ACP medicine, 3rd Edition
Disorders of Hair
David A. Whiting MD, FACP1
Associate Professor of Dermatology
1University of Texas Southwestern Medical Center at Dallas, Medical Director, Baylor Hair Research and Treatment Center
The author is a consultant and participates in the speakers' bureaus for Pharmacia & Upjohn, Merck & Co., Inc., and GlaxoSmithKline.
Oral contraceptives and antiandrogens discussed in this chapter have not been approved by the FDA for use in androgenetic alopecia; topical minoxidil discussed in this chapter has not been approved by the FDA for use in chronic telogen effluvium and cicatricial alopecia; diphencyprone, sulfasalazine, and cyclosporine discussed in this chapter have not been approved by the FDA for use in alopecia areata; and rifampin discussed in this chapter has not been approved by the FDA for use in folliculitis decalvans.
Physiology and Evaluation of Hair Growth
A basic knowledge of the hair growth cycle is needed to evaluate disorders of hair growth.1,2 Scalp hair follicles cycle independently of one another. At any given time, approximately 90% of scalp hairs are in the anagen (growing) phase and 10% are in the telogen (resting) phase. Anagen lasts an average of 3 years, with a range of 1 to 7 years. Telogen usually lasts 3 months, after which the resting hairs are shed and new hairs grow in. The average rate of scalp hair growth is approximately 0.35 mm/day, or 1 cm/month (1 in. every 2 to 3 months).
The scalp typically has about 100,000 hairs. An average loss of 100 hairs a day is normal, with larger numbers of hairs being lost on shampoo days. When obtaining a history, it is important to determine whether shedding is abnormal and whether the shed hairs break off or come out by the roots.3 Hair normally comes out by the roots; however, trauma or excessive fragility may cause hair to break.
Examination of the patient should include a routine check for broken-off hairs and the performance of hair-pull tests on the top, sides, and back of the scalp. The hair-pull test is performed by grasping groups of 10 to 20 hairs between the index finger and thumb and pulling steadily.4,5 Extraction of more than 20% of the grasped hairs indicates a potential for abnormal shedding, usually involving telogen hairs (club hairs). Telogen hairs are easily recognized by their whitish club-shaped bulbs and lack of root sheaths. Anagen hairs are normally difficult to detach and have blackish, indented roots with intact root sheaths.
Androgenetic alopecia is the common type of nonscarring hair loss affecting the crown. It results from a genetically determined end-organ sensitivity to androgens. It is often referred to as common baldness, male-pattern alopecia, and female-pattern alopecia.
Epidemiology and Pathogenesis
Androgenetic alopecia affects at least 50% of men by 50 years of age and 40% to 50% of women by 60 years of age.6 Males have more androgen than females and therefore are usually affected earlier and more severely. Male-pattern alopecia often starts between 15 and 25 years of age. Male-pattern alopecia has two characteristic components, bitemporal recession and vertex balding [see Figure 1], which in pronounced cases can progress to complete balding of the crown.6 Female-pattern alopecia is more likely to start between 25 and 30 years of age (or sometimes later, after menopause). It is characterized by an intact frontal hairline and an oval area of diffuse thinning over the crown [see Figure 2]. Bitemporal recession in women is much less obvious than it typically is in men, or it can be nonexistent. In general, androgenetic alopecia in women progresses to mild, moderate, or severe thinning but not to complete baldness. The best predictor of outcome is the degree of progression in affected relatives.
Androgenetic alopecia is an autosomal dominant disorder with variable penetrance. Susceptible hairs on the crown are predisposed to miniaturize under the influence of androgens, notably dihydrotestosterone. In both sexes, miniaturization results from a shortening of the anagen cycle, from years to months or weeks. Miniaturized hairs are characterized by reduced length and diameter; this accounts for the appearance of hair loss.7 Androgenetic alopecia largely spares the back and sides of the scalp.
The diagnosis of androgenetic alopecia is usually obvious from the clinical pattern of hair loss from the top of the head.8 In some men, a female pattern of alopecia (see above) causes diagnostic confusion but has no other significance. In women, a male pattern of alopecia (i.e., bitemporal recession and vertex balding) occurring with menstrual irregularities, acne, hirsutism, and a deep voice is significant. The virilism indicates significant hyperandrogenism, the cause of which must be identified and treated [see 3:IV The Adrenal and 16:V Polycystic Ovary Syndrome].
Scalp biopsies are rarely necessary to diagnose androgenetic alopecia. Biopsies cut horizontally are sometimes useful, however, in differentiating female-pattern alopecia from chronic telogen effluvium (see below).
Depending on the severity of the condition, management of androgenetic alopecia ranges from watchful inactivity to medical and surgical treatment; a hairpiece or wig may be used in the most refractory cases.
The Food and Drug Administration approved topical 2% minoxidil for use in men in 1987 and in women in 1989. Minoxidil is applied twice daily with a dropper, spread over the top of the scalp, and gently rubbed in. The drug should be tried for at least a year. Minoxidil acts by initiating and prolonging anagen. It produces visible hair growth in approximately one third of male and female patients, fine-hair growth in approximately one third, and no growth in approximately one third. It is more effective as a preventive agent, retarding hair loss in approximately 80% of patients.6
Figure 1. Male Pattern Androgenetic Alopecia
Bitemporal recession and vertex balding are present in this patient with male pattern androgenetic alopecia.
Figure 2. Female Pattern Androgenetic Alopecia
Intact frontal hairline and diffuse thinning over the crown are characteristic of female pattern androgenetic alopecia.
Topical 5% minoxidil, which was approved for use in men in 1997, produces visible hair growth in 45% of patients in less time than the 2% solution. Both concentrations are available over the counter. Side effects are not significant and include scalp irritation and increased facial hair.9 The medication has to be continued indefinitely.10 Topical 5% minoxidil foam, which is less irritating and easier to apply than standard minoxidil in propylene glycol, gained FDA approval for use in men in 2006.
Oral finasteride, at a dosage of 1 mg/day, was approved by the FDA for the treatment of male-pattern alopecia in 1997. Finasteride is a powerful type II 5α-reductase inhibitor that prevents formation of dihydrotestosterone in the prostate gland and in the hair follicle. It reduces circulating dihydrotestosterone by 65% to 70%. When administered at a dosage of 1 mg/day for 2 years to men with androgenetic alopecia who were between 18 and 41 years of age, finasteride resulted in the growth of visible hair in 66% of patients and prevented further hair loss in 83%.11 The efficacy of finasteride was maintained in a 5-year study.12 Hair-weight studies have shown that finasteride increases hair length and diameter, producing better coverage from existing hairs.13
Side effects in men are minimal and include lack of libido, lack of potency, and a mild reduction in semen in approximately 0.5% of patients. These effects are reversed when the drug is stopped and often disappear as the drug is continued. A 1-year trial of finasteride at a dosage of 1 mg/day in postmenopausal women failed to show any positive effects.14
Because of the likelihood of finasteride to cause severe side effects in the male fetus, the drug is contraindicated in fertile, premenopausal women.
Therapy for Hair Loss in Women
Topical minoxidil is currently the best available treatment for androgenetic alopecia in women.9,15 However, various antiandrogenic drugs have been used. Oral contraceptives (e.g., ethinyl estradiol-ethynodiol diacetate [Demulen], desogestrel-ethinyl estradiol [Desogen], ethinyl estradiol-norgestimate [Ortho Tri-Cyclen], and ethinyl estradiol-drospirenone [Yasmin]) can reduce hair loss and occasionally lead to slight hair growth.6 Oral spironolactone in dosages of 75 to 200 mg/day can produce androgen blockade. Dexamethasone in dosages of 0.125 to 0.5 mg/day can suppress adrenal overactivity. Cyproterone acetate, which is not available in the United States, is not as effective as minoxidil in female-pattern hair loss unless other signs of hyperandrogenism are present.16
Therapy for Refractory Cases
In patients who do not respond to pharmacologic treatment, the next step may be hair transplantation. Micrografts and minigrafts can produce a good cosmetic appearance in patients who have a sufficient reserve of hair on the back and sides of the scalp.17 If all therapies fail, a hairpiece may be an option.
Diffuse alopecia is generalized hair loss over the entire scalp. Because the loss is so diffuse, it is often unnoticeable until 30% to 50% of scalp hair is shed. Causes of diffuse alopecia include telogen effluvium, anagen arrest, drug reactions, and a number of systemic and nonsystemic conditions [see Table 1].18,19
Telogen effluvium is the most common form of diffuse alopecia.20 It presents as a generalized shedding of telogen hairs from normal resting follicles. The basic cause of telogen effluvium is a premature interruption of anagen, leading to an increase in the number of hairs cycling into telogen. When the 3-month telogen period ends, new anagen hairs grow in and numerous telogen hairs fall out. Patients may need reassurance that this apparent loss of hair is actually a sign of regrowth.
Acute telogen effluvium can be caused by childbirth, febrile illnesses, surgery, chronic systemic diseases, crash diets, traction, severe emotional stress, and drug reactions [see Table 2]. It can also be a physiologic reaction in neonates.21
During acute telogen effluvium, pull tests are positive all over the scalp, yielding two to 10 club hairs. Telogen effluvium is often accompanied by bitemporal recession; this is a useful diagnostic sign in women [see Figure 3]. The acute form usually ends within 3 to 6 months. The diagnosis is usually made on the basis of the history of an initiating event 3 months before the onset of shedding. Chronic telogen effluvium has a long, fluctuating course of 6 months to 7 years or more.22 By definition, no identifiable cause can be found.
Table 1 Causes of Diffuse Alopecia39
Table 2 Categories of Drugs That Can Cause Alopecia5
The diagnosis of telogen effluvium is usually clinical; biopsies may be necessary to distinguish telogen effluvium from an acute onset of widespread androgenetic alopecia or from diffuse alopecia areata.22 Other causes of hair loss should be excluded by a careful drug history and tests for iron deficiency, syphilis, and disorders of the thyroid, kidney, and liver.
No treatment is needed for acute telogen effluvium because the hair invariably regrows within a short time. In chronic telogen effluvium, topical minoxidil in a 2% or 5% solution may be indicated. The patient should be reassured that telogen effluvium rarely causes permanent baldness.
Anagen Arrest (Anagen Effluvium)
So-called anagen effluvium represents a diffuse loss of anagen hairs from growing follicles.23 The term anagen effluvium is a misnomer. Normally, hairs pass through a brief transition phase (catagen) between the anagen and telogen phases before falling out by the roots. In anagen arrest, inhibition of cell division in the hair bulb matrix leads to a progressive narrowing of the hair shaft and sometimes failure of hair formation. As the growing hair narrows near the skin surface, it may break off. The resultant shedding can occur within a few weeks, unlike in telogen effluvium, in which shedding takes 3 months to occur.
Causes of anagen arrest include reactions to cytostatic drugs and other toxic agents, radiation therapy, endocrine diseases, alopecia areata, cicatricial alopecia, trauma and pressure, and severe protein calorie malnutrition. Because 90% of scalp hairs are in anagen at any given time, this condition causes obvious and severe baldness [see Figure 4].
The diagnosis of anagen arrest is easily made by the history, evidence of extensive hair loss, and hair-pull tests that yield easily broken hairs with proximal tapering.
Figure 3. Bitemporal Recession in Female
In women, marked bitemporal recession is often a sign of telogen effluvium.
Figure 4. Diffuse Hair Loss Caused by Anagen Arrest
Anagen arrest causes severe, diffuse hair loss.
Treatment of anagen arrest lies in elimination of the underlying cause. Once the antimitotic influence is removed, the anagen hair will regrow promptly with a normally tapering shaft. Unbroken hairs that regrow often show the Pohl-Pinkus deformity (i.e., a constriction that results in a dumbbell shape).
Alopecia Caused by Drugs and Chemicals
Substance-induced alopecia is relatively common but is often hard to diagnose because of the large number of drugs and chemicals that can cause hair loss [see Tables 2 and 3]. Identification of the underlying cause often requires a time-consuming process of trial and error: many patients are exposed to several alopecia-inducing substances, and removal of the causative agent may not result in immediate regrowth of hair.
Other Causes of Diffuse Alopecia
Hypothyroidism and iron deficiency should be excluded in patients with diffuse hair loss [see Table 1]. Appropriate treatment may lead to hair regrowth.
Alopecia areata is typically characterized by patchy hair loss; however, involvement can vary from a single patch on the scalp or elsewhere to total body baldness (alopecia universalis).24
Epidemiology and Pathogenesis
In the United States, alopecia areata affects 1.7% of the population younger than 50 years.25 From 70% to 75% of cases are not associated with any other disease. In these patients, the onset of alopecia areata occurs when patients are in their 20s or 30s, although it can occur at any age. In only about 6% of these patients with alopecia areata does the disease progress to total loss of scalp hair. Even total alopecia can reverse itself.
Alopecia areata is currently regarded as an autoimmune disease. There is a genetic predisposition to alopecia areata, as indicated by the fact that 20% of alopecia areata patients have a positive family history for the condition. Certain HLA groups have been associated with mild or severe cases of alopecia areata.26 Although the exact cause is unknown, many researchers presume that an infectious agent such as a virus has an etiologic role. Stress, seasonal factors, and infection are among the factors that trigger active episodes of hair loss.
In approximately 5% of alopecia areata cases—usually those occurring in middle-aged patients—there is a history of autoimmune disease (e.g., thyroiditis) in the patient or in the patient's family. Approximately 10% of these patients will experience loss of all scalp hair in the course of the disorder. Approximately 20% to 25% of cases—often those occurring in childhood—may be associated with atopic disease (e.g., hay fever, asthma, or eczema). The incidence of complete scalp hair loss is much higher in these patients.
Despite its long course, often recurring over many years, the prognosis of alopecia areata is often favorable. Most patients will regrow hair at one time or another. In cases of extensive alopecia areata, alopecia totalis, and alopecia universalis, however, hair loss may be permanent.
Active alopecia areata is characterized by a spreading, annular area of hair loss; a smooth, depressed area of scalp that is slick to the touch is surrounded by hairs that often include so-called exclamation-point hairs (i.e., broken hairs 3 to 4 mm long, usually with an expanded tip and a telogen bulb). These hairs are not always seen but are diagnostic when present. They delineate the active spreading margin of alopecia areata. The bald patches generally affect the scalp but can also involve eyebrows, eyelashes, beard hair, and body hair. Spontaneous regrowth is common.
Table 3 Miscellaneous Chemicals That Can Cause Alopecia39
This condition is extremely unpredictable, often fluctuating without any obvious reason. However, seasonal outbreaks are noted in many patients. The initial patch may enlarge, or additional patches may develop and become confluent [see Figure 5]. The condition can progress to large irregular areas of baldness. In severe cases, patients lose all scalp hair or all body hair.
Ophiasis is a chronic and difficult to treat form of alopecia areata in which a band of baldness circles the scalp, very often around the inferior margin. This slowly extending lesion is often present for several years before any regrowth occurs. Permanent hair loss may result in some areas.
A scalp biopsy may be needed to confirm the diagnosis of alopecia areata.27
The treatment of alopecia areata depends on the severity of the disease.28 Small patches of alopecia areata often resolve spontaneously. If regrowth of hair does not occur, such patches usually respond to medium- or high-potency topical cortico-steroids or to intralesional injections of triamcinolone acetonide at a concentration of 5 mg/ml.
In more severe cases, intralesional corticosteroids may be tried; however, this approach may not be feasible in patients with extensive hair loss. Daily, short-contact topical therapy with 0.25% to 1% anthralin cream for up to an hour at a time may help and is suitable for children and adults. Psoralen and ultraviolet A (PUVA) therapy has also been used with some success.
Topical 5% minoxidil can be tried to speed hair regrowth and lengthen existing hairs. Minoxidil has no effect on the course of the disease but may improve hair coverage. It has few side effects and is often used in older children; however, the FDA has approved minoxidil for use only in persons 18 years of age and older. Systemic steroids are effective; however, they have shown a potential for side effects and do not prevent future recurrences. Prednisone (20 to 40 mg daily in the morning for 1 or 2 months, followed by slow tapering) has controlled the disease in adults; a change to alternate-day therapy is advisable whenever possible.
Topical immunotherapy with the sensitizing chemical diphencyprone has been used in some centers; it has a response rate comparable to that of systemic corticosteroids.29 Success with this treatment usually requires supervision in a specialized clinic. Sulfasalazine has been reported to have a 23% success rate in the treatment of severe alopecia areata.30 Other immunosuppressive drugs, such as oral cyclosporine, have been used experimentally. Such therapies are risky and expensive, however, and have not been approved in the United States for alopecia areata.
Traumatic alopecia may be caused by a variety of physical or chemical injuries to the hair and scalp. These injuries may be deliberate or accidental, inflicted by self or others, and acute or repetitive. The cause may be obvious or unclear.31 Potential causes include trichotillomania, habit tics, pruritic dermatoses, traction, pressure and friction, heat, radiation, and chemicals. In most cases of traumatic alopecia, management consists of removal of the underlying cause. In areas with permanent damage, hair transplantation may be necessary.
Trichotillomania is a compulsion to pull out one's hair. It is characterized by an increasing sense of tension before, and a sense of relief after, the hair is pulled. Trichotillomania is now classified as a specific disorder of impulse control.31,32 It is more common in children, in whom it is often caused by insecurity resulting from sibling rivalry, lack of attention, divorce of parents, learning disabilities, or unhappiness or teasing at school. In adolescents and adults, trichotillomania may be accompanied by mood disorders, anxiety disorders, or mental retardation and is often harder to treat than in children.
The diagnosis is based on the presence of irregular, broken-off hairs in patches on the scalp [see Figure 6]. The hairs are irregular in length because they are broken off at different times. The scalp itself is normal. Occasionally, biopsies are necessary to confirm the diagnosis. The best treatment is to explain cause and remedy to the patient in a nonconfrontational manner; usually, reassurance and understanding go a long way in the treatment of this condition. In more difficult cases, psychiatric consultation may be indicated.33 If habit tics or head rolling and banging are found to be causing traumatic hair loss, those behaviors should be treated.
Other Causes of Traumatic Alopecia
Pruritic dermatoses such as acne necrotica, folliculitis, lichen simplex chronicus, pediculosis capitis, prurigo nodularis, psoriasis, seborrheic dermatitis, and neurotic excoriations can lead to hair loss from excoriation. They need to be identified and treated.
Figure 5. Alopecia Areata
Circumscribed patches of hair loss are present in alopecia areata.
Traction Alopecia and Loose Anagen Syndrome
Traction alopecia may be acute (caused by accidental or deliberate avulsion of the scalp) or may arise from a familial condition, the loose anagen syndrome. Common causes of traction alopecia are excessive brushing and combing; backcombing and pulling the hair into braids, cornrows, and ponytails; weaving; and application of rollers.31
Loose anagen syndrome is usually seen in fair-haired children 2 to 5 years of age.34 It often presents as patchy hair loss following an incident of hair tugging. Prompt hair regrowth is the rule. The condition becomes asymptomatic with gentle hair care. Diagnosis is made on the basis of positive hair-pull tests showing many anagen hairs.
Alopecia Caused by Pressure and Friction
Prolonged pressure on a localized area of the scalp in immobilized neonates or patients under anesthesia, in coma, or with debilitating illness may result in ischemia leading to pressure alopecia. The hair usually regrows with time, but if the damage is severe, permanent hair loss and scarring may result.31 Alopecia caused by friction from vigorous massage has been described but is easily remedied.
Figure 6. Trichotillomania
Irregular, broken-off hairs are seen in trichotillomania.
Alopecia Caused by Heat, Radiation, and Chemicals
Excessive heat from hot oils and pomades, hot combs, and hot rollers is a common cause of chronic hair loss. Overheated hair dryers frequently cause the fluid droplets in wet hair shafts to expand, leading to the formation of bubble hairs.35 These brittle hairs are a frequent cause of follicle damage. The source of the overheating needs to be identified and removed.
Radiation dermatitis can cause hair loss. Permanent scarring alopecia is still seen in patients who were overtreated with x-rays for tinea capitis before oral antifungal agents became available.
Many chemicals can cause hair loss; the list includes hair dyes, moisturizers, oils and pomades, permanent waves, relaxers and straighteners, setting lotions, certain cationic and detergent shampoos, and saltwater.36 A careful history of hair care and grooming is needed to uncover these causes.
Cicatricial alopecia results from permanent scarring of the hair follicles. It may be widespread or localized and is sometimes difficult to identify. The causes of cicatricial alopecia may be primary or secondary and include hereditary or congenital conditions, infections, injuries, neoplasms, and dermatoses [see Table 4]. 37
On clinical examination, scarring is detected by the absence of follicular orifices and a pearly or scarred appearance of the skin. The scar may be depressed or hypertrophic. Associated lesions such as folliculitis, follicular plugs, scales, and telangiectasias may be found, along with broken, twisted, or easily extractable hairs. Other lesions may be present on skin or mucous membranes. If the disease is active, a specific diagnosis may be possible; in inactive cases, the initial cause is often inapparent.
The common variants of primary cicatricial alopecia of the scalp include central centrifugal cicatricial alopecia, discoid lupus erythematosus, lichen planopilaris, folliculitis decalvans, and nonspecific cicatricial alopecia (pseudopelade).38,39,40 The end phases of these conditions are similar; they are characterized by a lack of pores and by inflammation in white, scarred areas. For an accurate diagnosis, an early biopsy from an area of activity might show the identifying pathology. In the final scarring stage, it is usually not possible to identify the original cause.
Central centrifugal cicatricial alopecia
This condition usually affects middle-aged, African-American women, but it can occur in other races and in men. Central centrifugal cicatrical alopecia usually starts in the central vertex area of the scalp and gradually extends forward, assuming the outlines of a female-pattern alopecia. It is destructive and progressive. It is sometimes familial and is becoming more common. It may be aggravated by physical and chemical trauma—hence, its old name of hotcomb alopecia.
Discoid lupus erythematosus
The lesions of discoid lupus erythematosus are often itchy at onset and lead to erythema, scaling, telangiectasia, follicular spines, and atrophy [see Figure 7]. They often occur centrally in bare patches of scarring with an inactive border [see 15:IV Systemic Lupus Erythematosus].
Table 4 Causes of Cicatricial Alopecia40
Central scarring characterizes these lesions. The condition generally starts with bare, white patches that bud out from one another like pseudopods. Prominent follicular hyperkeratosis is present around the residual terminal hairs at the edges of the lesion, and varying degrees of erythema, scaling, and telangiectasia may occur. Itching may be present.
Crops of follicular pustules surrounding multiple, slowly expanding, and round or oval areas of alopecia characterize this condition. It may involve large areas of the skin. Secondary infection may be severe, with crusting and oozing. Eventually this condition gradually becomes less active and looks like other forms of chronic cicatricial alopecia.
Figure 7. Atrophic Scarring of Discoid Lupus
Atrophic scarring with erythema, scaling, telangiectasia, and follicular spines are characteristic of discoid lupus erythematosus.
Figure 8. Endothrix Tinea Capitis
In endothrix tinea capitis, black dots represent brittle, infected hairs snapped off flush with the scalp.
Figure 9. Diffuse Alopecia Caused by Syphilis
The characteristic irregular, so-called moth-eaten diffuse alopecia caused by syphilis is seen here.
Nonspecific cicatricial alopecia (pseudopelade)
The majority of cases previously classified as pseudopelade are in fact cases of nonspecific cicatricial alopecia in which the initial cause has not been established. In general, there is an insidious spread of a scarring process, which is apparently noninflammatory. It often involves the crown and occurs mainly in middle-aged women. It may represent the end result of lichen planopilaris or, less commonly, discoid lupus erythematosus or other disorders. It is characterized by patchy areas of alopecia with irregular extensions. The affected skin is smooth, white, and devoid of erythema, scaling, or pores; hence the descriptive term footprints in the snow. The course is variable and may last for a few years or several decades.
The original cases were described as a specific entity in the late 19th century and were reported as pseudopelade of Brocq. This eponym is rarely used currently, except perhaps for a small cohort of cases with no inflammatory phase at all, particularly occurring in children.
Treatment of cicatricial alopecia depends on the level of activity of the underlying disease. Central centrifugal cicatricial alopecia, discoid lupus erythematosus, and lichen planopilaris may respond to topical, intralesional, or systemic steroids; oral chloroquine therapy; or immunosuppressive agents such as mycophenolate mofetil or cyclosporine. Topical minoxidil is sometimes helpful in regrowing any surviving hairs, which may be normal, dystrophic, or in a resting stage. The application of a 2% or 5% solution twice daily should be tried for at least a year on scarred areas that show some hair. Folliculitis decalvans may respond to treatment with long-term antibiotics such as tetracycline (500 mg daily), minocycline (100 mg), erythromycin (250 mg), ciprofloxacin (750 mg), cephalexin (500 mg), trimethoprim-sulfamethoxazole (regular strength), or rifampin (300 mg, with regular-strength trimethoprim-sulfamethoxazole, given twice daily for at least 3 months). When the conditions have burned themselves out, either scalp reduction (i.e., surgical removal of a bald area of scalp and stretching of adjacent scalp over the removed area) or hair transplants may be helpful.
Miscellaneous Causes of Hair Loss
As mentioned earlier, less common causes of hair loss include infections (e.g., tinea capitis),41 infestations, hair shaft abnormalities, hereditary and congenital conditions, and various dermatoses involving the scalp.
In the United States, tinea capitis is now largely caused by Trichophyton tonsurans, an endothrix that infects the inside of the hair shaft. This makes the shaft brittle, which causes it to snap off flush with the skin, leaving a characteristic black dot of hair [see Figure 8]. The clinical diagnosis depends on this finding of black dots in patchy areas of hair loss. Removing the black dot with a small scalpel blade and dissolving it in potassium hydroxide (KOH) should reveal many spores packed inside the affected hair shaft. Ectothrix ringworm caused byMicrosporum canis and M. audouinii is much less common; it can usually be diagnosed by Wood light or by a finding of fungal spores around the hair shaft with KOH. Suitable oral antifungal treatments include griseofulvin, itraconazole, terbinafine, and fluconazole.
Secondary syphilis can cause a somewhat nondescript, moth-eaten type of diffuse alopecia [see Figure 9]. In such cases, a routine serologic test for syphilis is indicated.
Scalp lice should always be sought in cases of hair loss accompanied by pruritus. Lice are most likely to be found around and behind the ears and on the nape of the neck. Lymphadenopathy may also be present. Suitable treatment with permethrin shampoo or 0.5% malathion can be given. Ivermectine tablets may be useful in resistant cases.
Hair shaft abnormalities frequently present as broken-off hairs. Structural abnormalities of the hair shaft include fractures, irregularities, coiling and twisting, and extraneous matter.42,43 They can often be diagnosed by light microscopy.
There are many different types of congenital and inherited hair loss.44 These include congenital hypotrichosis with or without associated defects, congenital triangular alopecia, and many ectodermal dysplasias that affect the hair, teeth, nails, and sweat glands. One major form of congenital hypotrichosis is the Marie-Unna syndrome, which affects large families that have a dominant gene.45 Minor forms of hypotrichosis can occur in patients with other hereditary syndromes and chromosomal abnormalities. In most of these conditions, a reduction of hair follicles accounts for the hair loss. Some patients have surviving hairs that are often in telogen and may benefit from topical minoxidil.
Figures 2, 4, 7, and 8 D. A. Whiting and F. L. Howsden: Color Atlas of Differential Diagnosis of Hair Loss, rev. Canfield Publishing, Fairfield, New Jersey, 1998. Used with permission.
- Cotsarelis G, Millar SE, Chan EF: Embryology and anatomy of the hair follicle. Disorders of Hair Growth: Diagnosis and Treatment, 2nd ed. Olsen EA, Ed. McGraw-Hill, New York, 2003, p 1
- Krause K, Foitzik K: Biology of the hair follicle: the basics. Semin Cutan Med Surg 25:2, 2006
- Olsen EA: Clinical tools for assessing hair loss. Disorders of Hair Growth: Diagnosis and Treatment, 2nd ed. Olsen EA, Ed. McGraw-Hill, New York, 2003, p 75
- Rietschel RL: A simplified approach to the diagnosis of alopecia. Dermatol Clin 14:691, 1996
- Whiting DA, Howsden FL: Assessment of patient with hair loss. Color Atlas of Differential Diagnosis of Hair Loss, rev. Whiting DA, Howsden FL, Eds. Canfield Publishing, Fairfield, New Jersey, 1998, p 8
- Olsen EA: Pattern hair loss in men and women. Disorders of Hair Growth: Diagnosis and Treatment, 2nd ed. Olsen EA, Ed. McGraw-Hill, New York, 2003, p 321
- Birch MP, Messenger JF, Messenger AG: Hair density, hair diameter and the prevalence of female pattern hair loss. Br J Dermatol 144:297, 2001
- Whiting DA, Howsden FL: Androgenetic alopecia. Color Atlas of Differential Diagnosis of Hair Loss, rev. Whiting DA, Howsden FL, Eds. Canfield Publishing, Fairfield, New Jersey, 1998, p 18
- Shapiro J, Price VH: Hair regrowth: therapeutic agents. Dermatol Clin 16:341, 1998
- Olsen EA, DeLong ER, Weiner MS: Long-term follow-up of men with male pattern baldness treated with topical minoxidil. J Am Acad Dermatol 16:688, 1987
- Kaufman KD, Olsen EA, Whiting DA, et al: Finasteride in the treatment of men with androgenetic alopecia. Finasteride Male Pattern Hair Loss Study Group. J Am Acad Dermatol 39:578, 1998
- Kaufman KD: Long-term (5-year) multinational experience with finasteride 1 mg in the treatment of men with androgenetic alopecia. Eur J Dermatol 12:38, 2002
- Price VH, Menefee E, Sanchez M, et al: Changes in hair weight and hair count in men with androgenetic alopecia after treatment with finasteride, 1 mg, daily. J Am Acad Dermatol 46:517, 2002
- Olsen EA, Messenger AG, Shapiro J, et al: Evaluation and treatment of male and female pattern hair loss. J Am Acad Dermatol 52:301, 2005
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Editors: Dale, David C.; Federman, Daniel D.