Androgenetic Alopecia 

Updated: Feb 12, 2018
Author: Robert P Feinstein, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP 

Overview

Practice Essentials

Androgenetic (or pattern) alopecia is a genetically determined disorder characterized by the gradual conversion of terminal hairs into indeterminate, and finally into vellus, hairs. It is an extremely common disease that affects men and women.

Signs and symptoms

Signs of androgenetic alopecia include the following:

  • Gradual onset

  • Increased hair shedding

  • Transition in the involved areas from large, thick, pigmented terminal hairs to thinner, shorter, indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs

  • End result can be an area of total denudation; this area varies from patient to patient and is usually most marked at the vertex

Diffuse alopecia areata may mimic the androgenetic form. The presence of exclamation point hairs, pitted nails, or a history of periodic regrowth or tapered fractures noted on hair counts suggests the diagnosis of diffuse alopecia areata.

Males

  • Men note a gradual recession of the frontal hairline early in the process

  • Men present with gradual thinning in the temporal areas, producing a reshaping of the anterior part of the hairline

Females

  • Hair generally is lost diffusely over the crown; this produces a gradual thinning of the hair rather than an area of marked baldness; the part is widest anteriorly

  • The frontal hairline is often preserved in women

  • Bitemporal recession does occur in women but usually to a lesser degree than in men

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

History and the physical examination are the most important aspects of diagnosis in patients with androgenetic alopecia. The following laboratory tests, however, can play a role in patient assessment:

  • Dehydroepiandrosterone (DHEA)-sulfate and testosterone analysis: In women, if virilization is evident

  • Iron, total iron-binding capacity, and transferrin saturation: To test for iron deficiency, if telogen effluvium is present

  • Thyrotropin level: If a thyroid disorder is suspected

Biopsy and histology

A biopsy is rarely necessary to make the diagnosis of androgenetic alopecia. If a single biopsy specimen is obtained, it should generally be sectioned transversely if pattern alopecia is suspected.

In androgenetic alopecia, hairs are miniaturized. Although the condition is considered a noninflammatory form of hair loss, a superficial, perifollicular, inflammatory infiltrate is noted at times. A mildly increased telogen-to-anagen ratio is often observed.

See Workup for more detail.

Management

The following drugs have been approved by the FDA for the treatment of androgenetic alopecia:

  • Minoxidil: Androgen-independent hair-growth stimulator

  • Finasteride: 5-Alpha reductase type 2 inhibitor

The cosmetic results of surgical treatment for androgenetic alopecia are often satisfactory. Micrografting produces a more natural appearance than does the old technique of transplanting plugs.

See Treatment and Medication for more detail.

Background

Androgenetic alopecia, or pattern alopecia, is an extremely common disorder affecting both men and women. The incidence of androgenetic alopecia is generally considered to be greater in males than females, although some evidence suggests that the apparent differences in incidence may be a reflection of different expression in males and females.

Pathophysiology

Androgenetic alopecia is a genetically determined disorder and is progressive through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients with androgenetic alopecia have a reduction in the terminal-to-vellus hair ratio, normally about 4:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical patterned distribution of hair loss.

In androgenetic alopecia, studies have indicated a self-renewal of the hair follicle via keratinocyte stem cells located at the area of the bulge of the hair follicle. In addition, a series of studies using mice has indicated that interfollicular keratinocyte stem cells could generate de novo hair follicles in adult mouse skin. These regenerated hair follicles cycled through stages of telogen to anagen. However, these transitions between bulge and epidermal keratinocytes have not been seen yet in human studies.[1]

Another report has indicated that mice lacking in functional vitamin D receptors develop a functional first coat of hair, but lack the cyclic regeneration of hair follicles leading to the development of alopecia.[2] Whether these findings will lead to a new area of exploration into the cause of androgenetic alopecia in humans is unknown at this time.

A lymphocytic microfolliculitis targeting the bulge epithelium, along with deposits of epithelial basement membrane zone immunoreactants, are frequently seen in androgenetic alopecia in both sexes. Those cases with a positive immunoreactant profile respond better to combined-modality therapy than do those with a negative result.[3]

Numerous studies have identified 2 major genetic risk loci for androgenetic alopecia. These are the X-chromosomal AR/EDA2R locus and the PAX1/FOXA2 locus on chromosome 20. A recent genome-wide association study compared move than 1100 severely affected cases of androgenetic alopecia and controls to note differences in the 2 groups. The study indicated that HDAC9 is the third androgenetic alopecia susceptibility gene. The results of this German study were further analyzed by fine-mapping and then individually replicated in an Australian sample.[4]

A Japanese study of the sebaceous glands was performed to note whether the distribution of the bulge stem cells play a role in the development of androgenetic alopecia.[5] Biopsies from 250 cases of men with androgenetic alopecia were reviewed. Twenty-three vertical sections of areas of androgenetic alopecia were studied, and each sebaceous gland area was measured and statistically analyzed. For identification of the bulge area, immunochemical study was carried out in the cases of androgenetic alopecia. The result of the study was that the sebaceous gland area of the androgenetic alopecia group was noticeably increased, while the size of each sebaceous gland remained unchanged. This suggests that overgrowth of the sebaceous gland and relative preservation of the follicular stem cells could be an important factor in the pathology of androgenetic alopecia.

A study by Kaya Erdogan et al suggested that younger patients with early onset androgenetic alopecia have greater oxidative stress than do individuals without the disease. The study, on males aged 18 to 30 years, found higher total oxidant levels and oxidative stress index values in patients, all of whom had early onset androgenetic alopecia, than in healthy controls. The investigators also reported that within the patient group, the total antioxidant level was negatively correlated with patient age and disease duration.[6]

A literature review by Kim et al indicated that patients with androgenetic alopecia have abnormal lipid profiles, which may be a factor in the disorder’s association with cardiovascular disease. In the study, significantly higher levels of serum total cholesterol, serum triglyceride, and low-density lipoprotein cholesterol, as well as significantly lower levels of high-density lipoprotein cholesterol, were found in patients with androgenetic alopecia than in controls.[7]

Epidemiology

Frequency

Androgenetic alopecia is an extremely common disorder that affects roughly 50% of men and perhaps as many women older than 40 years. As many as 13% of premenopausal women reportedly have some evidence of androgenetic alopecia. However, the incidence of androgenetic alopecia increases greatly in women following menopause, and, according to one author, it may affect 75% of women older than 65 years.

A community-based study of androgenetic alopecia in 6 cities in China indicated that the prevalence of androgenetic alopecia in both Chinese males and females was lower than that seen in whites but similar to the incidence among Koreans.[8]

Race

The incidence and the severity of androgenetic alopecia tend to be highest in white men, second highest in Asians and African Americans, and lowest in Native Americans and Eskimos.

Age

Almost all patients with androgenetic alopecia have an onset prior to age 40 years, although many of the patients (both male and female) show evidence of the disorder by age 30 years.

Prognosis

The prognosis of androgenetic alopecia is unknown. Some patients progress to the point where they lose almost all of the hair on the scalp. Others have a patterned or nonpatterned thinning but retain a considerable number of scalp hairs. Women with androgenetic alopecia usually show thinning of the crown rather than developing truly bald areas.

Along with affecting the patient psychologically,[9] androgenetic alopecia is significant in that it allows ultraviolet light to reach the scalp and, thus, increases the amount of actinic damage. In addition, males with androgenetic alopecia may have an increased incidence of myocardial infarction.[10]

An increase in benign prostatic hypertrophy has also been associated with androgenetic alopecia.[11] Arias-Santiago et al measured prostatic volume by transrectal ultrasound and urinary flow by urinary flowmetry in order to study this hypothesis. Their findings suggest that a relationship exists between early onset androgenetic alopecia and prostate growth associated urinary symptoms, most likely owing to their pathophysiological similarity. They suggest that future studies may clarify whether treatment of patients with androgenetic alopecia might benefit concomitant benign prostatic hypertrophy.[12]

If these associations are proven conclusively, androgenetic alopecia will be of greater clinical significance.

A study by Sanke et al indicated that early androgenetic alopecia (ie, prior to age 30 years) in males is the phenotypic equivalent of polycystic ovarian syndrome (PCOS) and that these males may be at risk of developing complications found in association with PCOS, such as obesity, metabolic syndrome, insulin resistance, cardiovascular disease, and infertility. The investigators reported that the endocrinologic profile of the males with early androgenetic alopecia was similar to that of females with PCOS. Compared with controls, mean levels of testosterone, dehydroepiandrosterone (DHEA)-sulfate, luteinizing hormone, and prolactin were significantly higher in individuals with early androgenetic alopecia, while the mean free androgen index was also higher and mean levels of follicle-stimulating hormone were lower.[13]

A study by Polat et al indicated that men with androgenetic alopecia have a higher likelihood of developing urolithiasis than do those with no hair loss, with the risk being 1.3-fold greater in males with vertex-pattern alopecia, and 2.1-fold greater in those with total alopecia. The study included 200 men with urolithiasis and 168 males with no history of renal stones.[14]

Patient Education

For patient education resources, see the Skin, Hair, and Nails Center, as well as Hair Loss.

 

Presentation

History

The onset of androgenetic alopecia is gradual. Men present with gradual thinning in the temporal areas, producing a reshaping of the anterior part of the hairline. For the most part, the evolution of baldness progresses according to the Norwood/Hamilton classification of frontal and vertex thinning. Women with androgenetic alopecia usually present with diffuse thinning on the crown. Bitemporal recession does occur in women but usually to a lesser degree than in men. In general, women maintain a frontal hairline.[15]

Physical

In both males and females with androgenetic alopecia, the transition from large, thick, pigmented terminal hairs to thinner, shorter, indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs in the involved areas is gradual. As the androgenetic alopecia progresses, the anagen phase shortens with the telogen phase remaining constant. As a result, more hairs are in the telogen phase, and the patient may notice an increase in hair shedding. The end result can be an area of total denudation. This area varies from patient to patient and is usually most marked at the vertex.

Women with androgenetic alopecia generally lose hair diffusely over the crown. This produces a gradual thinning of the hair rather than an area of marked baldness. The part is widest anteriorly. The frontal hairline is often preserved in women with this disorder; in contrast, men note a gradual recession of the frontal hairline early in the process.

Causes

Androgenetic alopecia is a genetically determined condition. In 2008, 95 families were studied genetically, and the locus with strongest evidence for linkage to androgenetic alopecia was the 3q26 site on the X chromosome.[16] In addition, an association between androgenetic alopecia and chromosome 20pll and the androgen-receptor gene has been reported.[17]

Androgen is necessary for progression of androgenetic alopecia, as it is not found in males castrated prior to puberty. The progression of androgenetic alopecia is stopped if postpubertal males are castrated. Androgenetic alopecia is postulated to be a dominantly inherited disorder with variable penetrance and expression. However, it may be of polygenic inheritance. It has been noted that follicles from balding areas of persons with androgenetic alopecia are able to produce terminal hairs when implanted into immunodeficient mice.[18] This suggests that systemic or external factors may play a role in androgenetic alopecia. Interestingly, female androgenetic alopecia has been reported in a patient with complete androgen insensitivity syndrome. This suggests that factors other than direct androgen action contribute to patterned hair loss.[19]

As reported in 2005, it was noted in adult mouse skin that the hedgehog (Hh) family of intercellular signaling proteins can stimulate the transition from the resting (telogen) state to the growth phase (anagen) of the hair cycle.[20] Whether this will be helpful in the treatment of androgenetic alopecia remains to be seen.

As to the question of whether iron deficiency plays a role in female pattern hair loss, a study by Olsen et al indicated iron deficiency is common in women but is not significantly increased in patients with female patterns of hair loss or chronic telogen effluvium when compared with control subjects.[21]

Lattouf et al have described a case of connubial androgenetic alopecia in a 52-year-old woman secondary to contact with the skin of her husband who was being treated with topical testosterone for hypogonadism. She developed severe androgenetic alopecia involving the crown and the frontotemporal areas. Her spouse had been applying transdermal testosterone gel to his upper arms once daily. The patient was evaluated for evidence of hyperandrogenism, and no other signs of this disorder were identified. She was advised to ask her husband to apply his testosterone gel on a less exposed area of his body. The authors go on to state that it is possible that cases of connubial androgenetic alopecia may be underreported.[22]

 

DDx

Diagnostic Considerations

Also consider the following:

  • Alopecia of senescence
  • Alopecia associated with virilizing disorders of women, in whom it may be seen in association with hirsutism and menstrual problems
  • Anagen effluvium after exposure to toxic chemicals, including chemotherapeutic agents
  • Alopecia associated with hypothyroidism or hyperthyroidism
  • Telogen effluvium: This condition may accelerate androgenetic alopecia, and causes, such as iron deficiency and papulosquamous diseases of the scalp, must be considered.
  • Hypertension and/or smoking: A strong association of androgenetic alopecia with hypertension was noted in a study of 250 white men aged 35-65 years. In this French study, a definite familial tendency to androgenetic alopecia was also described, but no association was noted with diabetes mellitus, hyperlipidemia, or smoking. [23] However, a study of 740 Taiwanese men aged 40-91 years indicated an association between androgenetic alopecia and smoking. Smoking status, current amount of cigarette smoking, and smoking intensity were statistically significant in this report. [24]

Differential Diagnoses

 

Workup

Laboratory Studies

The most important aspects are the history and the physical examination. In the case of a woman, if virilization is evident, laboratory analysis of dehydroepiandrosterone (DHEA)-sulfate and testosterone may need to be obtained. Some authors have suggested that total testosterone level alone may be adequate to screen for a virilizing tumor. If a thyroid disorder is suspected, obtaining a thyrotropin level is indicated.

If telogen effluvium is present, laboratory analysis of serum iron levels or a biopsy to note an underlying papulosquamous disorder may be indicated. Telogen effluvium may accelerate the course of pattern alopecia. Iron deficiency is a common and reversible cause of telogen effluvium. A normal CBC count does not exclude iron deficiency as a cause of hair loss. While a low ferritin level is always a sign of iron deficiency, ferritin behaves as an acute phase reactant, and levels may be normal despite iron deficiency. Iron, total iron-binding capacity, and transferrin saturation are inexpensive and sensitive tests for iron deficiency.

Diffuse alopecia areata may mimic pattern alopecia. The presence of exclamation point hairs, pitted nails, or a history of periodic regrowth or tapered fractures noted on hair counts suggests the diagnosis of diffuse alopecia areata.

Schmidt et al used dermoscopy to study androgenetic alopecia. They noted brown peripilar casts and miniaturized hairs.[25]

Köse and Güleç examined the value of dermoscopy in the study of alopecias, finding that hair diameter diversity was seen in every patient with androgenetic alopecia. This was an essential but not specific finding of this alopecia because it was also present in alopecia areata, chronic telogen effluvium, and primary cicatricial alopecia. However, peripilar signs and empty follicles were indicative of androgenetic alopecia, as they were confined to this patient group.[26]

Procedures

A biopsy is rarely necessary to make the diagnosis of androgenetic alopecia. If a single biopsy specimen is obtained, it should generally be sectioned transversely if pattern alopecia is suspected. Some dermatopathologists recommend that if a biopsy is to be performed, a sample should be obtained from 2 sites: one for horizontal sectioning and one for vertical sectioning of the hair follicles. Other dermatopathologists point out that one may commonly obtain sufficient information from serial vertical sections to diagnose the condition.

Histologic Findings

In pattern alopecia, hairs are miniaturized. In evolving-pattern alopecia, the diameter of hair shafts varies. Fibrous tract remnants (so-called streamers) can be found below miniaturized follicles. Although androgenetic alopecia is considered a noninflammatory form of hair loss, at times, a superficial, perifollicular, inflammatory infiltrate is noted. A mildly increased telogen-to-anagen ratio is often observed.

 

Treatment

Medical Care

Only 2 drugs currently have US Food and Drug Administration (FDA)–approved indications for treatment of androgenetic alopecia: minoxidil and finasteride.

Minoxidil

Although the method of action is essentially unknown, minoxidil appears to lengthen the duration of the anagen phase, and it may increase the blood supply to the follicle.[27] Regrowth is more pronounced at the vertex than in the frontal areas and is not noted for at least 4 months. Continuing topical treatment with the drug is necessary indefinitely because discontinuation of treatment produces a rapid reversion to the pretreatment balding pattern.

Patients who respond best to this drug are those who have a recent onset of androgenetic alopecia and small areas of hair loss. The drug is marketed as a 2% or a 5% solution, with the 5% solution being somewhat more effective. A 48-week study compared the 2 strengths in men.[28] Findings indicated that 45% more regrowth occurred with the 5% compared with the 2% solution. In general, women respond better to topical minoxidil than men. The increase in effectiveness of the 5% solution was not evident for women in the FDA-controlled studies. Subsequent studies have shown at best a modest advantage to the higher concentration in women. In addition, the occurrence of facial hair growth appears to be increased with the use of the higher-concentration formulation.

Central chorioretinopathy has been associated with the use of minoxidil 2% for androgenetic alopecia. A 37-year-old man developed this adverse effect consisting of a positive elative scotoma, metamorphopsia, and impaired dark adaptation of the right eye after 8 months use of minoxidil for androgenetic alopecia. However, 1 month after cessation of the drug, normal findings were found upon reexamination.[29]

Finasteride

Finasteride is given orally and is a 5-alpha reductase type 2 inhibitor.[30] It is not an antiandrogen. The drug can be used only in men because it can produce ambiguous genitalia in a developing male fetus. Finasteride has been shown to diminish the progression of androgenetic alopecia in males who are treated, and, in many patients, it has stimulated new regrowth.

Although it affects vertex balding more than frontal hair loss, the medication has been shown to increase regrowth in the frontal area as well. Finasteride must be continued indefinitely because discontinuation results in gradual progression of the disorder. A study in postmenopausal women indicated no beneficial effect of the medication in treating female androgenetic alopecia.

A 10-year follow-up study of men using finasteride 1 mg daily for androgenetic alopecia reported that better improvements were noted in patients older than 30 years or men who had higher androgenetic alopecia grades. Interestingly, the efficacy of the medication was not reduced with time, and in some cases improved later on.[31]

A Japanese study of 3177 men noted the efficacy and safety of finasteride in the treatment of androgenetic alopecia. Photographs were assessed in 2561 men who completed the 42-month study. Of these men, 11.1% showed great regrowth, 36.5% moderate growth, and 39.5% had a slight increase in hair growth. Adverse effects occurred in 0.7% of the men, and there were no safety problems observed with long-term use. The authors concluded that in Japanese men with androgenetic alopecia, long-term use of oral finasteride maintained progressive hair regrowth without recognized adverse effects.[32]

Other drugs

Some drugs are not approved by the FDA but are potentially helpful medications.[33] In women with androgenetic alopecia, especially those with a component of hyperandrogenism, drugs that act as androgen suppressants or antagonists (eg, spironolactone, oral contraceptives) may be beneficial. Evidence exists of an association between androgenetic alopecia, hypertension, and hyperaldosteronism. Spironolactone could play a dual role in treatment.

Dutasteride is another possible treatment for androgenetic alopecia. This drug inhibits type I and type II 5-a reductase isoenzymes and is felt to be 3 times as potent as finasteride in inhibiting the type II enzyme and 100 times as potent in inhibiting the type I enzyme. A phase II study on the use of dutasteride in the treatment of alopecia was carried out in the United States, but no further trials are currently being conducted in the US. However, an ongoing trial is being conducted outside of the United States.

A report by Motofei et al suggested that finasteride is preferable to dutasteride as a therapy for androgenetic alopecia. The investigators stated that finasteride “preserves important physiological roles of dihydrotestosterone” unrelated to androgenetic alopecia and that it appears to have at least partially predictable adverse effects.[34]

A study by Singh et al suggested that botulinum toxin may be a viable treatment for androgenetic alopecia in males, since intramuscular infection of the drug into the scalp results in muscle relaxation and, therefore, increased blood flow. The study included 10 patients, with each of 30 sites in each patients’ scalp injected with 5 U of botulinum toxin. In eight patients, the investigators reported good to excellent results on photographic evaluation.[35]

Low-level laser light therapy, in particular a red light hairbrush–like device has been marketed as an over-the-counter technique for hair growth. In a double blind, sham-device controlled, multicenter, 26-week trial, 110 patients in the active treatment group who completed the study showed a significantly greater improvement in overall hair regrowth than did the sham group.[36] Marketed as the HairMax LaserComb, it has obtained 510K FDA approval for use as a medical device. Note that this approval refers to safety rather than actual efficacy and that the data required for medical devices are quite different from those required to demonstrate the safety and efficacy of drugs.

Topical latanoprost 0.1%, a prostaglandin analogue used to treat glaucoma, has been noted to cause an increase in the number, length, and thickness of eyelashes. Blume-Peytavi et al conducted a 24-week topical treatment with this agent to note the effect on androgenetic alopecia. Sixteen young men with mild androgenetic alopecia were studied. They applied latanoprost 0.1% and placebo daily on 2 minizones on the scalp. Measurements of the hair growth, density, diameter, pigmentation, and anagen/telogen ratio were performed throughout the study. At 24 weeks, an increase in hair density was noted at the latanoprost-treated site compared with baseline and the placebo site. They concluded that this medication could be useful for stimulating hair follicle activity and treating hair loss.[37]

Androgenetic alopecia is very common; therefore, not surprisingly, it may accompany other forms of hair loss. Cases of telogen effluvium often occur in patients with underlying androgenetic alopecia. Therefore, a search for treatable causes of telogen effluvium (eg, anemia, hypothyroidism), especially in patients with an abrupt onset or a rapid progression of their disease, is indicated.

Dawson et al, while discussing female androgenetic alopecia, list the following treatment options to arrest hair loss progression and stimulate partial hair regrowth in this disorder: the androgen receptor antagonists spironolactone and cyproterone acetate, the 5alpha-reductase inhibitor finasteride, and the androgen-independent hair growth stimulator minoxidil. These treatment are most effective when instituted early.[38]

A phase 1, double-blind clinical trial designed to evaluate the safety of a bioengineered, nonrecombinant, human cell–derived formulation containing follistatin, keratinocyte growth factor (KGF), and vascular endothelial growth factor (VEGF) was performed to assess the efficacy in stimulating hair growth. Twenty-six subjects were entered into the study and none showed an adverse reaction to the single intradermal injection. After 1 year, a statistically significant increase in total hair count continued to be seen.[39]

A 2015 study in Spain indicated that plasma rich in growth factors (PGRP) is effective in the treatment of androgenetic alopecia.[40] Over 100 patients were studied and were given two intradermal cycles of PGRF every 4 weeks. Anagen follicles significantly increased by 6.2% compared with baseline, and there was a decrease of 5.1% seen in telogen follicles. No adverse effects were noted in any of the patients.

Serena repens extract has been shown to inhibit both types of 5-α reductase and, when taken orally, has been shown to increase growth in androgenetic alopecia patients. A study by Wessagowit et al attempted to assess the efficacy of topical S repens in androgenetic alopecia.[41] Fifty male patients were studied and were treated with topical S repens products for 24 weeks. The result was that the average hair count increased at 12 and 24 weeks compared with baseline. They believe prolonged use of these products beyond 4 weeks is necessary for sustained efficacy.

Adipose-derived stem cells secrete various growth factors that promote hair growth. Using trichograms, Fukuoka and Suga evaluated the effects of adipose-derived stem cell‒conditioned medium on hair regeneration.[42] The studies were done on patients both on and off finasteride. It was their impression that combination therapy was preferable to single-agent treatment. They believe that using adipose-derived stem cell‒conditioned medium seems to represent a new avenue of therapy for hair regeneration, and they believe that long-term use (over a period of years) should be studied to note effects and histological changes.

Surgical Care

Surgical treatment of androgenetic alopecia has been successfully performed for the past 4 decades. Although the cosmetic results are often satisfactory, the main problem is covering the bald area with donor plugs (or follicles) sufficient in number to be effective. Micrografting produces a more natural appearance than the old technique of transplanting plugs.

A 2009 review of surgical procedures concluded that both patients and physicians alike are pleased with the results of contemporary hair transplantation.[36] Patients with less than 40 follicular units/cm2 in their donor areas are poor candidates for the procedure. Scalp reduction has been attempted to decrease the size of the scalp to be covered by transplanted hair. However, the scars produced by the reduction technique often spread and become more noticeable with time.

A South Korean study noted the effect of a 1550-nm fractional erbium-glass laser in women with androgenetic alopecia. The patients received 10 treatments at 2-week intervals. Global photographs taken at baseline and at the end of laser treatment showed improvement in 24 (87.5%) of the 27 patients studied. However, 2 patients reported mild pruritus after treatment.[43]

Hair weaving techniques are available, and, together with hairpieces, they offer the patient a prosthetic method of coverage.

Also see the Medscape article Hair Transplantation.

 

Medication

Medication Summary

Only 2 medications have been shown to be effective in the treatment of androgenetic alopecia: minoxidil and finasteride. Minoxidil is applied topically and available as 2% or 5% solutions. Finasteride is taken orally.

Vasodilators

Class Summary

This drug is indicated to improve hair growth by stimulating vasodilation.

Minoxidil topical (Rogaine)

Minoxidil topical relaxes arteriolar smooth muscle, causing vasodilation. Hair growth effects are secondary to vasodilation. It is available as 2% and 5% solutions.

Antiandrogens

Class Summary

Finasteride is the agent in this category known to promote hair growth.

Finasteride (Propecia)

Finasteride inhibits the conversion of testosterone to dihydrotestosterone, causing serum dihydrotestosterone levels to decrease. However, effects in hair growth are not clearly understood.

 

Questions & Answers

Overview

What is androgenetic alopecia?

What are the signs and symptoms of androgenetic alopecia?

What are symptoms of androgenetic alopecia in men?

What are the symptoms of androgenetic alopecia in women?

How is androgenetic alopecia diagnosed?

What is the role of biopsy in the diagnosis of androgenetic alopecia?

Which drugs have been approved by the FDA for the treatment of androgenetic alopecia?

What is androgenetic alopecia?

What is the pathophysiology of androgenetic alopecia?

What is the role of genetics in the pathophysiology of androgenetic alopecia?

What is the role of sebaceous glands in the pathophysiology of androgenetic alopecia?

What is the role of oxidative stress in the pathophysiology of androgenetic alopecia?

What is the role of lipids in the pathophysiology of androgenetic alopecia?

What is the prevalence of androgenetic alopecia?

What are the racial predilections of androgenetic alopecia?

Which age groups have the highest prevalence of androgenetic alopecia onset?

What is the prognosis of androgenetic alopecia?

Where can patient educations resources about androgenetic alopecia be found?

Presentation

Which clinical history findings are characteristic of androgenetic alopecia?

Which physical findings are characteristic of androgenetic alopecia?

What causes androgenetic alopecia?

DDX

Which conditions should be included in the differential diagnosis of androgenetic alopecia?

What are the differential diagnoses for Androgenetic Alopecia?

Workup

What is the role of lab studies in the workup of androgenetic alopecia?

What is the role of biopsy in the workup of androgenetic alopecia?

Which histologic findings are characteristic of androgenetic alopecia?

Treatment

Which drugs are approved by the FDA for treatment of androgenetic alopecia?

What is the role of minoxidil in the treatment of androgenetic alopecia?

What is the role of finasteride in the treatment of androgenetic alopecia?

Which treatments for androgenetic alopecia are not FDA approved?

How is telogen effluvium differentiated from androgenetic alopecia?

What are the treatment options for female androgenetic alopecia?

Which novel treatments for androgenetic alopecia have been investigated?

What is the role of surgery in the treatment of androgenetic alopecia?

Medications

Which medications are effective in the treatment of androgenetic alopecia?

Which medications in the drug class Antiandrogens are used in the treatment of Androgenetic Alopecia?

Which medications in the drug class Vasodilators are used in the treatment of Androgenetic Alopecia?