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Abstract

Alopecia is usually treatable and self-limited, but it may be permanent. Careful diagnosis of the type of hair loss will aid in selecting effective treatment. Reassurance is an important component of any treatment regimen.
CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 70 • NUMBER 8 AUGUST 2003
705
LOPECIA IS DISTRESSING to patients
because of its effect on appearance, but
the problem is often more than skin deep. We
physicians should not underestimate its impor-
tance, either as a cosmetic problem or as a sign
of a potentially serious underlying condition.
In most cases, alopecia is best managed
with reassurance and education, but other
cases require medical evaluation and therapy.
The evaluation includes a personal and family
history, physical examination, and sometimes
laboratory testing.
In this article, we give a brief overview of
the primary care management of the various
types of hair loss.
TYPES OF HAIR LOSS
Most hair loss can be categorized into three
types:
Noncicatricial (potentially reversible)
Cicatricial
Due to hair shaft abnormalities.
NONCICATRICIAL ALOPECIA
Noncicatricial alopecia, in turn, has several
subtypes:
Telogen effluvium (shedding)
Androgenetic alopecia (common bald-
ness)
Alopecia areata (isolated or recurrent
patchy hair loss)
Traction alopecia (caused by pulling hair),
and trichotillomania (compulsive hair-pluck-
ing). Although these cause temporary hair
loss, in chronic cases trauma can affect the fol-
licle stem cells, ie, the middle portion of the
hair follicle, producing scarring and perma-
nent hair loss.
1
FABIANE MULINARI-BRENNER, MD
International Scholar, Departments of Dermatology
and Pathology, The Cleveland Clinic
WILMA F. BERGFELD, MD
Head, Clinical Research, Department of Dermatology,
The Cleveland Clinic
Hair loss:
Diagnosis and management
REVIEW
ABSTRACT
Alopecia is usually treatable and self-limited, but it may be
permanent. Careful diagnosis of the type of hair loss will
aid in selecting effective treatment. Reassurance is an
important component of any treatment regimen.
KEY POINTS
Most alopecia is noncicatricial, meaning it is potentially
reversible. Subtypes include androgenetic alopecia, telogen
effluvium, alopecia areata, and traction alopecia.
To treat telogen effluvium, the cause or causes must be
isolated and treated. Patients should always be reassured
that their hair is being replaced, and that the chances of
becoming bald are remote.
Hair shaft abnormalities produce fragile or brittle hair.
Causes include traction, bleaching, perming, or blow-drying.
Tight braids, ponytails, elastic hair bands, rollers, or other
devices that place extreme and repetitive stress on the
scalp hair are responsible for most cases of traction
alopecia.
A
706
CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 70 • NUMBER 8 AUGUST 2003
Telogen effluvium
Telogen effluvium or shedding is the most
common type of hair loss. In this condition,
hair follicles prematurely convert from the
growth phase to the resting or shedding (telo-
gen) phase.
Presentation. The primary sign reported by
patients is an increase in the number of hairs
they are shedding, seen on the shower drain,
clothes, or pillow. Normally, people shed up to
about 100 hairs on days they do not shampoo;
people with telogen effluvium usually lose 150
to 400 hairs per day. Some patients notice a
decrease in hair volume only when hair density
is reduced as much as 30% to 50%.
2
Causes. Often, an event triggers the
process 3 to 6 months before the shedding
begins. Acute shedding was initially described
after febrile diseases, childbirth, chronic sys-
temic diseases, use of heparin, and emotional
distress.
3
Other factors identified as both acute and
chronic causes of telogen effluvium include
numerous drugs, endocrine disorders, severely
restrictive diets, surgical procedures, and anes-
thesia.
4–6
Recently, it was proposed that telogen
effluvium can herald androgenetic alopecia in
either sex.
7
Diagnosis. The key is to find the trigger,
with a careful clinical history. In addition,
the clinician should evaluate thyroid func-
tion and exclude anemia. Hormonal screen-
ing can help detect perimenopausal changes
and androgen excess.
The history and physical examination
should exclude infectious diseases (eg,
syphilis) and nutritional deficiencies (protein,
vitamins, and minerals) that are often associ-
ated with shedding.
Treatment. To treat telogen effluvium,
the cause or causes must be isolated and treat-
ed. Patients should always be reassured that
their hair is being replaced, and that the
chances of becoming bald are remote.
Androgenetic alopecia
Presentation. Androgenetic alopecia may
affect genetically predisposed men and women
at any time from puberty to senescence.
Thinning of the hair usually begins between
the ages of 12 and 40 years, and approximate-
ly half of the population expresses this trait to
some degree before age 50.
8
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 (ana-
gen) phase.
The pattern of hair loss is quite variable.
Common in both men and women is the M-
pattern, characterized by frontal recession
In shedding,
look for a
trigger that
occurred 3 – 6
months earlier
HAIR LOSS MULINARI-BRENNER AND BERGFELD
Androgenetic alopecia
FIGURE 1. Top, male pattern. Bottom,
female pattern.
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 1).
Causes. Androgens such as dehydrotestos-
terone and dehydroepiandrosterone sulfate
influence hair loss. Dehydrotestosterone, the
most potent androgen, reduces the amount of
scalp hair and increases the amount of body
and genital hair.
Whether androgenetic alopecia is inherit-
ed is controversial; it is either polygenic or
autosomal dominant with variable pene-
trance. Androgenetic alopecia affects equal
numbers of men and women. One-third of
people with a strong family history can expect
to be affected, irrespective of sex.
9
Diagnosis. The diagnosis is based on clin-
ical 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.
Treatment. Dehydrotestosterone is one of
the targets when treating androgenetic alope-
cia. Oral finasteride, a 5-alpha-reductase
inhibitor, produces local reductions in this hor-
mone in the scalp follicles. Studies with finas-
teride demonstrated good results in men, but
no improvement in postmenopausal women
with female androgenetic alopecia.
10,11
In women, topical minoxidil 2% or 5% is
the first option. (It is also used in men.
10
)
Women should take special care to avoid the
face when applying minoxidil, because it can
promote the growth of facial hair and worsen
hirsutism.
Systemic treatments for female androge-
netic alopecia, such as spironolactone and flu-
tamide, are controversial but are indicated to
block androgen uptake by the follicles.
12
For
the same reason, birth control pills and hor-
mone replacement therapy can be used as
adjuvant treatment.
Alopecia areata
Presentation. Alopecia areata causes iso-
lated or recurrent patchy hair loss (
FIGURE 2),
but multiple patches, complete scalp hair loss
(alopecia totalis), and complete scalp and
body hair loss (alopecia universalis) are other
clinical presentations.
The prognosis is unpredictable. The first
hair to regrow is thin and light in color (vel-
lus hair); this hair is often replaced by thick
white hair before the normal-colored hair
(terminal hair) regrows.
Causes. In alopecia areata, a deep inflam-
matory process around the follicle accelerates
the shedding phase.
13
The affected hair sheds,
and no replacement is seen while the inflam-
mation is present.
The exact cause of alopecia areata has not
been identified. However, growing evidence
suggests that it is an autoimmune disease
mediated by T lymphocytes. As an autoim-
mune disease, alopecia areata can be associat-
ed with other diseases of known or suspected
autoimmune origin, such as thyroid disease,
vitiligo, and atopy.
14
Other autoimmune dis-
orders such as lupus erythematosus, diabetes,
and pernicious anemia are common in the
family history.
Genetic factors have an important role in
alopecia areata, and a family history is found
in 10% to 42% of cases.
15
Treatment is based on the extent of the
disease and on the patient’s age.
CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 70 NUMBER 8 AUGUST 2003
709
Minoxidil is the
first option in
women with
androgenetic
alopecia
Alopecia areata
FIGURE 2
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CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 70 • NUMBER 8 AUGUST 2003
Intralesional corticosteroid injections are the
first-line therapy for adults with scalp involve-
ment of less than 50%.
15
Reducing the inflam-
mation is the main goal of corticosteroids.
Minoxidil is a biologic response-modifier
that enhances hair growth, but it produces
cosmetically acceptable results in fewer than
half of patients with alopecia areata.
16
Anthralin, a nonspecific immunomodulat-
ing agent commonly used in children, pro-
duces cosmetically acceptable regrowth in
20% to 25% of patients.
17
Topical immunotherapy with contact sensi-
tizers (dinitrochlorobenzene, squaric acid
dibutyl ester, or diphenylcyclopropenone) is
the most effective and accepted therapy for
chronic severe alopecia areata. However, the
rate of acceptable regrowth varies and depends
on the extent of the alopecia and on which
sensitizer is used.
15
The exact mechanism of
action of the topical sensitizers is unclear, but
they direct T lymphocytes away from the peri-
follicular area, causing a mild skin irritation
and allergic reaction.
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.
Presentation. Traction alopecia causes
the hair to be sparse and break in the frontal
area (
FIGURE 3). This condition is quite common
in women with curly hair, especially African
Americans.
Causes. Tight braids, ponytails, elastic
hair bands, rollers, or other devices that place
extreme and repetitive stress on the scalp hair
are responsible for most cases.
Treatment of traction alopecia involves
urging the patient to change her hairstyle and
explaining that the hair loss may be perma-
nent if the traction is not stopped.
Trichotillomania
Trichotillomania is the compulsive pulling out
of one’s own hair in a bizarre pattern.
Presentation. Trichotillomania clinically
presents as areas of incomplete hair loss and
short hair, most commonly on the scalp.
Eyelashes, eyebrows, and other hairy areas can
also be affected.
The condition is frequently seen in chil-
dren, in whom pulling is often due to insecu-
rity and is not a sign of psychiatric illness.
18
In both younger and older women, the con-
dition can be associated with depression or
anxiety.
19
Of note, it is unusual for the
patient to admit or report his or her own his-
tory of hair pulling.
Causes. The cause may not be obvious; it
can range from an underlying emotional prob-
lem to a definite mental disorder.
Treatment. Patients with trichotillomania
require psychological evaluation and counsel-
ing. Psychopharmacologic medications such
as fluoxetine are often necessary to control the
compulsive hair-pulling.
CICATRICIAL ALOPECIA
Cicatricial alopecia is irreversible hair loss
associated with destruction of the stem cell
reservoir located in the middle of the follicle.
Causes
Cicatricial alopecia is caused by a diverse
group of cutaneous disorders with a variety of
presentations. Common causes are fungal or
bacterial folliculitis, discoid lupus erythemato-
sus, and lichen planopilaris. Others include
trauma, scarring bullous disorders (epidermol-
ysis bullosa, bullous pemphigoid, porphyria
cutanea), and neoplastic disease (skin tumors
and cutaneous metastasis).
Traction
alopecia is
common in
women with
curly hair
Traction alopecia
FIGURE 3
HAIR LOSS MULINARI-BRENNER AND BERGFELD
712
CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 70 • NUMBER 8 AUGUST 2003
Diagnosis
The evaluation of cicatricial alopecia of
unknown origin starts with cultures for bac-
terial and fungal infection. The diagnosis is
based on scalp biopsy; 4-mm punch biopsy is
suggested.
Treatment
Even though the hair loss is irreversible, treat-
ment is always recommended to prevent the
process from spreading to unaffected areas.
These patients should be referred to a derma-
tologist who has a special interest in hair loss.
HAIR SHAFT ABNORMALITIES
Presentation
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.
Causes
Repeated trauma to the hair shaft from trac-
tion, bleaching, perming, or blow-drying is
most often the cause of the hair shaft abnor-
mality in adults.
In addition, inherited disorders (genoder-
matoses) and external hair shaft damage can
change the hair shaft structure.
A variety of hair shaft shapes may devel-
op. The most common hair shaft abnormali-
ty is trichorrhexis nodosa, a nodal area where
the hair splits into strands. Trichorrhexis
nodosa is more commonly acquired as a result
of external damage, but it may be associated
with genetic and metabolic disorders that
alter hair keratinization. Patients with these
latter conditions should be referred to a der-
matologist with a special interest in hair dis-
eases.
Treatment
Treatment is based on removing the cause, if
the problem is traumatically induced.
Leave-on conditioners that coat the hair
fibers may increase hair strength and pre-
vent breakage.
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ADDRESS: Wilma F. Bergfeld, MD, Department of
Dermatology, A61, The Cleveland Clinic Foundation, 9500
Euclid Avenue, Cleveland, OH 44195; e-mail bergfew@ccf.org.
HAIR LOSS MULINARI-BRENNER AND BERGFELD
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The safety and efficacy of 3% topical minoxidil were evaluated in the treatment of extensive patchy alopecia areata, alopecia totalis, and alopecia universalis. Patients with extensive patchy alopecia areata had greater than 50% scalp hair loss. In this double-blind study, thirty subjects applied minoxidil or placebo to half of the afflicted scalp area twice daily, with overnight petrolatum occlusion, for 1 year. Both male and female subjects, ranging in age from 9 to 65 years, were enrolled, fifteen subjects to each treatment group. Minoxidil applications were generally well tolerated except for three instances of scalp itching and dermatitis, two of which necessitated discontinuing the medication. Hair growth was seen in seven of eleven evaluable subjects (63.6%) in the minoxidil group and in five of fourteen evaluable subjects (35.7%) in the placebo group. Excellent, cosmetically acceptable hair growth was seen in three of eleven minoxidil-treated subjects (27.3%) and in one of fourteen placebo-treated subjects (7.1%). Examination of vital signs and laboratory measurements revealed no evidence of systemic effects of minoxidil. Seven of the twelve subjects assayed in the minoxidil group had detectable minoxidil serum levels, ranging from 0.4 to 7.5 ng/ml.
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So far, it is a widely accepted opinion that androgenetic alopecia is caused by an autosomal dominant gene with reduced penetrance in women. This view is essentially based on a family study performed by Osborn in 1916. She believed that balding men would be either heterozygous (Bb) or homozygous (BB), whereas balding women would be homozygous (BB). By contrast, we here present five arguments favoring a polygenic inheritance of the trait: (1) the high prevalence of the trait, (2) the distribution of balding patterns in the general population along a gaussian curve of variation, (3) the fact that the risk increases with the number of relatives already affected, (4) the slightly increased risk of relatives of severely affected women as compared to the relatives of mildly affected women, and (5) the fact that a predisposition inherited from an affected mother is of greater importance than that inherited from an affected father. In conclusion, the simple mendelian model of Bb and BB can no longer be upheld.
Article
Some individuals question whether any treatment is effective in severe alopecia areata. Certainly many patients, especially those with mild disease, experience spontaneous hair regrowth; however, results of double-blind studies clearly indicate that some treatments do promote hair regrowth even in those with extensive disease. Some patients never show either spontaneous or treatment-related hair regrowth; others experience hair regrowth only while maintained on treatment, repeatedly losing hair within a few weeks of discontinuing treatment and regrowing it within several weeks after restarting treatment. Some patients who have been responsive to treatment may experience exacerbation of their disease such that even high-dose systemic steroids do not prevent the development of alopecia universalis. Some treatments appear to work on some patients some or all of the time, but no treatment appears to work on all patients all of the time. We would suggest a few practical points that we find useful: To maximize the potential for cosmetic hair growth in alopecia areata that is extensive or flaring, treat the entire scalp instead of "chasing" patches. Do not change any topical treatment sooner than 3 months after starting it; early regrowth may first be present at 3 months. Cosmetic regrowth may take a year or more to achieve. Maintenance treatment increases the likelihood of maintenance of cosmetic hair growth, but patches of hair loss may still come and go. Atopic patients who experience seasonal hair loss may benefit (ie, have less severe hair loss flares or respond more readily to topical therapy) by using an antihistamine or mast cell stabilizer prophylactically. Whether one looks at the therapeutic cup as half full or half empty, most patients urge us to continue to try to find safe, effective long-term treatments for this disease.
Article
Chronic telogen effluvium is not uncommon. It is a form of diffuse hair loss affecting the entire scalp for which no obvious cause can be found. It usually affects women of 30 to 60 years of age who generally have a full head of hair prior to the onset of shedding. The onset is usually abrupt, with or without a recognizable initiating factor. The degree of shedding is usually severe in the early stages and the hair may come out in handfuls. Chronic telogen effluvium has distinctive clinical and histologic features that are usually diagnostic. Chronic telogen effluvium contrasts with classic acute telogen effluvium by its persistence and its tendency to fluctuate for a period of years. Patients are particularly troubled by the continuing hair loss and fear total baldness. Repeated reassurance that the condition represents shedding rather than actual hair loss and does not cause complete baldness is necessary. Chronic telogen effluvium does appear to be self-limiting in the long run.