CLINICAL OBSTETRICS AND GYNECOLOGY Volume 58, Number 1, 185–199 Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.

Hair Loss in Women KATYA L. HARFMANN, MD,* and MARK A. BECHTEL, MDw *The Ohio State University Wexner Medical Center, Columbus, Ohio; and w Division of Dermatology, Department of Medicine-Clinical, Ohio State University, College of Medicine, Gahanna, Ohio Abstract: Hair loss is a common cause of morbidity for many women. As a key member of the woman’s health care team, the obstetrician/gynecologist may be the first person to evaluate the complaint of hair loss. Common types of nonscarring hair loss, including female pattern hair loss and telogen effluvium, may be diagnosed and managed by the obstetrician/gynecologist. A systematic approach to diagnosis and management of these common forms of hair loss is presented. Key words: female pattern hair loss, androgenetic alopecia, telogen effluvium, minoxidil, 5-a reductase inhibitors, antiandrogens

overall well-being. As a result, it is paramount that the obstetrician/gynecologist feels comfortable assessing the types and patterns of hair loss commonly seen in women. This review will focus on the initial assessment of hair loss, as well as the management of female pattern hair loss (FPHL) and telogen effluvium (TE), 2 of the most common diagnoses in women with alopecia that may present to an obstetrician/gynecologist.


Diagnosing Hair Loss in Women

In current times, scalp hair has more social and psychological significance than biological importance. It serves as a social signal of sex, age, and status. For women, hair plays an important role in body image and self-identity. A 1993 Glamour magazine survey found that over half of women said ‘‘if my hair looks good, I look attractive no matter what I’m wearing or how I look otherwise,’’ and ‘‘if my hair isn’t right, nothing else can make me feel that I look good.’’1 This places the obstetrician/gynecologist, as a woman’s health care provider, in an important position in supporting her

When a woman presents with a complaint of hair loss, obtaining a thorough history is the key. A flowchart to guide the initial assessment has been provided in Figure 1. A brief look at the scalp to determine the presence or absence of follicular orifices in the affected areas can be helpful to guide questioning, as this is the critical distinction between forms of nonscarring and scarring alopecia.2 If follicular orifices are absent and the underlying scalp has a shiny white color, it is likely that the patient has a form of cicatricial, or scarring, alopecia that should undergo referral and evaluation by a specialist. If follicular orifices are present, a form of nonscarring alopecia is occurring, and further history taking may help elucidate the cause.

Correspondence: Mark Bechtel, MD, 540 Officenter Place, Suite 240, Gahanna, OH. E-mail: mark.bechtel@ The authors declare that they have nothing to disclose. CLINICAL OBSTETRICS AND GYNECOLOGY






MARCH 2015 | 185


Harfmann and Bechtel

FIGURE 1. Flowchart demonstrating the initial assessment of hair loss in women. FPHL indicates female pattern hair loss.

Ask the patient whether she is experiencing hair coming out at the roots or hair breakage. Hair breakage might indicate traumatic causes, and further questions regarding hair care practices are warranted. If her hair is coming out at the roots, determine whether her primary complaint is thinning of her hair and/or shedding of her hair. If she provides a history of excessive hair shedding, particularly on days that her hair is not washed, a medical history should be obtained

for the preceding 6 to 12 months. This should include any febrile illnesses, hospitalizations, surgeries, and traumatic events. A medication history should also be obtained, paying particular attention to use of oral contraceptive medications and hair loss that has occurred either during use or after stopping use.2 Nutritional information, including sources of dietary protein, should be sought in every patient, as numerous deficiencies have been associated with hair loss (Table 1).3 Ask the patient

Hair Loss in Women TABLE 1. Nutritional Deficiency

Nutritional Deficiencies that May Underlie Hair Disorders Clinical Setting Encountered


Weight loss diets consuming 6 hairs 50-60 hairs grasped extracted between thumb and forefinger, tugged firmly away from the scalp Fragile hair Cluster of hairs breaks into grasped with one small bits hand, distal ends pulled away with other hand

FIGURE 2. The upper image represents normal average duration of hair cycle phases. The lower image represents physiological changes seen with aging, with a decrease in anagen and increase in kenogen. Black—anagen. Medium gray—catagen. Light gray—telogen. White— kenogen

assess the hair density by comparing the part width on the top of the scalp to that on the occipital scalp, as more prominent thinning on the superior scalp is more suggestive of pattern hair loss, the common female equivalent of the better known male pattern baldness. Examine the appearance of the scalp in areas of hair loss. A peachcolored scalp in areas of patchy hair loss is a diagnostic clue for alopecia areata, whereas a shiny white color may represent scarring hair loss. Several tests easily performed during the office visit can also be helpful in categorizing the type of hair loss, although the results may be difficult to assess without the presence of light microscopy (Table 2).2 Although most women with hair loss will have normal laboratory studies, it may be reasonable to obtain a complete blood count, ferritin, thyroid-stimulating hormone, and vitamin D level, as abnormalities in these levels have been associated with different forms of alopecia.4,5 In addition, if there are signs of potential endocrine abnormalities, including severe acne, hirsutism, virilization, galactorrhea, menstrual irregularities, or infertility, a serum and free testosterone, dehydroepiandrosterone sulfate, and prolactin should be obtained.2 If at any point in the diagnostic workup of hair loss there is a concern for a progressive scarring condition, or if the presentation is not typical for any of the nonscarring conditions discussed below, the patient should be referred to a dermatologist for further evaluation.


Harfmann and Bechtel

Physiological Hair Changes in Women It is important to be able to distinguish between normal hair changes that occur with aging in every woman and changes that might represent a pathologic state. Unfortunately, these normal, physiological changes can resemble those seen in FPHL, which also occurs with increasing incidence as women age. There is not a clearly defined division between the more mild findings of normal aging and the more pronounced findings of FPHL.6 A schematic of normal hair cycling is presented in Figure 2. The anagen phase, or growth phase, is the longest phase of the hair cycle. Following anagen is a short regression phase termed catagen, during which the hair follicle regresses via apoptosis. The hair follicle then enters the resting phase, telogen. The point of actual shedding of the telogen hair, exogen,

further divides the telogen phase. Kenogen describes the phase of the hair cycle marked by an empty follicle after shedding of the telogen hair. As seen in Figure 2, the physiological changes in hair cycling with aging include a decrease in the duration of anagen and an increase in the duration of kenogen. The net result, when applied to the entire scalp, is an increased number of empty follicles.7 These physiological changes lead to a decrease in hair density, starting by the age of 35, although some sources report as early as age 20.6,8 When evaluating women complaining of hair thinning, it is important to remember that decreases in hair density are often not publicly perceived until the density has decreased by half.2 Therefore, it is important not to minimize a patient’s complaint of hair thinning, as she will likely appreciate early changes far before it is evident on exam. Hair density, however, is not the only

FIGURE 3. Thinning of scalp hair in female pattern hair loss, more prominent on the superior scalp (A) than the occipital scalp (B).

Hair Loss in Women TABLE 3.


Treatments for Female Pattern Hair Loss


Grade of Recommendation Dosing



















Spironolactone C

Side Effects


Not available in United States May be most useful in hyperandrogenic states Long half-life may 0.5 mg dailyHeadache, menstrual allow 2.5 mg daily irregularity, dizziness, intermittent increased body hair growth, dosing depression, nausea, hot flashes Topical Conflicting application evidence Response may take 1-5 mg daily Headache, menstrual 6 mo-2.5 y irregularity, dizziness, increased body hair growth, depression, nausea, hot flashes Topical Studies only in men application daily Maximum effect achieved within 90 d of use Approved for use in Europe (Czech and Slovak Republics) 62.5-250 mg daily Hot flashes, diarrhea, breast Black Box warning tenderness, headache for hepatotoxicity Laboratories must be monitored 2% shampoo 3 Dryness Studies only in men times weekly topical application Folliculitis, erythema, burning daily sensation Facial hypertrichosis, contact Takes 12 mo to Daily to twice assess efficacy dermatitis, pruritus, scaling, daily dryness 2% or 5% Transient—lethargy, nausea, Takes >6 mo to Initially 50 mg assess efficacy daily titrating up menorrhagia Persistent—hypotension, to 100-200 mg hyperkalemia, fatigue, daily headache, weight loss, urinary frequency, dry skin

Premenopausal— Weight gain, menstrual irregularities, breast 100 mg daily for tenderness, feminization of 10 d each month Postmenopausal— male fetus 50 mg daily

factor contributing to the perception of hair loss and hair thinning in aging women. At times, a thicker hair diameter can compensate for a decrease in density. Over time, however, just as with hair

density, hair diameter decreases, occurring after age 30.6,8 These changes of decreased hair density and hair diameter lead to physiological hair thinning in all aging women.


Harfmann and Bechtel


FPHL is the most common cause of diffuse hair loss in women, with a prevalence of 32% in white women over 20.9 While most women experience onset of their hair loss after age 50, it can occur any time after menarche. By age 70, more than half of women will have signs of FPHL. Heritability of graying and frontotemporal hairline recession in women has been demonstrated in twin studies, but it is yet to be verified that heritability plays a role in FPHL as it does in male pattern hair loss (MPHL).10 PATHOPHYSIOLOGY

The term ‘‘androgenetic alopecia’’ is often used interchangeably with FPHL, although the role of androgens, while clearly defined in MPHL, is less clear in FPHL. Women with hyperandrogenism often develop FPHL, but most women with FPHL have normal androgen levels.9 Despite normal systemic androgen levels, many women may have increased levels of androgens locally at the level of the follicle.10 The most important androgen appears to be dihydrotestosterone (DHT), which has a 5-fold higher affinity for the androgen receptor than testosterone. Its effect at the follicular level includes miniaturization of the hair and follicles by accelerating the mitotic rate in the hair matrix, shortening of the hair cycle, increasing telogen shedding, and increasing the duration of kenogen.11 Androgens alone are not sufficient for FPHL, as FPHL has been described in cases of complete androgen insensitivity syndrome and no detectable androgen levels.12,13 It is possible that estrogens may play an additional protective role in women, potentially through inhibition of 5-a reductase. This is supported by lower estrogen levels at menopause, postpartum, and with aromatase inhibitor therapy—all settings that may demonstrate FPHL.10 In addition, the frontal hairlines of women have higher levels of

aromatase than other areas of the scalp, and the resultant increased conversion of testosterone to estradiol in this region may partially explain the relative preservation of the frontal hairline in FPHL.14 Other potential pathophysiological mechanisms include insulin resistance, microvascular insufficiency, or inflammatory abnormalities.10 CLINICAL FEATURES

The typical pattern in FPHL consists of frontal hair thinning with widening of the midline part in a Christmas tree pattern (Fig. 3). The underlying scalp appears normal without visible signs of inflammation. The Ludwig scale and the Sinclair scale are 2 pictorial measurement systems to grade the severity of FPHL.9 Many women initially report increased hair shedding without a noticeable change in density, and a hair pull test may be positive for increased telogen hairs in active FPHL; this may be diagnostically difficult to distinguish from TE.9,14 Some women may report temporal thinning as the first manifestation. As in aging women, women with FPHL experience miniaturization of the hair follicles and a decrease in fiber length and diameter, resulting in replacement of their hair by short, fine, vellus hairs.14 DIAGNOSIS AND WORKUP

The diagnosis of FPHL is largely a clinical diagnosis, with biopsies reserved for atypical presentations. It is reasonable to consider routine blood work checking serum androgens, thyroid studies, iron studies with ferritin, prolactin level, and zinc level in all women, although some advise that these are best ordered on a case-by-case basis.10 In a premenopausal woman presenting with FPHL, it is important to exclude polycystic ovarian syndrome (PCOS). A history of menstrual disturbance, impaired fertility, or signs of hyperandrogenism during the history taking should alert the clinician to possible underlying PCOS. Approximately 20% of women with PCOS will

Hair Loss in Women have androgenetic alopecia, and in those women that do, they are also more likely to have hirsutism or moderate acne. Biochemical hyperandrogenism among patients with PCOS seems to have no impact on the development of FPHL in certain patients.15 The most likely conditions that may mimic FPHL are TE and alopecia areata incognita. TE should not be associated with a decreased hair density, but this can be difficult to distinguish from early FPHL, where there is not yet a decrease in density. A scalp biopsy may be useful to more firmly establish a diagnosis. Alopecia areata incognita involves abrupt, diffuse shedding of telogen hairs, rather than the patchy hair loss typical of classic alopecia areata. It is a very rare form of hair loss that has been described predominantly in young women.9 TREATMENT

Women presenting with FPHL often have different expectations regarding treating their hair loss; it is important to decipher whether a particular woman is wanting to reverse the process, halt progression, or simply camouflage with more cosmetic treatments. In many women, a multifaceted approach using a combination of treatments is indicated. An overview of potentially effective treatment options is supplied in Table 3. The most commonly used current treatments are discussed in more detail below.


effects from treatment may include facial hypertrichosis, contact dermatitis, pruritus, scale, and dryness.14 The 5% foam formulation, though not FDA approved for women, may be as effective as the 2% solution with a more favorable side effect profile.16 It is important to counsel patients that it may take up to 1 year to see its full effects, and hair loss will resume upon cessation. Unless it is not tolerated, it should be a component of every woman’s regimen for FPHL, as its beneficial effects are supported by several randomized controlled trials. Ketoconazole shampoo 2% is a reasonable adjunctive agent in regimens for FPHL. It is anti-inflammatory, reduces colonization by Malassezia on the scalp, and decreases DHT levels at the hair follicle.10 Oral ketoconazole has known antiandrogen effects, and topical ketoconazole shampoo may suppress androgen receptor activity. Although there are currently no studies in women, its use in MPHL has been associated with an increase in hair density and size of anagen follicles. While it does not have data to support its use as monotherapy, it can easily and safely be used in a combination regimen.17 Other potential topical pharmacologic agents that may be beneficial include the topical antiandrogen fluridil, topical estrogen preparations, and topical prostaglandin inhibitors like latanoprost, although these are either expensive or not yet readily available.14,18,19


Minoxidil 2% solution is the only medication approved by the Food and Drug Administration (FDA) for FPHL. The mechanism of action in FPHL is unknown, although its effect is an increase in anagen duration and hair diameter, as well as a shortening of the kenogen phase. Its effects are androgen independent, so it is a reasonable option for both premenopausal and postmenopausal women, with or without hyperandrogenism. Side


Finasteride is an inhibitor of 5-a reductase type 2, the isotype of the enzyme found most frequently in hair follicles. It, therefore, results in decreased levels of DHT at the follicle. Although FDA approved in MPHL at a dose of 1 mg daily, finasteride’s use in women is off-label. Unfortunately, the only large-scale multicenter, randomized, placebo-controlled trial of finasteride in FPHL failed to show a significant benefit


Harfmann and Bechtel

after 1 year of use at 1 mg daily.20 Importantly, this study included solely postmenopausal women; there have been subsequent case series and cohort studies of finasteride at higher doses of 2.5 to 5 mg daily that have shown finasteride to be efficacious, and these studies have included both premenopausal and postmenopausal women as well as both normoandrogenemic and hyperandrogenemic women.21–23 Fortunately, finasteride tends to be well tolerated, with minimal side effects consisting of headache, depression, nausea, and hot flashes. Proper patient selection must be employed, as teratogenicity is a concern; women of childbearing age should be counseled on the risk of pregnancy and ideally should also be on a contraceptive.14 There has been an association of 5-a reductase inhibitors and breast cancer in men taking the medication, though there is not longterm data in women to corroborate this. Reassuringly, a recent large case-control study in the urologic literature did not find an association and suggested that development of breast cancer not influence prescribing of reductase inhibitors.24 At this point in time, the successful use of finasteride is unpredictable. Further studies may better elucidate subsets of patients with FPHL that may be more likely to respond to treatment with finasteride. Dutasteride is a newer reductase inhibitor of both types 1 and 2 5-a reductase. Its inhibition of the type 2 isotype is more rapid and potent than that of finasteride, resulting in a 90% reduction in serum DHT, compared with 70% with finasteride.14 There is clear evidence of its successful use in MPHL, with some studies demonstrating its superiority over finasteride at certain dosages.25–27 There has been only 1 report of successful use of dutasteride 0.5 mg daily in FPHL.11 The side effects, teratogenicity, and possible association with breast cancer are the same as those for finasteride. A much longer half-life, however, may allow less frequent dosing.28

TABLE 4. Adjuvant Treatments for Hair Loss Adjuvant Treatment


Caffeine Cimetidine



Zinc Zinc pyrithium shampoo


Regulates mitochondrial carboxylase enzymes in hair roots No clinical trials showing efficacy May counteract testosterone effects on hair follicles Available in topical preparations Peripheral antiandrogen that may block binding of DHT to the androgen receptor 300 mg 5 times daily Suggested to maintain level >40 ng/dL Lack of ferritin may cause follicles to enter telogen phase May have antiandrogenic effects at the hair follicle No evidence that oral supplementation helps Can be compounded for topical use in alcohol and glycerin Supplement 8-15 mg daily Has anti-inflammatory and antioxidant effects May increase total visible hair counts

DHT indicates dihydrotestosterone.


Spironolactone has no FDA approval for any dermatologic conditions, although is a common treatment for acne, hirsutism, and FPHL. It competitively blocks androgen receptors and weakly inhibits adrenal androgen production.9 There are no randomized controlled trials supporting its use in FPHL, but case reports, case series, and an openlabel trial indicate that it may be a useful treatment for FPHL.29–31 Typical dosing should start at 50 mg daily and increase to 100 to 200 mg daily as tolerated. There may be some transient side effects of lethargy, nausea, breast tenderness, and menorrhagia that often improve after 3 months of treatment. More lasting side effects may include

Hair Loss in Women hypotension, hyperkalemia, headache, weight loss, increased urinary frequency, and dry skin.14 Spironolactone is pregnancy class D and should either be avoided in women of childbearing age or combined with a contraceptive agent. In addition to their contraceptive effect, concurrent oral contraceptive pills may increase the therapeutic effect and minimize menstrual irregularities while on spironolactone.9 Cyproterone acetate is a synthetic steroid that competes with DHT for androgen receptor binding. It is currently not available in the United States, but is approved for use in Europe and Canada. It may be beneficial in some cases of FPHL, particularly those with hyperandrogenism, although studies have shown conflicting results. As with other antiandrogens, side effects may include menstrual irregularities and breast tenderness; contraception is advised while on cyproterone due to teratogenicity.14 Flutamide is another competitive blocker of the androgen receptor. The best study supporting its use was an open-label study comparing flutamide to finasteride and cyproterone; flutamide 250 mg daily resulted in the most improvement of hair growth of the 3 agents.32 Its most serious side effect is hepatotoxicity and liver failure, and a black box warning exists for these potential adverse effects. Baseline liver function tests and periodic monitoring throughout treatment is recommended.14 LOW-LEVEL LIGHT THERAPY

Low-level light therapy consists of devices with light-emitting diodes (650 to 900 nm). Their exact mechanism in hair growth induction is unclear, although it is postulated that they may activate dormant hair follicles, increase follicular blood flow, or upregulate the production of ATP.14 The HairMax laser comb was approved for FPHL in 2011. This device has 9 laser beams aligned with hair combs that target the energy toward the scalp when the hair is parted with the comb. A


randomized controlled trial found efficacy with using the device 3 times weekly for 15 minutes.33 A newer device, the Oaze, is a helmet-shaped device that emits 3 wavelengths of light. A randomized controlled trial using the device for 18 minutes daily for 6 months improved hair diameter, although patient perception was that of no improvement.34 SUPPLEMENTS AND ADJUVANT TREATMENTS

Many times women with hair loss present either having been on over-the-counter supplements or desiring a more ‘‘natural’’ treatment as a first step. An overview of additional options is provided in Table 4. HAIR TRANSPLANTATION

Surgical treatment of FPHL may be an option for women that have failed traditional medical treatment or desire something more aggressive. Successful treatment relies on proper patient selection. Because the donor site of hair follicles typically lies over the occipital scalp, the ideal patient would have extensive frontal thinning with dense hair in the occipital region.9 This may be more difficult in women than men, as women often have some degree of thinning in the occipital area as well.10 COSMETIC TREATMENTS

In addition to the medical and surgical options discussed above, there are treatments for hair loss with the goal of simply masking the clinical appearance and making the hair loss less noticeable. Some women may desire these options as primary treatments, opting to forgo other more aggressive treatments to stabilize or reverse the hair loss. Other women who are attempting to find a successful medical regimen may be frustrated by the period of 6 to 12 months of treatment often required to assess efficacy, and they may desire some options while undergoing other treatments.


Harfmann and Bechtel

TABLE 5. Functional Type of TE

Headington Variants of Telogen Effluvium Mechanism

Immediate Follicles anagen stimulated to release leave anagen and enter telogen prematurely Prolongation of Delayed anagen results in anagen delayed, but release synchronous onset of telogen shedding Immediate Drug-induced telogen shortening of release telogen leading to follicles reentering anagen prematurely Short Idiopathic anagen shortening of syndrome anagen duration causing persistent telogen shedding Delayed Prolonged telogen telogen and delayed release transition to anagen


Acute TE

Physiologic stress Severe illness Drug-induced

Childbirth Interruption of longterm OCPs Systemic disease Fever Psychoemotional stress Weight loss

Telogen gravidarum OCP discontinuation Minoxidil initiation

Majority of CTE

Seasonal hair loss

CTE indicates chronic telogen effluvium; OCP, oral contraceptive pill; TE, telogen effluvium.

There are several leave-in products that aim to increase hair fiber diameter. A leave-on combination product including caffeine has been shown to increase hair cross-sectional area by 10%.35 Other leave-in conditioners may temporarily increase the hair shaft diameter by containing proteins that coat the hair shaft.36 Camouflaging options include hair building fibers and tinted hair sprays and lotions aimed to minimize the appearance of the scalp through thinning hair. Of course, hair pieces, wigs, and extensions are further options.

TABLE 6. Conditions Associated With Telogen Effluvium Chronic Diffuse Telogen Hair Loss

Thyroid disorders Iron deficiency Vitamin D deficiency Zinc deficiency Crash dieting, starvation Metabolic disturbances (renal failure, liver failure) Malignancy

Inflammatory scalp disorders—contact dermatitis to hair dye Seasonal variation HIV (July-October) Drugs Lithium Sodium valproate Lamotrigine SSRIs Anticoagulants (LMWH) b-blockers ACEi Oral retinoids Isoniazid HIV medications HPV vaccine

ACEi indicates angiotensin-converting enzyme inhibitors; HIV, human immunodeficiency virus; HPV, human papilloma virus; LMWH, low–molecular weight heparin; OCP, oral contraceptive pill; SSRI, selective serotonin reuptake inhibitor.

Women should be given tips on styling hair that may help mask the appearance of FPHL. They should avoid manipulating wet hair, as wet hair is most subject to trauma. Instead, hair should be detangled with the fingers and slightly dried before detangling with a wide-toothed comb. In general, the less that is done to thinning hair, the better. Any styling product that is used should be massaged into the base of the hair. The hair may then be dried while bending over, which gives the illusion of fullness. Hair spray is perhaps the most important product for hair loss, as it allows rearrangement of hair to cover thinning areas.36

Hair Loss in Women


FIGURE 4. Flowchart demonstrating the evaluation of telogen hair loss. ACEi indicates angiotensin-converting enzyme inhibitor; CBC, complete blood count; FPHL, female pattern hair loss; HIV, human immunodeficiency virus; HPV, human papilloma virus; LMWH, low– molecular weight heparin; OCP, oral contraceptive pill; SSRI, selective serotonin reuptake inhibitor; TE, telogen effluvium.


Chronic telogen effluvium (CTE), in contrast, seems to only affect women.38


The true incidence and prevalence of TE is unknown, as most cases are subclinical. In acute telogen effluvium (ATE), theoretically either men or women could present if a preceding inciting condition occurred. However, more women tend to present to their health care providers, likely because hair loss is more distressing in this population. Also, as hormonal changes in the postpartum period are a common cause of ATE, affecting nearly one third to one half of women after childbirth, it likely truly is seen more commonly in women than men.37


TE represents an abnormality of hair cycling during which a greater percentage of scalp hairs are in the telogen phase than normal. Headington described 5 different functional variants of TE that, despite different mechanisms, share a common endpoint of telogen shedding. These are reviewed in Table 5.39 Postpartum TE, or telogen gravidarum, deserves special mention, as the hair loss is directly attributable to the hormonal milieu surrounding pregnancy and the


Harfmann and Bechtel

postpartum period. Estrogens, which are known to prolong the anagen phase, are elevated during pregnancy. Following delivery, they abruptly return to normal levels within several days. This return is accompanied by a synchronous transition to the telogen phase and resultant shedding.40 The etiology of CTE remains to be determined, as women usually do not have a preceding trigger as they do in ATE. A majority of women with CTE do have evidence histologically of follicular miniaturization, which may indicate that early FPHL could be responsible for the excessive shedding seen.41 CLINICAL FEATURES

ATE Women with ATE generally present with the complaints of increased hair loss while washing hair and while combing or brushing hair. There is usually accompanying anxiety that this rate of hair loss will lead to baldness. Despite excessive hair shedding, there is an essentially normal visible hair density. History taking will elicit an inciting cause 2 to 3 months before onset in a third of cases. The usual cause is immediate anagen release, with the most common underlying causes presented in Table 6. Delayed anagen release is responsible for postpartum TE and hair loss occurring after cessation of oral contraceptive agents.39 In postpartum TE, time to hair loss often occurs 2 to 3 months postpartum, though can be delayed up to 6 months depending on the length of the telogen phase. Interestingly, the TE may be more pronounced if delivery occurs in the fall, as the time of postpartum TE would coincide with increased seasonal hair shedding occurring during the winter months. Breastfeeding may partially mitigate the TE due to the effects of prolactin, as lactating women continue to have an elevated anagen to telogen ratio at 4

months postpartum compared with nonlactating women.40 Telogen shedding usually remits within several months in most cases of ATE. Some women will notice continued shedding if the hair follicles do not convert back to asynchronous cycling. Postpartum TE often resolves by 12 months postpartum, even if the mother is breastfeeding.40 At times, an episode of ATE will unmask an underlying FPHL; likewise, some elderly women may not have a full recovery if they have concurrent FPHL.42 CTE Women with CTE experience a prolonged, fluctuating course of TE lasting >6 months. Usually, no trigger is identified, although some cases represent a continuation of ATE with a shortened anagen phase. This shortened anagen phase underlies a complaint of shortened hair, in addition to the hair shedding seen with all cases of TE.43 The natural history of CTE is poorly characterized. Although many believe it to be a self-limited disease, there are few longitudinal studies supporting this notion. Some women with the diagnosis of CTE eventually are reclassified as having FPHL after follow-up biopsies, but it does appear that women can have stable CTE for years without noticeable reduction in hair density.37,44 Chronic Diffuse Telogen Hair Loss (CDTHL) Women with CDTHL experience telogen hair loss lasting >6 months, just as in CTE. These women, however, have a reversible and reproducible cause of the telogen hair loss.37 Typical causes of CDTHL can be reviewed in Table 6, with further elaboration on some more common causes below. Both hypothyroidism and hyperthyroidism are associated with CDTHL. This is usually reversible upon reestablishment of the euthyroid state, although at times,

Hair Loss in Women longstanding hypothyroidism may cause hair follicle atrophy.45 Thyroid peroxidase antibodies have been found in a significant percentage of women with TE, although their significance and implications for treatment are not yet determined.46 Iron deficiency anemia is known to be 1 causative factor of CDTHL, as iron is required for follicles to enter the anagen phase of the hair cycle.39 Replacement with iron supplementation should reverse the hair loss. Iron deficiency without anemia is more controversial regarding its potential relationship to CDTHL.47 Drug-induced CDTHL occurs mechanistically through immediate anagen release in most cases.39 It typically occurs within 6 to 12 weeks of starting the medication, continues to progress while on the medication, and then subsides after stopping the offending medication.48 There are no controlled trials proving a causal relationship for specific medications, but if a medication is suspected, it should be stopped for a period of at least 3 months to test its relationship to the hair loss.37 DIAGNOSIS AND WORKUP

A guide to evaluating telogen hair loss is presented in Figure 4. ATE is a clinical diagnosis that can usually be made with a thorough history and physical examination alone. Because it, by definition, is self-limiting, no further workup is required. Occasionally, early FPHL may present with an ATE, but this does not need to be considered until the TE has persisted beyond 6 months. At that time, there may be other clinical signs of early FPHL and histologic findings of TE may be present. Any patient presenting with CTE requires exclusion of causes of CDTHL. Patients should routinely receive a laboratory workup that includes complete blood count and thyroid function tests.49 There is currently not evidence to support screening for iron deficiency for supplementation in hair loss in the absence of


anemia. However, treatment for hair loss tends to be more effective in the setting of a serum ferritin >70 ng/dL. It may be worthwhile, therefore, to screen and treat for iron deficiency in appropriate patients, including those that may not be responding to treatment.47 Other testing may be indicated for other causes of CDTHL in Table 6, but does not need to be done on a routine basis.49 The main diagnoses in the differential for TE include other causes of diffuse, nonscarring, hair loss including FPHL and alopecia areata incognita. Because clinically, they can appear quite similar, a punch biopsy can sometimes help make the distinction. The patient should be referred to a dermatologist if the hair loss is persisting and the diagnosis is not yet clear. TREATMENT

Treatment for TE consists primarily of reassurance, counseling, and correction of potential underlying causes.50 Women usually fear that they will lose all of their hair, and reassurance that TE does not lead to baldness can be very settling. There are currently no proven vitamins or supplements for any form of hair loss.50 A balanced diet with an adequate protein source and healthy weight are of utmost importance. In the setting of iron deficiency anemia, replacement with oral ferrous sulfate for 3 to 6 months to replenish iron stores is a reasonable first step.49 Patients with CTE should continue to be followed for development of FPHL, as this is the most common combination of hair loss. Treatment for FPHL can be initiated at the 6-month follow-up if thinning on the crown is seen on examination.49

Conclusions Women may frequently present to the obstetrician/gynecologist with a complaint of hair loss. It is important to not underestimate the emotional impact of this hair loss, which often seems out of proportion to its


Harfmann and Bechtel

clinical severity. Because studies have demonstrated that the burden of hair loss may be comparable with chronic or life-threatening diseases, being able to adequately assess and treat hair loss can make a profound difference in women’s lives.1 While progressive and scarring forms of hair loss should preferentially be managed by a dermatologist, nonscarring diffuse alopecias may be initially diagnosed and managed by the obstetrician/gynecologist. Careful attention to history taking and a brief examination are often all that is required to diagnose FPHL and TE. Even if successful treatment is not attained, women will often be grateful to the physician that takes the time to fully assess their devastating hair loss.

References 1. Cash TF. The psychology of hair loss and its implications for patient care. Clin Dermatol. 2001;19:161–166. 2. Jackson AJ, Price VH. How to diagnose hair loss. Dermatol Clin. 2013;31:21–28. 3. Finner AM. Nutrition and hair: deficiencies and supplements. Dermatol Clin. 2013;31:167–172. 4. Amor KT, Rashid RM, Mirmirani P. Does D matter? The role of vitamin D in hair disorders and hair follicle cycling. Dermatol Online J. 2010;16:3. 5. Kantor J, Kessler LJ, Brooks DG, et al. Decreased serum ferritin is associated with alopecia in women. J Invest Dermatol. 2003;121:985–988. 6. Messenger AG. Hair through the female life cycle. Br J Dermatol. 2011;165 (s3):2–6. 7. Courtois M, Loussouarn G, Hourseau C, et al. Ageing and hair cycles. Br J Dermatol. 1995;132: 86–93. 8. Mirmirani P. Hormonal changes in menopause: do they contribute to a ‘midlife hair crisis’ in women? Br J Dermatol. 2011;165 (s3):7–11. 9. Sinclair R, Patel M, Dawson TL Jr, et al. Hair loss in women: medical and cosmetic approaches to increase scalp hair fullness. Br J Dermatol. 2011;165 (s3):12–18. 10. Atanaskova Mesinkovska N, Bergfeld WF. Hair: what is new in diagnosis and management? Female pattern hair loss update: diagnosis and treatment. Dermatol Clin. 2013;31:119–127. 11. Olszewska M, Rudnicka L. Effective treatment of female androgenic alopecia with dutasteride. J Drugs Dermatol. 2005;4:637–640.

12. Cousen P, Messenger A. Female pattern hair loss in complete androgen insensitivity syndrome. Br J Dermatol. 2010;162:1135–1137. 13. Orme S, Cullen D, Messenger A. Diffuse female hair loss: are androgens necessary? Br J Dermatol. 1999;141:521–523. 14. Levy LL, Emer JJ. Female pattern alopecia: current perspectives. Int J Womens Health. 2013;5: 541–556. 15. Quinn M, Shinkai K, Pasch L, et al. Prevalence of androgenic alopecia in patients with polycystic ovary syndrome and characterization of associated clinical and biochemical features. Fertil Steril. 2014;101:1129–1134. 16. Blume-Peytavi U, Hillmann K, Dietz E, et al. A randomized, single-blind trial of 5% minoxidil foam once daily versus 2% minoxidil solution twice daily in the treatment of androgenetic alopecia in women. J Am Acad Dermatol. 2011;65: 1126–1134. 17. Pierard-Franchimont C, De Doncker P, Cauwenbergh G, et al. Ketoconazole shampoo: effect of long-term use in androgenic alopecia. Dermatology. 1998;196:474–477. 18. Sovak M, Seligson A, Kucerova R, et al. Fluridil, a rationally designed topical agent for androgenetic alopecia: first clinical experience. Dermatol Surg. 2002;28:678–685. 19. Blume-Peytavi U, Lonnfors S, Hillmann K, et al. A randomized double-blind placebo-controlled pilot study to assess the efficacy of a 24-week topical treatment by latanoprost 0.1% on hair growth and pigmentation in healthy volunteers with androgenetic alopecia. J Am Acad Dermatol. 2012;66:794–800. 20. Price VH, Roberts J, Hordinsky M, et al. Lack of efficacy of finasteride in postmenopausal women with androgenetic alopecia. J Am Acad Dermatol. 2000;43:768–776. 21. Iorizzo M, Vincenzi C, Voudouris S, et al. Finasteride treatment of female pattern hair loss. Arch Dermatol. 2006;142:298–302. 22. Shum K, Cullen D, Messenger A. Hair loss in women with hyperandrogenism: four cases responding to finasteride. J Am Acad Dermatol. 2002;47:733–739. 23. Yeon J, Jung J, Choi J, et al. 5 mg/day finasteride treatment for normoandrogenic Asian women with female pattern hair loss. J Eur Acad Dermatol Venereol. 2011;25:211–214. 24. Bird S, Brophy J, Hartzema A, et al. Male breast cancer and 5a-reductase inhibitors finasteride and dutasteride. J Urol. 2013;190:1811–1814. 25. Eun H, Kwon O, Yeon J, et al. Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: a randomized, double-blind, placebo-controlled, phase III study. J Am Acad Dermatol. 2010;63:252–258.

Hair Loss in Women 26. Olsen EA, Hordinsky M, Stough D, et al. The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. J Am Acad Dermatol. 2006;55:1014–1023. 27. Stough D. Dutasteride improves male pattern hair loss in a randomized study in identical twins. J Cosmet Dermatol. 2007;6:9–13. 28. Micromedex Healthcare Series. DRUGDEX System. Greenwood Village, CO: Truven Health Analytics; 2013Available at: http://www.micromedexsolutions. com/micromedex2/librarian. Accessed April 27, 2014. 29. Adamopoulos D, Karamertzanis M, Nicopoulou S, et al. Beneficial effect of spironolactone on androgenic alopecia. Clin Endocrinol (Oxf). 1997;47:759–760. 30. Burke B, Cunliffe W. Oral spironolactone therapy for female patients with acne, hirsutism or androgenic alopecia. Br J Dermatol. 1985;112:124–125. 31. Yazdabadi A, Green J, Sinclair R. Successful treatment of female-pattern hair loss with spironolactone in a 9-year-old girl. Australas J Dermatol. 2009;50:113–114. 32. Carmina E, Lobo R. Treatment of hyperandrogenic alopecia in women. Fertil Steril. 2003;79:91–95. 33. Leavitt M, Charles G, Heyman E, et al. HairMax LaserComb laser phototherapy device in the treatment of male androgenetic alopecia: a randomized, double-blind, sham device-controlled, multicentre trial. Clin Drug Ivestig. 2009;29:283–292. 34. Kim H, Choi J, Kim J, et al. Low-level light therapy for androgenetic alopecia: a 24-week, randomized, double-blind, sham device-controlled multicenter trial. Dermatol Surg. 2013;39:1177–1183. 35. Davis MG, Thomas JH, van de Velde S, et al. A novel cosmetic approach to treat thinning hair. Br J Dermatol. 2011;165 (s3):24–30.


36. Draelos ZD. Shampoos, conditioners, and camouflage techniques. Dermatol Clin. 2013;31:173–178. 37. Harrison S, Sinclair R. Telogen effluvium. Clin Exp Dermatol. 2002;27:389–395. 38. Whiting DA. Chronic telogen effluvium. J Am Acad Dermatol. 1996;35:899–906. 39. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol. 1993;129: 356–363. 40. Gizlenti S, Ekmekci T. The changes in the hair cycle during gestation and the post-partum period. J Eur Acad Dermatol Venereol. 2014;28: 878–881. 41. Patel M, Harrison S, Sinclair R. Drugs and hair loss. Dermatol Clin. 2013;31:67–73. 42. Chen W, Yang C-C, Todorova A, et al. Hair loss in elderly women. Eur J Dermatol. 2010;20: 145–151. 43. Sinclair R. Diffuse hair loss. Int J Dermatol. 1999;38 (s1):8–18. 44. Sinclair R. Chronic telogen effluvium: a study of 5 patients over 7 years. J Am Acad Dermatol. 2005; 52 (s1):12–16. 45. Church R. Hypothyroid hair loss. Br J Dermatol. 1956;77:661–663. 46. Baldari M, Guarrera M, Rebora A. Thyroid peroxidase antibodies in patients with telogen effluvium. J Eur Acad Dermatol Venereol. 2010;24:980–982. 47. Trost L, Bergfeld WF, Calogeras E. The diagnosis and treatment of iron deficiency and its potential relationship to hair loss. J Am Acad Dermatol. 2006;54:824–844. 48. Brodin M. Drug-related alopecia. Dermatol Clin. 1987;5:571–579. 49. Grover C, Khurana A. Telogen effluvium. Indian J Dermatol Venereol Leprool. 2013;79:591–603. 50. McMichael A. Approach to office visits for hair loss in women. Cutis. 2011;87:8–9.

Hair loss in women.

Hair loss is a common cause of morbidity for many women. As a key member of the woman's health care team, the obstetrician/gynecologist may be the fir...
342KB Sizes 5 Downloads 11 Views