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A. Miceli and K. Krishnamurthy
331© Springer International Publishing AG 2018
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-319-68379-9_20
Introduction
Alopecia (or hair loss) includes a group of disorders in which
there is an absence of hair where it is usually present. More
than 35 million men and 21 million women in the USA expe-
rience hair loss. The incidence is highest in Caucasians, fol-
lowed by Asians, African Americans, and Native Americans.
Though a common problem, hair loss can cause a consider-
able amount of emotional and social stress to patients.
Moreover, it presents a challenge for practitioners, as there
are multiple etiologies with similar clinical presentations.
A good understanding of the normal hair life cycle is
important when approaching alopecias. There are three main
phases of the hair follicle cycle: anagen (active growth), cata-
gen (regression), and telogen (rest). Approximately 85–90%
of hair follicles are in the anagen phase, while 10–15% are in
the telogen phase, and less than 1% in the catagen phase.
There are approximately 100,000 hair follicles on the scalp,
and, on average, 50–100 hairs are normally lost every day [1].
Chapter 20
Hair Loss
Alyssa Miceli and Karthik Krishnamurthy
A. Miceli, DO • K. Krishnamurthy, DO, FAOCD, FAAD (*)
Department of Dermatology, Orange Park Medical Center,
906 Park Avenue, Orange Park, FL, USA
e-mail: Alyssa.miceli@gmail.com; kkderm@gmail.com
332
Hair loss becomes a clinical problem when there are localized
patches of hair loss or when the number of hairs lost daily
exceeds the normal amount. The alopecias are divided into
two main categories: scarring (or cicatricial) and non-scarring
(or non- cicatricial) alopecias (Fig. 20.1). Female and male
pattern hair loss, or what most people refer to as “balding,” is
the most common type of hair loss. Other causes of hair loss
include autoimmune conditions, underlying systemic prob-
lems like thyroid disease and iron deficiency, infections of the
scalp, inflammatory processes, and habitual practices.
Regardless of the underlying cause, both physical and psy-
chological stress can exacerbate any form of hair loss.
Decision-Making/Differential Diagnosis
The first step to assessing hair loss is to determine whether a
scarring or non-scarring process is occurring. Generally
speaking, scarring alopecia includes forms of alopecia where
the hair follicles are permanently lost. Some alopecias,
including alopecia areata, androgenetic alopecia, and traction
alopecia, may demonstrate a non-scarring process early in the
disease course and permanent hair loss in later stages.
Non-scarring Alopecias
Pattern (Androgenetic)
Androgenetic Alopecia. Androgenetic alopecia represents the
most common subtype of the non-scarring alopecias and in
fact is the most common cause of hair loss overall. It can
begin any time after puberty, when androgens begin to be
synthesized [2, 3].
Features:
• Gradual thinning without noticeable shedding.
• Strong genetic disposition, with a high concordance
amongst monozygotic twins.
A. Miceli and K. Krishnamurthy
333
Alopecia
Non-Scarring
(Non-cicatricial)
Scarring
(Cicatricial)
Focal Diffuse
Telogen
Effluvium
Anagen
Effluvium
Female Pattern
Hair Loss (FPHL)
Female Pattern
Hair Loss (MPHL)
Lymphocytic
Disoid Lupus Dissecting
Cellulitis
CCCA
Neutrophilic Mixed
Pattern
(Androgenetic)
Alopecia
Areata
Traction Trichotillomania
Acne
Keloidalis
Fig. 20.1 Hair loss algorithm
20. Hair Loss
334
• Male pattern hair loss: symmetric and progressive, typi-
cally affecting the frontoparietal area with frontal reces-
sion as well as vertex thinning.
• Female pattern hair loss: diffuse central thinning of the
crown with preservation of the frontal hairline. A
“Christmas tree” pattern results with widening of the cen-
tral part width.
Focal Hair Loss
Alopecia Areata. This is usually a hair-specific autoimmune
phenomenon in which T-cells interact with follicular antigens.
Alopecia areata can be associated with other autoimmune
diseases, including Hashimoto’s thyroiditis, vitiligo, inflam-
matory bowel disease, and type I diabetes [4].
Characterized by:
• Discrete circular patches of hair loss.
• Loss of all scalp hair (alopecia totalis) or all scalp and
body hair (alopecia universalis) can occur.
• Ophiasis pattern: band-like pattern of hair loss that
occurs along the periphery of the temporal and occipital
scalp.
Traction Alopecia. Occurs due to physical stress on the
hair follicle secondary to tight hairstyles, including ponytails,
braids, and hair weaves:
• Occurs along the outer hairline, typically in the frontal and
temporal areas
• Mostly affects African Americans
Trichotillomania. Can have various presentations, but
there will be rough, irregular patches of hair loss with broken
or twisted hairs on closer examination. It is a result of inten-
tional pulling of hair from the scalp [1]:
• Often begins in childhood.
• More common in females than males.
A. Miceli and K. Krishnamurthy
335
• Patients may pull hairs out from other hair-bearing areas
such as the eyebrows, eyelashes, face, extremities, and
pubic area.
Diffuse Hair Loss
Telogen Effluvium. Patients experience excessive hair shed-
ding over the entire scalp:
• Often preceded by a physical or emotional stressor
approximately 3 months prior to the start of the hair loss.
• Causes include: severe infections, postsurgical, postpar-
tum, hypothyroidism, anemia, malnutrition, and drugs
(especially beta-blockers) [5].
• In many instances, a discernable precipitating cause can-
not be found.
Anagen Effluvium. Abrupt and striking loss of hair (90%
of hairs are in anagen phase):
• It typically is caused by chemotherapy.
• Occurs within days to weeks of initiation, and is entirely
reversible.
• Hair regrowth typically occurs after a delay of 3–6 months.
Scarring Alopecia
Generally refers to all forms of alopecia in which there is
permanent loss of hair follicles. Clinically, one will observe a
smooth scalp with absence of follicular ostia and replacement
with scar tissue. Patients may experience symptoms, including
pain, itching, erythema, and burning sensations. This occurs as
a result of continued inflammation that targets the follicle.
Histopathologic correlation is often needed. As such, the
classification scheme is typically divided into the type of
inflammatory infiltrate involved: lymphocytic, neutrophilic,
or mixed [6].
20. Hair Loss
336
Lymphocytic
Central centrifugal cicatricial alopecia (CCCA):
• A chronic, progressive disease that is centered on the
crown or vertex.
• Expands peripherally in a symmetric fashion.
• It is found almost exclusively in African Americans.
Discoid lupus erythematosus. A form of cutaneous lupus
erythematosus that occurs most commonly on the face, ears,
and scalp:
• Discoid lesions usually demonstrate erythema, epidermal
atrophy, and dilated, plugged follicular ostia.
• Central hypopigmentation with peripheral hyperpigmen-
tation is evident in dark-skinned individuals.
• Patients typically do not have systemic disease.
Mixed Neutrophilic and Lymphocytic
Acne keloidalis
• Presents with small, firm papules and pustules on the
occipital scalp and posterior neck.
• Usually affects young African American men and occa-
sionally women and rarely will be seen in Caucasians.
• Often seen in conjunction with CCCA, but the cause
remains uncertain.
Neutrophilic
Dissecting cellulitis. Involves multiple, firm scalp nodules
most often on the mid-posterior vertex and upper occiput:
• A part of the “follicular occlusion triad.
1
”
1 Group of disorders in which the hair follicle becomes blocked with
keratin, including hidradenitis suppurativa, acne conglobata, and
dissecting cellulitis.
A. Miceli and K. Krishnamurthy
337
• It most often affects young adult black men.
• Over time, the nodules become boggy, fluctuant, and inter-
connected and will discharge purulent material.
Key History and Physical Exam
Various diagnostic tools can help differentiate types of alope-
cia. A detailed history and physical will point to the diagnosis
of most non-scarring and some scarring alopecias, though a
skin biopsy may be required.
History
• Description: duration (acute vs. chronic), location, degree
of hair loss, distribution (diffuse vs. patchy), symptoms
including pruritus, redness, pain, or infection
• Hair practices: tight ponytails, braids, weaves, use of “hot
combs,” chemical treatment
• Recent changes to medications; chemotherapeutic agents
• Medical problems: recent illnesses or surgeries, pregnancy,
thyroid disorder, iron deficiency, autoimmune disorders,
malnutrition
• Emotional or psychological stressors
• Family history
Physical Exam
1. Gross inspection of hair
(a) Generalized, patterned, or focal hair loss
(b) Density of hair, presence of broken hairs, vellus (thin,
downy premature hair) vs. terminal hairs (thick, strong
mature hair)
2. Inspection of scalp
(a) Absence of follicular ostia and scar tissue: scarring
alopecias
20. Hair Loss
338
(b) Papules, pustules, scaling, perifollicular erythema
3. Diagnostic Procedures:
(a) Hair Pull Test: Useful for Telogen Effluvium [1]
• Performed by grasping a small portion of hair and
gently applying traction while sliding the fingers
along the hair shafts.
– Normal: 1–2 hairs removed
– Abnormal: ≥6 hairs
(b) Direct microscopic inspections of hair shaft: [1]
• Exclamation point hairs: distal end broader than
proximal end; seen in alopecia areata
• Anagen hairs: elongated, distorted bulb with
attached outer root sheath
• Telog39en hair: club-shaped bulb
(c) “Hair growth window”: Useful for Trichotillomania
• Repeatedly (weekly) shaving a small area of
involved scalp to demonstrate normal regrowth
(d) Scalp biopsy: Useful for scarring alopecias [1]
4. Laboratory testing: Useful for androgenetic alopecia
(females particularly)
(a) Total and free testosterone and dehydroepiandros-
terone sulfate
Treatment (Table 20.1) [1–6]
General Measures
• Treat underlying medical problems: thyroid disorder, iron
deficiency.
• Discontinue any possible contributing medications, espe-
cially in telogen effluvium.
A. Miceli and K. Krishnamurthy
339
Table 20.1 Non-scarring alopecia treatment
Androgenetic
alopecia
• Minoxidil 5% topical solution (1 mL BID)
• Finasteride 1 mg/day × at least
3 months (with oral contraceptives)
• Spironolactone 100–200 mg/day
• Surgical hair transplant
Alopecia areata • Intralesional steroid 2.5–5 mg/mL
(0.5–1 cm intervals)
• Topical clobetasol propionate 0.05%
ointment, desoximetasone 0.25% cream,
or betamethasone valerate foam BID
• Diphencyprone (DCP) and squaric acid
dibutyl ester (SADBE): (0.001% for
2 weeks and gradually increase weekly
over time (0.01%, 0.1%, 0.2%, 0.5%,
1% and 2%))
• Topical minoxidil
• Topical anthralin
• Systemic corticosteroids (for totalis
or universalis): 40 mg triamcinolone
IM monthly or daily oral prednisone
tapered over 6–8 weeks
Trichotillomania • Behavioral modification therapy, hypnosis,
insight-oriented therapy
• Clomipramine 25 mg daily, gradually
increase to 100 mg/day (divided with
meals) over 2 weeks.
Telogen effluvium • Treat underlying thyroid or iron deficiency
• Reassurance
Scarring alopecia treatment
Discoid lupus
erythematosus
Oral hydroxychloroquine
Topical, oral, or intralesional
corticosteroids
(continued)
20. Hair Loss