Chapter 20 Alopecia
1. How is alopecia classified?
Alopecia (hair loss) can be divided into: 1) disorders of the hair shaft and 2) all other forms of hair loss. Abnormalities of the hair shaft can produce alopecia because the shafts are fragile and “break off.” The other forms of alopecia can be divided into cicatricial (scarring) and noncicatricial alopecia. In cicatricial alopecia, hair is lost permanently. Both cicatricial and noncicatricial alopecia can be divided into diffuse and patterned hair loss. In diffuse hair loss, hair thins evenly from all parts of the scalp, and discrete “bald spots” do not occur. In patterned alopecia, certain areas of the scalp are affected more than others.
3. Can cicatricial and noncicatricial alopecia be differentiated clinically?
In the setting of alopecia, cicatricial means that there has been permanent destruction of hair follicles, and they have been replaced by fibrous tissue. Usually, an obvious scar, such as that seen after wounding, is not evident, but there is a loss of follicular openings that gives the scalp a smooth and shiny appearance (Fig. 20-1). The texture of the scalp may remain soft and supple, although sometimes induration or firmness is palpable.
4. What causes common balding?
People who become bald have hair follicles that are genetically programmed to miniaturize under the influence of postpubertal androgens. Probably, several genes (inherited from both mother and father) influence the severity of balding. Until very late in the balding process, the number of hairs does not decrease, but the hairs become progressively smaller until they are no longer visible to the naked eye. Except in very marked and long-standing balding, very fine, short hairs can be seen exiting from follicular orifices if a magnifying lens is used.
Randall VA: Androgens and hair growth, Dermatol Ther 21(5):314–328, 2008.
5. How effective are medical treatments for common balding?
About one third of balding patients who use topical minoxidil solution experience significant (cosmetically obvious) hair regrowth. Any regrowth that occurs is only maintained while the drug is used. If therapy is stopped, hair density reverts to its pretreatment state. Oral finasteride, a 5α-reductase inhibitor, is somewhat more effective, and can be used in combination with topical minoxidil.
6. Is common balding in women managed differently than in men?
Women whose balding is a manifestation of hyperandrogenism (excessive production of circulating androgens) may benefit from therapy directed at the cause of hyperandrogenism. Polycystic ovarian disease, late-on-set congenital adrenal hyperplasia, Cushing’s syndrome, and adrenal and ovarian neoplasms are potential causes of hyperandrogenism. In the absence of elevated circulating androgens, nonspecific therapy directed at suppressing ovarian androgen production or blocking the peripheral effect of androgens is sometimes tried. Oral contraceptive agents (to suppress ovarian androgen production) and spironolactone are most often utilized for this purpose. Topical minoxidil solution is also useful, but oral finasteride is seldom used in women.
7. What are the surgical options for treatment of balding?
Men, and occasionally women, can achieve permanent cosmetic improvement by undergoing a hair transplantation procedure. Hair follicles from the occipital area (donor site) are moved to the balding area (recipient site). The procedure is tedious and expensive, but the cosmetic results can be quite good. Various other surgical procedures, including scalp reductions (which involve excising the bald areas) and scalp flaps, are sometimes used in selected patients.
8. Discuss the common causes of circular bald spots.
Although many forms of alopecia can result in a circular bald patch, the most common causes are tinea capitis and alopecia areata. Tinea capitis is a superficial fungal infection with a predilection for children, especially black children. The surface of the skin is scaly and sometimes inflamed, and small dark stubs of hair (“black dots”) may be scattered within the affected area. In this condition, the hair shaft is invaded and replaced by myriad circular fungal spores. In the United States, Trichophyton tonsurans is usually the culprit. A circular, scaly, or crusted bald spot on the scalp of a black child should be considered to be tinea capitis until proven otherwise (Fig. 20-2A).
Alopecia areata also commonly affects children, but adults more often develop the condition. In alopecia areata, the affected areas may be totally hairless, but the scalp surface looks otherwise normal, without scaling and minimal, if any, erythema. A few short hairs may be present in the bald spot; these “exclamation mark” hairs tend to taper and lose pigment as they approach the scalp and may appear to float on the surface of the scalp (Fig. 20-2B).
9. What is alopecia totalis?
Alopecia areata may cause one or many bald spots. If it affects the entire scalp, it is called alopecia totalis (Fig. 20-3). If the entire body is affected, it is referred to as alopecia universalis.
10. How is alopecia areata treated?
When a solitary lesion of alopecia areata is small (<5 cm in diameter), no treatment may be needed. The prognosis for such a lesion is excellent, and spontaneous regrowth often occurs. Intralesional corticosteroids, and sometimes potent topical corticosteroids, may hasten regrowth. Larger or more numerous lesions carry a more guarded prognosis. Intralesional corticosteroid injections are often begun. For extensive hair loss involving 30% to 100% of the scalp surface, a short (e.g., 3-month) course of systemic corticosteroids (usually prednisone) may be tried. If hair regrowth does not resume or if hair loss recurs once corticosteroids are stopped, the prognosis is poor. The use of systemic corticosteroids to treat extensive alopecia areata is controversial. Appropriate risk-versus-benefit considerations must be carefully analyzed.
11. How is tinea capitis treated?
Although topical antifungal agents work well for tinea corporis, they are of little value in treating tinea capitis. Systemic antifungal agents are required to eradicate the spores that invade affected hair shafts. A course of treatment generally takes 1 to 3 months. Griseofulvin is the treatment of choice because it is safe and effective, rarely causing significant side effects. Ultramicrosized formulations of griseofulvin can be given in half the dose required with microsized forms of the drug. Fungal resistance to griseofulvin is rare. For the few patients whose tinea capitis is resistant to griseofulvin, or who cannot tolerate griseofulvin because of side effects (such as headache or gastrointestinal upset), terbinafine and itraconazole are acceptable alternatives.
Andrews MD, Burns M: Common tinea infections in children, Am Fam Physician 77(10):1415–1420, 2008.
13. Who is most likely to be affected by trichotillomania?
The typical patient is an adolescent girl, although the condition can affect children of both sexes as well as adults. In trichotillomania, hairs are forcibly plucked out of the scalp by the patient, usually as a mechanism for relieving tension or stress. Less often, trichotillomania is a manifestation of psychosis or an obsessive-compulsive neurosis. Although the patient may deny plucking, the often bizarre shape of the bald area, combined with the presence of short hairs of various lengths within the area of thinning, suggest the diagnosis (Fig. 20-4). The diagnosis may be confirmed by a scalp biopsy demonstrating diagnostic features, or by creating a “hair growth window.” This test is performed by weekly shaving of an involved area to prevent plucking; the hair will recover and regain normal density within the shaved area, resembling a “five o’clock shadow.”
14. Why do cancer patients lose their hair?
Cancer patients are susceptible to two forms of diffuse hair loss. Anagen effluvium is a direct effect of anticancer treatment. Patients receiving radiation therapy to the scalp or systemic chemotherapy can shed all or most of their hair within a few weeks of starting treatment. This hair loss is a direct effect of the chemotherapy or radiotherapy on the hair follicle, whose rapidly dividing cells are very susceptible to injury. When the hair matrix (the epithelial root that produces the hair shaft) is exposed to radiation or chemical toxins, it can only produce a thinned hair shaft that eventually tapers to a point (Fig. 20-5A). This marked tapering makes the shaft extremely fragile, and the hair shaft can literally be combed away or broken off by minor trauma. Unless the dose of radiation or chemotherapy is very high, regrowth of hair occurs once therapy is stopped.
In telogen effluvium the metabolic and emotional “stress” of severe, debilitating illness causes many of the actively growing (anagen) hairs to enter the shedding (telogen) phase of hair growth prematurely. The hairs remain in telogen for about 3 months before they are finally shed (Fig. 20-5B), so there is always a “lag” time between the onset of severe disease and actual hair loss. Seldom is more than 50% of the hair shed in telogen effluvium, so patients develop thin hair but do not become completely bald. If the patient recovers and is no longer debilitated, hairs reenter the actively growing phase and the hair regrows.
15. In what other clinical settings can a telogen effluvium occur?
Normally, about 10% of scalp hairs are in the telogen (preshedding) phase at any given time. Whenever an abnormally large number of otherwise normal telogen hairs are present, a telogen effluvium occurs. There are several clinical situations in which a telogen effluvium is found, including severe illness such as metastatic cancer, but any serious illness or major surgical procedure can also result in a telogen effluvium. The most common form of telogen effluvium occurs in women about 3 months after giving birth. In addition, virtually all newborn infants develop a telogen effluvium during the first 6 months of life, which is why many babies have more hair at birth than at 3 to 4 months after birth.
16. To what forms of hair loss are black patients susceptible?
• Hair shaft fragility disorders are also common among African-American women because of certain hair grooming techniques using chemical hair “relaxers.” These products are effective in straightening kinky or curly hair but are caustic and, with continued use, the hair shaft becomes frayed. The foci of fraying have a special appearance termed trichorrhexis nodosa, which looks like the bristles of two paint brushes that have been pushed together (Fig. 20-6). The hair shafts easily fracture at the points of trichorrhexis nodosa, leaving abnormally short hair shafts behind. Patients have scalp hair of very uneven length and may complain that their hair “falls out” with combing or “won’t grow.” In fact, their hair is growing but breaking off.
17. Discuss the mechanism of central, centrifugal, cicatricial alopecia (CCCA).
The most common form of cicatricial alopecia in black patients was once called “hot comb alopecia” but is now called central, centrifugal, cicatricial alopecia (CCCA). The condition more often affects adult women than men and typically causes hair loss that is most severe on the central crown of the scalp and slowly progresses centrifugally (see Fig. 20-1). When the bald patches are carefully examined, a few normal hairs may be found, but most follicular openings have been completely obliterated, suggesting a cicatricial process. Scattered inflammatory, perifollicular papules may be found in the peripheral zone where hair thinning has just begun. Scalp biopsy confirms that hair follicles are completely destroyed and replaced with fibrous tissue. “Hot combs” are rarely used nowadays for straightening hair, so hot comb alopecia is a misnomer. It is uncertain whether hair care products are primarily responsible for hair loss in these patients, but chemical relaxers and other cosmetics may exacerbate the condition.
Key Points: Alopecia
1. A circular, scaly, or crusted bald spot on the scalp of a black child should be considered tinea capitis until proven otherwise.
2. Women whose balding is a manifestation of hyperandrogenism (excessive production of circulating androgens) may benefit from therapy directed at the cause of hyperandrogenism.
3. When a solitary lesion of alopecia areata is small, no treatment may be needed. The prognosis for such a lesion is excellent, and spontaneous regrowth often occurs.
18. Name some medications that cause hair loss.
19. What is alopecia mucinosa?
This term actually refers to two entirely different causes of hair loss. The conditions have in common a similar histologic finding—follicular mucinosis, the accumulation of mucin (acid mucopolysaccharides) within the follicular epithelium, resulting in hair damage and hair loss.
The second form of alopecia mucinosa occurs in patients with mycosis fungoides, a form of cutaneous T-cell lymphoma. Patients are usually elderly, and numerous, often large, hairless, erythematous, and indurated plaques are found (Fig. 20-7). Histologically, follicular mucinosis is present, but an atypical lymphocytic infiltrate that often invades the epidermis and follicles is also seen. This atypical cellular infiltrate allows for the diagnosis of mycosis fungoides. The hairless lesions and histologic follicular mucinosis are merely manifestations of the underlying lymphoma.
Figure 20-7. Alopecia mucinosa occurring in a patient with mycosis fungoides.
(Courtesy of Fitzsimons Army Medical Center teaching files.)
Gibson LE, Brown HA, Pittelkow MR, Pujol RM: Follicular mucinosis, Arch Dermatol 138(12):1615, 2002.
20. What is meant by the term “moth-eaten alopecia”?
“Moth-eaten alopecia” is a form of noncicatricial, patterned hair loss in which there are myriad small foci of alopecia scattered over the scalp (Fig. 20-8). This pattern of alopecia is described as the classic form of alopecia seen in patients with secondary syphilis. However, other etiologies, such as alopecia areata and systemic lupus erythematosus, can result in the same pattern of hair loss. Furthermore, hair loss in syphilis can be diffuse as well as moth-eaten.
