Hair Diseases: Anatomy

C H A P T E R 2 4
Hair Diseases
CHAPTER CONTENTS
ANATOMY Female Pattern Hair Loss (Androgenic

PHYSIOLOGY Alopecia in Women)
Hirsutism
EVALUATION OF HAIR LOSS Alopecia Areata
GENERALIZED HAIR LOSS Trichotillomania
LOCALIZED HAIR LOSS Traction (Cosmetic) Alopecia
Androgenetic Alopecia in Men (Male Pattern Scarring Alopecia
Baldness) TRICHOMYCOSIS
Physicians are frequently confronted with hair-related forms a cylinder of uniform diameter. Short hairs with
problems. Most complaints are from patients with early- tapered tips either have short growth cycles or have
onset pattern baldness. The physician must be able to experienced the recent onset of anagen.
recognize this normal, inherited hair loss pattern so that The growing shaft is surrounded by several concentric
detailed and expensive evaluations can be avoided. Other layers (see Fig. 24.2). The outermost glycogen-rich layer
patients have complaints about abnormal hair growth; is called the outer root sheath. It is static and continuous
these diseases must be recognized and not dismissed as with the epidermis. The inner root sheath (Henle layer,
balding. The signs of hair loss or excess growth are at Huxley layer, and cuticle) is visible as a gelatinous mass
times subtle. The signs usually seen with cutaneous disease, when the hair is plucked. It protects and molds the growing
such as inflammation, may be absent. A systematic approach hair but disintegrates before reaching the surface at the
to evaluation is essential. infundibulum.
The hair shaft that emerges has three layers – an outer
cuticle, a cortex, and sometimes an inner medulla – all of
ANATOMY which are composed of dead protein. The cuticle protects
and holds the cortex cells together. Split ends result if
Types of Hair. There are three types of hair. Thick, the cuticle is damaged by brushing or chemical cosmetic
pigmented hairs are called terminal hairs. Terminal hairs treatments. The cortex cells in the growing hair shaft
on the top of the head and in the beard, axillary, and rapidly synthesize and accumulate proteins while in the
pubic areas are influenced by androgens. Androgens are lower regions of the hair follicle. Systemic diseases and
important in regulating hair growth. At puberty, androgens drugs may interfere with the metabolism of these cells
increase the size of follicles in the beard, chest, and limbs and reduce the hair shaft diameter. Pigment-containing
and decrease the size of follicles in the bitemporal region, melanosomes are acquired deep in the bulb matrix and
which reshapes the hairline in men and many women. are deposited in the cortical and medullary cells.
Lanugo hairs are the fine hairs found on the fetus;
similar fine hairs (peach fuzz) found on the adult are called Hair Follicle. Humans have about 5 million hair fol-
vellus hairs. Vellus hair is short, fine, and relatively licles at birth. No follicles are formed after birth, but
nonpigmented and covers much of the body. Hair on the their size changes under the influence of androgens. The
rest of the body is independent of androgens. hair follicle is formed in the embryo by a club-shaped
epidermal down-growth – the primary epithelial germ that
Hair Structure. The hair shaft is dead protein. It is is invaginated from below by a flame-shaped, capillary-
formed by compact cells that are covered by a delicate containing dermal structure called the papilla of the hair
cuticle composed of plate-like scales. The living cells in follicle. The central cells of the down-growth form the
the matrix multiply more rapidly than those in any other hair matrix, the cells of which form the hair shaft and
normal human tissue. They push up into the follicular its surrounding structures. The matrix lies deep within
canal, undergo dehydration, and form the hair shaft, which the subcutaneous fat. The mature follicle contains a hair
consists of a dense, hard mass of keratinized cells. Normal shaft, two surrounding sheaths, and a germinative bulb
hairs have a pointed tip. The hair in the follicular canal (Fig. 24.1). The follicle is divided into three sections. The
927
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928 Habif’s Clinical Dermatology
infundibulum extends from the surface to the sebaceous

gland duct. The isthmus extends from the duct down
Sebaceous
to the insertion of the erector muscle. The inferior
gland Infundibulum
segment, which exists only during the growing (anagen)
phase, extends from the muscle insertion to the base of
the matrix. The matrix contains the cells that proliferate
to form the hair shaft (Fig. 24.2). The mitotic rate of
the hair matrix is greater than that of any other organ.
The cells begin to differentiate at the top of the bulb. The
Isthmus inner and outer root sheaths protect and mold the growing
hair. The inner root sheath disintegrates at the duct of
the sebaceous gland. Hair growth is greatly influenced by
Erector any stress or disease process that can alter mitotic activity.
muscle
PHYSIOLOGY
Cycling of hair follicles depends on the interaction of the
follicular epithelium with the dermal papilla. The dermal
papilla induces hair-follicle formation from the overlying
epithelium at the onset of each new follicular cycle (Fig.
24.3). The bulge consists of cells in the outer root sheath,
Inferior
segment
which is located near the insertion of the arrector pili
muscle. The dermal papilla interacts with germ cells in
the hair-follicle bulge to regenerate the lower follicle.
Stem cells in the bulge portion of the outer root migrate
out of the follicle and regenerate the epidermis after injury.
Rapidly proliferating matrix cells in the hair bulb
Bulb produce the hair shaft. The matrix cells differentiate, move
Matrix upward, and are compressed and funneled into their final
shape by the rigid inner root sheath. The shape (curvature)
of the inner root sheath determines the shape of the hair.
The bulk of the hair shaft is called the cortex. Pigment
FIG 24.1 ■ Hair follicle. Longitudinal section showing
in the hair shaft is produced by melanocytes interspersed
the three sections: the infundibulum, the isthmus, and
among the matrix cells. The volume of the dermal papilla
the inferior segment.
determines the diameter of the hair shaft.
FIG 24.2 ■ Hair bulb. The outer and

inner root sheaths mold and protect Hair cuticle Outer root
the growing hair shaft. The hair sheath
shaft consists of the medulla, hair Hair cortex Cuticle of inner
cortex, and cuticle. Hair medulla
root sheath
Inner
Huxley layer root
sheath
Henle layer
Hyaline
basement Pool of
membrane undifferentiated
cells in shaft
Melanocyte
Matrix
Fibrous sheath
Papilla
24 Hair Diseases 929
Stage 1 FIG 24.3 ■ Stages 1, 3, 6, and 8

is represent the embryonic events of
nes
g e the development of the hair follicle.
Stage 3
ho
Epidermis rp The follicle then enters a three-
o
stage (anagen, catagen, and
m
r
la
telogen) growth cycle. The cycle
cu
Stage 6
lli
depends on the interaction of the
Fo
follicular epithelium and the dermal
Bulge papilla. The Roman numerals
Dermal Anagen VI
indicate morphologic substages of
papilla
anagen and catagen. Catagen III:
conclusion of the growth phase.
Stage 8
Catagen VII: transition phase; the
inferior segment separates from the
Bulge
papilla. Telogen: the hair ascends to
Sebaceous the level of the erector muscle.
gland Connective-tissue Anagen III: the growing cycle
sheath Anagen IV
resumes. Anagen IV: the growing
Outer root Club hair hair forces the club hair out.
Arrector
sheath
Hair shaft pili muscle Anagen VI: the mature follicle is
Inner root restored. The pie chart shows the
sheath proportion of time the hair follicle
Melanocytes spends in each stage. (Adapted from
Hair shaft Paus R, Cotsarelis G. The biology of
Hair matrix
hair follicles. N Engl J Med
Catagen III 1999;341:491–7.)
Bulb
Anagen III
Anagen
Initiation of
follicular cycling
Catagen VII
Catagen Telogen
Telogen
Sebaceous
gland
Involuting Arrector
epithelial column Club hair pili muscle
Hair Growth Cycle

phase), telogen (resting phase), and anagen (growing phase)
The average scalp has more than 100,000 hairs. The growth (Fig. 24.4). Approximately 90% to 95% of hairs are in the
phase of scalp hair is approximately 1000 days (range, 2 anagen phase, and 5% to 10% are in the telogen phase.
to 6 years). Hair in other areas, such as the eyebrows and Up to 100 telogen hairs are lost each day from the head,
eyelashes, has a shorter growth phase (1 to 6 months). and about the same number of follicles enter anagen. The
Scalp hair grows 0.3 to 0.4 mm/day, or approximately 6 duration of anagen determines the length of hair, and the
inches a year. volume of the hair bulb determines the diameter.
Humans have a mosaic growth pattern; hair growth Anagen and telogen hairs from hair-plucked preparation
and loss are not cyclic or seasonal, as in some mammals, are shown in Fig. 24.5.
but occur at random, so that hair loss is continuous (see
Fig. 24.3). Each hair follicle perpetually goes through Anagen (Growth). The anagen or growth phase begins
three stages in the hair growth cycle: catagen (transitional with resumption of mitotic activity in the hair bulb and
BOX 24.1 Systematic Approach to Evaluation

of Hair Loss
Telogen History Diagnostic procedures

2–3 months Sudden vs gradual loss Hair pull test
Anagen Presence of systemic disease or Daily counts
2–6 years
high fever Part width
Recent psychologic or physical Possible trichotillomania
stress Potassium hydroxide
Medication or chemical examination for fungi
exposure Scalp biopsy
Examination Hormone studies
Localized vs generalized
Catagen
2–3 weeks
Scarring vs nonscarring
Inflammatory vs
FIG 24.4 ■ Hair growth cycle – scalp. noninflammatory
Presence of follicular plugging
Skin disease in other areas
Anagen hair
begins. The outer root sheath degenerates and retracts

around the widened lower portion of the hair shaft to
become a club hair. The lower follicle shrinks away from
the connective tissue papilla and ascends to the level of
the insertion of the erector muscle. The dermal papilla
Telogen hair
condenses and moves upward, coming to rest underneath
the hair-follicle bulge. The completion of catagen is marked
by formation of the normal club hair.
Telogen (Rest). All activity ceases and the structure rests

during the telogen phase. The telogen phase in the scalp
lasts for 2 to 3 months before the scalp follicles reenter
FIG 24.5 ■ Hair pluck preparation showing anagen and the anagen stage and the cycle is repeated. The percentage
telogen hairs. of follicles in the telogen stage varies according to the body
region. Approximately 5% to 10% of scalp hairs are in the
telogen phase at any one time, and these follicles are
dermal papilla. Interactions between the dermal papilla randomly distributed. The telogen phase is much longer
and the overlying follicular epithelium are required for in eyebrow, eyelash, trunk, arm, and leg hair. Approximately
the onset of anagen. The follicle grows down and meets 40% to 50% of follicles on the trunk are in the telogen
the dermal papilla, recapitulating the embryonic events phase. The inactive dead hair, or club hair, has a solid,
of development of the hair follicle. A new hair shaft forms hard, dry, white node at its proximal end; the white color
and forces the tightly held club hair out. During anagen, is due to a lack of pigment. The club hair is firmly held in
hair grows at an average rate of 0.35 mm/day, or 1 cm in place and then ejected. A new anagen hair grows and
28 days; this rate diminishes with age. replaces the shed telogen hair. Approximately 25 to 100
Hair follicles in different areas of the body produce telogen hairs are shed each day; possibly twice this number
hairs of different lengths. The length is proportional to are lost on the days the hair is shampooed. Seasonal shed-
the duration of the anagen cycle. Scalp hair remains in ding occurs in other animals but is random in humans.
an active growing phase for an average of 2 to 6 years.
The active growing phase is much shorter and the resting
stage is longer for hair on the arms, legs, eyelashes, and EVALUATION OF HAIR LOSS
eyebrows (30 to 45 days), which explains why these hairs
remain short. Approximately 90% to 95% of scalp hairs The causes of hair loss (alopecia) are numerous. Most
are in an active growing phase at any one time. Continuous hair problems seen by the practitioner are due to changes
anagen occurs in some dogs (e.g., poodles) and in merino in hair-follicle cycling. Many inflammatory conditions
sheep; these animals do not lose or shed hair. permanently damage the hair follicle, resulting in scarring
alopecia. A classification is used here that is based primarily
Catagen (Involution). Catagen is a process of involution on distribution and scarring (i.e., localized [patchy] versus
that occurs with cell death in follicular keratinocytes. It generalized and scarring versus nonscarring). A systematic
is the phase of acute follicular regression that signals the approach for evaluation of hair loss is outlined in Box
end of anagen. Less than 1% of scalp hairs are in this 2 24.1 and Table 24.1. The evaluation of the woman who
to 3 week transitional phase at any one time. Cell division observes that “My hair is falling out in large amounts” is
in the hair matrix stops, and the resting, or catagen, stage presented in Fig. 24.6. Alopecia occurs when hair shafts
TABLE 24.1 A Simplified Tool for the Diagnosis of Alopecia

(This scheme will diagnose 97% of cases of alopecia.)
Disease Scalp Pattern Pull Test Laboratory Treatment
DIFFUSE LOSS (NONSCARRING)
Telogen effluvium Normal Diffuse Increased telogen Disease specific Disease specific
Diffuse alopecia Normal Irregularly diffuse Increased telogen – Topical
areata immunotherapy
Androgenetic Normal Hamilton (Fig. 24.8) Negative – Minoxidil
alopecia (men) Finasteride 1 mg
Surgery
Androgenetic Normal Ludwig (Fig. 24.9) Negative Testosterone Minoxidil
alopecia (women) DHEA-S Oral contraceptives
Spironolactone
Systemic disease Normal in most Diffuse Normal or Thyroid function Disease specific
(thyroid, iron increased Iron/IBC
deficiency, telogen ANA
systemic lupus
erythematosus,
dermatomyositis)
PATCHY LOSS (SCARRING)
Discoid lupus Atrophy, Patchy Negative Biopsy Intralesional steroids
erythematosus dyspigmentation, Hydroxychloroquine
follicular
plugging
Lichen planopilaris Hairs trapped in Patchy Negative Biopsy Intralesional steroids
“islands” Immunofluorescence Hydroxychloroquine
Frontal fibrosing Advancing edge Develops on frontal Negative Biopsy Same as lichen
alopecia perifollicular hairline, extends Immunofluorescence planopilaris
papules backward
Pseudopelade Scarring, Moth-eaten pattern Negative Biopsy Topical steroids
noninflammatory Immunofluorescence Hydroxychloroquine
Central centrifugal Scarring in Patchy over crown Negative Biopsy Avoid hair traction
cicatricial alopecia localized pattern
Folliculitis Pustules at Patchy Negative Biopsy Antibiotics
decalvans periphery Immunofluorescence
Bogginess
Dissecting cellulitis/ Abscess formation Diffuse Negative Biopsy, culture Antibiotics
folliculitis
Acne keloid Pustules and dense Occipital scalp Negative Biopsy, culture Antibiotics
follicular papules
Tufted folliculitis Many hairs arise Occipital scalp Negative Biopsy Antibiotics
from a giant
follicle
PATCHY LOSS (NONSCARRING)
Alopecia localized Normal Patchy + May be + at KOH (children) Intralesional steroids
exclamation mark margins Minoxidil
hairs Anthralin
Tinea capitis Scale or papules Patchy Hair breakage KOH Oral antifungal
or pustules Fungal culture antibiotics
Traction alopecia ± Scarring Patchy, marginal Hair breakage – Avoid
Trichotillomania ± Scarring, normal Patchy with stubble Usually negative – Fluoxetine, others
Psychotherapy
Syphilis Normal Moth-eaten Increased telogen RPR Penicillin
Hair breakage Normal Patchy or marginal Broken hairs – –
ANA, antinuclear antibodies; DHEA-S, dehydroepiandrosterone sulfate; IBC, iron-binding capacity; KOH, potassium hydroxide; RPR, rapid
plasma reagin.
EVALUATION OF HAIR LOSS
“My hair is falling out in large amounts”

Acquired diffuse Frontoparietal
scalp hair thinning “I am afraid to thinning
wash or brush my hair”
“I am going bald” Androgenetic

alopecia
Less common
Anagen effluvium
Hypothyroidism
Iron deficiency Onset – Teens, 20s, 30s, 40s
May bring doctor
Renal and hepatic failure 50% of women <age 50 have androgenetic alopecia
bag of shed hair
Nutritional disturbances two thirds of all hair loss in women
(e.g., hypervitaminosis A)
History
Systemic diseases
1. Gradual diffuse thinning

Common causes 2. No increased shedding
Acute telogen effluvium 3. Family history maybe +
Chronic telogen effluvium 4. Patient cuts hair shorter
Drugs and other chemicals 5. Not taking drugs that cause hair loss
Hair thinning as part
of the aging process Scalp exam
50s, 60s, 70s
1. Increased spacing between hairs
Child birth, acute 2. Thinning in frontal or parietal areas
illness, fever, chronic 3. Rim of hair along the frontal hairline is retained
systemic disease, 4. May have mild bitemporal recession
emotional stress, Idiopathic 5. “Central part” looks wider in front
heparin, drugs, 6. Pony tail is thinner
hypothyroidism, 7. Pull test normal
surgical operations, 8. Miniaturized hairs of varying diameter and length
anesthesia, crash diets
Acute telogen effluvium Chronic telogen effluvium History and PE

(middle-aged women) for
Thinning 1–3 months after ? Due to shortened anagen signs of androgen excess
event
Lasts <6 months 30–60-year-old women
Diffuse thinning entire scalp Increased shedding
Hair shedding by roots Thinning – abrupt onset No signs
No miniaturized hairs Long fluctuating course >6 mon Irregular menses
Positive telogen pull test Diffuse mild thinning Infertility
Usually no
Bitemporal recession Hirsutism
laboratory studies
Hair shedding by roots Severe cystic acne
required
No miniaturized hairs Virilization
Positive telogen pull test Galactorrhea
Pull test (20–40 hairs) Scalp biopsy Total testosterone

Two 4 mm punches Rx DHEA-S
Normal 1–4 hairs Horizontal sections Prolactin
CTE 2–8 hairs Vertical sections ?TSH
ATE >4 hairs
AGA Normal Chronic telogen effluvium Heavy or long
Terminal/vellus-like ratio 9:1 lasting menses
Anagen/telogen % 89:11 Iron
(normal or slightly increased) Iron-binding
Minoxidil capacity
(Rogaine) Ferritin
Androgenetic alopecia
Terminal/vellus-like ratio 2:1
Anagen/telogen % 83:17
FIG 24.6 ■ Evaluation of hair loss. AGA, androgenetic alopecia; ATE, acute telogen effluvium; CTE, chronic
telogen effluvium; DHEA-S, dehydroepiandrosterone sulfate; PE, physical examination; TSH, thyroid-stimulating
hormone.
are fragile and break due to many inherited and acquired remaining hair. Cut the hair short; then shave a 2.0 cm2
disorders. area. Cover the area with an occlusive dressing and remove
it in 1 week if trichotillomania (TTM) is suspected. Normal
growth is 2.5 mm in 1 week and 1 cm in 1 month. This
Diagnosis of Hair Disease
test proves to the patient that the hair is growing.
History. Inquire about medication use, calorie restriction,
vitamin A supplementation, and thyroid symptoms. Hair Pluck – Trichogram. This is a painful technique
Determine the precise onset and the duration of hair loss. but is still used by some clinicians. Abruptly extract hairs
Abrupt-onset telogen effluvium is most often related to from the scalp with a rubber-tipped needle holder. Cut
a specific traumatic event. Gradual or imperceptible onsets the excess hair 1 cm from the roots, float the hairs onto
are more complicated and involve possible shortened a wet microscope slide or Petri dish, and examine with a
anagen, as well as a differential diagnosis that includes hand lens (see Fig. 24.5).
alopecia areata (AA), androgenetic alopecia, and diffuse Telogen hairs have small, unpigmented, ovoid bulbs
primary scarring alopecias. and do not contain an internal root sheath. Anagen hairs
have larger, elongated, pigmented (if hair is pigmented)
Physical Examination. Examine the scalp surface and bulbs shaped like the end of a broom, surrounded by a
hair shafts. Microscopically examine hair ends and hair gelatinous internal root sheath.
shaft diameters. Hair density may be reduced by 50% There are diseases in which hair fragments with absent
before hair thinning becomes clinically apparent; therefore bulbs are obtained during a hair pull. Processes that
observation is an inaccurate method of evaluating hair interfere with cell division cause the shaft to be poorly
density and loss. Examine all nonglabrous skin, teeth, and formed and therefore apt to break under tension. Alopecia
nails. Findings in these areas may lead to diagnostic clues. areata, antimetabolite therapy, and small doses of ionizing
radiation interrupt the mitotic activity in the cells that
Hair Pull Test. For the hair pull test, obtain a sample normally contribute to the growing hair.
3 cm above the auricle. Tightly grasp 20 to 40 hairs firmly
between the thumb and forefinger. Exert a slow, constant Trichoscopy. Magnification of the scalp with a derma-
traction to slightly tent the scalp, and slide the fingers up toscope allows for in situ observation of the follicular
the hair shafts. There should be fewer than six club hairs ostia, hair shafts, blood vessels, and for the presence or
extracted. Repeat the count on the opposite side of the absence of subtle scale and erythema.
head and in two other areas. Examine the hair bulbs.
Daily Counts. The patient collects hair lost in the first GENERALIZED HAIR LOSS
morning combing and includes those lost during washing
for 14 days, saving them in clear plastic bags. The patient Diffuse hair loss (Box 24.2 and Table 24.2) usually occurs
counts the hairs and records the number on the bags. without inflammation or scarring. The loss affects hairs
Examine the hairs under the microscope to determine if throughout the scalp in a more or less uniform pattern.
the bulbs are anagen or telogen. Daily hair shed counts The hair pull test is important for differential diagnosis.
are not necessary if the pull test is positive. It is normal
to lose up to 100 hairs daily and 200 to 250 hairs on the Telogen Effluvium. A number of events have been
day of shampooing. If the hair is shampooed daily, the documented that prematurely terminate anagen and cause
counts should be less than 100. an abnormally high number of normal hairs to enter the
resting, or telogen, phase (see Box 24.2). The follicle is
Part Width. Make a coronal part with a comb over the not diseased but has had its biologic clock reset and
vertex. Note the part width. Make a series of parallel parts undergoes a normal involutional process. Usually no more
over the vertex and visually compare the part diameter. than 50% of the patient’s hair is affected. Scarring and
Do the same over the occipital and temporal scalp. Visually inflammation are absent. Resting hairs on the scalp are
compare the part diameters in the different anatomic scalp retained for approximately 100 days before they are lost;
areas. Hair density is greatest in childhood and decreases therefore telogen hair loss should occur approximately 3
progressively with age. The hair is less dense in the vertex months after the event that terminated normal hair growth.
in both genders, and thinning increases with age. Kligman explained this process and identified the various
precipitating events (see Box 24.2). The most common
Hair Shaft Examination (Clip Tests). Grasp 25 to 30 causes are briefly discussed here. High fever from any
hairs between the thumb and forefinger just at the scalp cause may result in a sudden, diffuse loss of club hairs 2
surface. Cut the hair between the fingers and the scalp. Hair to 3 months later. Hair loss begins abruptly and lasts for
just above the fingers is cut and discarded. Float the hairs approximately 4 weeks. Hair pluck tests show telogen
onto a wet microscope slide and cover with another slide. counts that vary from 30% to 60%. Full recovery can be
Evaluate hair shaft diameter and structure. There are many expected.
rare diseases that produce shaft structural abnormalities, Severe emotional and physical traumas have been
such as pili torti in which the hair is twisted on its axis. documented to cause diffuse hair loss. Hair loss has been
reported to occur 2 weeks after severe psychologic or
Hair Growth Window. Select an area where the hair physical trauma, but because that is too short a time for
fails to grow and an area that can be covered by the the induction of the telogen phase, the loss must have
BOX 24.2 Hair Loss
GENERALIZED* • Poisoning
• Acute blood loss • Thallium (rat poison)
• Childbirth • Arsenic
• Crash diets (inadequate protein) • Radiation therapy
• Drugs • Secondary syphilis: “moth eaten” alopecia
• Coumarin
LOCALIZED†
• Retinoids (isotretinoin, acitretin)
• Anticoagulants (particularly heparin) • Androgenetic alopecia
• Amantadine • Male pattern
• Lithium • Female pattern
• Penicillamine • Hirsutism
• Βeta-blockers (e.g., propranolol) • Alopecia areata
• Amiodarone • Trichotillomania
• Vitamin A excess • Traction alopecia
• Captopril • Scarring alopecia
• Antiinflammatories (e.g., colchicine, cimetidine) • Developmental defects: aplasia cutis
• Antineoplastic agents • Physical injury: burns, pressure
• Antihyperlipidemics • Infection
• Antithyroid (e.g., propylthiouracil, methimazole) • Fungal: kerion
• Anticonvulsants (e.g., valproic acid, carbamazepine, • Bacterial: folliculitis, furuncle
phenytoin) • Viral: herpes zoster
• High fever • Neoplasms
• Hypothyroidism and hyperthyroidisms • Metastatic carcinoma
• Physical stress (e.g., surgery) • Sclerosing basal cell carcinoma
• Physiologic stress (e.g., neonate) • Lupus erythematosus
• Psychologic stress • Lichen planus
• Severe illness (e.g., systemic lupus erythematosus) • Cicatricial pemphigoid
• Cancer chemotherapeutic agents • Scleroderma
*Diffuse, uniform loss, but many hairs left randomly distributed in area of loss.
†
Most or all hair missing from involved area.
by its long fluctuating course and from androgenetic

TABLE 24.2 Features Differentiating Telogen
alopecia by its clinical and histologic findings. CTE lasts
Effluvium and Anagen Effluvium
from 6 months to 7 years.
Clinical Presentation Telogen Anagen Many physicians test patients with hair loss for iron
deficiency and thyroid abnormalities. Iron deficiency is
Onset of shedding 2–4 months 1–4 weeks
after insult
commonly found in CTE but treatment for it seldom
reverses the hair loss. Perform a ferritin and a transferrin
Percent of hair loss 20–50 80–90 saturation evaluation if iron deficiency is suspected. The
Type of hair loss Normal club Anagen hair long, fluctuating course is different than that seen in acute
(white bulb) (pigmented bulb) telogen effluvium. The presence of 20% to 30% telogen
Hair shaft Normal Narrowed or hairs and 15% to 35% dystrophic hairs on the trichogram
fractured (plucked hair) confirms the diagnosis. A biopsy can support
the diagnosis but is usually not necessary. CTE is distin-
guished from androgenetic alopecia by distribution,
occurred by another mechanism. Some individuals may trichogram and a biopsy.
experience increased shedding caused by idiopathic Men are treated with 5% minoxidil solution. Premeno-
shortening of anagen (a short anagen syndrome). They pausal women are prescribed 5% minoxidil solution plus
have increased shedding and decreased hair length. For cyproterone acetate (CPA) (not available in the United
every 50% reduction in the duration of anagen, there is States) 50 mg, from day 5 to day 15 of their menstrual
a corresponding doubling of follicles in telogen. cycle, always taken together with ethinyl estradiol
0.035 mg/day. Postmenopausal women are treated with
Chronic Telogen Effluvium. Chronic telogen effluvium 5% minoxidil solution plus CPA 50 mg/day. Alterna-
(CTE) refers to a diffuse hair loss all over the scalp and tives to CPA 50 mg/day could be spironolactone 50 to
persists for more than 8 months. Patients present with 100 mg/day.
hair loss with increased shedding and thinning of abrupt Biopsies confirm the diagnosis but are usually not
onset and fluctuating course. There is diffuse thinning necessary. Two 4-mm punch biopsy specimens are taken
over the entire scalp, frequently accompanied by bitemporal from the mid or posterior parietal scalp. Specimens are
recession. CTE usually affects 30- to 60-year-old women. sectioned horizontally and vertically. The findings are
It may be distinguished from classic acute telogen effluvium shown in Fig. 24.6.
BOX 24.3 Drugs Probably Associated With

Telogen Effluvium
Acitretin
Aminosalicylic acid
Amphetamines
Bromocriptine
Captopril
Carbamazepine
Cimetidine
Coumadin
Danazol
Enalapril
Levodopa
Lithium
Metoprolol
Propranolol
Pyridostigmine
Trimethadione
Postpartum Hair Loss. The percentage of follicles in FIG 24.7 ■ Chemotherapy-induced alopecia. 1 month
telogen progressively decreases during pregnancy, par- after treatment with paclitaxel and carboplatin. The
ticularly during the last trimester. Diffuse but primarily only hairs left are those in the telogen phase. (From
frontotemporal hair loss occurs in a significant number Chon SY, Champion RW, Geddes ER, Rashid RM.
of women 1 to 4 months after childbirth. The loss can Chemotherapy-induced alopecia. J Am Acad Dermatol
be quite significant, but recovery occurs in less than 1 2012;67(1):e37–47.)
year. Hair growth usually returns to the pre-pregnancy
state. Postpartum hair loss is thought to be due to a
prolongation of the anagen phase due to stimulating factors; Scalp hypothermia decreases the amount of chemo-
when the factors are removed, more hairs enter the telogen therapy delivered to the scalp and minimizes anagen
phase and hair falls out at once (delayed anagen release). effluvium, especially in breast cancer patients. DigniCap
(www.dignicap.com, Food and Drug Administration
Drugs. Cytotoxic drugs that directly affect hair matrix approved in the United States) and Paxman Scalp Cooling
cell proliferation cause profound hair loss, inducing an System are two available devices.
anagen effluvium. A large number of drugs probably cause Minoxidil 2% topical has no benefit in the prevention
telogen effluvia. These are listed in Box 24.3. of chemotherapy-induced alopecia.
Anagen Effluvium. Anagen effluvium (see Box 24.2 and Loose Anagen Hair Syndrome. The loose anagen hair
Table 24.2) is the abrupt loss of hair from follicles that are syndrome (LAS) is a rare sporadic or familial hair disorder
in their growing phase.1 An abrupt insult to the metabolic that affects children but may be seen in adults. The
and follicular reproductive apparatus must be delivered female-to-male ratio is 6 : 1. LAS is due to a defective
to create such an event. Cancer chemotherapeutic agents anchorage of the hair shaft to the follicle that results in
and radiation therapy are capable of such an insult. The easily and painlessly pluckable hair.
rapidly dividing cells of the matrix and cortex are affected. LAS may result from premature keratinization of the
The insult causes a change in the rate of hair growth but inner root sheath that produces an impaired adhesion
does not convert the follicle to a different growth phase, between the cuticle of the inner root sheath and the cuticle
as occurs in telogen effluvium. High concentrations of of the hair shaft.
antimetabolites or radiation bring the entire metabolic The typical patient with LAS is a young girl with short
process to an abrupt halt, and the entire hair and hair blond hair that does not grow long, but LAS can affect
root are shed intact. The only hairs left are those in the children with dark hair. The signs are reduced hair length,
telogen phase (Fig. 24.7). These are dead, wedged into increased hair shedding, and altered hair texture. These
the hair canal, and unaffected by any acute event. The patients may have sparse hair that does not grow long
stem cells of the hair follicles are spared because of their and have patches of dull, unruly hair. Others just have
slow cycling, and they generate a new hair bulb. Insults of increased hair shedding. The child needs few haircuts,
less intensity slow the mitotic rate of the bulb and cortex and the hair is difficult to manage. Examination shows
cells, causing bulb deformity and narrowing of the lower diffuse thinning and irregular bald patches attributable
hair shaft. Narrow, weakened hair shafts are easily broken to traumatic painless extraction of hair tufts. Hair is dull,
and shed without bulbs. Since 90% of scalp hairs are in unruly, or matted. Up to 300 hairs are shed daily. Most
the anagen phase, a large number of hairs can be affected. cases are isolated, but it can occur in hereditary or devel-
Patients with 10% to 20% of their hair remaining after opmental disorders including coloboma, Noonan syndrome,
an insult almost certainly have had an anagen effluvium. and hypohidrotic ectodermal dysplasia.
Microscopic examination shows anagen hair without

sheath. The bulb is often misshapen, and its proximal LOCALIZED HAIR LOSS
portion often shows a visible ruffled cuticle. The pull test
in children with LAS shows more than 3 and often more Androgenetic Alopecia in Men
than 10 loose anagen hairs. The pull test in normal children (Male Pattern Baldness)
shows one or two loose anagen hairs. The trichogram in
LAS shows at least 70% loose anagen hairs and no telogen Baldness in men is not a disease, but rather a physiologic
hairs. Most patients improve with age. reaction induced by androgens in genetically predisposed
Short anagen syndrome due to a short duration of the men. The pattern of inheritance is probably polygenic.
anagen phase (4 to 10 months) results in short hair and Thinning of the hair begins between the ages of 12 and
has a similar presentation to loose anagen syndrome. The 40 years, and about half the population expresses this trait
short duration of anagen causes synchronization of the before the age of 50.
hair cycle with periods of diffuse hair shedding. Parents
often note that the child’s hair remains short despite not Hamilton Patterns. The progression and various patterns
having a haircut. After a hair pull test, hairs have pointed of hair loss are classified by the Hamilton male baldness
tips and do not have hockey stick–shaped hair bulbs with classification system (Fig. 24.8). Triangular frontotemporal
proximal ruffling of the cuticle as is seen in loose anagen recession occurs normally in most young men (type I)
syndrome. Table 24.3 compares loose anagen and short and women after puberty. The first signs of balding are
anagen syndromes.2 Patients may see improvement in hair increased frontotemporal recession accompanied by
density, but most patients do not grow long hair. midfrontal recession (type II). Hair loss in a round area
TABLE 24.3 Short Anagen Syndrome vs Loose Anagen Syndrome

Short Anagen Syndrome Loose Anagen Syndrome
Chief complaints Hair that does not grow long Hair that does not grow long
Excessive shedding Patchy, diffuse hair loss
Unruly hair
Pull test Positive Usually negative
Physical examination Very short hair (<6 cm) Short hair (<shoulder length)
Trichoscopy No specific features Black rectangular structures
Microscopic examination Short tapered telogen hairs Anagen hairs devoid of sheaths, ruffled cuticles
Treatment Reassurance, minoxidil Reassurance, minoxidil, gentle styling
Prognosis Improves with age Improves with age
Unlikely to grow long hair
From Oberlin KE, Maddy AJ, Martínez-Velasco MA, et al. (2018). Short anagen syndrome: Case series and literature review. Pediatr
Dermatol 2018;35(3):388–91.2
I III IV Va
II IIIa IVa VI
IIa III V VII

vertex
FIG 24.8 ■ Hamilton classification of male pattern baldness.
on the vertex follows, and the density of hair decreases, brands of the 2% solution are available. One milliliter of
sometimes rapidly, over the top of the scalp (types III solution is applied twice daily and spread lightly with a
through VII). Approximately 10% of men have hair loss finger. An applicator conveniently and effectively applies
that looks like female pattern hair loss with sparing of the medication. Minoxidil increases nonvellus hairs.
the frontal hairline and hair loss on the central scalp. Spontaneous reversal to the pretreatment state occurs in
1 to 3 months after stopping treatment. Ideal candidates
Pathophysiology. Androgenetic alopecia is due to the are men younger than 30 years of age who have been
progressive shortening of successive anagen cycles. There losing hair for less than 5 years. The solutions produce
are two populations of scalp follicles: androgen-sensitive a modest increase in hair on scalps of young men and
follicles on the top and androgen-independent follicles women with mild to moderate hair loss, with continuous
on the sides and back of the scalp. In genetically predis- twice daily application for years to maintain the effect.
posed individuals, and under the influence of androgens, In men with androgenetic alopecia, 5% topical minoxidil
predisposed follicles are gradually miniaturized, and large, was clearly superior to 2% topical minoxidil in increasing
pigmented hairs (terminal hairs) are replaced by thin, hair regrowth, and the magnitude of its effect was marked
depigmented hairs (vellus hairs). (45% more hair regrowth than 2% topical minoxidil at
Inflammation surrounds the bulge area of the outer week 48).3
root sheath. The inflammation may damage the follicle One 48-week study in women showed that 5% topical
stem cells, which results in a decrease in hair-follicle minoxidil was superior to 2% topical minoxidil in the
density. Hair follicles are still present, but removing patient assessment of treatment benefit. Application of
androgens or treatment with minoxidil or finasteride does 2% topical minoxidil in this study showed that differences
not result in the conversion of miniaturized follicles back in patient assessment of hair growth at week 48 were not
to terminal ones. significantly different from those for the placebo.4 A
Skin Androgen Metabolism. Testosterone (T) is 48-week study in men found a mean increase in hairs per
converted to the more potent dihydrotestosterone (DHT) square centimeter of 12.7 with 2% minoxidil, and 18.5
by 5α-reductase. Skin cells contain 5α-reductase (types I with 5% minoxidil. One study found that topical use of
and II). The type I enzyme is found in sebaceous glands, 2% minoxidil caused small but statistically significant
and the type II enzyme is found in hair follicles and the increases in left ventricular end-diastolic volume, cardiac
prostate gland. Testosterone and DHT act on androgen output, and left ventricular mass. Dizziness and tachycardia
receptors in the dermal papilla. They increase the size of have been reported with 2% solution. Local irritation,
hair follicles in androgen-dependent areas such as the beard itching, dryness, and erythema may occur and are likely
area during adolescence, but later in life DHT binds to attributable to the vehicle of alcohol and propylene glycol.
the follicle androgen receptor and activates transformation The medication is applied to a dry scalp twice a day. The
of large, terminal follicles to miniaturized follicles. The hair should not be wet for at least 1 hour afterward. About
duration of anagen shortens with successive hair cycles, one third of these patients grow hair that is long enough
and the follicles become smaller, producing shorter, finer to be cut or combed. Hair growth is evident in 8 to 12
hairs. Androgenetic alopecia does not develop in men with months. Minoxidil may stop or retard the progression of
a congenital absence of 5α-reductase type II. Finasteride, male pattern baldness. In one large study of long-term
which inhibits 5α-reductase type II, slows or reverses the use, almost all patients gradually avoided continuing the
progression of androgenetic alopecia. treatment. The causes of discontinuation in the majority
of patients were the insignificant cosmetic effect and an
Treatment. The desire for treatment varies. Some men aversion to this topical treatment method.5
accept the inevitable; others find baldness intolerable. Finasteride. Finasteride (Propecia 1 mg) taken daily
Topical treatment (minoxidil), oral treatment (finasteride), is an effective oral therapy for androgenetic alopecia in
and several surgical procedures are available. The drugs men. Some physicians prescribe finasteride (Proscar 5 mg)
can enlarge existing hairs and retard thinning in the vertex and instruct patients to split the 5-mg tablet with a pill
and the frontal regions. They have no benefit for men splitter into four equal parts. The cost savings is consider-
who are bald or those with bitemporal recession without able. Based on global photographic assessment, finasteride
hair. Benefits are seen in 6 to 12 months. Treatment must (1 mg) is able to increase hair growth in all areas of the
be continued indefinitely. If treatment is stopped, benefits scalp affected by male pattern hair loss.6
are lost within 6 to 12 months, and hair density will be Androgenetic alopecia (male pattern hair loss) is caused
the same as before treatment. Patients who begin balding by androgen-dependent miniaturization of scalp hair
at an early age are most distressed and are tempted to follicles, with scalp DHT level implicated as a contributing
consult nonphysician “experts” at hair clinics. These clinics cause. Finasteride blocks 5α-reductase type II, which
offer a variety of topical preparations, none of which has inhibits the conversion of T to DHT and decreases serum
any value. Selected patients may be referred for hair and cutaneous DHT concentrations. This slows further
transplants, plastic surgical rotation flaps, or wigs. hair loss, inhibits androgen-dependent miniaturization of
Minoxidil. Minoxidil was developed to treat hyperten- hair follicles, and improves hair growth and hair weight
sion. It increases the duration of anagen, causes follicles in men with androgenetic alopecia.
at rest to grow, and enlarges miniaturized follicles. These In men with male pattern hair loss, finasteride 1 mg/
effects occur in only a minority of patients. Minoxidil 2% day slowed the progression of hair loss and increased hair
(Rogaine) and 5% (Extra Strength Rogaine) are available growth in clinical trials over 2 years. Therapy leads to
over the counter in a solution or foam preparation. Generic slowing of further hair loss.
Efficacy is evident within 3 months of therapy. The Dutasteride. Dutasteride (Avodart) is a dual inhibitor
drug produces progressive increases in hair counts at 6 of both type I and type II 5α-reductases, and thus inhibits
and 12 months. Finasteride treatment for 4 years leads conversion of T to DHT. Finasteride inhibits only type
to sustained improvement in hair weight. Hair weight II 5α-reductase. Dutasteride is three times more potent
increased to a larger extent than hair count.7 Finasteride than finasteride at inhibiting type II 5α-reductase. A study
is effective in men with vertex male pattern hair loss and of men with male pattern hair loss, 20 to 50 years old,
hair loss in the anterior/mid area of the scalp. It may not treated with dutasteride (0.5 mg) and finasteride 1 mg was
be effective for men who are older than 60 years of age conducted. In this study, dutasteride 0.5 mg was statistically
because type II 5α-reductase activity in the scalp may not superior to finasteride 1 mg and placebo.9 Dutasteride
be as high as that in younger men. improved hair growth and was well tolerated.
In postmenopausal women with androgenetic alopecia,
finasteride 1 mg/day taken for 12 months did not increase Hair Transplants. Hair transplants have been used
hair growth or slow the progression of hair thinning. successfully for years to permanently restore hair. Age is
Finasteride is contraindicated in women who are or may not a determining factor. Androgen-independent hairs
potentially be pregnant because of the risk that inhibition from the lateral and posterior areas of the scalp are used.
of conversion of fetal T to DHT could impair virilization The surgeon must have a sense of aesthetics to properly
of a male fetus. Approximately 20% to 30% of men do design the anterior hairline. There are many techniques
not respond. Treatment must be continued indefinitely. used for harvesting and implanting the grafts. The tech-
Side Effects. Approximately 1.5% of men will experience niques are constantly changing and improving.
sexual problems (impotence, decreased libido, and ejacula-
tory dysfunction) with finasteride use. In most men, these Scalp Reduction and Flaps. An anterior–posterior
side effects resolve when the medication is stopped, elliptic excision of bald vertex scalp with primary closure
however in some, the sexual symptoms and others persist. can provide an instant hair effect. The procedure can be
These persistent symptoms and physical findings are repeated every 4 weeks until hair margins converge or
referred to as post-finasteride syndrome (Table 24.4). The scalp tissue becomes too thin. Grafts or flaps may be used
mechanism for post-finasteride syndrome is unknown, but later to fill any remaining void. Alternately, several types of
may be related to decreased production of central neuros- flaps can be designed by the creative surgeon to fill voids.
teroids, which regulate sexual desire and function, impaired
T metabolism, and a relative excess of estrogen. The risk Hair Weaves. Hair weaves have been refined by the Hair
for finasteride sexual difficulties appears to increase with Club (www.hairclub.com) in the United States. They create
age and other side effects such as gynecomastia, testicular a matrix of crisscrossing, transparent fibers, fitted and
pain, and depression appear to be more common at higher shaped to the client’s thinning area. The matrix is porous,
doses (5 mg/day) used to treat benign prostatic hypertro- allowing the scalp to “breathe.” New hair is added to the
phy. Further studies are needed to evaluate the true inci- matrix strand by strand to recreate the pattern and hair
dence and risk factors for post-finasteride syndrome. flow of the client’s own hair. The matrix is then fused to
Minoxidil Versus Finasteride. A study showed that the client’s remaining growing hair using a medical adhesive
2% minoxidil produced faster initial improvement in called Polyfuse. The client returns to Hair Club for haircuts
midfrontal/vertex AA in up to one third of treated patients, and to replace the Polyfuse every 5 weeks.
whereas finasteride produced marginally better results with Newer treatments include low level laser light therapy
increasing duration of treatment. Both agents were equally and platelet-rich plasma. Further studies will determine
effective in stopping the progression of AA.8 the efficacy to these treatments.
TABLE 24.4 Reported Symptoms of Post-Finasteride Syndrome

Mental and Neurologic
Sexual Symptoms Physical Symptoms Symptoms
Decreased or complete loss of sex drive Female-like breast development and Severe memory/recall
Erectile dysfunction, impotence enlargement impairment
Loss of morning and spontaneous Chronic fatigue, listlessness Slowed thought processes
erections Muscle atrophy, weakness Impaired problem solving,
Sexual anhedonia, loss of pleasurable Decreased oil and sebum production decreased comprehension
orgasm Chronically dry, thinning of skin Depression
Decreased semen volume/force Melasma Anxiety
Penile shrinkage and numbness Tinnitus Suicidal ideation
Peyronie disease Increased fat deposition, obesity, and Emotional flatness and
Scrotal shrinkage and numbness elevated body mass index anhedonia
Decrease in body temperature Insomnia
Reduced HDL cholesterol, raised fasting Attempted suicide
glucose and triglycerides Completed suicide
HDL, high density lipoprotein.

Post-Finasteride Syndrome Foundation. Global Public Health Advisory – US National Institutes of Health recognises post-finasteride
syndrome. https://www.pfsfoundation.org/; 2015.29
alopecia. Women with increased androgens may benefit

Female Pattern Hair Loss (Androgenic with an antiandrogen treatment such as spironolactone
Alopecia in Women) and finasteride.
Chronic, progressive, diffuse hair loss in women in their

twenties and thirties is a frequently encountered complaint.
Hirsutism
These women, who usually have a normal menstrual cycle Hirsutism is defined as excessive terminal hair that appears
and lack any abnormalities on physical examination and in a male pattern (i.e., sexual hair) in women. Hirsutism
have normal androgen levels, have been classified as having affects 5% to 10% of women. The differential diagnosis
“male pattern baldness,” a genetic trait, and have been is shown in Box 24.4.
dismissed without further evaluation. Studies have shown
that some of these women have increased levels of the Idiopathic Hirsutism. Hirsute patients with normal
serum adrenal androgen dehydroepiandrosterone sulfate ovulatory function and circulating androgen levels have
(DHEA-S) and a distinct pattern of central scalp alopecia, idiopathic hirsutism (IH). A history of regular menses is
which has been called adrenal androgenic female pattern not sufficient to exclude ovulatory dysfunction, since up
alopecia. Female pattern hair loss is more common in to 40% of hirsute women with menses are anovulatory.
endocrine disorders resulting in androgen excess, such as The excessive body hair is due to increased sensitivity of
polycystic ovarian syndrome (PCOS). the pilosebaceous unit to normal plasma levels of androgen.
Male pattern baldness results in a gradual regression of These women may have increased numbers of androgen
the hair on the central scalp and gradual frontotemporal receptors and increased 5α-reductase activity. These
recession, as well as a gradual decrease in hair shaft diam-
eter in the areas of hair loss. In contrast, most women
with diffuse alopecia experience a gradual loss of hair on BOX 24.4 Etiology and Differential Diagnosis
the central scalp, with retention of the normal hairline for a Patient Presenting With
without frontotemporal recession. There are a variety of Hirsutism
anagen hair diameters. With advancing age, the central
thinning becomes more pronounced; in contrast to male • Ferriman–Gallwey scale (Fig. 24.10)
pattern baldness, a fringe of hair along the frontal hairline • Score of 8 to 15 – mild hirsutism
persists (Fig. 24.9). In exceptional cases, a course similar to • 50% have idiopathic condition*
that in men is seen, with deep frontotemporal recession. • 50% have elevated androgen levels
• Hyperandrogenism
Laboratory Findings. The laboratory investigation of • Polycystic ovary syndrome – most cases
female patients with diffuse alopecia with both female • Nonclassic congenital adrenal hyperplasia – 2%
and male patterns is outlined in Table 24.5. Laboratory • Androgen-secreting tumors – 0.2%; 50% are
evaluation for some androgenetic alopecia patients should malignant
initially include determination of the serum DHEA-S and • Primary presenting symptoms (not hirsutism)
• Cushing syndrome†
total serum T levels, testosterone–estradiol binding • Hyperprolactinemia
globulin (TeBG) level for the T/TeBG ratio, and serum • Acromegaly
prolactin levels. • Thyroid dysfunction
• Hyperandrogenism, insulin resistance + acanthosis
Treatment. In a 48-week study of 381 women with nigricans†
female pattern hair loss, 5% topical minoxidil applied • Mild, idiopathic hyperandrogenism – 8%
twice a day demonstrated statistical superiority over the
2% topical minoxidil group in the patient assessment of *Hirsutism in a patient with normal androgen levels and normal
ovarian function (normo-ovulation and no polycystic ovaries on
treatment benefit. Once-daily 5% minoxidil topical foam ultrasound).
is as effective for stimulating hair growth as twice-daily †
If clinical findings are highly suggestive of these rare disorders,
2% minoxidil topical solution in women with androgenetic further biochemical testing might be needed.
TABLE 24.5 Laboratory Values for Evaluation of Diffuse Female Alopecia

Female Pattern Alopecia Male Pattern Alopecia
Laboratory Parameter Female Pattern Alopecia With Hirsutism (Frontotemporal Recession)
DHEA-S Normal or elevated Normal or elevated Elevated
T Normal Normal or elevated Elevated
TeBG Normal Decreased or normal Decreased or normal
T/TeBG prolactin† Normal Elevated Elevated
DHEA-S, dehydroepiandrosterone sulfate; T, total serum testosterone; TeBG, testosterone–estradiol binding globulin; T/TeBG, androgenic
index.
†
If elevated, suspect pituitary disease (e.g., pituitary prolactin secreting adenoma).
FEMALE PATTERN – ALOPECIA
C D
FIG 24.9 ■ Female pattern – alopecia. A, Ludwig pattern. Evolution of the female type of
androgenetic alopecia. B, Widening of the hair part is an initial change. C, More extensive
widening of the hair part. D, Diffuse hair loss over the crown. The frontal hair line is preserved.
patients respond to antiandrogen or 5α-reductase inhibitor have more body hairs per unit area than Asians. Hair
therapy (finasteride). Less than 20% of all hirsute women follicles cover the entire body except for the lips, palms,
have IH. and soles. There are two types of hair follicles: vellus and
terminal. Most women have some terminal hair in the
Virilization. Virilization is the combination of hirsutism so-called male sexual pattern around the areolae and
plus other signs of masculinization, such as deepening of extending from the pubis in the midline of the abdomen.
the voice and temporal balding (Box 24.5). Virilization In women, excess androgen production stimulates vellus
may be the sign of an ovarian or adrenal tumor. Virilization hairs to develop into long, coarse, pigmented terminal
is associated with markedly increased androgen production hairs in most areas of the body except the scalp, where
by the ovaries or adrenal glands (or both) and markedly terminal hairs are converted to vellus hairs, resulting in
increased levels of plasma androgens. balding. Women in whom hirsutism develops after puberty,
especially if accompanied by signs of virilization such as
Body Hair. The number of hairs per unit area is deter- infrequent or absent menses, have an abnormal condition
mined by genetic factors. Mediterranean men and women and require further evaluation.
and ethnicity are important factors. Asian women have

BOX 24.5 Hirsutism and Virilization –
less dense hair than white women.
Clinical Findings in Women
Testosterone is the major circulating androgen. It is
produced by the ovaries and adrenal glands. Testosterone
HIRSUTISM: EXCESSIVE HAIR GROWTH IN WOMEN IN
9 KEY ANDROGEN-SENSITIVE ANATOMIC SITES: levels are highest in the early morning. Measuring plasma-
free T level is more sensitive than total T level in detecting
Face
excess androgen production.
Chest
Areola
Linea alba Documenting Hirsutism. The presence of hirsutism is
Lower back determined by the modified Ferriman–Gallwey scoring
Upper back system (mFG) for hirsutism. This grades the hair growth
Buttocks between 0 (absence of terminal hairs) and 4 (extensive
Inner thigh terminal hair growth) at nine different body sites (upper
External genitalia lip, chin, chest, upper and lower back, upper and lower
VIRILIZATION: THE COMBINATION OF abdomen, arm, and thigh) (Fig. 24.10).
HIRSUTISM PLUS: Less than 5% of black or white women of reproductive
age have a total score greater than 7. In a white or a black
Acne and increased sebum production
Clitoral hypertrophy woman, hirsutism is said to be present when the mFG
Decrease in breast size score is 6 to 8.
Deepening of the voice Medications that cause hirsutism include anabolic
Frontotemporal balding or androgenic steroids and valproic acid. If hirsutism is
Increased muscle mass moderate or severe or if mild hirsutism is accompanied
Infrequent or absent menses by features that suggest an underlying disorder, elevated
Heightened libido androgen levels should be ruled out. Disorders to consider
Hirsutism are neoplasm and endocrinopathies (PCOS is the most
Malodorous perspiration common). Measure plasma T level in the early morning on
days 4 to 10 of the menstrual cycle. Plasma total T level
should be rechecked along with free T level if the plasma
total T level is normal in the presence of risk factors or
Hirsutism Is Not Hypertrichosis. Hypertrichosis is progression of hirsutism on therapy. Simultaneous assay of
excessive hair growth in a nonsexual pattern stimulated by 17-hydroxyprogesterone level may be indicated in subjects
medications such as glucocorticoids, phenytoins, minoxidil, at high risk for congenital adrenal hyperplasia.
or cyclosporine; or it exists as a result of heredity.
History and Physical Examination. The prepubertal
General Guidelines. Test for elevated androgen levels onset of hirsutism with progression over years suggests
in women with moderate or severe hirsutism or hirsutism functional disorders such as PCOS. Rapid progression of
of any degree when it is sudden in onset, rapidly progres- excess terminal hair growth and signs of virilization are
sive, or associated with other abnormalities such as indications of an ovarian or adrenal androgen-producing
menstrual dysfunction, obesity, or clitorimegaly. Polycystic tumor (Box 24.6).
ovary syndrome (PCOS) is the most likely diagnosis in a Determine the Existence of Hirsutism. Unwanted hair
woman with moderate or severe hirsutism and elevated growth may just represent an increased ethnic and genetic
T level. Women who desire treatment are treated with predisposition for facial hair growth. It is important to
oral medication or hair removal methods such as lasers establish that the excess hair is terminal and not vellus
or photoepilation. Oral contraceptives are first-line drugs. and that a male pattern distribution exists.
Add an antiandrogen after 6 months if the response is Initial investigations are shown in Box 24.7. Pelvic
poor. Antiandrogen monotherapy is used only with ultrasonography and 17-hydroxyprogesterone levels
adequate contraception. Insulin-lowering drugs are not may be ordered to exclude related disorders. Thyroid-
recommended. stimulating hormone (TSH) and prolactin levels are
More than 80% of patients with hirsutism have PCOS ordered if oligomenorrhea or amenorrhea is present.
whereas about 10% have IH or nonspecific functional Determine androgen levels for moderate to severe hirsutism
hyperandrogenism. Less than 10% have other disorders, or in those with hirsutism and menstrual dysfunction.
such as those listed in Box 24.4, as specific identifiable Basal levels of total T >6.9 nmol/L (>200 ng/dL) and of
disorders. DHEA-S >18.9 nmol/L (>7000 ng/mL) suggest an ovarian
or adrenal androgen-producing tumor. Patients with these
Pathogenesis of Hirsutism. The growth of sexual hair tumors have the sudden onset and rapid progression of
is dependent on the presence of androgens. Androgens hirsutism and the presence of virilization. For a detailed
induce vellus follicles in sex-specific areas to develop into algorithm, see references 10 and 11.
terminal hairs, which are larger and more heavily pig-
mented. Hirsutism is caused by increased androgen produc- Polycystic Ovary Syndrome. Polycystic ovary syndrome
tion and/or an increased sensitivity of the hair follicles to (PCOS) is the most frequent cause of anovulatory infertil-
androgens. Vellus hair is transformed irreversibly to ity and hirsutism. It is a heterogeneous syndrome that
terminal hair in androgen-sensitive areas of the skin. Race affects 6% of women of reproductive age. The etiology
1 2 3 4 1 2 3 4
FIG 24.10 ■ Ferriman–Gallwey hirsutism scoring system. Each of the nine body areas most sensitive to androgen
is assigned a score from 0 (no hair) to 4 (frankly virile). The numbers in each area are added to obtain the total
score. A score of 6 to 8 generally defines hirsutism.
is unknown. The onset is in the peripubertal years. There Diagnosis of PCOS. In the absence of pregnancy and
is insulin resistance, androgen excess, and abnormal when amenorrhea or oligomenorrhea has persisted for 6
gonadotropin secretion. There are signs and symptoms months or longer without a diagnosis, a history and physical
of elevated androgen levels, menstrual irregularity, and examination should be undertaken, with particular attention
amenorrhea. to patterns of hair distribution and a search for acanthosis
A genetic defect may cause an increase in the concentra- nigricans.
tions of intraovarian androgens and stop ovulation. The The diagnosis of PCOS is primarily clinical (Fig. 24.11).
polycystic ovary forms when an anovulatory state exists. Many women have elevated levels of T, LH, and fasting
Bilaterally enlarged polycystic ovaries develop, defined insulin and reduced levels of sex hormone–binding
by the presence of more than eight follicles per ovary, globulin. Conditions to exclude in the diagnosis of PCOS
with the follicles less than 10 mm in diameter. These are listed in Table 24.6.
findings are seen on ultrasound examinations in more Patients with hirsutism and PCOS should have an
than 90% of women with PCOS, but they are also present assessment and management of all risk factors shown in
in up to 25% of normal women. Serum T and luteinizing Fig. 24.11.
hormone (LH) levels are elevated in most affected women. Treatment of PCOS. Reducing body weight and
Women present with menstrual irregularities, infertility, adhering to a strict diet and exercise program are essential.
and androgen excess symptoms of hirsutism and acne. Low-dose oral contraceptive pills prevent endometrial
Some women have normal cycles. Virilizing signs such hyperplasia and cancer and treat hirsutism and acne.
as clitorimegaly, deepening of the voice, temporal balding, Antiandrogens may be combined with oral contraceptive
or masculinization of body habitus are almost always absent. pills for the treatment of hirsutism (see hirsutism treatment
Obesity is present in up to 70% of patients. in the following section).
PCOS is associated with hyperinsulinemia, insulin
resistance, an increased risk for type 2 diabetes mellitus, Hirsutism Treatment (General Guidelines). Hirsutism
acanthosis nigricans, lipid abnormalities, and hypertension. improves with weight loss. Women with hirsutism often
Hyperinsulinemia may be the cause of the overproduction have anxiety and depression related to their appearance
of ovarian androgens. The risk of endometrial cancer is and this needs to be addressed. A decrease in hirsut-
three times higher than that in normal women. ism while the woman participates in both medical and
psychologic therapy may require 6 to 24 months. Women

BOX 24.6 History and Physical Examination
with PCOS may have anovulatory infertility, type 2
for a Patient Presenting With
diabetes, and an increased risk of cardiovascular disease
Hirsutism
and of endometrial cancer. Impaired glucose tolerance
or type 2 diabetes is observed in up to 40% of patients
HISTORY
with PCOS.
• Time course of hair growth Oral Medications. See Box 24.8 for a listing of
• Other androgenic symptoms oral medications used to treat hirsutism. Oral contracep-
• Menstrual and reproductive history
• Symptoms of virilization*
tives are the first-line treatment for patients with hirsutism
• Changes in weight and PCOS. They control hyperandrogenic skin changes,
• Changes in the size of the patient’s extremities, changes
in head size, or changes in body contour
• Medications (e.g., androgenic drugs, skin irritants)
• Psychosocial issues
• Family history (particularly androgen excess disorders BOX 24.7 Initial Investigations in a Patient
and/or type 2 diabetes) Presenting With Hirsutism
PHYSICAL EXAMINATION • Exclusion of related disorders

• Standard scoring of the excess body hair (modified • Basal or stimulated 17-hydroxyprogesterone levels
Ferriman–Gallwey score) • TSH levels
• Blood pressure • Prolactin levels
• Anthropometric measurements • Determination of biochemical hyperandrogenemia
• Skin: signs of acne, androgenetic alopecia, or acanthosis • Total and free testosterone levels,
nigricans dehydroepiandrosterone sulfate levels
• Signs of virilization* • Free androgen index (calculated as the ratio of
• Thyroid total testosterone divided by SHBG and multiplied
• Evidence of galactorrhea by 100)
• Adrenal or ovarian masses • Confirmation of ovulatory function
• Features of Cushing syndrome or of acromegaly • Progesterone levels on days 20 to 22
• Pelvic ultrasonography
*Clinical features of virilization include hirsutism, acne, androgenetic
alopecia, clitorimegaly, deepening of the voice, increased muscle SHBG, sex hormone–binding globulin; TSH, thyroid-stimulating
mass, breast atrophy, and amenorrhea. hormone.
POLYCYSTIC OVARY SYNDROME
Any 2 of the following 3 disorders All of the following disorders ruled out:
confirmed: • Hyperprolactinemia
• Oligomenorrhea or amenorrhea • Nonclassic congenital adrenal hyperplasia
• Hyperandrogenism (e.g., hirsutism, • Cushing syndrome
acne, alopecia) or hyperandrogenemia • Androgen-secreting neoplasm
(e.g., elevated levels of total or free • Acromegaly
testosterone)
• Polycystic ovaries on ultrasonography
Polycystic ovary
syndrome
Ancillary studies
Risk assessment Risk assessment Fasting cholesterol, Risk assessment

for endometrial for glucose HDL cholesterol, for obstructive
carcinoma intolerance triglycerides, sleep apnea
LDL cholesterol
Endometrial Oral glucose- Polysomnography

biopsy if risk tolerance test if if risk increased
increased risk increased
FIG 24.11 ■ Polycystic ovary syndrome. HDL, high-density lipoproteins;

LDL, low-density lipoproteins.
TABLE 24.6 Conditions for Exclusion in the Diagnosis of Polycystic Ovary Syndrome
Hyperandrogenemia, Distinguishing Features
Hyperandrogenism, Oligomenorrhea
Condition or Both or Amenorrhea Clinical Hormonal or Biochemical
Nonclassic congenital Yes Not often Family history of infertility, Elevated (basal) level of
adrenal hyperplasia hirsutism, or both; 17-hydroxyprogesterone in
caused by deficiency common in Ashkenazi morning or on stimulation
of 21-hydroxylase Jews
Cushing syndrome Yes Yes Hypertension, striae, easy Elevated 24-h urinary free
bruising cortisol level
Hyperprolactinemia or None or mild Yes Galactorrhea Elevated plasma prolactin level
prolactinoma
Primary None or mild May be present Goiter may be present Elevated plasma thyrotropin
hypothyroidism and subnormal plasma
thyroxine levels; prolactin
level may also be increased
Acromegaly None or mild Often Acral enlargement, coarse Increased plasma insulin-like
features, prognathism growth factor I
Premature ovarian None Yes May be associated with Elevated plasma follicle-
failure other autoimmune stimulating hormone level
endocrinopathies and normal or subnormal
estradiol level
Simple obesity Often Not often Diagnosed by exclusion None
Virilizing adrenal or Yes Yes Clitorimegaly, extreme Extremely elevated plasma
ovarian neoplasm hirsutism, or male androgen level
pattern alopecia
Drug-related Often Variably Evidence provided by None
condition* history
*A drug-related condition is a condition attributable to the use of androgens, valproic acid, cyclosporine, or other drugs.
From Ehrmann DA. Polycystic ovary syndrome. N Engl J Med 2005;352(12):1223–36.30
BOX 24.8 Oral Medications for Hirsutism* oral contraceptives. The four antiandrogens listed in Box
24.8 are equally effective. The combination of oral
contraceptives and antiandrogens provides contraception,
ORAL CONTRACEPTIVES
reduces the risk of irregular menstrual bleeding, and
Antiandrogens suppresses androgen levels by a different mechanism.
• Cyproterone acetate 50–100 mg/day on menstrual Liver function tests are performed before taking oral
cycle days 5–15, with ethinyl estradiol 20–35 mcg on contraceptives and antiandrogens. Kidney function and
days 5–25 serum potassium levels are measured when spironolactone
• Spironolactone 100–200 mg/day (given in divided doses
is used, especially in patients with diabetes or hypertension.
[twice daily])
• Finasteride 2.5–5 mg/day Glucocorticoids and long-acting gonadotropin-releasing
• Flutamide 250–500 mg/day (high dose), 62.5 to hormone analogues are used as second-line therapy in
<250 mg (low dose) patients with severe hirsutism who do not respond to
antiandrogens.
GLUCOCORTICOIDS Treatment consists of pharmacologic therapy or direct
• Hydrocortisone 10–20 mg twice daily hair removal, or both. Hirsutism is caused by increased
• Prednisone† 2.5–5 mg nightly or alternate days levels of circulating androgens and the response of the hair
• Dexamethasone 0.25–0.50 mg nightly follicle to local androgens. Treatment options include either
LONG-ACTING GONADOTROPIN-RELEASING (1) drugs that target androgen production and action or
HORMONE ANALOGUES (2) lasers and intense pulsed light (IPL) therapy, or both.
• Combination therapy
Cosmetic Measures. Cosmetic measures to manage
*At least 6 months of treatment are needed for a response. hirsutism include shaving, chemical depilatory agents to
†
Prednisone is preferable to dexamethasone because the dose can be dissolve the hair, and epilation methods, such as plucking
more finely titrated to avoid side effects. or waxing. Scarring, folliculitis, and hyperpigmentation
may occur with plucking or waxing. Bleaching with
regulate menstrual cycles, and provide contraception. Oral products containing hydrogen peroxide and sulfates masks
contraceptives that contain antiandrogenic progestins (CPA dark hair. Bleaching can cause irritation.
and drospirenone) may be preferred. Eflornithine Cream. Topical eflornithine (Vaniqa) is
Antiandrogens may also be used as first-line treatment. an irreversible inhibitor of ornithine decarboxylase, an
These have teratogenic potential and may be used with enzyme that catalyzes the rate-limiting step for follicular
is rare. It may cause diuresis, postural hypotension, and

TABLE 24.7 Selection of Photoepilation
dizziness early in treatment. Antiandrogens may cause
Methods – Laser and Intense
fetal male pseudohermaphroditism if used in pregnancy.
Pulsed Light (IPL) Therapy
Cyproterone Acetate. Cyproterone acetate (CPA) is
Skin/Hair Color Choice of Photoepilation Device not available in the United States. CPA is a progestogenic
compound with antiandrogen activity that inhibits the
Light skin/dark hair Relatively short wavelength
androgen receptor and 5α-reductase activity. It suppresses
Dark skin/dark hair Relatively long wavelength or IPL serum gonadotropin and androgen levels. Because of its
Light/white hair IPL + radiofrequency long half-life, CPA is usually administered in a reverse
sequential way. Doses of ethinyl estradiol (20 to 50 mcg/
IPL, intense pulsed light.
Adapted from Martin KA, Chang RJ, Ehrmann DA, et al. day) are given for 3 weeks (days 5 to 25) to ensure normal
Evaluation and treatment of hirsutism in premenopausal menstrual cycling, and CPA is administered for the first
women: an endocrine society clinical practice guideline. J Clin 10 days (days 5 to 15) of the cycle. Doses of 50 to 100 mg/
Endocrinol Metab 2008;93(4):1105–20.11 day of CPA are often prescribed until the maximal effect
is obtained, and then lower doses (such as 5 mg/day) are
prescribed for maintenance. CPA is also available as an
polyamine synthesis, which is necessary for hair growth. oral contraceptive at lower daily doses of 2 mg of CPA
The topical preparation reduces the rate of hair growth. with 35 mcg of ethinyl estradiol. CPA is generally well
Results take about 6 to 8 weeks, but hair regrows once tolerated, but there are dose-dependent metabolic effects
the cream is stopped. similar to those of higher doses of oral contraceptives.
Photoepilation. Light source–assisted hair reduction Finasteride. Finasteride is second-line therapy. Spi-
(photoepilation) is effective. Methods include lasers and ronolactone is the preferred drug. Finasteride inhibits
nonlaser light sources, such as IPL therapy. type II 5α-reductase activity. Enhanced 5α-reductase
Vellus hair follicles may remain and can be converted activity in hirsutism probably involves both type I and
into terminal hairs when androgen excess is present; this type II 5α-reductase enzymes. Therefore finasteride
explains why many women experience hair regrowth. These produces only a partial inhibitory effect. There are no
techniques are particularly effective in the hands of major adverse effects. Spironolactone 100 mg daily may
experienced therapists who are aggressive enough to be more effective than finasteride 5 mg daily with more
produce lasting results. Eflornithine cream during treat- prolonged treatment. The optimal dose of finasteride has
ment may produce a more rapid response. Cost is a not been determined; 5 mg of finasteride is the most
significant limiting factor for many patients. Different commonly used dose but 7.5 mg may be more effective.
skin types require different approaches (Table 24.7). These Doses of 2.5 and 5 mg may be equally effective.
techniques are more effective than electrolysis. Flutamide. Flutamide is second-line therapy. It is
not used for the routine management of hirsutism. The
Pharmacologic Therapy. Most women are treated potential for hepatotoxicity and its high cost limit its
with oral contraceptives. Antiandrogens have teratogenic value. Flutamide is a pure antiandrogen with a dose-
potential. Therefore antiandrogen monotherapy is avoided response inhibition of the androgen receptor. Doses
unless contraception is used. Reducing insulin levels ranging from 250 to 750 mg/day are similar in efficacy
pharmacologically attenuates both hyperinsulinemia and to spironolactone 100 mg/day and finasteride 5 mg/day.
hyperandrogenemia. However, drugs such as metformin The most frequently used dose is 500 mg/day; 250 mg/
have been shown to be less effective than antiandrogens. day may be just as effective. Hepatic toxicity resulting in
Oral Contraceptive Monotherapy. Oral contraceptives liver failure and death is reported. The effect may be dose
contain a synthetic estrogen, ethinyl estradiol, in combina- related; no hepatotoxicity was observed in adolescent girls
tion with a progestin. Most of these progestins are derived and women receiving flutamide 62.5 to 250 mg/day or
from T and exhibit mild degrees of androgenicity. Other in young women receiving up to 375 mg/day. Therefore
progestins, including CPA and drospirenone, are structur- the lowest effective dose should be used, and the patient
ally unrelated to T and function as androgen receptor should be monitored.
antagonists. Oral contraceptives reduce hyperandrogenism Glucocorticoid Therapy. Glucocorticoids are not
by suppression of LH secretion (and therefore ovarian first-line therapy. They have the potential for significant
androgen secretion) and stimulation of hepatic production adverse effects and are less effective than antiandrogens.
of sex hormone–binding globulin (SHGB) (thereby Low dosages of glucocorticoids reduce adrenal androgen
increasing androgen binding in serum and reducing serum secretion without significantly inhibiting cortisol secretion.
free androgen concentrations). The evidence from studies Unfortunately, suppression of serum T concentration is
supporting the effectiveness of oral contraceptives is weak. not optimal. Glucocorticoids are used to suppress adrenal
Antiandrogen Monotherapy. Spironolactone is an androgens in women with classic congenital adrenal hyper-
aldosterone antagonist that exhibits dose-dependent plasia caused by 21-hydroxylase deficiency (CYP21A2). In
competitive inhibition of the androgen receptor and these patients, glucocorticoids help prevent hirsutism. In
inhibition of 5α-reductase activity. Studies show that women with the nonclassic form of CYP21A2 deficiency,
spironolactone 100 mg/day can significantly lower the glucocorticoids produce ovulation induction, but their role
Ferriman–Gallwey scores. Spironolactone’s effects are in the management of hirsutism is less clear.
dose dependent. Spironolactone is well tolerated but has Gonadotropin-Releasing Hormone (GnRH) Ana-
a dose-dependent association with menstrual irregularity logues. GnRH agonist therapy is second-line therapy. It
unless an oral contraceptive is also used. Hyperkalemia has no therapeutic advantages when compared with oral
contraceptives and antiandrogens. It is expensive and stubs of hair. The hair shaft in AA is poorly formed and
complicated to use. breaks on reaching the surface (Fig. 24.12). Some patients
complain of itching, tenderness, or a burning sensation
before the patches appear. The ophiasis type presents as
Alopecia Areata band-like hair loss in the parietotemporo-occipital area
Alopecia areata (AA) is a common asymptomatic disease (Fig. 24.13). The ophiasis pattern has a poor prognosis
characterized by the rapid onset of total hair loss in a for spontaneous recovery.
sharply defined, usually round, area. The diagnosis is made AA appears to progress as a wave of follicles prematurely
by observation. Any hair-bearing surface may be affected. enters telogen. The event weakens or narrows the hair
The cause is unknown. An interaction between genetic shaft, which continues to grow before the telogen phase is
and environmental factors may trigger the disease. Alopecia complete. Most weakened hairs fracture when they reach
areata is a partial loss of scalp hair, alopecia totalis is 100% the surface. The affected hairs that are often found retained
loss of scalp hair, and alopecia universalis is 100% loss of at the periphery of a lesion have a normal upper shaft and
hair on the scalp and body. a narrowed base – “exclamation point” hair (Fig. 24.14).
Regrowth begins in 1 to 3 months and may be followed
Prevalence. The incidence of AA in the United States by loss in the same or other areas. The new hair is usually
is 0.1% to 0.2% of the population. Sixty percent of patients of the same color and texture, but it may be fine and
present with their first patch before 20 years of age. white. Occasionally the white color remains. The eyelashes,
Familial incidence is 37% in patients who had their first beard (Fig. 24.15), and, rarely, other parts of the body
patch by 30 years of age and 7.1% in patients who had may be involved. Total hair loss of the scalp (alopecia
their first patch after 30 years of age. totalis), seen most frequently in young people, may be
accompanied by cycles of growth and loss, but the prognosis
Clinical Presentation. A wide spectrum of involvement for long-term regrowth is poor. Total body hair loss
is seen. Most patients report the sudden occurrence of (alopecia universalis) is very rare.
one to several 1- to 4-cm areas of hair loss on the scalp
that can be easily concealed by covering with adjacent Psychologic Implications. Hair plays an important role
hair. The skin is smooth and white or may have short in one’s appearance and self-image, and sudden hair loss
A B
C D
FIG 24.12 ■ Alopecia areata. A, Multiple round and oval patches of hair loss. B, The regrown hair is white.
C, Loss of eyelashes and eyebrows is a common finding. D, Alopecia totalis. The hair has regrown for short
periods. The prognosis for normal regrowth is poor.
FIG 24.13 ■ Ophiasis pattern of alopecia areata. Presents

as a band-like hair loss in the parietotemporo-occipital
area. (From Alkhalifah A, Alsantali A, Wang E, et al.
Alopecia areata update: part I. Clinical picture,
histopathology, and pathogenesis. J Am Acad Dermatol
2010;62(2):177–88, quiz 189–90.14)
FIG 24.15 ■ Alopecia areata. The beard area is the
second most common area to be affected.
A B
FIG 24.14 ■ A, Close view showing multiple exclamation mark hairs that are often found retained at the
periphery of a lesion. B, Exclamation mark hairs seen under folliscope examination have a normal upper shaft
and a narrowed base. (Courtesy Sometech Inc., Seoul, Korea; original magnification, ×350. From Alkhalifah A,
Alsantali A, Wang E, et al. Alopecia areata update: part I. Clinical picture, histopathology, and pathogenesis. J Am
Acad Dermatol 2010;62(2):177–88, quiz 189–90.14)
regrowth in cases with limited involvement is excellent.

Most patients entirely regrow hair within 1 year without
treatment; 10% develop chronic disease and may never
regrow hair. Patients with a family history of AA, young
age at onset, immune diseases, nail dystrophy, atopy, and
extensive hair loss have a poor prognosis.
Differential Diagnosis. The differential diagnosis

includes TTM, tinea capitis, and telogen effluvium. In
TTM, there are short and broken hairs. A 4-mm punch
biopsy may be required. Hair loss occurs over the entire
scalp with telogen effluvium. The “moth-eaten” or diffuse
alopecia of secondary syphilis may be confused with AA.
Etiology. The etiology is unknown. Genetic factors

are important. There is a higher incidence of a family
history in patients with AA. Stress is frequently cited.
One study concludes that there is little evidence that
emotional stress plays a significant role in the pathogenesis
of AA.
Immunologic Factors. AA may be an autoimmune disease

mediated by T lymphocytes directed to hair follicles. Atopy
is twice as common in AA patients compared with the
general population. There are associations between AA
and autoimmune disorders. An incidence of 8% to 11.8%
in the frequency of thyroid disease has been reported. AA
patients have an increased prevalence of antithyroid and
FIG 24.16 ■ Shallow pitting of the nail occurs in some thyroid microsomal antibodies. AA patients have a 4-fold
patients with alopecia areata. greater incidence of vitiligo. The significance of these
findings is unknown.
Pathology. A peribulbar lymphocytic infiltrate (“swarm

in a bizarre pattern is psychologically painful. It affects of bees”) with no scarring is characteristic. The acute
the quality of life and limits social freedom. Those affected follicular inflammation attacks the hair bulb in the sub-
equate partial hair loss with balding and fear total hair cutaneous fat. This inflammation terminates the anagen
loss. The appearance is striking, and people stare. AA is stage, forcing the follicle into catagen. Since the bulge
devastating for image-conscious teenagers. Patients make area is spared, a new hair bulb and shaft grow at the start
attempts to hide bald spots by covering them with adjacent of the anagen stage, once the inflammation has subsided
long hairs. Those with extensive loss who cannot adequately or has been controlled with glucocorticoids. Large numbers
camouflage the spots may hide or obtain a wig. A network of catagen and telogen hairs are present in subacute cases
of support groups across the country is available to help and follicle miniaturization with minimal or no inflam-
people cope with fears, loneliness, and concerns. The mation is seen in chronic cases.
National Alopecia Areata Foundation (www.naaf.org)
provides informational brochures, newsletters, research, Treatment. Treatments control but do not cure and do
updates, sources of scalp prostheses, videotapes for not prevent the spread of AA. Treatments according to
schoolchildren, and locations of support groups and holds age and severity are listed in Boxes 24.9 and 24.10. Treat-
an annual conference to help patients cope with the ment options depend on the patient’s age and extent of
condition. The physician can provide continuing support the disease (Fig. 24.17). For children younger than 10
for this difficult problem. years of age, a combination of 5% minoxidil solution
twice daily with a midpotent topical corticosteroid is the
Nail Changes. Nail dystrophy may be associated with first line of therapy. If there is no response after 6 months,
AA. The incidence is 10% to 66%. Pitting with an irregular short-contact anthralin can be tried. Most adults have
pattern, or in organized transverse or longitudinal rows less than 50% scalp involvement and are treated with
and longitudinal striations, may result in a sandpaper intralesional injections of triamcinolone acetonide (see
appearance seen in one or all of the nails of some patients Boxes 24.9 and 24.10 for details); 5% topical minoxidil
with AA (Fig. 24.16). Dystrophy precedes, coincides with, twice a day, potent topical corticosteroid under occlusion
or occurs after resolution of AA. at night, and short-contact anthralin are alternative treat-
ments if there is no response to intralesional injections
Prognosis. The course is unpredictable; recovery may after 6 months.
be complete or partial. Several episodes of loss and Observation. The majority of patients with a few small
regrowth are typical. The prognosis for total permanent areas of hair loss can be assured that the prognosis for
BOX 24.9 Treatment for Patients With Alopecia Areata According to Age and Severity of Condition
PATIENTS <10 YEARS OF AGE >50% of scalp affected

5% topical minoxidil solution, topical glucocorticoid, or • 5% topical minoxidil solution, with or without topical
both glucocorticoid
Anthralin (short contact)* • Topical immunotherapy
• Anthralin (short contact)*
PATIENTS ≥10 YEARS OF AGE • Oral glucocorticoid
<50% of scalp affected • Scalp prosthesis
• Intralesional glucocorticoid, 5% topical minoxidil EYEBROWS AND BEARD AFFECTED
solution, or both, with or without topical
glucocorticoid Intralesional glucocorticoid, 5% topical minoxidil solution,
• Anthralin (short contact)* or both
*Anthralin is left on the scalp for 20 to 60 minutes.

From Price VH. Treatment of hair loss. N Engl J Med. 1999;341(13):964–73.31
TREATMENT FOR ALOPECIA INVOLVING THE SCALP
Scalp Alopecia Areata
10 yr old 10 yr old
Topical midpotent 50% scalp 50% scalp

corticosteroids + 5% involvement involvement
minoxidil solution
or ILCS ± 5% minoxidil Topical

± topical immunotherapy
Short contact corticosteroids DPCP or SADBE
anthralin
6–12 months 6–12 months
Good Poor Good Partial Poor

response response response response response
Continue PRN 1% Anthralin Continue PRN Add ILCS to Combination of

± minoxidil refractory minoxidil 5% solution
5% solution patches every 4 twice daily + potent
weeks topical corticosteroids
under occlusion
or
Short contact
Anthralin
FIG 24.17 ■ Treatment for alopecia involving the scalp. DPCP, diphenylcyclopropenone;
ILCS, intralesional corticosteroids; PRN, as needed; SADBE, squaric acid dibutyl ester.
(From Alkhalifah A, Alsantali A, Wang E, et al. Alopecia areata update: part II. Treatment. J Am
Acad Dermatol 2010;62(2):191–202, quiz 203–4.15)
regrowth is excellent. If there is great anxiety or if bald valerate foam, clobetasol ointment, or clobetasol foam
areas cannot be concealed, then intralesional injections may be used. Foam-based medications are convenient and
should be considered. have a lower incidence of folliculitis following occlusion. A
Topical Steroids. Topical midpotent corticosteroids are shower cap can be used for occlusion. In a study of patients
the treatment of choice in children. Some authors combine with alopecia areata totalis, patients applied clobetasol
topical corticosteroids with minoxidil 5% solution applied propionate every night under occlusion with a plastic film
twice a day. Adults can be treated with potent topical 6 days a week for 6 months.12 Glucocorticoid-induced
steroids under occlusion; alternatively, 0.1% betamethasone folliculitis is a common adverse effect.
BOX 24.10 Suggested Methods of Treatment for Alopecia Areata
INTRALESIONAL GLUCOCORTICOID apply 2% solution of selected contact allergen in acetone

All Sites to a 4 cm2 area on one side of the scalp. After initial
sensitization, apply diluted solution of contact allergen
The preferred compound is triamcinolone acetonide weekly to same half of scalp in two coats. For both the
(10 mg/mL), administered with a 1-mL Luer-Lok syringe sensitizing application and the subsequent weekly
with a 30-gauge 1 1 2 -inch-long needle. Concentrations of 2.5 applications, the patient washes off the allergen after 48
to 8 mg/mL may also be used; 2.5–5 mg/mL is used for the hours. The patient should be instructed to keep the
beard area and eyebrows. Inject 0.1 ml or less into the treated areas protected from the sun while the product is
mid-dermis at multiple sites 1 cm apart; do not raise wheal on it. Adjust concentration of allergen according to the
or inject into subcutaneous tissue. Repeat every 4 to 6 response to the previous week’s treatment. Desired
weeks; if atrophy of the skin occurs, do not reinject affected responses include mild itching, erythema, and scaling.
site until atrophy resolves. Optional topical anesthesia may • Concentrations of allergen that elicit responses range
be used: apply a mixture of 2.5% lidocaine and 2.5% from 0.0001%, 0.001%, 0.01%, 0.025%, 0.05%, 0.1%,
prilocaine (EMLA cream) in a thick layer to intact skin and 0.25%, 0.5%, and 1.0%, to 2.0%. After hair growth is
cover with occlusive dressing for 1 hour before injections established on the treated side (in 3 to 12 months), then
are given; remove cream immediately before injections. both sides of the scalp are treated. Apply contact
Scalp sensitizer with wooden applicator tipped with generous
amount of cotton (the physician or nurse applying
The maximal dose is 20 mg per visit. When more than 50% weekly treatment must wear gloves). To minimize side
of scalp is affected, inject only selected sites. effects, it is recommended that the allergen be applied in
Beard a physician’s office and not be given to the patient for
use at home.
The maximal dose is 1.25 mg per visit injected into the
mid-dermis of each brow at five or six sites (for a total of ORAL GLUCOCORTICOIDS
2.5 mg to both brows).
The maximal dose is 7.5 mg per visit. Active, Extensive, or Rapidly Spreading Alopecia Areata
• For patients weighing >60 kg the recommended
5% TOPICAL MINOXIDIL SOLUTION treatment is 40 mg of oral prednisone daily for 1 week;
Scalp and Beard then 35 mg daily for 1 week; 30 mg daily for 1 week;
The maximal dose is 1 mL per application. Apply twice 25 mg daily for 1 week; 20 mg daily for 3 days; 15 mg
daily to affected sites. Spread solution with fingers. Wash daily for 3 days; 10 mg daily for 3 days; and 5 mg daily
hands afterward. This treatment is not effective for patients for 3 days. Prednisone may be used with 5% topical
with total (100%) loss of scalp hair. minoxidil solution twice daily and intralesional
triamcinolone acetonide injections, given as previously
Eyebrows described, every 4 to 6 weeks. Topical therapy should be
Using a finger, apply two applications to each eyebrow continued twice daily with or without intralesional
twice daily using a mirror to ensure precise placement. injections every 4 to 6 weeks after prednisone is tapered.
Hold a cotton ball over the eye for protection. Wash hands
Active, Less Extensive Alopecia Areata
afterward.
• Twenty milligrams of oral prednisone should be given
ANTHRALIN (SHORT CONTACT FOR 20–60 MINUTES) daily or every other day; dose should be tapered slowly
• Apply 0.5% to 1% anthralin cream to affected scalp once by increments of 1 mg after the condition is stable.
daily; leave on 20 to 30 minutes daily for 2 weeks, and
then 45 minutes daily for 2 weeks, up to a maximum of 1 Other Therapies Being Researched
hour daily. Wash hands afterward, and avoid getting These methods of therapy are currently being researched
anthralin in the eyes. for their efficacy and safety:
• Remove from scalp with mineral oil; then wash off with • JAK/STAT inhibitors, such as tofacitinib (5 to 10 mg
soap and water. Do not use on brows or beard. Some twice daily) and ruxolitinib (20 mg twice daily or 0.6%
patients tolerate overnight application. cream twice daily for 12 weeks)
• Anthralin may stain the skin, clothing, and hair brown. • Sulfasalazine (0.5 g twice daily for one month, then 1 g
Wash hands immediately after application with lukewarm twice daily for one month, then 1.5 g twice daily for at
water. least 3 months). For the first 3 months of therapy,
monitor blood cell counts and liver function tests.
TOPICAL GLUCOCORTICOID Continue to monitor blood cell counts and liver function
• Apply twice daily. every three to six months.
• Evaluate growth after three months of therapy. • Azathioprine 2.5 mg/kg daily. Adjust to thiopurine
methyltransferase (TMPT) levels
TOPICAL IMMUNOTHERAPY • Hydroxychloroquine 200 mg twice daily
• Use diphencyprone or squaric acid dibutyl ester to • Cyclosporine
induce contact sensitization. For initial sensitization, • Methotrexate
JAK, Janus kinase inhibitors; STAT, signal transducer and activator of transcription.
Adapted from Price VH. Treatment of hair loss. N Engl J Med 1999;341(13):964–73.31
Intralesional Injections. Intralesional corticosteroid affecting more than 50% of the scalp are the best candi-
injections (triamcinolone acetonide 5 to 10 mg/mL) are dates. Poor long-term outcome of severe AA in children
first-line therapy for patients with less than 50% of scalp treated with high-dose pulse corticosteroid therapy has
involvement. Regrowth is seen in 4 to 8 weeks. This agent been reported.16 A 6-week taper of prednisone resulted
stimulates localized regrowth in 60% to 67% of cases. in 25% regrowth in 30% to 47% of patients with mild
Repeat injections every 4 to 6 weeks. Atrophy occurs with to extensive AA, alopecia totalis, or alopecia universalis,
larger volumes and concentrations of triamcinolone and with predictable and transient side effects. Patients with
with injections that are too superficial. Children younger recent-onset AA (1 year) and a bald surface of greater than
than 10 years do not tolerate the pain. Stop treatment if 30% of the scalp were given 250 mg of methylprednisolone
there is no response after 6 months of treatment. Intra- intravenously twice a day on 3 successive days. Another
lesional steroid injections do not alter the course of the study using the same dosages supports these findings.17
disease, and the hair may once again be shed. The course of the ongoing episode of AA was stopped
Minoxidil (Topical Solution or Foam). Minoxidil in eight patients. At the 6-month follow-up, a regrowth
(Rogaine 2% or 5% solution or foam) must be applied on 80% to 100% of the bald surfaces was observed in
twice daily. Many patients prefer the foam. The 5% con- six patients. The addition of 2% topical minoxidil three
centration is more effective. The response is variable. Hair times daily may alleviate poststeroid relapse.
regrowth occurs in 20% to 45% of patients with 20% to Cyclosporine. Oral cyclosporine is effective for
99% scalp involvement. The response is slow and requires treatment of AA. However, the side effects, high recurrence
months of treatment. Initial hair regrowth is usually seen rate, and long treatment periods limit the use of this drug.
after 12 weeks. Minoxidil does not change the course Hair Weaves and Wigs. See treatment section under
of the disease, and continual use is required to sustain androgenetic alopecia in men. High-quality wigs are
growth. Instruct patients that applications must continue available.
twice daily with the recommended dose to gain maximal
clinical effect. Anthralin or betamethasone dipropionate
enhances the efficacy of minoxidil solution. Anthralin is
Trichotillomania
applied 2 hours after the second minoxidil application. Trichotillomania (TTM) is a chronic impulse control
Betamethasone dipropionate cream is applied twice daily, disorder characterized by repetitive hair-pulling, resulting
30 minutes after each use of minoxidil. These treatments in alopecia. Others feel it should be classified more
are not effective for alopecia totalis/universalis. appropriately as a disorder on the obsessive–compulsive
Anthralin. Anthralin 0.5% to 1% short-contact therapy spectrum.
is used as alternative treatment. Anthralin results in There is increased tension immediately before pulling
regrowth in 20% to 25% of patients. Mild irritation should or when attempting to resist the behavior. Feelings of
develop in order for it to be effective, and short-contact pleasure, gratification, or relief from pulling out the hair
therapy is effective. Side effects include irritation, scaling, are characteristic.18
folliculitis, and regional lymphadenopathy. Protect treated
skin from sun exposure. Anthralin temporarily stains the Prevalence. Prevalence rates range from 0.6% to 13%.
skin. It may have a nonspecific immunomodulating effect. This conscious or subconscious habit or tic is most
The treatment is safe and may be considered for refractory commonly performed by young children, adolescents, and
cases. Combination therapy with 5% minoxidil plus 0.5% women. Many children have a benign, self-limited form
anthralin is more effective than when either drug is used of hair pulling. The average age of onset is 11 to 13 years.
as a single agent. New hair growth is seen within 3 months. The female-to-male ratio is 2.5 : 1. Increased prevalence
Treatment is stopped if there is no response by 3 months. has been documented in adults with anxiety and with
Anthralin is a good choice for children. See Box 24.10 affective disorders.
and Fig. 24.17. Anthralin can be made by a compounding
pharmacist. Dermatologic Manifestations. Hair is twisted around
Topical Immunotherapy. Diphenylcyclopropenone the finger and pulled or rubbed until extracted or broken.
(DPCP) is the treatment of choice for adults with more The favorite site is the easily reached frontoparietal region
than 50% scalp involvement. The treatment is also reported of the scalp, but any scalp area or the eyebrows and
in children.13 Sensitization with DPCP 2% is followed eyelashes may be attacked (Fig. 24.18). The affected area
by weekly application of the lowest concentration that has an irregular angulated border, and the density of hair
can cause mild irritation. Squaric acid dibutyl ester is an is greatly reduced; but the site is never bald, as in AA.
alternative in patients who do not develop allergic reaction Several short, broken hairs of varying lengths are randomly
to DPCP. Treatment should be stopped if there is no distributed in the involved site. Hair that grows beyond
improvement after 6 months. The success rate in the most 0.5 to 1 cm can be grasped by small fingers and extracted
experienced hands is approximately 60% in patients with (Figs. 24.19 and 24.20).
25% to 99% scalp involvement. This is not routine therapy
and is not available in some teaching centers. See Box Psychiatric Manifestations. The symptom may first
24.10 and Fig. 24.17 for details of preparation.14,15 manifest during inactive periods in the classroom, while
Systemic Corticosteroids. Systemic corticosteroids are watching television, or in bed while waiting to fall asleep.
effective but rarely used. The side effects, high relapse rate, Parents seldom notice the behavior. In many children TTM
long treatment periods, and inability to change prognosis is triggered by hospitalizations or medical interventions,
limit their use. Young adult patients with active disease problems at home, or difficulties at school. Cases also
FIG 24.18 ■ Trichotillomania. Extraction of the eyelashes

may produce a clinical presentation that is identical to
alopecia areata. FIG 24.20 ■ Trichotillomania. Several short hairs are
randomly distributed in the involved site.
BOX 24.11 DSM-5 Diagnostic Criteria for

Trichotillomania
1. Hair loss resulting from recurrent pulling out one’s

hair.
2. Repeated attempting to decrease or stop hair pulling.
3. Significant distress or impairment in occupational,
social, or other areas of functioning is experienced as a
result of the pulling.
4. The hair pulling or hair loss is not attributable to
another medical condition, such as a dermatologic
condition.
5. The pulling is not better explained by the symptoms of
another mental disorder, such as body dysmorphic
disorder.
American Psychiatric Association. Diagnostic and statistical manual

of mental disorders (5th ed.). Arlington, VA: American Psychiatric
Publishing, 2013.32
FIG 24.19 ■ Trichotillomania. Hair has been manually
extracted from a wide area of the scalp. There is no
inflammation or scarring.
rules out noninflammatory tinea capitis. Areas of AA are
completely devoid of hair. In questionable cases, a hair
pluck can be performed from the diseased areas; in TTM,
occur with severe sibling rivalry, a disturbed parent–child it shows no telogen hair roots. Nearly 100% of the hairs
relationship, and intellectual disability. Comorbidity with are in the active-growing, anagen phase. The absence of
mood and anxiety disorders and in patients with a primary telogen hairs is the reason no hair is released on gentle
depressive illness increases in incidence, with TTM arising hair traction. Skin biopsy specimens (4 or 5 mm punch
in adolescence and adulthood. Some psychiatrists classify extending into the subcutaneous tissue) show normal
it as an obsessive–compulsive disorder in adults. hairs, absence of hairs in follicles, and no infiltration of
The course is chronic, with remissions and exacerba- leukocytes. Catagen hairs are present in 74%, pigment casts
tions. Patients can spend 1 to 3 hours per day pulling in 61%, and traumatized hair bulbs in 21% of patients;
hair, resulting in severe hair loss, suffering, and loss of these findings are most evident in areas affected for less
productive social and work relationships. Shame is a than 8 weeks.
prominent component. Hair pullers fear discovery, avoid
health care visits, and worry about being critically judged. Treatment. A summary of treatment strategies is listed
Psychologic suffering is intense. in Box 24.12. Many patients are psychologically stable
and require only a discussion of the problem with an
Diagnosis. The diagnostic criteria are listed in Box 24.11. understanding physician or parent. Many of these cases
First, the patient should be asked if he or she manipulates resolve spontaneously. Advise parents to divert the child’s
the hair. Parents or teachers may be aware of the habit. attention when hair is being pulled and to be accept-
A potassium hydroxide and Wood’s light examination ing and supportive rather than judgmental or punitive.
BOX 24.12 Guidelines for the Treatment of BOX 24.13 Primary Scarring Alopecia
Trichotillomania (Classification Based on Clinical
Presentation and Histology)
• Establish adequate physician–patient relationship to
improve insight, acknowledgment of disease, and INITIALLY LYMPHOCYTIC
compliance with treatment. • Chronic cutaneous lupus erythematosus
• Evaluate all sites of pulling. • Lichen planopilaris (LPP)
• Assess motivation for treatment. • Classic lichen planopilaris
• Inquire about trichophagia. • Frontal fibrosing alopecia
• Consider psychiatric referral. • Lassueur–Graham–Little syndrome (LPP and lichen
• Evaluate and treat comorbid conditions (e.g., skin planus and spinous lesions)
picking, mood disorders, anxiety disorders). • Pseudopelade (Brocq)
• Guide patient to educational and support groups. • Central centrifugal cicatricial alopecia (follicular
• Evaluate for habit-reversal therapy. degeneration syndrome, hot comb alopecia)
• Institute modified habit reversal.
• Evaluate pharmacotherapy: clomipramine (evaluate the NEUTROPHILIC
adverse effects of clomipramine). • Folliculitis decalvans
• Consider introducing posthypnotic suggestions. • Dissecting cellulitis/folliculitis
• Institute relapse-prevention strategies.
MIXED
Modified from Koran LM. Trichotillomania. In: Obsessive-
compulsive and related disorders in adults. A comprehensive clinical • Acne keloid
guide. Cambridge, UK: University Press, 1999:185.33 • Tufted folliculitis
• Acne necrotica
• Erosive pustular dermatosis
Patients with extensive involvement or those who persist
in the habit should undergo psychiatric evaluation. The Adapted from Whiting DA. Cicatricial alopecia: clinico-pathological
findings and treatment. Clin Dermatol 2001;19(2):211–25.34
relative effectiveness and long-term benefits of behavioral
and drug treatments are not established. A meta-analysis
demonstrated that habit-reversal therapy was superior BOX 24.14 Secondary Scarring Alopecia
to pharmacotherapy with clomipramine. Clomipramine
was more efficacious than placebo, while there was no INHERITED AND CONGENITAL DISORDERS
evidence to demonstrate that selective serotonin reuptake Aplasia cutis, chondrodysplasia punctata, cutis verticis
inhibitors (SSRIs) are more efficacious than placebo in the gyrata, Darier disease, eccrine hamartoma, epidermal
treatment of TTM.19 Many other oral medications have nevi, epidermolysis bullosa, hair-follicle hamartoma,
been tried. For more information visit the TLC Foundation hypotrichosis congenita, ichthyosis (sex-linked recessive),
for Body-Focused Repetitive Behaviors at www.bfrb.org. incontinentia pigmenti, keratosis pilaris spinulosa
decalvans, neurofibromatosis, polyostotic fibrous dysplasia,
porokeratosis of Mibelli, scarring follicular keratosis
Traction (Cosmetic) Alopecia
PHYSICAL/CHEMICAL AGENTS
Prolonged tension created by certain hairstyles (such as
braids or ponytails), hair rollers, and hot hair-straightening Chemical burns, insect bites, mechanical trauma or
laceration, radiation dermatitis, thermal burns
combs may result in temporary or, rarely, permanent hair
loss in an area corresponding exactly to the stressed hair. SCLEROSING DISORDERS
The scalp may appear normal or may show evidence of Lichen sclerosus et atrophicus, morphea, scleroderma,
inflammation or scarring. scleroderma en coup de sabre and facial hemiatrophy,
sclerodermoid porphyria cutanea tarda
Scarring Alopecia DERMAL GRANULOMATOUS INFILTRATIONS
The cicatricial or scarring alopecias cause destruction of Actinic granuloma; amyloidosis; infections caused by
follicles and result in irreversible hair loss. They occur fungi, protozoa, syphilis, tuberculosis, viruses, etc.;
with either destruction of the follicle or scarring of the Miescher granuloma; necrobiosis lipoidica; sarcoidosis
reticular dermis. Scarring alopecias are classified as primary DERMAL NEOPLASTIC INFILTRATIONS
or secondary. In primary scarring alopecias (Box 24.13), Adnexal tumors, basal cell carcinoma, dematofibrosarcoma
the follicle is the target of inflammation. In secondary protuberans, lymphoma, melanoma, metastatic carcinoma,
scarring alopecias (Box 24.14), the follicle is destroyed by squamous cell carcinoma, etc.
a nonfollicular process. In primary scarring alopecias, the
inflammation is either primarily lymphocytic or neutro- Adapted from Whiting DA. Cicatricial alopecia: clinico-pathological
philic. All parts of the follicle can be involved, but the findings and treatment. Clin Dermatol 2001;19(2):211–25.34
bulge area of the follicle, where the arrector pili muscles
insert, is the primary target of the inflammatory process. Central Centrifugal Cicatricial Alopecia (Follicular
This bulge contains the stem cells for regeneration of the Degeneration Syndrome). Central centrifugal cica-
lower follicle during normal follicular cycling. The end tricial alopecia (CCCA) (previously known as hot comb
stage is smooth skin with no follicular orifices. The primary alopecia, follicular degeneration syndrome) can result
cause may be related to sebaceous glands. in the permanent destruction of hair follicles. It is the
BOX 24.15 Central Centrifugal Scarring BOX 24.16 Chronic Cutaneous Lupus
Alopecia (Follicular Degeneration Erythematosus
Syndrome, Hot Comb Alopecia)
• Young to middle-aged women
• Middle-aged black females, some black males • Lesions on sun-exposed areas – face, ears, scalp
• Some have history of hot comb usage • Well-circumscribed, erythematous, scaly plaques
• Scarring alopecia starts on the vertex, spreads forward • Follicular plugging, telangiectasia, atrophy, and
and outward and gradually assumes the central, dyspigmentation
elongated configuration of female pattern alopecia; • Early, active lesions may be sensitive and pruritic
most active disease at the periphery; eventual burnout • Developed lesion – scaly crust with follicular spines
• Lymphocytic inflammation (carpet tack scale attached to the undersurface)
• Premature disintegration of the inner root sheath • No active border like lichen planopilaris and others
• Release of hair fragments into the dermis, causing • Patches without visible inflammation may resemble
granulomatous inflammation alopecia areata or pseudopelade
• Differential diagnosis – discoid lupus erythematosus, • Interface alteration at dermoepidermal junction
lichen planopilaris, folliculitis decalvans, pseudopelade, • Lymphocytic infiltrates – perifollicular + between
tufted folliculitis follicles, around superficial and deep blood vessels, and
• Treatment – minimal hair grooming; no oily scalp in and around eccrine glands
preparations, traction, heat, chemicals, straighteners, • Diagnosis is difficult at fibrosis stage
perming, or dyeing; treat with topical or intralesional • Immunofluorescence – IgG, IgM, or complement
steroids, topical minoxidil deposits in a band at dermoepidermal junction
• Treat with topical clobetasol propionate once or twice
daily; intralesional triamcinolone acetonide suspension
most common form of cicatricial hair loss among black 10 mg/mL repeated every 4 to 6 weeks (very effective);
imiquimod cream35; tacrolimus ointment 0.1%
women. The ideology is unknown. Hair styles causing
• Oral corticosteroids such as prednisone 10 to 20 mg
traction and inflammation from bacterial infection may daily in morning, and later reduce to alternate-day
be contributing factors. The increase in diabetes mellitus therapy with a gradually reducing dosage for multiple
type 2 among those with CCCA supports the theory that itchy lesions
cicatricial alopecia may be a manifestation of metabolic • Use hydroxychloroquine sulfate, retinoids (isotretinoin,
dysregulation. CCCA presents on the vertex of the scalp acitretin), azathioprine, and cyclosporine for more
and can be divided into early (inflammatory) and late extensive disease
(scarring) stages (Box 24.15). Erythema and scaling indicate
the presence of inflammation around hair follicles. Pruritus
and scalp tenderness are common. Early in the disease
process, there is decreased hair density in an area measuring
a few centimeters. The disease progresses slowly. Histologi-
cally there are varying levels of inflammation, ranging
from minimal to intense perifollicular lymphohistiocytic
infiltration involving the infundibulum and isthmus leading
to replacement of terminal hair follicles with fibrous tracts.
There is a spectrum of severity from slowly progressive
(over decades) and relatively noninflammatory disease to
rapidly progressive (over years) and highly inflammatory
disease. Patients with highly inflammatory disease would
have been described as having folliculitis decalvans. The
end stage may be described as pseudopelade. High-potency
topical corticosteroid foam or ointment may be applied
nightly. Intralesional triamcinolone 5 mg/mL every 4 to 6
weeks for approximately 1 to 3 sessions is more effective
than topical corticosteroids. Doxycycline may be considered
for inflammatory disease.
Chronic Cutaneous Lupus Erythematosus

Chronic cutaneous lupus erythematosus (discoid lupus
erythematosus) is a common cause of scarring alopecia
(see p. 676) (Box 24.16). Women are more often affected.
Early discrete bald patches look like pseudopelade or lichen
planopilaris (LPP). Late lesions are more pronounced and
clinically diagnostic. The combination of diffuse scaling, FIG 24.21 ■ Discoid lupus erythematosus. Red,
erythema, telangiectasias, and mottled hyperpigmentation scaly plaques that evolve to irregular atrophic
within areas of scarring is highly characteristic. Follicular hypopigmented or hyperpigmented plaques. Scales fill
plugging and epidermal atrophy occur (Figs. 24.21 and dilated hair follicles and form “carpet tack scale.”
BOX 24.17 Classic Lichen Planopilaris
• Adult women
• Lesions show a centrifugal pattern centered on the
vertex, but can occur all over the scalp
• Spinous, hyperkeratotic, follicular papules with
perifollicular erythema
• Smooth, atrophic, polygonal-shaped patches of alopecia
with activity at the margins of the lesions that are
spreading outward; leaving central scarring behind is
typical
• Lichenoid dermatitis at the dermoepidermal junction
• Concentric lamellar fibrosis around follicles in
advanced lesions
• Immunofluorescence is positive in 50% of patients;
highlights cytoid bodies with IgG, IgA, IgM, or C3
• Differential diagnosis – lupus erythematosus,
FIG 24.22 ■ Discoid lupus erythematosus. Lesions pseudopelade, and folliculitis decalvans
eventually form smooth atrophic scars as seen in the • Treat with clobetasol propionate topical steroid
• Intralesional triamcinolone acetonide suspension
middle of this lesion.
10 mg/mL for active lesions
• Oral agent: tetracycline20
• Other oral agents – corticosteroids, long-term
hydroxychloroquine sulfate, tetracycline, azathioprine,
and cyclosporine
involved. Large areas of the scalp may be involved. Lesions

are most active at the expanding border. LPP is more
active at the periphery of the plaque than is discoid lupus
erythematosus. Other skin and mucosal lesions of lichen
planus may be present. Patients complain of pain, stinging,
or burning in active areas.
Histologic verification is required for diagnosis. Biopsy
of early lesions shows lichenoid interface inflammation
involving only the follicles and the perifollicular dermis.
Immunofluorescence in active stages shows cytoid body
FIG 24.23 ■ Patchy hair loss in lichen planopilaris. staining by anti-IgM and anti-IgA.
Note loss of follicular ostia in central bare areas and LPP is difficult to treat. Superpotent topical steroids,
perifollicular scale and perifollicular erythema at intralesional steroids, and short courses of oral steroids
periphery of patches. (From Chiang C, Sah D, Cho BK, are common first-line treatments. Doxycycline and tet-
et al. Hydroxychloroquine and lichen planopilaris: efficacy racycline20 have been tried for their antiinflammatory
and introduction of Lichen Planopilaris Activity Index effects. Hydroxychloroquine,21 isotretinoin, dapsone,
scoring system. J Am Acad Dermatol thalidomide, and cyclosporine have all been tried.
2010;62(3):387–92.21) Mycophenolate mofetil was effective in 83% of patients
(10 of 12) who had failed multiple prior treatments includ-
ing hydroxychloroquine and cyclosporine.22
24.22). With time, plugged follicles disappear, and the
skin becomes smooth, atrophic, and scarred. Biopsy of Lichen Planopilaris With Frontal
early lesions shows follicular inflammatory changes; late Sclerosing Alopecia
lesions show scarring in the reticular dermis. Treat-
ment includes intralesional steroids and antimalarials Frontal fibrosing alopecia (FFA) is felt to be a variant of
(hydroxychloroquine). LPP (Figs. 24.24 to 24.27). Postmenopausal women present
with a scarring process that develops on the frontal hairline
and then gradually extends backward. Eyebrow loss and
Lichen Planopilaris
hair loss in other body sites, especially the upper limbs,
Follicular lichen planus of the scalp (LPP) (Fig. 24.23) is may also occur.23 All patients had frontotemporal involve-
more common in women. There are several clinical ment, with follicular hyperkeratosis, scarring, and variable
presentations (Box 24.17). Typical lesions present with perifollicular erythema. The advancing edge of the area
erythema and perifollicular scaling or as scattered foci of of alopecia may demonstrate minute perifollicular papules
partial hair loss. It may be insidious or fulminate. The at the bases of terminal hairs. Biopsy findings are those
frontal–central scalp and crown are most commonly of LPP. The prognosis for recovery is poor.
24 Hair Diseases 955.e1
FIG 24.26 ■ Frontal fibrosing alopecia. Perifollicular FIG 24.27 ■ Frontal fibrosing alopecia showing
erythema is absent with perifollicular depression being perifollicular erythema and recession along frontal
marked. (From MacDonald A, Clark C, Holmes S. Frontal hairline. Note presence of freckles on lower chronically
fibrosing alopecia: a review of 60 cases. J Am Acad sun-exposed forehead. (From Chiang C, Sah D, Cho BK,
Dermatol 2012;67(5):955–61.28) et al. Hydroxychloroquine and lichen planopilaris: efficacy
and introduction of Lichen Planopilaris Activity Index
scoring system. J Am Acad Dermatol 2010;62(3):
387–92.21)
FIG 24.24 ■ Frontal sclerosing alopecia. Degree of

inflammation along hairline is variable. Perifollicular
erythema is evident. (From MacDonald A, Clark C,
Holmes S. Frontal fibrosing alopecia: a review of 60 cases.
J Am Acad Dermatol 2012;67(5):955–61.28)
BOX 24.18 Classic Pseudopelade of Brocq

(Nonspecific Cicatricial Alopecia)
• A noninflammatory, progressive scarring alopecia of A

unknown origin
• Original patch is usually on the crown
• Occurs primarily in young to middle-aged women
• Lesions are round or oval; several may coalesce to form
irregular, bald, slightly depressed patches
• No areas of folliculitis; hairs at periphery are easily
extracted
• Patches spread slowly over decades or progression is rapid
• May become bald in a few years
• Biopsy hair-bearing skin at the edge of a scarred plaque
• Lymphocytic infiltrates occur around follicular
infundibulum and mid follicles in early lesions
• Differential diagnosis – lupus erythematosus, lichen
planopilaris, folliculitis decalvans, follicular
degeneration syndrome; may have originated as these
diseases but with time have burned out and lost their
diagnostic clinical and histologic features B
• Treatment resistant to topical steroids, 5% minoxidil,
intradermal steroids; oral medications usually FIG 24.25 ■ A–B, Frontal fibrosing alopecia showing
ineffective perifollicular erythema and recession along the frontal
and temporal hairline.
Pseudopelade
Pseudopelade (Fig. 24.28) is an archaic term that designates 24.19, Figs. 24.29 and 24.30). Late-stage lesions show
a rare, slowly progressive cicatricial alopecia without wide areas of scarring with active pustular lesions at the
clinically evident folliculitis (Box 24.18). The disease margins. The etiology is unknown. Chronic bacterial fol-
process spreads centrifugally from the crown. It does not liculitis or altered host immune responses are proposed
describe any one disease entity but may represent the end mechanisms. Staphylococcus aureus may be cultured from
stage of various forms of scarring alopecia. Pseudopelade pustular lesions. Biopsy specimens of early lesions show
of Brocq was a term originally used to describe white follicular neutrophilic abscesses in the infundibula or upper
adult males with asymptomatic, irregularly shaped, widely or middle levels of the follicle. Late lesions show dermal
distributed clusters of hairless patches that are at times lymphocytes, destruction of follicles, and dermal scarring.
atrophic. Periods of disease progression are followed by Systemic and topical antibiotics (mupirocin) and daily
dormant periods. bactericidal antibiotic treatment of the nasal vestibules
to eliminate the carrier state of Staphylococcus may help.
One, two, or three 10-week courses of a combination of
Folliculitis Decalvans
300 mg of rifampicin and 300 mg of clindamycin twice
Folliculitis decalvans is a chronic pustular eruption of daily for 10 weeks arrested the disease. Dapsone 100 mg
the scalp resulting in patchy permanent alopecia (Box per day was effective. Some patients have areas of tufted
FIG 24.28 ■ Pseudopelade. Asymptomatic, skin-colored

bald area is present over the parietal scalp. Lesion
coalesced to form irregular, atrophic bald patches with
a “footprints in the snow” appearance. Atrophy rather
than scarring is present.
FIG 24.30 ■ Folliculitis decalvans. Chronic folliculitis

leads to progressive scarring.
BOX 24.19 Folliculitis Decalvans
• Occurs in adults and runs a very long course

• Crops of pustules surround multiple expanding oval
areas of alopecia
• Episodes of folliculitis can occur for years, causing
tufted folliculitis in some cases
• Sometimes found in beard, pubic and axillary areas,
inner thighs
• Initial neutrophilic infiltration
• Moderate perifollicular dermal fibrosis
• Differential diagnosis – bacteria, fungal, or viral
folliculitis; follicular degeneration syndrome; and acne
necrotica
• Treatment – culture pustules; povidone–iodine
shampoo, topical antibiotics (Cleocin or mupirocin);
topical steroids sometimes effective; oral antibiotics:
tetracycline, minocycline, cephalosporins, ciprofloxacin;
rifampin with clindamycin, or sulfamethoxazole/
FIG 24.29 ■ Folliculitis decalvans. Well-defined irregular trimethoprim; oral corticosteroids
to oval atrophic plaques of alopecia with follicular
pustules at the advancing margins.
There may be little or no pain. The presence of hair

folliculitis (TF). Tufted hair folliculitis (a possible variant follicles appears to be essential for disease progression.
of folliculitis decalvans) is characterized by follicular fusion Eventually, dense dermal fibrosis, sinus tract formation,
in which multiple hair tufts emerge from a single dilated hypertrophic scarring, and permanent hair loss occur. The
follicular orifice. These two entities may form part of a “follicular occlusion triad” consists of dissecting folliculitis,
spectrum of a single disease. hidradenitis suppurativa, and acne conglobata. Isotretinoin
is sometimes effective. Adalimumab is reported to be
effective.24
Dissecting Cellulitis
This rare disease most often affects young black men (Box Acne Keloidalis
24.20 and Figs. 24.31 and 24.32). Multiple inflammatory
nodules are concentrated on the crown, vertex, and occiput. Acne keloidalis usually affects young black men. Small,
They evolve into coalescing, boggy, fluctuant, oval, and follicular papules with occasional pustules occur on the
linear ridges that eventually discharge purulent material. occipital scalp and posterior neck (Box 24.21). They
BOX 24.20 Dissecting Cellulitis
• Young black men

• Presents as follicular rupture with abscess formation
• Painful fluctuant draining scalp nodules form extensive
interconnected abscesses with sinus tracts
• Scarring is extensive
• Part of the follicular occlusion triad (dissecting
folliculitis, acne conglobata, hidradenitis suppurativa)
• Neutrophilic, lymphohistiocytic, granulomatous
inflammation
• Fibrosis in dermis and in subcutis
• Differential diagnosis – folliculitis decalvans, acne
keloid, fungal kerion
• Treatment – early cases: tetracycline, doxycycline,
minocycline, cephalosporins, ciprofloxacin; advanced
cases: isotretinoin, oral corticosteroids, dapsone;
drainage of large abscesses
BOX 24.21 Acne Keloid (Acne Keloidalis

Nuchae)
• Young black men on the occipital scalp and neck; much

less common in white men FIG 24.32 ■ Dissecting cellulitis. End stage is extensive
• Presents as follicular papules or pustules progressing thick scarring alopecia.
to fibrosis papules and extensive keloidal plaques that
lack hair
• Inflammation is initially neutrophilic
• Differential diagnosis – folliculitis decalvans; acne
necrotica; dissecting folliculitis; bacterial, fungal, or
viral folliculitis
• Treatment – povidone–iodine shampoo, topical
antibiotics (clindamycin, mupirocin); oral antibiotics
(doxycycline, minocycline, cephalexin,
sulfamethoxazole/trimethoprim); many weeks of
suppression with oral antibiotics may be necessary;
topical and intralesional steroids may help; excisional
surgery may be necessary in advanced cases
FIG 24.33 ■ Acne keloidalis. Follicular papules and

pustules are concentrated on the back of the scalp
above the hairline.
FIG 24.31 ■ Dissecting cellulitis. Superficial and deep FIG 24.34 ■ Acne keloidalis. Follicular papules and
intercommunicating abscesses and widespread pustules without scarring are present in the early
scarring alopecia. stages of this process.
FIG 24.36 ■ Tufted folliculitis. Initial inflammatory

folliculitis stage may be any one of several scarring
alopecia variants (folliculitis decalvans, acne keloidalis,
common staphylococcal folliculitis, and dissecting
FIG 24.35 ■ Acne keloidalis. End-stage disease with cellulitis) that leads to tufts of hairs emerging from the
large, firm keloidal papules confined to the nape. same ostium. End-stage disease with several hairs
(tufts) emerging from the same ostium.
BOX 24.22 Tufted Folliculitis

Tufting of hair is caused by clustering of adjacent
• A number of hairs emerging from a single follicular
orifice may be seen in any scarring folliculitis; this is
follicular units attributable to a fibrosing process
called tufted folliculitis and to retention of telogen hairs within the involved
• A total of 3 to 10 hairs arise from a giant follicle follicular units.
• Controversial whether tufted folliculitis is an entity or
is secondary to other forms of scarring alopecia (lichen Acne Necrotica
planopilaris, discoid lupus erythematosus, folliculitis
decalvans) Acne necrotica is a severe form of scalp folliculitis. Papules
• Follicular rupture and abscess formation and pustules evolve to form crusts leaving depressed scars
• Fibrosis around upper and mid follicles (Fig. 24.37). Acne necrotica may also appear on the face.
• Neutrophils present around upper follicles
• Differential diagnosis – discoid lupus erythematosus,
lichen planopilaris, pseudopelade, folliculitis decalvans, Erosive Pustular Dermatosis
dissecting folliculitis, syndrome de Lassueur–Graham–
Little, follicular degeneration syndrome Erosive pustular dermatosis is a disease of unknown origin
• Treatment – same as that for folliculitis decalvans that occurs in the elderly and often in actinically damaged
scalp skin. Lesions may follow trauma or destructive
procedures for actinic keratoses. Patients present with
red, pustular, crusted, and eroded plaques on the scalp (Fig.
24.38). Removal of crusts reveals purulent material. The
coalesce into firm papules and become thick and elevated lesions progress slowly and heal with scarring alopecia.
(Figs. 24.33 to 24.35). Abscesses and sinuses with pus may Then adjacent areas become affected. Biopsy shows patchy
develop. There may not be any symptoms, or there may or diffuse inflammatory infiltrates with lymphocytes and
be mild burning or itching. Histologically, there is inflam- plasma cells in the dermis.25 Potent topical steroids, topical
mation, fibroplasia, and disappearance of sebaceous glands. tacrolimus ointment, calcipotriol (calcipotriene) cream,
Treatment is discussed on p. 354. isotretinoin (0.75 mg/kg/day), acitretin, and topical 5%
dapsone gel (for months)26 are some of the reported
Tufted Folliculitis. Tufted folliculitis (TF) may not be treatments.27
a specific disease but an end stage of other diseases such
as folliculitis decalvans or acne keloidalis (Box 24.22 and
Fig. 24.36). Patients present with an inflamed scalp with TRICHOMYCOSIS
pustules from which S. aureus can be cultured. It leads
to patches of scarring alopecia within which multiple Trichomycosis is an asymptomatic infection of axillary or
hair tufts emerge from dilated follicular orifices. Tufted pubic hair caused by Corynebacterium. The hair shaft
folliculitis can be differentiated from folliculitis decalvans becomes coated with adherent yellow (occasionally red
only by finding several hair tufts scattered within patches or black), firm concretions (Fig. 24.39). Hyperhidrosis is
of scarring alopecia. often present. The hair is shaved, and hyperhidrosis is
A B
FIG 24.37 ■ Acne necrotica miliaris. A–B, The patient was treated with minocycline and topical clobetosol.
FIG 24.38 ■ Erosive pustular dermatosis. Diffuse FIG 24.39 ■ Trichomycosis axillaris. Yellow concretions
crusting associated with multiple pustular, exudative, are adherent to the axillary hair. These concretions are
and erosive lesions. The pustular lesions progressively composed of a mass of diphtheroid organisms and not
merge. fungi.
Bonus Ebook Content controlled with antiperspirants. Naftifine hydrochloride

1% cream (Naftin) is effective for superficial fungal
Fig 24.26 Frontal fibrosing alopecia.
infections and also has antibacterial properties. It is report-
Fig 24.27 Frontal fibrosing alopecia showing edly effective for trichomycosis.
perifollicular erythema and recession along frontal
hairline. Please see ExpertConsult.com for references and additional online
content.
24 Hair Diseases 960.e1
17. Luggen P, Hunziker T. High-dose intravenous

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Hair Diseases: Anatomy

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Hair Diseases: Anatomy

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C H A P T E R 2 4

ANATOMY Female Pattern Hair Loss (Androgenic

infundibulum extends from the surface to the sebaceous

FIG 24.2 ■ Hair bulb. The outer and

Stage 1 FIG 24.3 ■ Stages 1, 3, 6, and 8

Hair Growth Cycle

BOX 24.1 Systematic Approach to Evaluation

Telogen History Diagnostic procedures

begins. The outer root sheath degenerates and retracts

Telogen (Rest). All activity ceases and the structure rests

TABLE 24.1 A Simplified Tool for the Diagnosis of Alopecia

EVALUATION OF HAIR LOSS

“My hair is falling out in large amounts”

“I am going bald” Androgenetic

1. Gradual diffuse thinning

Acute telogen effluvium Chronic telogen effluvium History and PE

Pull test (20–40 hairs) Scalp biopsy Total testosterone

BOX 24.2 Hair Loss

by its long fluctuating course and from androgenetic

BOX 24.3 Drugs Probably Associated With

Microscopic examination shows anagen hair without

TABLE 24.3 Short Anagen Syndrome vs Loose Anagen Syndrome

IIa III V VII

FIG 24.8 ■ Hamilton classification of male pattern baldness.

TABLE 24.4 Reported Symptoms of Post-Finasteride Syndrome

HDL, high density lipoprotein.

alopecia. Women with increased androgens may benefit

Chronic, progressive, diffuse hair loss in women in their

TABLE 24.5 Laboratory Values for Evaluation of Diffuse Female Alopecia

FEMALE PATTERN – ALOPECIA

and ethnicity are important factors. Asian women have

psychologic therapy may require 6 to 24 months. Women

PHYSICAL EXAMINATION • Exclusion of related disorders

POLYCYSTIC OVARY SYNDROME

Risk assessment Risk assessment Fasting cholesterol, Risk assessment

Endometrial Oral glucose- Polysomnography

FIG 24.11 ■ Polycystic ovary syndrome. HDL, high-density lipoproteins;

is rare. It may cause diuresis, postural hypotension, and

FIG 24.13 ■ Ophiasis pattern of alopecia areata. Presents

regrowth in cases with limited involvement is excellent.

Differential Diagnosis. The differential diagnosis

Etiology. The etiology is unknown. Genetic factors

Immunologic Factors. AA may be an autoimmune disease

Pathology. A peribulbar lymphocytic infiltrate (“swarm

PATIENTS <10 YEARS OF AGE >50% of scalp affected

*Anthralin is left on the scalp for 20 to 60 minutes.

TREATMENT FOR ALOPECIA INVOLVING THE SCALP

Scalp Alopecia Areata

10 yr old 10 yr old

Topical midpotent 50% scalp 50% scalp

or ILCS ± 5% minoxidil Topical

Good Poor Good Partial Poor

Continue PRN 1% Anthralin Continue PRN Add ILCS to Combination of

BOX 24.10 Suggested Methods of Treatment for Alopecia Areata

INTRALESIONAL GLUCOCORTICOID apply 2% solution of selected contact allergen in acetone

FIG 24.18 ■ Trichotillomania. Extraction of the eyelashes

BOX 24.11 DSM-5 Diagnostic Criteria for

1. Hair loss resulting from recurrent pulling out one’s

American Psychiatric Association. Diagnostic and statistical manual

Chronic Cutaneous Lupus Erythematosus

BOX 24.17 Classic Lichen Planopilaris

involved. Large areas of the scalp may be involved. Lesions

FIG 24.24 ■ Frontal sclerosing alopecia. Degree of

10 yr old 10 yr old

Topical midpotent 50% scalp 50% scalp