acad Dermatol 2009;61:157-8.  Back to cited text no. 86
Moreno-Ramírez D, Ferrándiz L, Camacho FM. Diagnostic and therapeutic assessment of frontal fibrosing alopecia. Actas Dermosifiliogr 2007;98:594-602.  Back to cited text no. 87
Tosti A, Piraccini BM, Iorizzo M, Misciali C. Frontal fibrosing alopecia in postmenopausal women. J Am Acad Dermatol 2005;52:55-60.  Back to cited text no. 88
Katoulis A, Georgala, Bozi E, Papadavid E, Kalogeromitros D, Stavrianeas N. Frontal fibrosing alopecia: treatment with oral dutasteride and topical pimecrolimus. J Eur Acad Dermatol Venereol 2009;23:580-2.  Back to cited text no. 89


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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