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Female pattern hair loss (androgenetic alopecia in females): Management

Female pattern hair loss (androgenetic alopecia in females): Management
Author:
Amy McMichael, MD
Section Editor:
Maria Hordinsky, MD
Deputy Editor:
Abena O Ofori, MD
Literature review current through: Jan 2024.
This topic last updated: Dec 21, 2021.

INTRODUCTION — Female pattern hair loss (FPHL; female pattern alopecia, androgenetic alopecia in females) is a common form of nonscarring hair loss that most frequently occurs in adult females and primarily involves the frontal scalp and vertex of the scalp (picture 1A-C). Untreated, FPHL results in a slow, progressive decline in the density of scalp hair but does not typically progress to baldness.

Hair loss related to FPHL can be distressing, and many patients desire treatment. Topical minoxidil; oral antiandrogenic drugs; and other topical, oral, and procedural therapies have been used for FPHL (algorithm 1). Hair transplantation surgery is an option for patients who have inadequate responses to medical therapy.

The management of FPHL will be reviewed here. The pathogenesis, clinical manifestations, and diagnosis of FPHL; the diagnosis and management of male pattern hair loss (androgenetic alopecia in males); and the general evaluation of patients with hair loss are discussed separately.

(See "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis".)

(See "Male pattern hair loss (androgenetic alopecia in males): Pathogenesis, clinical features, and diagnosis".)

(See "Male pattern hair loss (androgenetic alopecia in males): Management".)

(See "Evaluation and diagnosis of hair loss".)

TREATMENT PRINCIPLES — Female pattern hair loss (FPHL) typically progresses over time, resulting in diminishing hair coverage over affected areas of the scalp. The primary goals of treatment are to minimize additional hair loss and to induce regrowth of terminal hairs.

Responses to treatment vary, ranging from no effect, to improvement limited to the inhibition of further hair loss, to a variable degree of regrowth of hair. A favorable response may be considered cessation of the progression of hair loss and improvement in hair density that is cosmetically satisfactory for the patient. Initiating treatment early, prior to the development of extensive hair loss, is preferred given the potential for incomplete responses.

Counseling of patients should involve a discussion of the therapeutic options as well as realistic expectations for the duration of treatment and expected outcomes. At least several months of treatment are usually required to achieve initial clinical signs of a response, and effective pharmacologic therapy typically must be continued indefinitely to maintain improvement.

ASSESSING RESPONSE — Given that responses to treatment are delayed, periodic follow-up is reasonable. Provided that patients are tolerating treatment well, we typically reassess patients every four to six months.

The physical examination is the primary method of assessing the response to treatment. Serial photographs are valuable for identifying improvement in hair coverage on the scalp. Use of grading scales, such as the Ludwig or Sinclair scales, may be helpful for documenting baseline severity (figure 1 and picture 2). Additional methods commonly used in clinical studies include measurements of hair density and hair diameter.

INITIAL THERAPY — We aim to incorporate topical minoxidil in the treatment of all patients for female pattern hair loss (FPHL) (algorithm 1). Compared with other interventions, topical minoxidil has the strongest evidence for efficacy and is generally well tolerated [1,2]. We also typically prescribe an oral antiandrogenic agent (usually spironolactone). The addition of an oral antiandrogen is based upon limited data that suggest benefit of oral antiandrogenic therapy. (See 'Topical minoxidil' below and 'Adjunctive oral therapy' below.)

Hyperandrogenism and concomitant inflammatory scalp disorders that may contribute to hair loss should be treated. (See 'Patients with hyperandrogenism' below and 'Patients with concomitant scalp disorders' below.)

Topical minoxidil — Topical minoxidil is available in a variety of formulations. In the United States, minoxidil may be obtained commercially as a 2% solution, 5% solution, or 5% foam:

Product selection – All three commercial formulations of minoxidil (2% solution, 5% solution, and 5% foam) are effective for FPHL. Historically, many clinicians recommended use of minoxidil 5% solution or foam based upon a perception of greater efficacy than minoxidil 2% solution; however, data to support this assertion are lacking. In a systematic review of randomized trials evaluating interventions for FPHL, none of the four trials that compared minoxidil 2% with minoxidil 5% found a significant difference in efficacy between the two concentrations [2].

Minoxidil 5% foam offers drug delivery in a vehicle that may be preferred by some patients and is associated with a reduced risk for side effects (eg, scalp pruritus, dandruff, sideburn hypertrichosis) compared with twice-daily application of the 2% solution [3]. In a vehicle-controlled, randomized trial (n = 404), the incidences of scalp irritation and hypertrichosis with once-daily use of minoxidil 5% foam were comparable with vehicle [4].

AdministrationMinoxidil 2% solution (1 mL) is usually applied twice daily. Minoxidil 5% solution (1 mL) or foam (one-half capful) is usually applied once daily. Patients should be instructed to apply minoxidil to the scalp, not the hair. The patient should massage minoxidil onto the scalp with fingers, and hands should be washed after application. Patients should apply the product at least two hours before bed to allow adequate time for drying. This may help to avoid the inadvertent spread of the solution to other body sites during sleeping.

Treatment with minoxidil takes at least four months to exhibit a visible effect. We typically assess patients for initial signs of response after six to nine months. Use of the product for at least 12 months prior to concluding inefficacy is recommended [5].

Efficacy – The exact mechanism through which minoxidil improves FPHL is not completely understood. It is theorized that the drug may prolong the anagen (growth) phase of hair follicles, shorten the telogen (resting) phase, and induce enlargement of miniaturized follicles, thereby contributing to the conversion of miniaturized hairs to terminal hairs [6]. (See "Male pattern hair loss (androgenetic alopecia in males): Management".)

The efficacy of topical minoxidil for FPHL is supported by a systematic review and meta-analysis of randomized trials that found that patients treated with topical minoxidil (1%, 2%, or 5% formulations) were more likely to report clinically significant hair regrowth than patients in the placebo groups (risk ratio 1.93, 95% CI 1.51-2.47) [2]. In addition, the mean increase in hair counts within treated areas was higher in patients treated with minoxidil than in patients in the placebo groups. A subsequent, randomized trial that compared minoxidil 5% foam with placebo also supports the efficacy of minoxidil [4].

Adverse effects – Shedding of hair commonly occurs during the first two to eight weeks of minoxidil treatment [3,5], an event likely due to the release of telogen hairs, as follicles are stimulated to transition from telogen to the anagen phase [7]. Patients should be warned about this side effect to avoid the premature cessation of treatment.

Potential local adverse effects of minoxidil include scalp pruritus, flaking, and facial hypertrichosis. The low risk for scalp irritation with use of the 5% foam formulation may be related to the absence of propylene glycol, a common contact allergen, in this formulation. Hypertrichosis usually resolves within four months if treatment is discontinued [5]. (See "Male pattern hair loss (androgenetic alopecia in males): Management".)

Oral minoxidil may be an alternative for patients who are unable to tolerate topical minoxidil. (See 'Oral minoxidil' below.)

Adjunctive oral therapy — Our initial treatment protocol typically consists of topical minoxidil plus an oral antiandrogenic agent for patients who can tolerate oral antiandrogenic therapy (algorithm 1). Androgens are postulated to play a role in FPHL, although the nature and degree of androgen involvement in the pathogenesis of FPHL are unclear. (See "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis", section on 'Androgens'.)

Spironolactone is our preferred antiandrogen based upon data that suggest benefit for FPHL and the extensive experience with this drug for other indications in females (eg, hirsutism, acne, polycystic ovarian syndrome). Alternatives include finasteride (a 5-alpha-reductase inhibitor) or cyproterone acetate. We tend to use finasteride when patients do not tolerate spironolactone, prefer to avoid spironolactone, or have a poor response to spironolactone. Cyproterone acetate is not available in the United States. Use of all antiandrogenic agents should be avoided in pregnancy. (See 'Spironolactone' below and 'Finasteride' below and 'Cyproterone acetate' below.)

Spironolactone — Spironolactone is an aldosterone antagonist that competitively blocks androgen receptors and weakly inhibits androgen synthesis [8,9]:

Administration – The typical dose of spironolactone utilized for adults with FPHL is 100 to 200 mg per day. Treatment is usually begun at a lower dose (eg, 50 mg per day) to support tolerance of the drug. Provided that patients tolerate the 50 mg dose, we increase the dose to 100 mg per day after two to four weeks.

Spironolactone should be continued for at least six months prior to assessing its efficacy. For insufficient responses, the daily dose may be increased up to a maximum daily dose of 200 mg.

Efficacy – Data in support of the use of spironolactone for FPHL include open-label and retrospective studies, case reports, and case series [10-15]. In a retrospective study of 79 adults with FPHL treated with spironolactone (average dose 100 mg per day, range 25 to 200 mg per day) alone or in combination with topical minoxidil or low-level laser therapy (LLLT) for at least six months, all patients improved or maintained their initial Sinclair score (picture 2) [16].

An open-label study did not find a significant difference in efficacy between spironolactone and cyproterone acetate [10]. In the study, 80 patients with FPHL (ages 12 to 79, most with normal androgen levels) were treated with spironolactone (200 mg per day) or cyproterone acetate (50 mg per day for postmenopausal patients and 100 mg per day for 10 days per month in conjunction with an oral contraceptive pill for premenopausal patients). All patients were treated for at least 12 months, and the average duration of treatment was 16 months. Overall, 44 percent of patients had regrowth, 44 percent had no change in hair density, and 12 percent had continued hair loss.

Adverse effects – Potential side effects of spironolactone include headache, decreased libido, menstrual irregularities, orthostatic hypotension, fatigue, and hyperkalemia. There is a theoretical concern that spironolactone may cause feminization of a male fetus; therefore, the drug should not be administered during pregnancy.

Spironolactone is often given in conjunction with oral contraceptives in premenopausal patients to prevent pregnancy, as well as to reduce menstrual irregularity. Serum potassium levels should be followed periodically in patients over the age of 45 years; in patients with multiple medical problems, cardiac disease, or renal disease; and in patients who are taking medications that may increase risk for hyperkalemia [17,18]. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults", section on 'Adverse effects'.)

Although there is a theoretical concern for an elevation in breast cancer risk based upon the estrogenic effects of spironolactone, there is no definitive evidence linking human breast tumors, or other estrogen-dependent tumors, to spironolactone therapy [19-21].

Finasteride — Finasteride is a type 2 5-alpha-reductase inhibitor that is frequently used in the treatment of male pattern hair loss. Finasteride inhibits the conversion of testosterone to dihydrotestosterone, thereby reducing the effects of dihydrotestosterone on hair follicles [22] (see "Male pattern hair loss (androgenetic alopecia in males): Management", section on 'Oral finasteride'):

Administration – Typical dosing for finasteride for FPHL is 2.5 to 5 mg per day [23]. Clinical signs of response are expected within six months.

Efficacy – Few studies have evaluated the efficacy and safety of finasteride in patients with FPHL, and the available studies have utilized varied treatment regimens and have yielded different results [24]. Although a 12-month, placebo-controlled, randomized trial of 137 postmenopausal patients with FPHL and normal serum androgen levels found that treatment with finasteride 1 mg per day did not seem to be of benefit [25], uncontrolled studies utilizing higher doses of finasteride (2.5 or 5 mg per day) have suggested that finasteride may be of benefit in some patients without hyperandrogenism [26-28].

The value of finasteride in hyperandrogenemic patients with FPHL is also uncertain. A one-year, open-label trial in which 36 premenopausal patients with FPHL and hyperandrogenism were randomized to receive finasteride (5 mg per day), flutamide (250 mg per day), or cyproterone acetate (50 mg per day for 10 days per month) plus ethinyl estradiol (25 mcg for 20 days per month) found that the results achieved with finasteride were similar to those seen in 12 patients who were recruited to the study but refused therapy [29]. In contrast, in a case series of four patients with hyperandrogenism and hair loss (two premenopausal and two postmenopausal), the condition appeared to stabilize or improve during finasteride therapy [30].

Adverse effectsFinasteride is usually well tolerated in female patients [25]. Studies in male patients have included reports of reduced libido and breast swelling or tenderness [22]. Finasteride is also teratogenic; the drug may induce feminization of a male fetus. Thus, treatment with finasteride should be avoided in patients who are pregnant or considering becoming pregnant. When the drug is given to premenopausal patients who may become pregnant, the use of reliable contraception is indicated.

Cyproterone acetate — Cyproterone acetate is an antiandrogen that may be effective for FPHL. Cyproterone acetate is not available in the United States:

Administration – The dosing regimen for cyproterone acetate for FPHL is not standardized. When used in the treatment of FPHL, some authors have suggested the following regimens for premenopausal patients [31]:

100 mg per day on days 5 to 15 of the menstrual cycle and 50 mcg of ethinyl estradiol on days 5 to 25

Or

50 mg of cyproterone acetate on days 1 to 10 and 35 mcg on ethinyl estradiol on days 1 to 21

Postmenopausal patients may be treated with 50 mg daily [10].

Efficacy – The efficacy of cyproterone acetate in FPHL is difficult to assess since studies evaluating the efficacy of the drug have used variable treatment regimens and have yielded mixed results [10,29,32-34]. As mentioned above, an open-label study of 80 premenopausal and postmenopausal patients (most with normal androgen levels) that compared treatment with cyproterone acetate and spironolactone found that both treatments appeared to be effective and did not find a significant difference in efficacy between the two groups [10]. (See 'Spironolactone' above.)

In contrast, a randomized trial raised questions about the efficacy of cyproterone acetate for FPHL. In the one-year trial, 66 premenopausal patients (many with acne, hirsutism, or menstrual cycle irregularities) were randomized to receive either topical minoxidil 2% solution plus an oral contraceptive containing ethinyl estradiol and gestodene or cyproterone acetate (50 mg per day for 20 days per menstrual cycle) plus an oral contraceptive containing ethinyl estradiol and 2 mg of cyproterone acetate [32]. While minoxidil appeared to be effective for inducing hair regrowth (change in hair count between first and last measurement = 7.7±9.3 per 0.36 cm2), statistically significant hair regrowth did not occur in the cyproterone acetate group (change in hair count between first and last measurement = -0.2±6.7 per 0.36 cm2). Among patients treated with cyproterone acetate, patients with irregular menstrual cycles seemed to respond better than patients without irregular menstrual cycles; however, this difference was not statistically significant.

Adverse effects – Potential side effects of cyproterone acetate include menstrual cycle irregularity, weight gain, breast tenderness, reduced libido, depression, and nausea [31]. Cyproterone acetate should not be taken during pregnancy.

Additional interventions

Patients with hyperandrogenism — Treatment of the underlying, hyperandrogenic state is important for improving FPHL associated with hyperandrogenism. FPHL therapies that are not antiandrogenic, such as topical minoxidil, may also be beneficial [23]. A frequent approach to FPHL related to polycystic ovarian syndrome (a common cause of hyperandrogenism in females) is the addition of topical minoxidil and spironolactone when oral contraceptive therapy yields insufficient improvement. (See "Clinical manifestations of polycystic ovary syndrome in adults" and "Treatment of polycystic ovary syndrome in adults", section on 'Androgen excess'.)

Patients with concomitant scalp disorders — Treatment of coexisting inflammatory scalp conditions, such as seborrheic dermatitis, is generally advised to minimize additional hair loss related to scalp inflammation. In our experience, successful treatment of seborrheic dermatitis seems to reduce risk for skin irritation from topical minoxidil. (See "Seborrheic dermatitis in adolescents and adults", section on 'Management'.)

FAILURE OF INITIAL THERAPY

General approach — When hair density fails to improve despite combination treatment with topical minoxidil and an oral antiandrogen, we incorporate other therapies, such as platelet-rich plasma (PRP) injections, low-level laser therapy (LLLT), and oral minoxidil (algorithm 1). We typically continue topical minoxidil and oral antiandrogenic drugs, with the exception of the discontinuation of topical minoxidil for patients starting oral minoxidil. Efficacy of these therapies may be assessed after six months. Hair transplantation is an alternative for patients who fail medical therapy. (See 'Platelet-rich plasma' below and 'Low-level laser therapy' below and 'Oral minoxidil' below and 'Hair transplantation' below.)

Patient preference strongly influences the selection among these therapies. PRP and LLLT may be favored by patients who prefer to avoid systemic therapy. Oral minoxidil may be favored by patients who experience skin irritation from topical minoxidil or dislike daily application of topical minoxidil therapy. The cost of PRP therapy, LLLT devices, and hair transplantation can be limiting for some patients.

Although combination antiandrogenic therapy is used by some clinicians, data to confirm superior efficacy of combination antiandrogenic therapy (eg, spironolactone and finasteride) over antiandrogen monotherapy are lacking. We treat most patients with a single antiandrogenic agent, reserving combination therapy for occasional, treatment-refractory cases.

Platelet-rich plasma — Platelet-rich plasma (PRP) has been utilized for the treatment of male and female pattern hair loss (FPHL). PRP therapy is based upon the concept that growth factors released from platelets may modulate hair cycle signaling pathways that contribute to regrowth of hair [35]. Additional study is necessary to confirm the effects of PRP and determine optimal treatment regimen:

Administration – Approaches to PRP vary [36]. In general, whole blood drawn from the patient is centrifuged to separate platelets and plasma from other blood products. In some protocols, calcium chloride is used to activate PRP to stimulate the release of growth factors. The PRP is subsequently injected into the patient's scalp.

Efficacy – Although there are data that suggest benefit, studies evaluating this approach for FPHL are limited, and uncertainty remains regarding the role of this treatment [36-42]. Randomized trials evaluating PRP have generally been small and have used widely varying treatment regimens and PRP devices.

Examples of trials assessing the efficacy of PRP include:

A 24-week trial in which 30 patients with FPHL were randomly assigned to three monthly treatments with PRP or placebo found patients treated with PRP more likely to demonstrate improvement in clinical photographs (57 versus 7 percent) and found greater improvement in hair density and hair caliber in the PRP group, suggesting benefit of PRP [43].

A placebo-controlled, randomized, split-scalp trial that included 12 males and 13 females with androgenetic alopecia found a greater increase in the mean total hair density in sites treated with PRP compared with control sites six months after the first of three monthly PRP treatments [42]. However, differences in percentage of anagen hairs, percentage of telogen hairs, anagen/telogen hair ratio, terminal hair density, and hair count between the treated and control areas were not statistically significant.

A split-scalp trial in which 17 females and 18 males with androgenetic alopecia received three monthly treatments with PRP in one scalp area and saline treatments in a second scalp area did not find a difference in hair density change between the two groups three months after the last treatment [35]. Both PRP- and saline-treated areas demonstrated increased hair density. The authors postulated that diffusion of PRP from relatively large treatment areas or a beneficial effect of wounding from injections may have contributed to the absence of a significant difference in effect between the groups.

Adverse effects – The injections for delivery of PRP into the scalp can cause discomfort [35]. Other potential adverse events include headache; postinjection bleeding; and scalp discomfort, redness, or swelling [43].

Low-level laser therapy — Low-level laser therapy (LLLT), also referred to as "photobiomodulation therapy," may be of benefit for FPHL [44]. The mechanism of effect is unclear. Acceleration of cellular mitosis, stimulation of hair follicle stem cells or follicular keratinocytes, effects on cell metabolism leading to increased adenosine triphosphate production and cellular activity, and anti-inflammatory effects are postulated to contribute [45]. LLLT has also been used for male pattern hair loss [46]. (See "Male pattern hair loss (androgenetic alopecia in males): Management", section on 'Photobiomodulation'.)

Two 26-week trials in which a total of 141 patients with FPHL were randomly assigned to use of either one of two models of an LLLT comb device three times per week or to similar treatment with a sham device found greater improvements in terminal hair density among patients treated with LLLT combs than among patients given sham treatment [45]. Similarly, a 24-week trial in which 20 males and 20 females with androgenetic alopecia were randomly assigned to treatment with a laser helmet or sham device found the laser helmet more effective for increasing hair density and hair diameter [47]. Other studies suggest greater efficacy of combined topical minoxidil and LLLT therapy over topical minoxidil monotherapy [48,49].

Oral minoxidil — Limited data suggest oral minoxidil may be an alternative treatment for FPHL [50-53]. A 24-week, open-label trial that randomly assigned 52 patients with FPHL to either oral minoxidil (1 mg per day) or once-daily application of minoxidil 5% solution did not find a statistically significant difference in effect on total hair density (12 versus 7 percent increase, respectively) [50]. However, the adverse event of mild hypertrichosis occurred more frequently in the oral minoxidil group than in the topical minoxidil group (27 versus 4 percent). Other adverse events in the oral minoxidil group included a slight increase in mean heart rate at rest and one occurrence of pretibial edema.

HAIR TRANSPLANTATION — Surgical interventions similar to those performed for male pattern hair loss are an option for patients with female pattern hair loss (FPHL) who do not achieve a satisfactory response with pharmacologic therapy (algorithm 1) [54-57]. Through the transplantation of terminal hairs from unaffected areas of the scalp to affected sites, patients can achieve cosmetically favorable improvements.

Disadvantages of hair transplantation include high cost; significant time investment for patients; side effects such as early, temporary hair loss, pain, and infection; and the potential for transplant failure. Some patients with FPHL are poor candidates for hair transplantation, including patients with diffuse hair loss or in whom hair density in the donor area (typically the posterior scalp) is insufficient [55]. (See "Male pattern hair loss (androgenetic alopecia in males): Management".)

OTHER THERAPIES — Insufficient efficacy data or concern for adverse effects inhibit the routine use of other therapies:

Prostaglandin analogsLatanoprost 0.1%, a topical prostaglandin analog, was reported to increase hair density in a small, randomized trial of male patients with androgenetic alopecia [58]. In a case report, injections of bimatoprost, another prostaglandin analog, were not effective in a patient with female pattern hair loss (FPHL) [59].

Topical finasteride – In a 24-week trial in which 30 postmenopausal females were randomly assigned to either topical finasteride 0.25% combined with minoxidil 3% solution or minoxidil 3% solution alone, combination therapy was associated with a greater increase in hair diameter compared with minoxidil alone [60]. Of note, serum dihydrotestosterone levels decreased in the combination therapy group.

Dutasteride – Oral dutasteride, a type 1 and type 2 5-alpha-reductase inhibitor, appeared effective in a 46-year-old female patient who had attained only minimal improvement in FPHL with finasteride [61].

FlutamideFlutamide is an antiandrogenic agent infrequently utilized for the treatment of FPHL. A few studies have found evidence in support of its efficacy [29,62-64]. In a prospective cohort study of 101 premenopausal patients with FPHL (including 12 with elevated testosterone levels at baseline) who were treated with flutamide (250 mg for one year, 125 mg for one year, then 62.5 mg per day for two years), statistically significant improvement in hair loss severity scores was detected within six months, and continued improvement was noted up to two years [63]. The mean percentage improvement was 15 percent at six months and 28 percent at two years.

Potential side effects of flutamide include reduced libido, gastrointestinal distress, and liver function test abnormalities [63]. Hepatic failure is a rare side effect, and concern regarding this possibility has limited the use of flutamide therapy. However, significant elevations in transaminases were seen in only 4 percent of patients in the prospective cohort study, and the transaminase abnormalities resolved rapidly after treatment cessation [63].

Other – Although biotin supplementation is commonly marketed for hair loss, evidence to support efficacy in FPHL is lacking. We do not use biotin supplementation for the treatment of FPHL.

Similarly, the efficacy of other supplements (eg, iron, ginseng, saw palmetto, green tea, and caffeine), mesotherapy, microneedling, topical estrogens, and topical progesterone on FPHL are unclear [7,65].

COSMETIC OPTIONS — Patients with female pattern hair loss (FPHL) who are bothered by the appearance of hair loss may benefit from cosmetic interventions. Consultation with a cosmetologist may be helpful for identifying techniques to minimize the cosmetic impact of hair loss. Interventions such as hair styling techniques, hair dyeing, hair fibers, scalp micropigmentation, thickening shampoos, and wigs or other hair prostheses may be helpful.

PROGNOSIS — Once female pattern hair loss (FPHL) develops, the condition typically progresses over time, resulting in diminishing coverage of affected areas of the scalp by hair. Unlike male pattern hair loss, progression to complete baldness usually does not occur.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Alopecia".)

SUMMARY AND RECOMMENDATIONS

Overview – Female pattern hair loss (FPHL) is a common form of nonscarring hair loss that typically occurs in adult females (picture 1A-C). The characteristic feature is the progressive loss of terminal hairs over the frontal and vertex regions of the scalp, leading to a visible reduction in hair density. Topical, systemic, and surgical therapies have been used for the management of FPHL. (See 'Introduction' above and 'Prognosis' above.)

Treatment principles – The goals of treatment of FPHL include cessation of progression of hair loss and improvement in terminal hair density that is cosmetically satisfactory for the patient. Responses to treatment vary, and at least several months of treatment are often necessary to achieve a noticeable response. Initiating treatment early, prior to the development of extensive hair loss, is preferred given the potential for incomplete responses. Topical minoxidil and oral antiandrogenic therapy are the mainstays of treatment. (See 'Treatment principles' above.)

Patients with hyperandrogenism – A minority of patients with FPHL have associated hyperandrogenism. Identification and treatment of the underlying, hyperandrogenic state is an important component of the treatment of FPHL in these patients. (See 'Patients with hyperandrogenism' above.)

Initial treatment – For patients with FPHL, we recommend topical minoxidil (Grade 1B) (algorithm 1). We also suggest the addition of spironolactone to topical minoxidil, rather than topical minoxidil monotherapy (Grade 2C).

Topical minoxidil has the strongest evidence for efficacy and is generally well tolerated. Spironolactone is our preferred oral antiandrogen for FPHL based upon data that suggest benefit and the extensive experience with this drug in females for other indications.

Finasteride and cyproterone acetate are alternative oral antiandrogens. We tend to use finasteride when patients do not tolerate spironolactone, prefer to avoid spironolactone, or have a poor response to spironolactone. Cyproterone acetate is not available in the United States. (See 'Adjunctive oral therapy' above.)

Failure of initial treatment – The best approach to patients who fail to achieve sufficient improvement with topical minoxidil plus an oral antiandrogen is unclear. Our typical approach consists of the addition of platelet-rich plasma (PRP) injections, the addition of low-level laser therapy (LLLT), or the replacement of topical minoxidil with oral minoxidil (algorithm 1). Patient preference strongly influences treatment selection. (See 'Failure of initial therapy' above.)

Hair transplantation – Hair transplantation surgery can provide cosmetically favorable results in patients with FPHL. Surgical intervention is an option for patients who fail to achieve satisfactory improvement with pharmacologic therapy (algorithm 1). (See 'Hair transplantation' above.)

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Topic 86648 Version 11.0

References

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