Female pattern hair loss:
A review of diagnosis and treatment

Melissa Raue, PA-C

Ms. Raue works in a dermatology practice in Ridgefield, Conn. The author has indicated no relationships to disclose relating to the content of this article.

Most medical treatment is minimally effective, but all patients will benefit from gaining an understanding of their diagnosis and from the reassurance and support provided by a concerned and knowledgeable clinician.

Alopecia, the excessive or abnormal loss of hair, can occur in both men and women. Many men experience androgenetic alopecia (AGA), known to the general public as male pattern hair loss or baldness. Women can develop a similar condition, known as hereditary thinning or female pattern hair loss (FPHL). Since the influence of androgens may be only one of several paths leading to patterned hair loss in women, FPHL may be a more accurately descriptive term until other mechanisms involved in normal aging and hair cycle disruption are clarified.¹

Women may develop AGA at any time after puberty, although onset peaks in the third and fifth decades, in perimenopause, or at other times of hormonal change.² Women with FPHL do not become completely bald but instead experience diffuse thinning with an emphasis on the top of the scalp. Women often notice first a more visible central scalp or a widening part in addition to reduced overall hair volume. AGA represents the gradual transformation of normal (long, thick, pigmented) terminal hairs to miniaturized (short, fine, hypopigmented) hairs.

The true prevalence of FPHL is difficult to determine because the diagnostic criteria and particular patterns of loss are described differently by different authors.^3-5 An episode of sudden hair loss, as after childbirth or major illness, may uncover a latent predisposition to hereditary hair thinning. This type of sudden loss can also occur repeatedly, overlapping clinically with both AGA and the thinning that comes with menopause. A commonly cited statistic is that 50% of women will experience some degree of thinning by age 50 years; some other studies put this number as high as 87%.^6,7 Thirty million women have hereditary hair thinning; this figure is overlaid by the number of postmenopausal women who experience a normal degree of senescent hair loss.

Other less common causes of hair loss are the effects of inflammatory cells on hair follicles, physiologic factors other than androgens, and mechanical factors. Before investigating the causes, the clinician must determine whether the loss is of the scarring or nonscarring type and whether it is diffuse, patchy, or patterned. Scarring indicates that there has been permanent destruction of hair follicles, which were replaced by fibrous tissue. Hair will never regrow in such areas. The scalp, which may remain soft and supple, looks smooth and shiny. By contrast, in nonscarring alopecia, follicles are visible and may be empty or have abnormal hair. In a diffuse pattern, hair is lost evenly from all parts of the scalp rather than in patches, a pattern characterized by considerable loss in a defined area. In patterned hair loss, certain areas are affected more than others.

Anatomy and pathophysiology

Hair is a modified type of keratin produced by the hair matrix. Short, fine vellus hair covers all of the body except the palms and soles. Terminal hair is the long, coarse, pigmented hair found on the scalp and in the eyebrows and eyelashes, as well as in the axillae and pubic area after puberty. The scalp contains between 100,000 and 150,000 hairs. The hair cycle–the three phases of hair production and shedding–occurs randomly in each follicle over the scalp, resulting in the loss of up to 100 hairs daily. Each scalp follicle goes through the cycle 10 to 20 times in a lifetime. Over time, telogen, the third or resting phase, becomes longer and the rate of hair growth slows; thus, hair density gradually decreases, and the hairs become finer with age.

AGA in women can be inherited both maternally and paternally. In this condition, the hairs are genetically programmed to miniaturize under the influence of postpubertal androgens, with terminal hairs gradually being replaced during telogen by vellus hairs. In females, these androgens are produced systemically by the ovaries and adrenal glands and peripherally by endocrine-sensitive hair follicles and sebaceous glands. In genetically marked follicles, reduction of testosterone to dihydrotestosterone (DHT) by the enzyme 5α-reductase is increased. The same process takes place in both males and females, although its expression is milder in females because of their lower levels of circulating testosterone and higher levels of aromatase, an enzyme that aromatizes testosterone to estradiol. Increased hair shedding and mild inflammation can also be parts of this process.

Anagen effluvium is a diffuse loss of anagen hairs from growing follicles. Since 90% of hairs are in anagen (the growing phase) at any given time, processes that interfere with this phase can cause massive hair loss. Anagen effluvium occurs within a few weeks of the inhibition of cell division in the hair bulb. Causes include cytotoxic drugs, radiation therapy, endocrine diseases, scarring alopecias, and severe protein malnutrition. Although the diffuse alopecia that occurs is severe, if it is not due to a scarring process,hair growth will resume once the inhibitory influence is removed.

Telogen effluvium is a disruption to hairs in the telogen phase of the cycle. Postpartum telogen effluvium is familiar to many women who have been pregnant. During pregnancy, the anagen phase is interrupted, causing many hairs to cycle into telogen and increasing the telogen proportion from the normal 5% to 10% of hairs to 20% to 30% or more. The cycle resumes at delivery, leading to considerable shedding 2 to 3 months later. Interestingly, patients taking oral contraceptives and those who have discontinued hormone replacement therapy can experience the same phenomenon. In addition to childbirth, common causes of acute telogen effluvium include febrile illnesses, surgery, chronic systemic diseases, crash diets, mechanical traction from tight hairstyles, severe emotional stress, and drugs. Ninety-five percent of cases of acute telogen effluvium resolve within the year following the crisis, but if chronic disease or stress is present, hair loss can continue longer. In chronic telogen effluvium, the clinician should rule out thyroid disorder, syphilis, and iron deficiency.

Alopecia caused by drugs and chemicals may be telogen or anagen effluvium or nonspecific. Some of the drugs known or suspected of causing hair loss are listed in Table 1. Chemical causes include arsenic in pesticides, lead, and thallium salts found in rodent poison.

The scalp is vulnerable to various dermatoses, including tinea capitis, which produces a patchy alopecia with broken-off hairs and variable degrees of inflammation, scaling, and crusting. Although children are most affected, this condition can also occur in adults, particularly in wrestlers or other persons having close skin contact. Alopecia areata, another cause of a patchy alopecia, can occur at any age. Of unknown cause, it is manifested by smooth, round patches of scalp with follicles present and is an example of a nonscarring alopecia. In rare cases, the hair loss can be complete, although in milder cases the hair usually returns. Chronic cutaneous (discoid) lupus causes one form of scarring alopecia, although during acute toxic exacerbations of systemic disease, a diffuse nonscarring hair loss can occur. Frontal alopecia with short, broken-off hairs has been referred to as lupus hair. Secondary syphilis can also cause a diffuse alopecia, and although these are uncommon causes of alopecia in the absence of other symptoms, keeping syphilis and systemic lupus erythematosus (SLE) in the differential diagnosis is prudent.

Improper hair care can damage either the hair shaft or the follicle. African-American patients are particularly at risk because of hair-grooming techniques that may involve the use of harsh chemical straighteners. These products can fray the hair shaft and also increase the risk for a type of scarring alopecia called follicular degeneration syndrome, or "hot comb alopecia." Most chemical treatments are safe unless they are employed too frequently or incorrectly, but tightly pulled hairstyles such as fine cornrow braids can lead to damage of the follicle, resulting in permanent hair loss. Trichotillomania, the habit of pulling out hair when under stress, can also damage both the hair shaft and (if chronic) the hair follicle. Although this practice is more common in children, it can also occur in adult women

History

The clinician should determine exactly what the patient means when she complains of hair loss. If she has noticed an increased number of hairs falling out daily but no bald areas are seen, an irregularity in the hair cycle (telogen or anagen effluvium) may be to blame. A patient who has not noticed excessive hair loss but complains of having less hair may be experiencing a diffuse loss from genetic FPHL or normal senescent thinning. However, a careful history is needed to rule out the less obvious causes of hair loss, such as thyroid disease or other endocrine disorders, poor nutritional status, iron deficiency, drugs, severe infection, and systemic disease (particularly secondary syphilis and SLE). The next series of questions should explore signs, symptoms, and patient habits to distinguish between normal and pathologic hair loss. Ask about pregnancy, menstrual irregularities or heavy menses, recent illness, weight change, nausea, and altered bowel habits. Determine whether urinary changes such as hematuria or oliguria, heat or cold intolerance, or joint pain or stiffness is present. If questioning reveals a probable reversible process such as pregnancy, strict dieting, or surgery, you can reassure the patient that her hair will most likely regrow after the crisis has passed. A fluctuant course with showers of hair loss every few years, however, may be a sign of the inexorable progression of AGA; a woman with the genetic predisposition to hereditary hair thinning may not fully regrow her hair following the shedding episode.⁸ Since 20% of hair can be lost before the loss becomes evident, follow-up is crucial.

Drugs, particularly anticancer agents, anticoagulants, anticonvulsants, thyroid drugs, β-blockers, and tricyclic antidepressants, can cause diffuse thinning. Although pesticides are not a common cause, determine whether the patient has been exposed to these toxins. If a drug or chemical exposure is the cause, discontinuing the offending agent is usually followed by hair regrowth.

A history of thinning or balding on both sides of the family is important. AGA is autosomal recessive and so may show on either the maternal or the paternal side in the immediate family and in aunts, uncles, and grandparents. The patient’s hairstyle history can also be revealing. She will know whether she has had to use smaller hair clips, style her hair shorter, or arrange it to hide thinning toward the top. These are all signs that FPHL is implicated in a gradual transition to shorter, finer hair. Explore the possibility that chronic tension on the hair shaft has led to follicular damage and hair loss. Although this type of damage is most common in African-American patients, it can also result from tight chignons, ponytails, or other chronic forceful hair pulling in patients of any race.

The patient’s menstrual history is important. A history of heavy menses may signify the presence of anemia or other hormonal causes, while irregular or absent menses may indicate excessive androgen production. This is most likely if the loss pattern is masculine (recession back from the temples) or if other signs of virilization, such as hirsutism, cystic acne, infertility, or galactorrhea, are present.

Finally, inquire whether there seems to be less hair on other parts of the body. Diffuse loss of body hair is a normal part of aging, but discrete patchy loss indicates pathology, not AGA. Similarly, skin and nail changes suggest a general pathologic process involving the skin and its appendages (hair and nails).

Physical exam

Examination should begin with the hair and scalp, evaluating the hair density and pattern of loss. Female pattern AGA manifests as diffusely thinner and finer hair at the centroparietal area, but as normal density at the back and sides with a normal frontal hairline. Evaluate this by parting the hair and looking for a wider part on the top of the head than on the sides. The presence of many miniaturized hairs of varying length and diameter is another important sign of AGA.⁹ Although short hairs along the frontal hairline are normal, note whether they are blunt, which would indicate breakage, or tapered, a sign of new growth. Gently pull on a clump of hair with the thumb and two fingers. To see up to four hairs leaving the follicle is normal, but five or more may indicate telogen effluvium rather than AGA. Severe bitemporal recession may signal a hormonal disorder. Hair loss in discrete patches, whether completely free of hair or with broken, twisted, or easily extractable hairs, indicates a problem that may require dermatologic evaluation.

Note any changes in the scalp itself. Folliculitis, follicular plugging, inflammation, obliteration of the follicular orifices, and atrophy are also signs that a dermatologic referral is necessary. Seborrhea alone does not cause hair loss, but it may be a symptom of female AGA.

The rest of the skin should be examined at least briefly, and any lesions, jaundice, pallor, edema, or hyperpigmentation noted. Also note any nail changes, especially pitting, which may be a sign of alopecia areata. Hirsutism may not be evident if only the face is examined, because many female patients regularly remove excess facial hair.

Laboratory studies

The diagnosis of FPHL is usually made from the history and clinical exam alone (see "Quick guide: Clinical and laboratory evaluation of hair loss" and Table 2). However, certain laboratory studies are indicated to rule out other causes, either primary or overlying. If menses are regular and no other signs of hormonal imbalance are present, hormonal tests are unnecessary. When indicated, testing of free and total testosterone, dehydroepiandrosterone sulfate (DHEAS), and prolactin may suggest the need for further endocrine workup. In all cases, order a CBC and serum ferritin, total iron-binding capacity (TIBC), thyroxine (T₄), and thyroid-stimulating hormone (TSH) tests to rule out underlying thyroid or iron deficiency. In a sick patient, VDRL and an antinuclear antibodies (ANA) test are needed to rule out syphilis or SLE. In the absence of other clear causes, iron studies and the TSH are the most likely to produce positive results.

Treatment and follow-up

All cases of patchy or scarring hair loss should be referred for dermatologic diagnosis. Symptoms of tinea capitis are erythema, crusting, and scaling, although the diagnosis should be confirmed with a KOH (potassium hydroxide) preparation. Treatment requires an oral antifungal agent. Biopsy may be necessary to exclude other causes of patchy alopecia, such as alopecia areata and trichotillomania. The presence of scarring indicates that alopecia is permanent because hair follicles have already been destroyed. Note as well that potentially reversible nonscarring patchy alopecias may develop into the scarring with permanent loss type if not treated correctly. Even in cases clearly attributable to chronic traction or use of harsh hair-straightening techniques, a biopsy will indicate whether hair can still regrow once the insult to the follicle is discontinued.

If testing reveals an underlying disorder or deficiency, the hair may regrow once the problem is corrected. The patient with telogen effluvium following pregnancy, severe stress, crash dieting, or febrile illness needs only to be reassured that the increased shedding will stop as telogen renormalizes to the stable anagen, or growing, phase. In fact, in 95% of patients this type of loss is reversed within a year.

A more difficult problem is the patient with a chronic telogen loss in the absence of these triggering events. Such patients may report having had thick hair before the onset of continuous or fluctuating periods of increased shedding. This condition is probably due to a shorter anagen phase resulting in shorter hair that traverses the hair cycle more quickly and is shed more often. While understandably alarmed at the handfuls of hair that have been shed, these patients usually do not have much thinning. Although the practitioner can reassure them that the condition represents shedding rather than hair loss, indicating that the shed hair is being replaced, the condition remains distressing since it may persist for 6 months to 7 years before remitting. In the majority of people who do not have concomitant AGA and are not at an age when normal senescent hair loss is occurring, a cosmetically acceptable amount of hair will be retained.⁵

AGA can be treated medically, surgically, cosmetically, or not at all. Medical treatment is aimed at promoting growth and retarding further thinning. The only treatment currently approved by the FDA for women with AGA is minoxidil 2% solution (Rogaine For Women); the 5% solution may lead to hirsutism of the face and is not approved for females. Minoxidil must be used consistently for at least 3 to 4 months before new growth is seen, and for up to 6 months to evaluate its true effect. The patient must continue to use minoxidil, or she will return to her previous state within 3 months. Unfortunately, new growth is usually poor, with only one third of patients seeing a significant effect.¹⁰

Some patients may ask about antiandrogens such as spironolactone (Aldactone) and cyproterone acetate; these agents have only been evaluated in small, uncontrolled trials without well-defined end points.¹ Although these substances bind to androgen receptors and block DHT, they are probably only effective in the case of androgen excess, which is not the situation in AGA. Similarly, finasteride (Propecia, Proscar) is not approved for use in women, is highly teratogenic, and is ineffective in postmenopausal women.¹¹ Surgical treatment, which includes follicular unit transplant or multiple punch grafts from androgen insensitive areas, should always be preceded by a trial of minoxidil.

The patient can explore aesthetic improvement with different styling, waving, thickening products, swatches, or weaving. However, care must be taken not to pull on the hair or overtreat it, which would only worsen the problem. The practitioner should also reassure the patient that a wig will not damage the scalp. Once treatable causes have been ruled out, the most important treatment may simply be counseling. The clinician should advise the patient that some degree of hair loss is inevitable as aging and hormonal changes take place; that genetically driven changes are inexorable but unpredictable; and that she is unlikely to become as bald as a man would.

Conclusion

The diagnosis of FPHL can be confusing. The androgen-dependent path may be only one of several leading to similar hair loss patterning, thereby causing problems in both research and diagnosis. A chronic form of telogen effluvium may overlie androgenetic loss. Normal senescent loss also easily combines with truly androgenetic hair loss. Most medical treatment is minimally effective, and the patient is understandably frustrated when told that there is little to be done. Symptoms should be taken seriously because hair loss can be devastating to the patient's self-image and self-confidence. The diagnosis should include consideration of the patient’s age, the duration and timing of the loss, a thorough examination of the scalp, observation of the overall pattern of hair loss, the results of a pull test, and pertinent diagnostic tests. Even though the available treatments offer help to only some patients, all will benefit from an understanding of their diagnosis and the reassurance and support of a concerned and knowledgeable medical practitioner.

REFERENCES

1. Olsen EA. Female pattern hair loss. J Am Acad Dermatol. 2001;45(3 suppl):S70-S80.

2. Olsen EA. Androgenetic alopecia. In: Olsen EA. Disorders of Hair Growth: Diagnosis and Treatment. New York, NY: McGraw-Hill; 1994:257-283.

3. Hamilton JB. Patterned loss of hair in man: types and incidence. Ann NY Acad Sci. 1951;53:708-728.

4. Norwood OT. Male pattern baldness: classification and incidence. South Med J. 1975;68:1359-1365.

5. Birch MP, Messenger JF, Messenger AG. Hair density, hair diameter and the prevalence of female pattern hair loss. Br J Dermatol. February 2001;144:297-304.

6. Venning VA, Dawber RP. Patterned androgenic alopecia in women. J Am Acad Dermatol. 1988;18(5 pt 1):1073-1077.

7. Price VH. Treatment of hair loss. N Engl J Med. 1999;341:964-973.

8. Whiting DA. Chronic telogen effluvium: increased scalp hair shedding in middle-aged women. J Am Acad Dermatol. 1996;35:899-906.

9. de Lacharriere O, Deloche C, Misciali C, et al. Hair diameter diversity: a clinical sign reflecting the follicle miniaturization. Arch Dermatol. 2001;137:641-646.

10. Price FH, Menefee E. Quantitative estimation of hair growth: comparative changes in weight and hair count with 5% and 2% minoxidil, placebo and no treatment. In: Van Neste D, Randall VA, eds. Hair Research for the Next Millennium. New York, NY: Elsevier Science; 1996:67-71.

11. Price VH, Roberts JL, Hordinsky M, et al. Lack of efficacy of finasteride in postmenopausal women with androgenetic alopecia. J Am Acad Dermatol. 2000;43(5 pt 1):768-776.

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