Female Pattern Baldness

As medical /scientific research continues, current expert opinion expressed herein may change.

Androgen-related hair loss

Permanent hair-loss caused by the action of androgens on genetically susceptible follicles.

Androgenetic Alopecia is non-reversible genetically determined hair loss. Androgen presence is necessary for its progression. It is genetically either:
i) dominant – a single gene is inherited.
ii) polygenic – a number of genes are inherited.

Androgenic Alopecia in women is caused by follicular miniaturisation associated with endocrine changes and increased androgen presence. Accompanying factors may include: Polycystic ovarian syndrome, virilisation (and hirsutism), irregular menstruation, infertility, acne, seborrhoea oleosa.
Menopausal Alopecia (androgenic alopecia) is associated with hormone changes. As estrogen reduces, hair-follicles become increasingly vulnerable to the effects of androgen exposure. Anti-androgen therapy may reduce further hair loss, but is currently unlikely to initiate the return of the lost hair.
Androgenic Alopecia in women is a multi-factorial condition in which genetic predisposition + circulating androgens viz testosterone androsteinedione, and dihydrotestosterone (DHT) are key factors in a process of progressive hair follicle miniaturisation and reduction in the anagen (hair growing) phase. Follicles effectively ‘shrink’ to produce vellus hairs. Caucasoids have a higher susceptibility than Afroid’s or Mongoloids. This condition may warrant endocrinological investigation.

How the condition differs from that in men:
i) The progression is slower – possibly due to a level of ‘follicular protection’ afforded by estrogen.
ii) Hairloss is diffuse and does not conform to the traditional patterns of loss in males.
iii) Hairloss may worsen following menopause with the development of baldness especially at the vertices.
iv) In men the condition is due to genetic predisposition and is usually age related.
v) In women the condition can present at any time associated with underlying medical conditions. viz: polycystic ovarian syndrome, thyroid disorders, anaemia, chronic illness, use of certain medications.

Expert opinion currently doubts that the condition in women is the same as that in men.

Correct diagnosis is essential, and may require blood tests, or scalp biopsy.

Things to do
Until recently, no effective treatments have been available for certain alopecias in women.
Current options however may include the following drugs which may limit hair loss:
Systemic anti-androgen drugs e.g.
Spironolactone: Aldactone® Spiroctan®, Diatensec®.
Cyproterone acetate (Androcur®) Diane® or
Flutamide (Eulexin®).

Minoxidil: Regaine®
Finasteride: Propecia® is not currently indicated in women. However 5-alpha-reductase inhibitors (which prevent testosterone conversion and subsequent baldness in men) are currently being considered for female use. This may bring renewed possibilities in the treatment of this distressing disorder

Surgical Hair Restoration may be an option (see transplantation techniques)

                                                                                           © Prof. B Stevens FTTS (Contact the author)



A detailed overview- Inga Zemite MD MTTS

Female pattern hair loss (FPHL) is a term used to describe the decrease in central scalp hair density that occurs in number of females after puberty. This decrease is meant to be caused by action of androgen hormones. Decrease in hair density happens in central (frontal, vertex and mid) scalp, and bitemporal and parietal regions can also be affected.
There are several synonyms for this condition – Female Pattern Hair Loss (FPHL); androgenetic alopecia (AGA – used to imply a specific androgen related etiology); androgenic alopecia, (used for genetic etiology); FAGA – female androgenetic alopecia; common baldness in women, etc. By some authors female alopecia with androgen increase is called female androgenetic alopecia (FAGA) and without androgen increase is called female pattern hair loss (FPHL). I will use FPHL as general term in this essay.
Hamilton describes male pattern of alopecia in women but in his report from 1951 he noted that hair loss in women never progressed further that pattern IV in his own classification of MAGA. Ludwig has described diffuse hair loss patterns in women. Olsen described Christmas tree pattern with frontal accentuation. It is still a question what are behind these patterns, as it is found that pathogenesis and therapy results differs in different pattern.  
In susceptible hair follicles, dihydrotestosterone binds to the androgen receptor, and the hormone-receptor complex activates the genes responsible for the gradual transformation of large terminal follicles to miniaturized follicles. Women with FPHL have higher levels of 5alpha reductase and androgen receptor in frontal hair follicles compared to occipital follicles. At the same time, women have high levels of cytochrome p-450 aromatase in frontal follicles and in occipital follicles that saves the hair. This leads to specific pattern of hair loss.

The condition is very emotionally devastating for affected women.

  • Epidemiology

FPHL is quite common beginning in the late 20s and reaching its peak after 50 years of age. It affects more as 50% of women after the age of 50 years.
There are two ages of onset described:

  • early – post-puberty to third decade; and
  • late – age 40 and after.

FPHL can occur alone and may be seen together with other androgen-related conditions. Sometimes signs of hyperandrogenism (hirsutism, irregular periods) or hyperandrogenemia occur may be observed but most often women with FPHL have neither.
Many affected women respond to antiandrogens or 5α-reductase inhibitors with increased hair growth that indicate an androgen etiology in at least some cases of FPHL.
Women suffer from a more diffuse hair loss in the vertex region that starts after menopause due to the relative increase of androgens.

  • History

Beek in 1950 noted that baldness in women increased from the fourth to the sixth decades.
Ludwig in 1977 described the progressive centrifugal hair loss with preservation of the frontal hair line to which he assigned three pictorial graduations of severity. 
Olsen described Christmas tree pattern of FPHL with frontal accentuation.
More recently in consensus meeting of specialists in hair proposed the term FPHL to describe the hair phenotype in women with or without obvious androgen relatedness.

  • Pathophysiology

FPHL is induced by androgens in genetically susceptible women. Hair follicles of women with FPHL have increased 5alpha-reductase activity and increased levels of dihydrotestosterone (DHT). DHT, which is formed by the peripheral conversion of testosterone by 5alpha-reductase, is thought to be responsible for the characteristic miniaturization of scalp hair follicles in FPHL. In genetically susceptible hair follicles, DHT binds to the androgen receptor, and the hormone-receptor complex then activates the genes responsible for the gradual transformation of large, terminal follicles to small, miniaturized follicles.
FPHL are a consequence of:

  • increased central or peripheral androgens and/or
  • a fault in the follicle hormonal transformation and/or
  • a genetic predisposition to permit these to act on follicular target cells which are specially sensitized by binding to specific intracellular androgen receptors.

Over successive hair cycles in FPHL, the duration of anagen shortens and matrix size decreases, resulting in smaller follicles that produce shorter, finer, miniaturized hairs that cover the scalp less and less well. These miniaturized hairs of various lengths and diameters are the hallmark of androgenetic alopecia. The number of follicles per unit area remains the same.
In women with FPHL, the extent of hair loss is usually less than in men. The androgen receptors are on the X chromosome, which would explain why women show a mosaic pattern of alopecia and are relatively mildly involved.
It has been assumed that the hormonal basis for androgenetic alopecia is similar in women as in men. The milder expression of androgenetic alopecia in women if compared with men may in part be the result of lower levels of 5alpha reductase and androgen receptors in frontal follicles of women; additionally, higher levels of aromatase in women may result in increased local formation of estradiol from testosterone, and less formation of 5alpha-reduced products such as DHT. Aromatase is capable of converting testosterone to estradiol.
Circulating androgens in women come from three potential sources:

  • adrenal,
  • ovary and
  • peripheral conversion.

Primary androgens causing cellular androgen- related effects are testosterone (T) and dihydrotestosterone (DHT). Their availability in the hair follicle depends on an intact central (gonadal or adrenal) steroid biosynthetic pathway that will take synthesis to at least dehydroepiandrosterone sulfate (DHEA-S); as well as the presence of the terminal conversion enzymes of steroid sulfatase, 17β-hydroxysteroid dehydrogenase, 5α-reductase, and 3β-hydroxysteroid dehydrogenase. All these enzymes are available in the hair follicle.
Androgens circulate in the blood either free or preferentially bound to sex-hormone-binding globulin (SHBG) (78%), albumin (20%) or cortisol-binding globulin or acid α-2 glycoprotein (<1%). Hairs are affected by free androgens.
Androgen action in the tisues is determined by:

  • the amount and type of androgen delivered to the tissue;
  • the amount and type of androgen synthesized in the tissue;
  • the amount of local androgen receptor;
  • the relative binding affinity to the androgen receptor of the androgens present in the tissue and
  • relative metabolism ot these androgens.

Circulating androgen levels are age dependent – both adrenal and gonadal sources increasing with puberty and decreasing after menopause.
The mechanism of androgen action in hair follicles is well known in female androgenetic alopecia:

  • FAGA is related to the excess of  β-4-androstenedione serum levels of ovary or adrenal origin and
  • FAGA.M with the increase of dehydroepiandrosterone (DHEA) or DHEA-S of adrenal origin.

Androstenedione and DHEA-S are peripherally transformed into testosterone (T), and this in turn is converted into 4 main metabolites, of which hairs are affected mainly by 5-α-dihydrotestosterone (DHT). Conversion of T in DHT requires free T that is not bound to sex-hormone-binding globulin (SHBG).
In balding scalp hair follicles, the androgen receptor is a specific protein known as “caspase,” which binds 5-α-DHT. Once the hormone have been bound, the receptor complex undergoes a conformational change, exposing DNA binding sites, and the hormone-receptor complex, in conjunction with other coactivating proteins, to specific hormone response elements in the DNA altering the expression of specific androgen-dependent genes and starting apoptosis.
Once DHT has been metabolized in the follicular target organ, it is transformed into its metabolite 3-α-androstanediol glucuronide by the enzyme 3-β-hydroxysteroid dehydrogenase; therefore, the serum level of this metabolite is an indicator of the intracellular androgenic metabolism.
Prolactin may be also involved in FPHL. It is thought that hyperprolactinemia is associated with an increase in DHEA-S as the result of the action of prolactin on the adrenal cortex.
Another important enzyme is aromatase that is located in outer root sheath. Aromatase converts androstenedione to estrone and testosterone to estradiol, decreasing both – the levels of circulating and tissue T and DHT. This explains the differences between AGA of male and female pattern. It is found that in women there are 2- to 5-fold greater amounts of aromatase in the scalp than in men. In FPHL there is 3 to 5 times more aromatase in frontal and occipital scalp areas than in MAGA what explains the maintenance of the frontal hairline in women.
As an etiopathogenic factor of FAGA, one should also consider the decrease of SHBG, as this would result in free T, which could act then at the follicular level. For different authors, the biochemical marker of FPHL would be:

  • the decrease of SHBG and the increase of 3α- androstanediol glucuronide or
  • the decrease of SHBG that would proportionally increase the T/SHBG ratio.

In hypothyroidism, there is decreased synthesis of SHBG, which is why women with hypothyroidism with a history of FPHL could see an increase of their alopecia.

The hair follicle has also estrogen receptors that makes it estrogen sensitive organ. Effects of estrogens on human hair are still not studied enough. In vitro experiments it is found that estrogens inhibit elongation of hairs from the female occipital scalp but can stimulate male frontotemporal hairs. Differences in estrogen’s action in various tissues are thought to be related with differences in estrogen receptor distribution and the tissue levels of co-regulatory proteins.

A high percentage of women with FPHL without any overt clinical sign of hyperandrogenism had no biochemical evidence of androgen excess.
Two genes have been shown to be related to alopecia.

  • CYP17 is a steroid metabolism gene that codifies P450 aromatase enzyme helping to release more estradiol. This gene was found in women with PCOS and their brothers with early balding.
  • A new gene on chromosome locus 3q26 has been found in androgenetic alopecia families.

It is likely that early and late FPHL differs genetically, and it seems that hair loss in women is polygenic and multifactorial with the additional influence of environmental factors.

  • Clinical features and Classification

FPHL in women is characterised by early or late age of onset, the pattern of increased thinning over the frontal/parietal scalp with greater density over the occipital scalp, retention of the frontal hairline, and the presence of miniaturized hairs. Most women have normal menses and pregnancies.
Women first notice hair thinning over the frontal area, and gradually the scalp becomes more and more visible. Over time the thinning increase. Thinning is often diffuse and may involve most of the scalp; nevertheless usually it is patterned with most marked thinning over the frontal and parietal scalp, and with greater density over the occipital scalp. Women typically retain hairs along the frontal hairline, even when the scalp is visible behind the hairline.
Miniaturized hairs, the shorter and finer hairs of various lengths and diameters, are the hallmark of AGA and result from the shortening of anagen phase and reduction in matrix size. Increased spacing between hairs makes the central part appear wider over the frontal scalp compared to the occipital scalp.
The patient may note that her pony tail is smaller and the hair is cut to shorter lengths in order to give a fuller appearance. Rarely, advanced thinning occurs with loss of the frontal hairline, but this is associated with markedly elevated circulating androgens.
Androgenetic alopecia in women is not usually accompanied by increased shedding. However, in some instances, an episode of telogen effluvium following childbirth, major illness or other causes may uncover a latent predisposition to FPHL.

Female pattern hair loss is a condition characterized clinically by a decrease in hair density in the central scalp and histologically by miniaturization of some follicles and an increased percentage of hair in telogen in the affected area. Patterns in FPHL are much less obvious than in MPHL and examination of the scalp shows three different patterns:

  • vertex/frontal (male pattern) -thinning associated with bitemporal recession – Hamilton-Norwood type
  • diffuse central  
      • the commonly used 3-point Ludwig scale
      • the 5-point Sinclair scale
  • frontal accentuation (“Christmas tree” pattern) – thinning and widening of the central part of the scalp with breach of frontal hairline – assessed by Olsen scale

Many women develop a minor degree of postpubertal recession at the temples whether or not they have diffuse hair loss.

The classification system for the female pattern designed by Ludwig is less complex and can be easily used in practice. It includes three degrees of hair loss localized on the crown.
In Ludwig’s classification, the 3 patterns represent stages or progressive types of FAGA (Pic. 5.1).
FAGA Degree I (Minimal)
It is considered as the beginning of FAGA. There is a perceptible thinning of hair from the anterior part of the crown with minimal widening of the part width. Ludwig described the earliest change as rarefaction of the hair on the crown. This produces an oval area of alopecia encircled by a band of variable breadth with normal hair density. Hair loss can be hiden by combing the hair forward, thus, exposing a visible area of alopecia in the anterior centroparietal area while the frontal hairline is maintained. This type of alopecia is observed in young women with SAHA syndrome (SAHA for – seborrhea, acne, hirsutism, alopecia), generally of ovarian origin. It is accompanied by other hyperandrogenism manifestations. Because SAHA syndrome is constitutional, there are not increases of blood biochemical levels.

FAGA Degree II (Moderate)
Some time later, the “crown” area of thinning will be more evident as a number of thin and short hairs increases. Progression to Ludwig grade II results in further rarefaction of the crown, with preservation of the fringe. This makes it more difficult, although still possible, to camouflage the alopecia with combing the hair forward. This pattern of alopecia is a marker of excess androgens, generally of ovarian origin. The stage of SAHA syndrome has passed. Blood biochemical studies usually demonstrante an excess of androstenedione, free testosterone, and androstanediol glucuronide.
FAGA Degree III (Intense)
Grade III is near-complete baldness of the crown. In some perimenopausal or menopausal women, the “crown” becomes practically denuded, with significant widening of the part width, but the frontal hairline is maintained. Although women comb their hair forward trying to cover the alopecia, it will always be possible to see hair loss. This type of alopecia also can be seen in women with adrenal diseases, tumoral or not, with very high levels of androstenedione, DHEA-S, free testosterone, sometimes of prolactin, and always of androstanediol glucuronide.

Ludwig also described female androgenetic alopecia with male pattern (FAGA.M) that should be subclassified according to Ebling’s or Hamilton-Norwood’s classification. FAGA.M may be present in 4 conditions: persistent adrenarche syndrome, alopecia caused by an adrenal or an ovarian tumor, posthysterectomy, and as an involutive alopecia.
A more recent classification is Olsen’s classification of FPHL and it proposes 2 types: early- and late-onset with or without excess of androgens in each. The Olsen’s patterns incorporate the accentuation of the frontovertical alopecia, which has a triangular or “Christmas tree” form.
Not all women who develop FPHL maintain their frontal hair line. By some authors bitemporal recession occurs in 13% of premenopausal women and 37% of postmenopausal women. There is number of women with hair loss confined to the vertex scalp, but in a significant proportion hair loss also occurs diffusely over the parietal scalp.

Most women who present with FPHL have no other evidence of virilization.  It is important:

  •  if the hair loss is of sudden onset,
  • is rapidly progressive and
  • advanced,

a full medical history must be taken, and examination and endocrinological investigation are needed to exclude virilization, which can rarely be caused by a virilizing tumour. Investigation is also indicated in women with FAGA of gradual onset accompanied by menstrual disturbance, hirsutism or recrudescence of acne.

  • Laboratory investigations and Pathology

A correct diagnosis, which is based on the clinical history, clinical examination, and biochemical investigation, is essential for successful treatment. In practice FPHL usually is a visual diagnosis confirmed by examination and history. Measurable hormonal changes are rare. In such conditions as polycystic ovary syndrome (PCOS), adrenal hyperplasia, androgen-producing neoplasms, or intake of exogen androgens (anabolics) increase in hormones can be found. In these cases often other symptoms of androgenization such as oligo-or amenorrhea, infertility of women, acne vulgaris, severe unresponsive cystic acne, hirsutism, galactorrhea and virilization are observed.
The clinical history consists of an in-depth examination of factors that may exacerbate the alopecia, such as chronic illnesses, nutritional alterations, metabolic and endocrinologic alterations, lack of vitamins, and recent surgical interventions and other treatments. It is always important to take a menstrual history.
In the clinical examination, a photograph should be taken to document the baseline condition. It is important in evaluating the therapeutic results. Physical examination should include all aspects of the scalp, especially to see whether hair loss excludes the occipital area.
The specific maneuvers that may be performed include noninvasive, semi-invasive, and invasive methods.
Noninvasive Methods
Traction test or “Sabouraud’s sign,” evaluate the number of hair that are shedding after slight traction on scalp hair, “pull-out sign” let to know the strength of a tuft of hairs, and “standardized wash test.”
In the wash test the woman refrains from shampooing for 5 days, and then she shampoos and rinses her hair in the basin with the hole covered by gauze. After collecting all the hairs remaining in the water and the gauze, they are examined. Hairs are counted and divided into less as 5 cm and more as 5 cm in length. This is an important technique to differentiate telogen effluvium from female pattern hair loss.
Other photographic methods, such as macrophotographic analysis in microcalibrated hair tubes, phototrichogram, traction phototrichogram, and the methods that use an image analyzer, are obsolete. These still can be used in hair research practices. Dermoscopy has replaced them in the diagnosis of androgenetic alopecia.
Dermoscopic features are:

  • hairs with different caliber reflecting progressive hair miniaturization;
  • brown halo, roughly 1 mm in diameter, at the follicular ostium around the emergent hair shaft;
  • small bald areas with numerous empty follicles in postmenopausal women;
  • scalp pigmentation because of sun exposure.

Semi-Invasive Methods
Semi-invasive methods include the trichogram, unit area trichogram, and trichoscan.
The trichogram is the most criticized technique, but still vary useful in practice. To perform the technique correctly, one must observe 50 – 100 hairs from the temporoparietal, occipital, and vertex areas (some 25 hairs from each area). Once the dermatologist has experience, he/she can evaluate FPHL even with approximately 10 to 15 hairs from the vertex. It is a quantitative technique that provides information about the growth capacity of hair and the alterations of its growth. The trichogram also permits measurement of the diameter of the hair shaft. The “coefficient of variability”of the hair shaft diameter can be determined. It expresses the percentage of variation between the diameters of each individual. The coefficient of variation in women without hair problems is 20.41%, with a standard deviation of 6.3%, whereas in women with FAGA.M, the coefficient of variability reaches 41.7% with a standard deviation of 4%.
Rushton described the “unit area trichogram” in 1983. With this technique one can determine the hair density in a specific area (hairs/cm2), the diameter of the hair (mm), and the linear growth (mm/d).
Trichoscan is a new technique consisting in shaving a transitional balding area of 0.661 cm2 and evaluating several parameters with an epiluminescence microscopy: number of hairs in the area, density of hairs (hairs/cm2), anagen hairs, telogen hairs, density of vellus (vellus/cm2), density of terminal hairs (terminal hairs/cm2), and vellus and terminal hairs. This technique is only a screening tool and is not useful for diagnostic purposes.
Invasive Methods
There are two invasive methods for hair diagnostic – scalp biopsy and folliculogram Folliculogram is used to evaluate the action mechanism of several treatments in animals used as models in alopecia, and is not useful in practice.
Biopsies from the involved area can be taken when the diagnosis is in doubt, especially to differentiate from CTE or to know the possibility of reversing hair loss. With biopsy, Whiting demonstrated the different features between controls, CTE and FPHL patients:





Terminal hairs








terminal hair/vellus ratio




Percentage of telogen




Table 5.1. Features demonstrated by biopsy (Whiting 1996)
A biopsy is rarely necessary to make the diagnosis of androgenetic alopecia. It is usually taken when differentiaton from other conditions is needed. Biopsy is taken from active, representative sites, and horizontal sectioning is preferred because of the larger number of follicular structures that can be studied.
Biopsy of FPHL has similar features to male pattern hair loss. A decrease of terminal hair and anagen hair and an increase of vellus-like hair, telogen hairs, and fibrous residual tract that ends in the superficially located miniaturized follicle must be found. Slight perifollicular lymphohistiocytic infiltrate is another microscopic feature. A mildly increased telogen-to-anagen ratio is often observed. Sebaceous glands remain intact.
Biochemical Tests
Among the laboratory tests, most important is androgenic determination. Levels of free testosterone, 5-α-DHT, DHEA-S, 17-β-hydroxyprogesterone, prolactin, androstenedione, SHBG, and 3-β-androstanediol glucuronide are useful.
Cortisol levels will be increased in Cushing’s disease. When cutaneous signs of Cushing’s disease are present, a 24-hour urinary free cortisol and creatinine excretion must be determined, and the overnight “dexamethasone suppression test” also can be performed.
Gonadotropins luteinizing hormone (LH), follicle-stimulating hormone (FSH), and the ratio of LH:FSH must be determined to confirm PCOS because an increase in serum LH is pathognomic of a diagnosis of PCOS, and ratio LH:FSH can be increased in up to 95% of subjects.
When HAIRAN syndrome is suspected, insulin serum levels must be also determined.
When androgen levels are normal, screening should include TSH, T4, antimicrosomal and antithyroglobulin antibodies, and ferritin or total iron binding capacity.

        • Differential diagnosis

The diagnosis of AGA in women is supported by early age of onset, the pattern of increased hair thinning over the frontal/parietal scalp with greater hair density over the occipital scalp, retention of the frontal hairline, and the presence of miniaturized hairs.
When these features are present, the diagnosis is not problematic. However, FPHL is common and other causes of hair loss may coexist and need to be recognized or excluded.
Chronic telogen effluvium (CTE) may present a difficult differential diagnosis even though the features of CTE seem different. In CTE, women with average hair density, describe sudden onset of shedding from the entire scalp. Hair pull test may extract increased numbers of telogen hairs easily. Scalp hair density appears normal or minimally decreased even if the shedding may be prolonged. Miniaturized hairs are not seen. Acute telogen effluvium may occur in a woman with long-standing FPHL or unmask latent FPHL. A history usually identifies the cause of profuse hair shedding such as high fever, severe dietary protein deficiency, drugs or chronic blood loss as in women with prolonged heavy menses.
Both patchy and diffuse alopecia areata may mimic or coexist with FPHL. 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 alopecia areata.  Also scalp biopsy can be used; it shows a peribulbar lymphocytic infiltrate around anagen hair bulbs.
An adult with loose anagen syndrome has a history of decreased hair density since early childhood, and the pull test is strongly positive. Low power microscopy of the easily extracted hairs shows misshapen anagen bulbs, a “ruffled” cuticle just distal to the bulb, and absent inner root sheath.
Frontal fibrosing alopecia is a condition where hair loss almost exclusively presents in postmenopausal women although a few reports in younger women have been published. A gradual recession follows perifollicular erythema with or without associated follicular keratosis. The hair loss progresses backward to about 8 cm maximum. Frontal fibrosing alopecia is characterized histologically by a lymphocytic infiltrate around the isthmus and infundibular region of the hair follicles as well as concentric perifollicular lamellar fibrosis.
Central centrifugal cicatricial alopecia (CCCA) is a common type of hair loss. This particular hair loss is described first in African Americans; most commonly in African American women who use hot combs (a method by which oiled or greased hair is straightened with a heated iron). Others also can be affected by this condition.

        • Treatment

As FPHL is a biological process determined by sensitivity to androgens and is genetically mediated there three main treatment approaches to interrupt its course are used:
1) modification of the biological response through nonhormonal mechanisms;
2) modification of the androgen action by
a) altering the production,
b) transport, or
c) metabolism of androgens, such as preventing binding to androgenic receptors; and
3) transplanting follicles to balding areas by surgical procedures.

Topical Treatment

One topical treatment used in the management of FPHL is minoxidil. Proposed mechanism of action of minoxidil is due to its influence on hair cycling, causing premature termination of telogen, and probably prolonging anagen, minoxidil is also a potent peripheral vasodilator. Effects of minoxidil are currently the subject of research and some debate.
Topical minoxidil solution is the only approved drug available for promoting hair growth in women with FPHL. Minoxidil is available in both 2% and 5% preparation. Studies show a mild non-significant advantage for the 5% solution. 1 ml of minoxidil is applied twice daily to dry scalp with a dropper.
Efficacy has been shown in studies using hair counts and hair weight analysis. Minoxidil-treated women had significantly higher hair counts and an increase in hair weight compared to women who received placebo. It should be noted that clinical perception of improved scalp coverage is not immediate; it can take up to 6–12 months, until hair length and mass are increased sufficiently. Treatment should be continued for at least 12 months.
Most frequent side effects are irritation dermatitis, contact eczema, pruritus, scaling, dryness, headaches, a non-virilizing hypertrichosis, which affects the face (the cheeks and forehead), shoulders, arm, and legs of women, including the scalp. Hypertrichosis usually is temporary. Patients should be warned that in the first 2–8 weeks, a temporary telogen effluvium may occur. This shedding is self-limiting and subsides when anagen regrowth begins. Hair loss recurs with interruption of application.

Other Local Therapeutics. Twice-daily applications of tincture of progesterone are useful in women. Also both spironolactone and its metabolite canrenone are used for the topical treatment of FPHL. In menopausal women, a solution of estradiol valerate has demonstrated improvement of anagen/telogen ratio and a decrease in hair loss. Topical finasteride showed a 40% decrease of DHT serum levels, but does not increase the hair growth.

Systemic Treatment

When FPHL is associated with high levels of androgens, systemic anti-androgenic therapy is needed.

Persistent adrenarche syndrome – adrenal SAHA and FPHL in adrenal hyperandrogenism is treated with two types of drugs – corticosteroids for adrenal suppression and anti-androgens, central or peripherals, to avoid the production of adrenal androgens or their effects on the target follicular organ.
Adrenal suppression is achieved with glucocorticosteroids. Antiandrogens therapy includes cyproterone acetate, drospirenone, spironolactone, flutamide, and finasteride.

Excess release of ovarian androgens – ovarian SAHA and alopecia of ovarian hyperandrogenism is treated with ovarian suppression and antiandrogens.
Ovarian suppression includes the use of contraceptives containing an estrogen, ethinylestradiol, and a progestogen.
Gonadotropin-releasing hormone agonists such as leuprolide acetate suppress pituitary and gonadal function through a reduction in luteinizing hormone and follicle-stimulating hormone levels. Subsequently, ovarian steroid levels also will be reduced, especially in patients with polycystic ovary syndrome. When polycystic ovary syndrome is associated with insulin resistance, metformin must be considered as treatment.
Antiandrogenic therapy includes cyproterone acetate (CA), spironolactone, drospirenone, flutamide, finasteride, and dutasteride. Central antiandrogens competitively inhibit binding of 5-α-DHT to the androgen receptor and peripheral antiandrogens acts by inhibiting the 5-α-reductase, blocking the conversion of testosterone to 5-α-DHT. It is recommended to accompany antiandrogens by tricyclic contraceptives.
Hyperprolactinemic SAHA and alopecia of pituitary hyperandrogenism should be treated with bromocriptine or cabergoline.
FPHL in Postmenopausal hyper or normoandrogenic women is treated with antiandrogens (mentioned above).

Postmenopausal alopecia, with previous high levels of androgens or with prostatic-specific antigen greater than 0.04 ng/mL, improves with finasteride or dutasteride.
Androgen-dependent medications
The use of androgen-dependent medications can cause abnormalities in the genitalia of the male fetus. These medications are contraindicated in women who are pregnant. All androgen-dependent medications need to be used for at least 1 year before an accurate appraisal of efficacy can be made.
Finasteride inhibits 5α-reductase II enzyme, which is responsible for catalyzing the conversion of testosterone to the much more active chemical DHT. Finasteride suppresses overall androgen activity by restricting total circulating androgen activity. Finasteride is generally well tolerated. Rare side effects in female patients include increased libido and breast tenderness, usually in the beginning of therapy, and it is reversible on dose reduction, and diminishes over time.
Evidences show that postmenopausal alopecia in normoandrogenic women also improves with finasteride at a dose of 2.5 mg per day. There are also studies that confirm that in postmenopausal women with AGA, finasteride 1 mg/day taken for 12 months did not increase hair growth or slow the progression of hair thinning. Finasteride does appear to be successful in some patients, but further studies are required to determine its efficacy and optimal dosing regimes.
Cyproterone acetate
This medication works by inhibiting gonadotropin-releasing hormone (GnRH) and blocks androgen receptors. Other uses include hirsutism, severe acne and prostate cancer. It is commonly used combined with estradiol as an oral contraceptive pill named Diane-35.
Efficacy is greater in patients with evidence of hyperandrogenism. CA clearly decrease the loss of hair, hair thinning, and seborrhea but without actual increased hair regrowth.
Study where two antiandrogen medications was compared (ie, spironolactone and cyproterone acetate) involved 80 women with biopsy confirmed FPHL. The authors found that 88% of women either experienced improvement of hair or had no progression of their hair loss with no significant difference in efficacy between individual medications.
Treatment doses utilized vary. It can be used in regime 100 mg/day on days 5–15 of the menstrual cycle supplemented by 50 μg ethinyl estradiol on days 5–25.
The side effects are weight gain, loss of libido, menstrual disturbances, breast tenderness, depression, and gastrointestinal upsets.
Spironolactone is used to treat FPHL and hirsutism. It works as an androgen antagonist by competitively blocking androgen receptors in hair cells, as well as inhibiting ovarian androgen production.
The usual daily dose is 100–200 mg/day twice a day.
In my own practice it is most often used antiandrogen.  
The side effects of spironolactone vary, due to its additional actions as an aldosterone antagonist. These include menstrual irregularities, breast tenderness, postural hypotension, electrolyte disturbances, fatigue, urticaria, and hematological disturbances. These side effects must be monitored, especially in the first months of treatment. Further caution with its use needs to be exercised in the patient with renal abnormalities since it can potentially cause electrolyte disturbances.
Flutamide is a potent antiandrogen. It is acting via androgen receptor antagonism. It is used to treat advanced prostate cancer and hirsutism. It is new antiandrogen therefore it lacks experience in using it in FPHL. One randomized study suggested that flutamide at a dose of 250 mg/day could lead to greater improvements in stemming hair loss after 1 year of treatment compared with finasteride and cyproterone acetate. Another randomized controlled trial found a significant treatment advantage for flutamide over spironolactone in the treatment of hirsutism, the reduction of total acne and seborrhea, and the slowing or halting of hair loss.
Side effects of flutamide are severe. These include hepatotoxicity (3 in 10,000 users) and breast tenderness, both of which are dose-related. It is recommended that serial liver transaminases are checked in the first months of treatment, and it must be stopped or if transaminase levels exceed twice the normal limits.
Cosmetic aids are very useful part of management options. Hair styling techniques, camouflage products, hair accessories, hair replacements can be succesfully used to manage visual condition of hair.
Hairstyling – useful tips:

  • getting greater hair volume and lift from shorter styles;
  • disguising central thinness by a side or zigzagging part;
  • adding soft layers at the top to allow pulled back hair to have more style;
  • taking some weight off the top;
  • using wide-toothed combs or brushes to allow thin hair to flow through without breakage;
  • using a friction-free towel that blots hair and absorbs most of the moisture rather than damaging thin hair with towel drying;
  • coloring hair to make hair look thicker and appear to give it more volume;
  • styling with a body wave with soft or tight curls to give hair more bounce and fullness;
  • and using hair sprays and foams that are light and nondrying to give volume and prevent breakage.

Camouflaging products cover affected areas on the scalp and hide visible hair loss, and adds volume. The most commonly used products include hair building fibers, scalp spray thickeners, alopecia masking lotion, and topical shading.
Hair extensions can be useful for women with mild hair loss if more length and volume are needed. These can be clipped on daily or attached permanently.
Weight loss undoubtedly improves hair loss in hyperandrogenic women.
There is also the possibility of surgical hair restoration, which includes follicular grafting, scalp reduction, and flap rotations. These techniques may apply to any form of focal alopecia.


        • References
  • Blume-Peytavi, U. at all. Hair Growth and Disorders. Springer-Verlag Berlin Heidelberg. 2008.
  • Burns, T. at all.  Rook’s Textbook of Dermatology. Blackwell Publishing Ltd. 2010.
  • Buxton, P.K. Eczema and Dermatitis. British Medical Journal. 1987.,Vol. 295., pp. 1048-1051.
  • Camacho-Martínez, F,M. Hair Loss in Women. Semin Cutan Med Surg 28:19-32 © 2009 Elsevier Inc.
  • Dinh, Q,Q; Sinclair, R. Female pattern hair loss: Current treatment concepts. Clin Interv Aging. 2007 June; 2(2): 189–199 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684510/
  • Norwood, O,T. at all. Incidence of Female Androgenetic Alopecia. Dermatol Surg. 2001;27:53-54.
  • Price, V, H.  Androgenetic Alopecia in Women Journal of Investigative Dermatology Symposium Proceedings (2003) 8, 24–27 http://www.nature.com/jidsp/journal/v8/n1/full/5640087a.html
  • Sinclair R. Br J Dermatol.2008
  • Olsen, E, A.  Female Pattern Hair Loss and its Relationship to Permanent/Cicatricial Alopecia: A New Perspective Journal of Investigative Dermatology Symposium Proceedings (2005) 10, 217–221 http://www.nature.com/jidsp/journal/v10/n3/full/5640208a.html
  • Vexiau, P. at all. Role of Androgens in Female-Pattern Androgenetic Alopecia, Either Alone or Associated With Other Symptoms of Hyperandrogenism. Arch Dermatol Res. 2000;292:598-604.
  • http://www.medscape.com/viewarticle/483591_4
  • http://www.uptodate.com/contents/patient-information-hair-loss-in-men-and-women-androgenetic-alopecia/abstract/3