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Hair Loss and its Management in Children

Vibhu Mendiratta, Masarat Jabeen

Expert Rev Dermatol. 2011;6(6):581-590.

Abstract and Introduction


Hair loss in children can cause psychological stress to the parent and patient alike. Alopecia can be
classified into congenital and acquired. Commonly encountered causes of pediatric alopecia (tinea
capitis, alopecia areata, traction alopecia and trichotillomania) are reversible if diagnosed early. Special
note should be made of the extent and type of alopecia (scarring or nonscarring), any hair shaft
anomalies and signs of inflammation. Diagnostic evaluation includes a bewildering array of age-old
simple bedside tests (e.g., potassium hydroxide preparation) to state-of-the art accurate instruments
(e.g., trichoscan). Systemic antifungal therapy is required for tinea capitis. Topical and systemic
immunomodulators are currently being employed for treating alopecia areata. A holistic approach would
include not just therapeutic intervention but also an active search for associated nutritional deficits,
underlying psychosocial disturbances and behavioral problems, the latter two requiring counseling and
behavior therapy. Children with permanent hair loss can be offered surgical hair transplantation or
camouflage devices, such as wigs.

Though losing hair is not usually health threatening, it can scar a young child's vulnerable self esteem by
causing immense psychological and emotional stress; not just to the patient, but also to the concerned
parents and siblings. Thus, management of hair disorders can be quite a daunting task for the attending
physician and mandates a holistic approach to the patient. Nevertheless, an organized diagnostic and
management strategy can turn this challenging task into an interesting and fruitful exercise.
To fully understand hair loss in childhood, a basic knowledge of normal hair growth is necessary. The
normal hair cycle is divided into four phases: the active growth anagen phase, followed by a brief
catagen phase, the resting telogen phase and finally the shedding exogen phase. [1] Typically, 8595% of
hairs are in the anagen phase, which lasts approximately 3 years. Less than 1% of hairs are in catagen,
the transitional phase, which lasts from a few days to weeks. The telogen phase (which accounts for 5
15% of hairs and lasts about 3 months) ends when the new anagen hair emerges from the follicle.
For the classification of pathological hair loss in children, two major groups should be differentiated:
congenital and acquired hair loss.[2,3] This distinction is the first step in diagnosis ( & Figure 1).
Pathological hair loss, although rare in the first year of life, may be a symptom of an underlying
congenital syndrome or clue to an underlying metabolic disorder which may have a bearing on the
mental and physical development of a child.[46]
Box 1. Age-wise distribution of common causes of alopecia.



Congenital aplasia cutis

Alopecia areata

Occipital alopecia

School going

Tinea capitis

Alopecia areata


Telogen effluvium

Traction alopecia


Telogen effluvium

Alopecia areata

Androgenetic alopecia

Hair cosmetic-induced alopecia

Triangular alopecia

Figure 1.

Approach to common causes of pediatric alopecia.

Hair loss on the scalp can also be classified as focal or diffuse (). Focal hair loss is secondary to an
underlying disorder that may cause nonscarring or scarring alopecia. [3]
Box 2. Classification of pediatric alopecia.

Diffuse alopecia

Isolated hair shaft anomalies presenting with hair breakage (in some cases with
associated defects):

Trichorrhexis nodosa



Pili torti

Genetic syndromes with hair shaft anomalies:


Netherton's syndrome

Menkes syndrome


Ectodermal dysplasia


Congenital hypotrichosis and atrichia with papular lesions (can be associated with

Production decline:

Patterned hair loss

Alopecia due to abnormal hair cycling:


Anagen loss:

Anagen effluvium

Loose anagen syndrome

Telogen loss:

Telogen effluvium

Focal alopecia



Aplasia cutis

Nevoid condition

Syndromic associations

Folliculitis decalvans


Postinfections (e.g., kerion)


Alopecia areata

Tinea capitis

Traction alopecia


DLE: Discoid lupus erythematosus; LPP: Lichen planopilaris.

Patient's personal and family history, a thorough clinical examination, as well as general and specific
diagnostic procedures aid in correct diagnosis and early treatment. [3]
The key points in a patient's history are:

Age of onset of the patient: congenital or acquired;

Onset of hair loss: sudden or insidious;

Extent of alopecia: localized or diffuse;

Subsequent development of the disease and associated symptoms;

Physical and mental development (may be affected as a part of a genotrichosis);

Psychological problems of the child;

Obvious physical or emotional triggers in the previous 25 months, and any accompanying
complaints (e.g., fatigue, weight changes, and nail or skin abnormalities);

Past medical history including chronic illnesses, surgeries, medication, autoimmune,

dermatologic and psychiatric disorders (e.g., anxiety and obsessivecompulsive tendencies);

Family history of alopecia, autoimmune disease, dermatologic or psychiatric disorders;

Hair grooming practices (chemicals, tight braiding).

Examination should have the following components:

Sparsing of hair (hypotrichosis) or loss of hair (alopecia);

Thorough examination of scalp as well as the other hair-bearing areas of the body, especially
loss of axillary and pubic hair, eyelashes, eyebrows and body hair;

Type of alopecia: localized or diffuse, scarring or nonscarring;

Any hair shaft anomalies, hair quality, color, roughness and tendency to breakage, 'exclamationpoint' hairs;

Presence of erythema, edema, papules, pustules, scaling, atrophy, telangiectasias, follicular

hyperkeratosis, ulceration and scarring;

Hair pull test:


Approximately 20 hairs are grasped and firmly tugged away from the scalp;

The number of extracted hairs is counted;

>10% of grasped hairs or two hairs suggests positive pull test and active hair shedding.

The skin, nails, oral or genital mucous membranes (e.g., for evidence of associated dermatoses,
such as lichen planus);

Thorough clinical examination of the entire head and body is necessary in order to evaluate
impaired vision, defective hearing, dysmorphic features, clues to autoimmune or metabolic
diseases, or ectodermal anomalies.

Diagnostic Procedures
When tinea capitis is suspected:

Fungal culture by scraping the affected areas with a blunt scalpel, a sterile brush or moistened
gauze to gather affected hairs;

Woods lamp examination: as screening to detect flourescing species, such as Microsporum;

A potassium hydroxide preparation (to reveal hyphae): a scalp scraping or plucked hairs from
the affected area.

When alopecia areata is suspected:

Thyroid function

When telogen effluvium is suspected:

Hair pull test (already described);

If there is no obvious trigger of telogen effluvium tests include:


Sedimentation rate, complete blood count;

Serum ferritin;

Antinuclear antibody;

Thyroid function test;

Serology for syphilis.

When scarring alopecias are suspected:

4-mm punch scalp biopsy

When hereditary hair shaft disorders are suspected:

Serum biochemistry: for metabolic disorders;

To analyze hair structure:

Hair mount examination by light and polarizing microscopy;

Scanning or transmission electron microscopy, or both.

To analyze biochemical composition of affected hair.


Amino acid analysis by chromatography, spectroscopy (cysteine and sulfur content);

Keratin analysis.

Newer techniques:[714]

Videodermoscopy: the magnified images of hair follicle are useful for the differential diagnosis
between cicatricial and noncicatricial alopecia and between alopecia areata and trichotillomania;

Trichoscan: it is an automated software program for the accurate analysis of hair growth and
useful in monitoring the response to treatment;

Contrast-enhanced phototrichogram: a technique used to analyze hair growth activity using

photographic records and a scalp immersion proxigraphy method.

Frequent causes of alopecia encountered in general practice are discussed below.

Focal Noncicatricial Alopecia (Acquired)

Tinea Capitis

Tinea capitis is the commonest cause of patchy hair loss in children in the developing world owing to
poor socioeconomic conditions.[15] It is an infection of the scalp and associated hair, caused by
dermatophytes (generaTrichophyton and Microsporum except Trichophyton concenticum). The most
common cause is Trichophyton tonsuransin the USA and UK and Microsporum canis in the rest of the
world.[16,17] A clinician should be aware of its variable morphological presentations such as circular patches
of alopecia and marked scaling (grey patch type), black dots indicating broken hair (black dot type),
diffuse widespread scaling (seborrheic type), boggy nodules studded with pustules (kerion type) and
yellow crusts (scutula) that surround hair follicles with a peculiar musky odour (favus type caused
by Trichophyton schoenleinii).
Tinea capitis, once proven by culture or potassium hydroxide, requires systemic treatment. Flouroscence
by woods lamp is only displayed by a few species, so it is not a very sensitive tool in detection of tinea
capitis. Treatment is outlined in .[1821]
Table 1. Treatment options for tinea capitis.



The only oral US FDA approved treatment


Dose: 2025 mg/kg (micronized) or 15 mg/kg (ultramicronized) taken

with a fatty meal for 68 weeks


5 mg/kg/day in 68 weeks


6 mg/kg for 20 days or weekly pulse of 8 mg/kg for 816 weeks

Dose: 36 mg/kg for 48 weeks


A RCT comparison of 4 weeks of terbinafine with 8 weeks of griseofulvin

showed no statistically significant difference overall. However, a
subgroup of Trichophyton responded better to terbenafine
and Microsporum audouinii responded better to griseofulvin

Topical selenium
sulphide shampoo
Zinc pyrithone

Use by patients as well as all household members reduces transmission

Povidone Iodine
RCT: Randomized controlled trial.

Alopecia Areata

Alopecia areata (AA) is a chronic, organ-specific autoimmune disease, mediated by autoreactive T cells,
which affects hair follicles and sometimes the nails. Evidence of the autoimmune nature includes
reported associations between AA and other autoimmune disorders (e.g., Hashimoto thyroiditis) and,
histopathologically, the presence of lymphocytes around the hair bulb in a pattern resembling a swarm of
The characteristic lesion of AA is commonly an oval, totally bald, smooth patch involving the scalp or any
hair-bearing area on the body. A characteristic feature of an AA patch is 'exclamation-mark' hairs (broken,
short hairs that taper proximally) that may be present at its margin. The clinical presentation of AA is
subcategorized according to pattern or extent of the hair loss. It can be classified according to pattern as
classical patchy AA (most common), reticulated pattern of AA, ophiasis band like AA (hair loss in the
parietal temporo-occipital scalp) and sisaphio (a band of hair loss in the frontal parieto-temporal scalp).
If categorized according to extent of involvement, the following forms may be seen: alopecia areata
with partial loss of scalp hair; alopecia totalis (100% loss of scalp hair) and alopecia universalis (100%
loss of hair on the scalp and body).[22]
Indicators of a poor prognosis are the presence of other immune diseases, atopy, family history of AA,
young age at onset, nail dystrophy, extensive hair loss and ophiasis pattern. [23]
In the majority of patients, hair regrows entirely within 1 year without treatment. Because of the chance
for spontaneous resolution, it is often reasonable to do watchful waiting and reassurance initially. Should
the alopecia continue to worsen or persist, a therapy can be considered. It is helpful to get the patient
involved in a support group and/or counseling from the very first visit. The treatment of alopecia depends
on the extent of involvement and the age of the patient. In localized involvement, commonly used agents
include topical and intralesional corticosteroids, topical anthralin and minoxidil. In widespread
involvement, contact sensitization (e.g., diphenylcyclopropenone) and oral immunosuppressives are
usually resorted to.
Various treatment options are discussed in .[22,2552]
Table 2. Treatment options for alopecia areata.




Nonsystemic therapy
Easy to apply at home
Topical corticosteroids

Can be used for large


Poor data to support efficacy

Potential for skin atrophy

Intralesional corticosteroids

Can quickly regrow hair


Fairly reliable efficacy

Useful for only limited areas

Potential for skin atrophy

Multiple sittings required

Good evidence for
Contact sensitization (e.g., with
squaric acid)
Can be used for large

Good response in
majority cases

Topical irritants (e.g.,


Potential for itchy reaction

Not an approved medication
High relapse rate
Pruritus can be troublesome
Long response time
Pruritus can be troublesome


26% hair regrowth


Dermal irritation

Prostaglandin analogue
(latanoprost, bimatoprost)

Well tolerated

Poor results in RCTs



Variable results

Calcineurin inhibitors

Poor results
Easy to use

Laser (excimer, pulse infrared


Excellent results


No side effects reported

Fractional photothermolysis

Single case report

Complete regrowth
reported after multiple

Expensive option

Systemic therapy

Systemic corticosteroids

Can be used for large


Potential for serious adverse

High relapse rate
High relapse rate


Response rate >50%

Cumulative radiation exposure


Response rates >60%

Side effect profile


Relatively safe

Response rate <30%


Safe in pregnancy

Scanty data

Biologicals (alefacept,
adalimumab, etanercept,

Poor response
Side effect profile


Useful in widespread

Infrared irradiation

Some success reported

Few reports showed

development of alopecia areata
while on ciclosporin
Confirmatory larger RCTs

IVIG: Intravenous immunoglobulin; PUVA: Psoralen plus UVA; RCT: Randomized controlled trial.

Sometimes preferentially referred to as trichotillosis (as the suffix mania can connote insanity)
trichotillomania refers to compulsive habit or desire to pull out the hair.[5355] The clinical manifestation is
usually quite distinctive, with a confluence of twisted and broken off hairs within an otherwise normal area
of the scalp. Counselling, psychotropic drugs such as clomipramine or sertraline, N-acetyl cysteine and
behavior modification techniques (e.g., habit-reversal therapy) are effective treatment options. [5662] As
glutamatergic dysfunction has been implicated in the pathogenesis of obsessivecompulsive disorder; Nacetylcysteine, a glutamate modulator, is a novel therapeutic agent found to be effective in
Traction Alopecia

Traction alopecia is caused by prolonged traction of scalp hair by use of hair styles, such as tight braids
and high pony tails, among others. Though usually the alopecia is reversible, if the traction is continued
over years, mechanical damage to hair follicles may result in permanent hair loss. [63,64] Cessation of the
offending hair practice is the treatment.
Syphilitic Alopecia

It may be the first sign of syphilis and can present as typical motheaten alopecia, generalized thinning of
the hair or may mimic alopecia areata. A high index of suspicion is required to diagnose this entity,
especially in sexually active adolescents.[65]

Focal Cicatricial Alopecia (Acquired)

Cicatricial alopecia damages hair follicles without regrowth. Stem cell failure at the base of the follicles
inhibits follicular recovery from the telogen phase, thus leading to an irreversible loss of hair. Common
causes of acquired focal cicatricial alopecia in the pediatric population are discussed below.
Lichen Planopilaris

Although predominantly a disease of adults, children can rarely be affected. Clinical hallmarks of active
disease include perifollicular violaceous papules and follicular hyperkeratosis. Histopathology
demonstrates the diagnostic features of lichenoid interface alteration. Limited disease is managed with
topicalor intralesional steroids. For those with rapidly progressive or extensive lesions, steroids, retinoids
or antimalarials are considered.[6669]

Linear Scleroderma

Most often seen in the first decade of life, linear scleroderma can present on the frontal scalp extending
to the forehead (en coup de sabre) as a linear shiny plaque with binding down of skin. It may be
associated with underlying bony, eye and CNS defects and requires a complete radiological work up to
exclude associated abnormalities. Histopathology reveals increased collagen in dermis with reduced
pilosebaceous appendages. Early diagnosis is important to halt the active inflammatory phase by
instituting treatment in the form of immunomodulators, such as steroids and hydroxychloroquine. [70]

Focal Cicatricial Alopecia (Congenital)

Common causes of congenital focal cicatricial alopecia are discussed below.
Temporal (Congenital) Triangular Alopecia

It presents as well-circumscribed triangular or ovoid patch of alopecia that involves the temporal region.
Vellus hair is present in the affected area. There is no effective treatment.
Aplasia Cutis Congenita

Aplasia cutis congenita constitutes a group of disorders that present at birth with eroded areas in the
scalp or body with or without other developmental anomalies.[72,73] The scalp erosions are characterized
by absence of a part of skin which heals spontaneously over a period of time and manifests as a patch of
cicatricial alopecia.
Nevus Sebaceous

Nevus sebaceous of Jadassohn is a common clinical entity which belongs to the group of epidermal nevi,
usually manifesting early in life in the form of an orange, waxy hairless circumscribed plaque most
commonly localized on the head and neck area.[74] It may be part of epidermal nevus syndrome in
association with other development anomalies. Excision is recommended in view of potential to develop
cutaneous malignancies.
Keratosis Follicularis Spinulosa Decalvans

Inherited as X-linked disease, keratosis follicularis spinulosa decalvans is characterized by widespread

follicular hyperkeratosis followed by atrophy, cicatricial alopecia of the scalp and photophobia. Topical
and intra-lesional corticosteroids and oral retinoids have been used with usually unsatisfactory results. [75]

Diffuse Alopecia (Congenital)

Common causes of congenital diffuse alopecia are discussed below.
Congenital Hypotrichosis & Atrichia

Hereditary simple hypotrichosis is a rare group of familial nonscarring hypotrichosis and atrichias without
associated internal abnormalities. Most of them are inherited in an autosomal dominant pattern. [7678]
Woolly Hair Hypotrichosis

It is characterized by tightly coiled, markedly curly and short hair. It may be associated with eye and teeth
defects, deafness, palmoplantar keratoderma and cardiac abnormalies (Naxos disease).

Ectodermal Dysplasias

These genodermatoses are characterized by absent or inadequate development of one or more of the
epidermal appendages namely hair, sweat glands, sebaceous glands, nails and teeth.
Genetic Syndromes With Hair Shaft Anomalies

Netherton Syndrome Netherton syndrome is a severe, autosomal recessive form of ichthyosis

associated with mutations in the SPINK5 gene with characteristic hair microscopy showing typical nodes
resembling bamboo joints. Other features include erythroderma, ichthyosis linearis circumflexa, failure to
thrive and atopic state.[7982]
Menkes Kinky Hair Syndrome Menkes kinky hair syndrome is an X-linked recessive disorder of copper
metabolism, characterized by microcephaly, pale skin, silvery brittle scalp hair and progressive
neurological deterioration.[8388]
Trichothiodystrophy Trichothiodystrophy is characterized by trichorrhexis-nodosa like hair fractures due
to a defect in synthesis of high-sulfur proteins. It can present as brittle hair, intellectual impairment,
decreased fertility, short stature (BIDS), ichthyosis and BIDS or photosensitivity and ichthyosis and BIDS.
Polarized microscopy reveals a characteristic tiger-tail pattern. [89]
Isolated Hair Shaft Anomalies

Trichorrhexis Nodosa In light microscopy, trichorrhexis nodosa, shows hair fracture with individual
cortical cells and their fragment splaying-out resembles two brushes whose ends are pushed together. [90

Monilethirix Monilethirix is characterized by uniform elliptical nodes and intermittent constrictions

('internodes') along the hair shaft. Clinically it presents as scalp follicular keratosis and hypotrichosis. It
can rarely be associated with koilonychia, mental retardation or ectodermal defects. [93]
Pili Torti Pili torti consists of closely grouped twists of hair, occurring in groups of three to ten at irregular
intervals along the shaft.

Diffuse Alopecia (Acquired)

Common causes of acquired diffuse alopecia in the pediatric population are discussed below.
Alopecia Due to Abnormal Hair Cycling

Loose Anagen Syndrome Loose anagen syndrome is a disorder of anagen hair anchorage to the hair
follicle, characterized by the ability to easily and painlessly pull out large numbers of anagen hairs from
the scalp. Physical examination shows sparse growth of thin, fine hair and diffuse or patchy alopecia
without inflammation or scarring. Trichogram demonstrates 98100% of plucked hairs to be anagen
hairs. Light microscopy may reveal ruffling of the cuticle adjacent to the anagen bulb giving a 'floppy
sock' appearance. In most patients the condition improves spontaneously.[9496]
Telogen Effluvium

Telogen effluvium refers to an abnormality of the normal hair cycle leading to excessive loss of telogen
hair. Frequent triggers include physiologic effluvium of the newborn, febrile illnesses, catabolic illnesses,
such as malignancies, hypothyroidism, medications (e.g., retinoids and valproate), stress, surgery, caloric

or protein deprivation and chronic iron deficiency. Assuming there is no intervening pathological process,
the loss is usually replaced in 612 months. Treatment revolves around addressing the underlying cause.

Anagen Effluvium

Anagen effluvium is the abrupt loss of 8090% of hair, which occurs when the anagen phase is
interrupted. Radiotherapy to the head, systemic chemotherapy especially alkylating agents (e.g.,
cyclophosphamide) and exposure to toxic agents are usually the inciting events. These agents disrupt
the anagen cycle and cause varying degrees of hair follicle dystrophy. Replacement with a normal pelage
usually occurs rapidly after discontinuation of chemotherapy, but radiotherapy can cause permanent
scarring alopecia.[99103]

Decline in Hair Production

Androgenetic Alopecia

Androgenetic alopecia encompasses male pattern hair loss and female pattern hair loss and is identified
as the most frequent cause of hair loss in adolescents (male:female ratio of 2:1). It is usually due to
action of dihydrotestosterone on a genetically susceptible hair follicle leading to progressive hair
miniaturization. In adolescent girls the most common patterns of hair loss are centrifugal loss at the
crown and the frontal accentuation or 'christmas tree' pattern. In adolescent boys it commonly manifests
as bitemporal recession and thinning in the frontal and vertex. Although the pathogenesis remains
speculative, endocrine evaluation and a strict follow-up are recommended in prepubertal patients with
androgenetic alopecia. Topical minoxidil and finasteride (only in male patients) is effective. [102]

Expert Commentary
Diagnosing a given case of childhood alopecia is not just crucial for preventing irreversible hair loss, but
may also turn out to be the necessary clue to an otherwise unfathomable multisystem illness or an
explanation for an unexplained developmental delay. The most frequent causes of childhood alopecia
(tinea capitis, alopecia areata, traction alopecia and trichotillomania) are usually reversible if detected
early. The evaluation of a child with scalp hair loss should always include a detailed history, physical
examination and microscopic examination of the hair. A thorough examination of scalp, skin, mucosa,
teeth, nails and relevant systemic examination can be helpful in clinching accurate diagnosis. Newer
techniques, such as videodermoscopy, trichoscan and contrast-enhanced phototrichogram aid in solving
clinical dilemmas.
Congenital alopecia remains a largely neglected area with not many treatment options. There is a well
perceived need for hair clinics dedicated solely to the study of disorders causing hair loss. Newer
therapeutic armentatorium for alopecia areata, such as baxarotene, lasers (excimer, pulse infrared diode,
fractional photothermolysis) and infrared irradiation has been found to be useful while biologicals and
prostaglandin analogues (latanoprost, bimatoprost) has been found to be ineffective. N-acetylcysteine
has been found useful in trichotillomania. Counseling and support groups can be invaluable to reduce
psychological sequelae. Promising modalities for scarring alopecias are alginate gel implantation with
microencapsulation of hair follicle stem cell and dermal papilla cells.

Five-year View

Recent advances in epithelial stem cell biology have led to successful isolation of hair follicle stem cells,
which creates the opportunity to bioengineer hair follicles for the treatment of hair loss.
Utilizing effectiveness of alginate gel in cell implantation, microencapsulation of the hair follicle stem cells
and dermal papilla cells can be implanted into the bald scalp of the patient. As both follicle stem cells and
dermal papilla cells have strong proliferative capacity, the patient's own cells could be expanded
considerably in vitro.[103105] A genome-wide association study, which implicates T-cell and natural killer cell
activation pathways, has opened the window for new approaches in future clinical trials of alopecia
areata. Future treatment approaches for alopecia areata include use of drugs that block the NKGDactivating ligand and NKG2D receptor interaction, halt activated T cells, or modification of the
inflammatory cytokine network (e.g., anti-CD25, anti-CTLA-4, Jak 1/2 inhibitor, anti-NKG2D, Syk
Congenital alopecias remain a domain of orphan diseases with little to offer in terms of treatment except
camouflage and wigs. Research to refine knowledge of genes controlling the differentiation of hair
follicles is likely to develop treatment breakthroughs, such as gene therapy.

Key Issues

Acknowledging patients' concerns and having an empathetic approach to hair loss goes a long
way. Patients often appreciate a supportive diagnostic and therapeutic approach.

Although alopecia has myriad causes, a careful study of history, close attention to the
appearance of the hair loss and a few simple tests can quickly narrow the potential diagnoses.

Scarring alopecias, although rare, are considered true trichologic emergencies as hair loss can
be irreversible if prompt appropriate therapy is not instituted.

Focal alopecia is more likely to be acquired than diffuse alopecia.

Frequent causes of nonscarring focal alopecia are usually treatable (tinea capitis, alopecia
areata, traction alopecia and trichotillomania).

Evaluation of alopecia in infants should include recording of family history to exclude genetic
disorders and examination of teeth, nails, skeletal system and the eyes, along with a thorough
systemic examination.

Androgenetic alopecia can be the presenting sign of an underlying endocrine disorder in preadolescents.

Offering psychosocial support and nonpharmacologic techniques to help the child appear more
like their peers should be part of care.



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The authors have no relevant affiliations or financial involvement with any organization or entity with a
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No writing assistance was utilized in the production of this manuscript.
Expert Rev Dermatol. 2011;6(6):581-590. 2011 Expert Reviews Ltd.