HAIR LOSS

Fabiane Mulinari-Brenner, M.D.

International Scholar, Departments of Dermatology and Pathology
The Cleveland Clinic Foundation

Wilma F. Bergfeld, M.D., F.A.C.P.

Head, Clinical Research, Department of Dermatology
The Cleveland Clinic Foundation

Address: 9500 Euclid Avenue

Cleveland, OH 44195
FAX: 216/231-5448
E-MAIL: [email protected]
ABSTRACT

Hair loss is a common problem in men and women. Correct diagnosis of hair

disorders is complex and requires evaluation of clinical presentation, history, physical

examination, and laboratory tests. Hair loss may be categorized as non-cicatricial

alopecia, cicatricial alopecia, or hair shaft abnormalities. Non-cicatricial alopecia is the

most common group and includes androgenetic alopecia, telogen effluvium, alopecia

areata, and traction alopecia. The hallmark of this group is the possibility of regrowth

with adequate treatment.

INTRODUCTION

Hair loss, or alopecia, is one of the most distressing disorders for both adults and

children because our society places a great emphasis on physical appearance. The

importance of the patient’s cosmetic concerns should not be underestimated.

Alopecia may be associated with a wide variety of causes. Some cases are best

managed with reassurance and education, whereas others require medical evaluation and

therapy. This article reviews the causes of hair loss emphasizing the most common ones

– adrogenetic alopecia, telogen effluvium, alopecia areata, and traction alopecia.

CAUSES OF HAIR LOSS

Most cases of hair loss can be divided into three categories: non-cicatricial

alopecia, cicatricial alopecia, and hair shaft abnormalities (Table 1).

1. NON-CICATRICIAL ALOPECIA

Non-cicatricial alopecia is hair loss with chances for regrowth. Types of non-cicatricial

alopecia include telogen effluvium (TE), androgenetic alopecia (AGA), and alopecia

areata (AA). Traction alopecia (caused by pulling hair) and trichotillomania (compulsive

hair-plucking) are also included in this group. However, in chronic cases, trauma can

affect the follicle stem cells (follicle midportion), producing scarring and permanent hair

loss.1

Shedding

The most common cause of hair loss is shedding or telogen effluvium (TE), which

is the premature conversion of growth-phase hair follicles to the resting or shedding

(telogen) phase. Acute shedding was initially described after febrile diseases, childbirth,

chronic systemic diseases, administration of heparin, and emotional distress.2 Other

factors have been identified as acute and chronic causes of TE, including numerous

drugs, endocrine disorders, severely restricted diets, surgical procedures, and

anesthesias.3,4,5 Recently, it has been proposed that TE can herald androgenetic alopecia

(AGA) in both sexes.6

The primary sign reported by the patient is shedding. Patients usually report

increased hair on shower drain, clothes, or pillow. The daily hair-shed counts are higher
than the normal. Hair shed counts on a non-shampoo day is up to about 100 in normal

individuals. Decreased hair volume may be noticeable when hair density is reduced as

much as 30% to 50%.7

A good clinical history may find the trigger 3 to 6 months before the shedding

started. When evaluating shedding, clinicians must evaluate thyroid function and exclude

anemia. Hormonal screening can be helpful detecting perimenopausal changes and

androgen excess. History and examination should exclude infectious disease such as

syphilis. Nutritional deficiencies (protein, vitamins, and minerals) are often associated

with shedding.

To treat TE, the cause or causes must be isolated and treated. Patients should

always be reassured that the shedding is being replaced and that the chances of becoming

bald are remote.

Androgenetic alopecia

Androgenetic alopecia (AGA) or common baldness is prominent central-pattern

scalp alopecia induced by androgens, and it may affect genetically predisposed men and

women at any time between puberty to senescence. Inheritance of AGA is controversial,

it is eigther polygenic or autosomal dominant with variable penetrance. It is known that

AGA affects equal numbers of men and women. One third of the individuals with a

strong family history of AGA can expect to be affected, irrespective of sex.8 Thinning of

the hair usually begins between the ages of 12 and 40 years old, and approximately half

of the population expresses this trait to some degree before the age of 50.9
 The initiating event may be a telogen shed, but the primary sign reported by the

patient is thinning. The progressive thinning results from both a gradual miniaturization

of the hair follicle and a shortened growth phase (anagen).

The pattern of hair loss is quite variable. One common pattern in both men and

women is the M-pattern, characterized by frontal recession with thinning or absent hair in

the temples (figure 1). Another pattern, more common in women, is decreased density of

scalp hair in the central area, with retention of the frontal hairline (figure 2).

Diagnosis of AGA is based on clinical presentation and family history. Hormonal

evaluation is necessary if androgen excess is suspected by the presence of acne,

hirsutism, and, in women, irregular menstrual periods. Androgens, such as

dehydrotestosterone (DHT) and sulfonated dehydroepiandrosterone, influence hair loss.

The most potent androgen, DHT, reduces the amount of scalp hair and increases the

amount of body and genital hair. This hormone has been one of the targets when treating

AGA.

Oral finasteride, a 5-alpha-reductase inhibitor, produces local reductions in DHT

in the scalp follicles. Studies with finasteride demonstrated good results in males,

however, no improvement was noted in post-menopaused women with female AGA.10,11

In women, topical minoxidil is the first option. Systemic treatments for female AGA,

such as spirinolactone and flutamide, are controversial but indicated to block androgen

uptake by the follicles.12 For the same reason, birth control pills and hormone

replacement therapy can be used as adjuvant treatment. Topical preparations of 2% or

5% minoxidil are also used for AGA in both sexes.10 Special care should be taken to
avoid facial skin when applying minoxidil, because it can promote the growth of facial

hair and worsen hirsutism.

Alopecia areata

Alopecia areata (AA) is hair loss of suspected autoimmune origin with an

unpredictable prognosis. AA causes isolated or recurrent patchy hair loss (figure 3).

Multiple patches, complete scalp hair loss (alopecia totalis), and complete scalp and body

hair loss (alopecia universalis) are other clinical presentations of AA.

A deep inflammatory process around the follicle accelerates the shedding phase in

AA.13 The affected hair sheds and no replacement is seen while the inflammation is

present. The first hair to regrow is thin and light in color (vellus hair), this hair is often

replaced by thick white hair before the normal color hair (terminal hair) regrows.

Alopecia areata occurs in 1.7% of the population.14 Genetic factors have an

important role in the origin of AA and family history of AA occurs in 10% to 42% of the

cases.15

The exact cause of AA is not clearly identified. However, there is growing

evidence to suggest that AA is an autoimmune disease mediated by T-lymphocytes. As

an autoimmune disease, AA can be associated with other diseases of known or suspected

autoimmune origin, such as thyroid disease, vitiligo and atopy.16 Other autoimmune

disorders such as lupus erythematosus, diabetes, and pernicious anemia are frequent in

these patients’ family.

Treatment options for AA are based on the extent of the disease and on the

patient’s age. Intralesional injections of corticosteroids are the first-line therapy for
adults with less than 50% scalp involvement.15 Reducing the inflammation is the main

goal of corticosteroids. Minoxidil is a biologic response-modifier that enhances hair

growth. However, it produces cosmetically acceptable results in fewer than half of AA

patients.17 Anthralin, a nonspecific immunomodulating agent commonly used in

children, produces cosmetically acceptable regrowth ranging from 20% to 25% of the

cases.18

Topical immunotherapy with contact sensitizers (dinitrochlorobenzene, squaric

acid dibutyl ester or diphenylcyclopropenone) is the most effective and accepted therapy

for chronic severe AA. However, the frequency of acceptable regrowth is variable,

depending on the extension of the AA and on the sensitizer.15 The exact mechanism of

action of the topical sensitizers is unclear, but it is known that they direct T-lymphocytes

away from the perifollicular area causing a mild skin irritation.

Traction alopecia

Traction can physically damage the hair shaft and also alter the hair growth cycle.

If traction is repetitive and chronic, cicatricial alopecia may result. Practices such as tight

braiding, wearing ponytails or elastic hair bands, using rollers, or other devices that place

extreme and repetitive stress on the scalp hair are responsible for most cases. Traction

alopecia causes sparse hair and hair breakage in the frontal area (figure 4). This

condition is quire common in women with curly hair, especially African-Americans.

Trichotillomania (TM) is a traction alopecia where the patient repeatedly pulls or

plucks the hair in a bizarre pattern. The cause may not be obvious; it can range from an

underlying emotional problem to a definite mental disorder. It is unusual for the patient
to admit or report his or her own history of hair pulling. The condition is frequently seen

in children, when pulling is often due to insecurity and not a sign of psychiatric illness.19

Young and old women can present TM associated with depression or anxiety.20 TM

clinically presents as areas of incomplete hair loss and short hair, most commonly on

scalp. Eyelashes, eyebrows and other hairy areas can also be affected.

To treat traction alopecia, urge the patient to change her hairstyle and explain the

possibility of permanent hair loss if the traction is not removed. Patients with

trichotillomania require psychological evaluation and counseling. Psychopharmacologic

medications, such as fluoxetine, are often necessary to control the compulsive hair

pulling.

2. CICATRICIAL ALOPECIA

Cicatricial alopecia is irreversible hair loss associated with the destruction of stem

cell reservoir located in the midportion of the follicle. Cicatricial alopecia is caused by a

diverse group of cutaneous disorders with a variety of presentations.

Common causes of cicatricial alopecia are fungal or bacterial folliculitis, discoid

lupus erythematosus, and lichen planopilaris. Other causes are skin diseases, trauma,

scarring bullous disorders (epidermolysis bullosa, bullous pemphigoid, porphyria

cutanea), and neoplastic disease (skin tumors and cutaneous metastasis). To evaluate

cicatricial alopecia of unknown origin, clinicians should start with cultures for bacteria

and fungus. Diagnosis is based on a scalp biopsy, a 4-mm punch is suggested. Even

though this group presents with irreversible alopecia, treatment is always recommended
to prevent the process from spreading to unaffected areas. These patients should be

referred to a dermatologist interested in hair loss.

3. HAIR SHAFT ABNORMALITIES

Hair shaft abnormalities produce fragile and brittle hair. Patients may present with

diffuse or patchy areas of short hair and a history of hair that will not grow beyond a

certain length. Inherited disorders (genodermatoses) and external hair shaft damage can

change the hair shaft structure. Repeated trauma to the hair shaft in the form of traction,

bleaching, perming, or blow drying is most often the cause of the hair shaft abnormality

in adults.

A variety of hair shaft shapes may develop. The most commonly found hair shaft

abnormality is trichorrexis nodosa, a nodal area where the hair splits into strands.

Trichorrexis nodosa is more commonly acquired as a result of external damage, however

it may be associated with genetic and metabolic disorders that alter hair keratinization.

These patients should be referred to a dermatologist interested in hair diseases. Treatment

is based on removing the cause, when traumatically induced. Leave-on conditioners that

coat the hair fibers may increase hair strength and avoid breakage.
SUMMARY

In summary, hair loss comes in many different ways. Alopecia is usually treatable

or self-limited, however, it may be permanent or cicatricial. Careful diagnosis of the type

of hair loss will aid in selecting effective treatment. Reassurance is an important

component of any treatment regimen.

FIGURES

Figure 1. Androgenetic alopecia, male pattern.

Figure 2. Androgenetic alopecia, female pattern.

Figure 3. Alopecia areata.

Figure 4. Traction alopecia.

Table 1. Causes of hair loss

Non-cicatricial alopecia Cicatricial alopecia Hair shaft disorders

Telogen effluvium Trauma or local surgery External agents: traction

bleaching, perming, and
Androgenetic alopecia Skin or follicular infection: blow drying
fungal, bacterial, viral
Alopecia areata Inherited disorders:
Autoimmune diseases: discoid argininosuccinicaciduria,
Traction alopecia lupus erythematosus, lichen trichothiodystrophy syndrome
planopilaris, morphea
Trichotillomania
Neoplastic diseases:
skin tumors and cutaneous
metastases
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