Hair loss (alopecia) is a disorder in which the hair falls out from skin areas where it is usually present, such as the scalp and body. This loss interferes with the many useful biologic functions of the hair, including sun protection (mainly to the scalp) and dispersion of sweat gland products. Because hair has psychological importance in our society, patients with hair loss suffer tremendously. This chapter will focus on the most common causes of hair loss.

A number of factors are involved in hair disorders. Genetic factors, diet, endocrine abnormalities, systemic illnesses, drug intake, and hair shaft abnormalities may cause hair loss. Most alopecia cases are due to hair cycle changes.

Normal Hair Cycling
Understanding the basic facts about normal hair growth is essential for correct interpretation of hair loss events. The average rate of hair growth for a normal scalp is 0.35 mm a day,³ however, slower growth occurs in elderly people and in patients with chronic illness. Scalp hair grows in an asynchronous pattern, with approximately 80% of hair follicles in an active growing phase (anagen) and 10% to 20% in an involuting and resting phase (catagen and telogen).³ Figure 1 summarizes the hair growth cycle. Telogen hair fibers shed in 3 to 5 months and are responsible for daily hair shed. Average daily hair loss is 25 to 100 hair fibers.³

Alteration of hair growth cycling manifests clinically as increased shedding of scalp hair. In androgenetic alopecia, the hair cycle is shorter, and the hair follicle becomes progressively thinner (miniaturization) as a result of an androgen effect. Telogen effluvium is the result of an increased number of resting follicles, usually a few weeks after a trigger. Alopecia areata, an autoimmune disease, presents as an anagen effluvium. Autoimmune inflammation around the hair follicle aborts hair growth. Changes in chemical or physical structure of the hair shafts result in hair shaft abnormalities (trichodystrophies). Inherited trichodystrophies are associated with keratinization defects and are less frequent than acquired ones (from external trauma).

Hair stem cells are localized in the midportion of the follicles, on the middermis.⁴ If this area remains undisturbed, the follicles recycle throughout one's life. However, inflammation in this area can destroy the stem cells. In that case, a cicatricial alopecia is established, and no follicle is able to regrow.⁵ Examples of cicatricial alopecia are infectious folliculitis, discoid lupus erythematosus, and lichen planus (Table 1).

Clinical history should include duration of hair loss, family history, affected areas (localized or diffuse scalp, scalp alone, or other hair-bearing areas), associated nail changes, and hair care habits (shampooing, bleaching, perming).

The way the hair falls out is important to establishing the nature of the problem. One has to determine whether the hair is falling by the roots (shedding), is thinning, or whether the hair shafts are fracturing. Each of these complaints is meaningful because each points to a type of hair disorder (Table 2).

The clinical presentation of hair loss caused by androgenetic alopecia, telogen effluvium, trichodystrophy, or alopecia areata varies from a localized area of thinning on top of the head in androgenetic alopecia (Figure 2) to a total body hair loss (alopecia areata universalis). The most common history in patients with alopecia areata is abrupt onset of patchy circular areas of hair loss (Figure 3). The incidence of progression to a more widespread loss causing alopecia totalis (total scalp) or alopecia universalis (total body) is about 1%.⁶

The diagnosis of hair disorders is complex, and an evaluation of the clinical presentation, history, and physical examination is necessary. Laboratory work-up may be helpful. Diagnostic office techniques include visual examination of all the hair-bearing skin areas as well as examination of the nails. Inherited keratinization disorders and alopecia areata may be associated with nail dystrophy. Clinical examination should include scalp condition, pattern of hair loss, and length and diameter of hair fibers. Additional examinations are hair pulls, clippings, plucks, and collections (shed hair), light microscopy examination of hair fibers, scrapings of scalp scales for bacterial and fungal culture, and a scalp punch biopsy (Table 3).

A hair clipping for light examination is diagnostic in patients with trichodystrophies. Trichorrhexis nodosa, a node-like fragile area in the hair shaft, is the most common finding and can be associated with acquired and inherited hair shaft abnormalities (Figure 4).

Hair collections of the shed hair can be diagnostic in patients with telogen effluvium. These patients commonly bring amazingly large hair collections, literally bags of shed hair (Figure 5).

Male androgenetic alopecia is usually genetically predisposed, and no additional investigation is necessary. Female androgenetic alopecia often appears in women with a strong family history of baldness or a personal history of hirsutism, acne, or abnormal menses (signs of androgen excess). Genetically predisposed women may present with androgenetic alopecia in adolescence (puberty), perimenopause, or postmenopause. Young women have a higher incidence of acquired adrenal hyperplasia and polycystic ovaries. In general, postmenopausal women have lower levels of hormones, especially estrogen. However, testosterone levels in postmenopausal women are relatively high when compared with levels in adolescents. Androgen excess screening for women with hair loss should include measurements of total testosterone and dehydroepiandrosterone sulfate.

Other laboratory tests, such as a complete blood count, ferritin measurement, and thyroid screening, may be helpful. Ferritin level should usually be higher than 40 µg/L to ensure normal hair growth. A hair pluck test and a scalp biopsy may be helpful in any hair loss case. Cicatricial alopecias are difficult to differentiate clinically and often require a scalp biopsy for correct diagnosis. A 4-mm punch is recommended.

Androgenetic Alopecia
In men, medical treatment of androgenetic alopecia includes topical minoxidil 2% or 5% (Rogaine for Women and Rogaine for Men) twice a day and selected antiandrogens. Oral finasteride 1mg (Propecia), a 5-a-reductase inhibitor, blocks the peripheral conversion of testosterone to dihydrotestosterone. Serum and tissue (scalp) dihydrotestosterone concentrations are decreased in men taking finasteride, resulting in a progressive increase in hair count. Additional results can be achieved with creative hair styles, hair pieces, hair transplantation, and scalp reduction.

Women have more treatment options. Minoxidil 2% and 5% (Rogaine for Women and Rogaine for Men) can also be used, the 5% being more effective. In addition to antiandrogens, estrogen replacement therapy can be used.⁷ These agents include the estrogen-dominant oral contraceptive ethynodiol diacetate and ethinyl estradiol (Demulen 1/50) or conjugated estrogen (Premarin) given daily or in conjunction with a progesterone, such as medroxyprogesterone (Provera). Spironolactone (Aldactone) in doses of 50 to 200 mg has successfully been used as an antiandrogen. If adrenal suppression is needed for androgen excess, dexamethasone (Decadron) in doses of 0.125 to 0.25 mg may be taken at bedtime for 4 months or longer.

Telogen Effluvium
In general, telogen effluvium is self-limited, and no treatment is necessary after the initial cause is removed. Identifying the trigger is helpful to avoid relapses and new shedding periods. Common triggers for telogen effluvium are medications, illness, childbirth, and crash diets. The etiology of telogen effluvium is generally elucidated by history, with special concentration on events that have preceded the shed by 6 weeks to 4 months.

Chronic or persistent telogen shed heralds androgen alopecia or other metabolic or disease states, such as thyroid disorders.³ If telogen shedding persists, a more intense medical evaluation is needed.

Alopecia Areata
Treatment of alopecia areata depends on the extent of the hair loss and age of the patient. For mild to moderate patchy disease, topical corticosteroids are the preferred treatment. For more extensive or recalcitrant disease, triamcinolone acetonide suspension (Kenalog 10 mg per mL) can be injected into the involved sites with a 30-gauge needle, delivering tiny injections of 0.1 mL to each small site. The total amount of triamcinolone should not exceed 10 to 15 mg per visit every 6 to 8 weeks.

Other options for marked to severe disease are topical minoxidil (Rogaine), anthralin (Dritho-Scalp, Micanol), and topical contact sensitizers such as diphenylcyclopropenone (DPCP), dinitrochlorobenzene, and squaric acid dibutylester. The expected result of sensitization therapy is about 40% to 58% cosmetically acceptable regrowth of hair.⁶ DPCP is difficult to obtain in the United States, but is more readily available in Europe and Canada. Other treatment options include psoralen plus ultraviolet A radiation and systemic corticosteroids. Use of systemic corticosteroids is controversial because of their prolonged duration of therapy and potential side effects, including cataracts, osteopenia, osteoporosis, and growth retardation.

Patients with alopecia areata need a source of disease-specific information and support therapy, such as the National Alopecia Areata Foundation.

Trichodystrophies
Excessive sunlight, hair care techniques, (such as hot combing and blow drying) and chemical processes, (including coloring, straightening, and perming) may result in fragile hair. They should be avoided in patients with trichodystrophies. Treatment consists of gentle handling and normal shampooing with the use of leave-on conditioners and volumizers. If damage is not repeated, the hair normally regrows within a few months.

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5. Bergfeld WF. Alopecia: histologic changes. Adv Dermatol. 1989;4:301-320.
   
   
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7. Price VH. Treatment of hair loss. N Engl J Med. 1999;341:964-973.

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