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An Approach to Hair Loss in Pediatric Primary Care

      Abstract

      Pediatric hair loss is a cause of concern for patients and families. Early diagnosis and treatment are crucial, as delays in care for certain diagnoses can cause permanent scarring alopecia. The evaluation of hair loss includes a thorough history, physical examination, and other potential tests. The causes of hair loss can be classified as either acquired versus congenital. Acquired causes of hair loss can be subdivided into scarring and nonscarring; however, some conditions may present as nonscarring and progress to scarring alopecia. Recommendations for the evaluation and treatment of pediatric hair loss for the primary care practitioner will be summarized.

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      OBJECTIVES

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        To identify the physical findings of pediatric hair loss associated with underlying hair disorders.
      • 2.
        To classify hair disorders on the basis of presentation, outcomes, and associated risks, including, but not limited, to scarring.
      • 3.
        To illustrate findings on examination that warranted additional care by a dermatologist and suggested treatment recommendations.
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      INTRODUCTION

      Dermatologic concerns among the pediatric population account for up to 30% of pediatric outpatient visits (
      • Castelo-Soccio L.
      • McMahon P.
      Pediatric dermatology.
      ). In the United States, 3% of all pediatric primary care visits are for hair loss (
      • Chandrashekar B.S.
      IADVL textbook of trichology.
      ). Hair loss is alarming to parents and patients alike and may reflect a variety of etiologies. Depending on the presentation, the initial evaluation may warrant laboratory analysis for underlying pathology or infection, empirical treatment, or referral to pediatric dermatology. The shortage of pediatric dermatologists has increased wait times for evaluation which has been implicated in adverse outcomes (
      • Fogel A.
      • Teng J.
      A complex course: Referral paths to pediatric dermatology.
      ;
      • Vernacchio L.
      • Muto J.M.
      • Young G.
      • Risko W.
      Ambulatory subspecialty visits in a large pediatric primary care network.
      ). Poor outcomes are most notable in the setting of an inflammatory and terminal scarring process underlying the hair loss disorder, as these outcomes can be permanent (
      • Colavincenzo M.L.
      Practice and educational gaps in dermatology: Disorders of the hair.
      ) and impair patient quality of life (
      • Toussi A.
      • Barton V.R.
      • Le S.T.
      • Agbai O.N.
      • Kiuru M.
      Psychosocial and psychiatric comorbidities and health-related quality of life in alopecia areata: A systematic review.
      ). Recommendations for evaluation and treatment of pediatric hair loss for the primary care practitioner will be summarized.

      PHYSIOLOGY

      The normal hair cycle consists of three phases: anagen (growth), catagen (regression), and telogen (resting phase). Under normal circumstances, 85% of the scalp hair is in anagen and 15% is in the telogen phase (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). On the scalp, anagen persists for 2–6 years, catagen for 2–3 weeks, and the telogen phase for 3 months (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).
      In some instances, parents may be concerned about hair loss in their newborn; however, they should be reassured that this is normal physiology because of hair cycling. During the fetal stage, hair follicles on the scalp are all in the same phase. A few weeks after birth, synchronous cycling to the telogen stage results in uniform hair loss, which is followed by hair regrowth in an asynchronous pattern. This can lead to an area of brief, focal alopecia on the occiput at 8–12 weeks (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). This occipital neonatal alopecia is referred to as transient neonatal hair loss and is benign with spontaneous regrowth of hair (
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).

      PRIMARY EVALUATION

      The presentation of hair loss in a pediatric patient requires an evaluation of past medical, social, and family history. Medications may be a potential cause of iatrogenic hair loss, and those often implicated can be found in the Box. In addition, inquiry about family history of hair, nail, and teeth disorders may be useful as alopecia is implicated in ectodermal genetic conditions (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Hair products and styling practices have been implicated in hair loss. Evaluation of products used and styling of hair is useful in determining the cause of hair loss.
      Medications associated with hair loss
      Tabled 1
      Medications associated with hair loss
      AcitretinColchicine
      AmantadineHeavy metals
      AmiodaroneHormone therapy
      AnticoagulantsIsotretinoin
      AnticonvulsantsLithium
      CaptoprilPenicillamine
      Cholesterol-lowering agentsPropranolol
      Cimetidine
      Note. This list is not exhaustive, and any medications an individual is taking should be evaluated.
      Physical examination findings, specifically the extent, pattern, and distribution of hair loss, are all diagnostic clues in addition to examination of teeth and nails. The hair pull test is commonly used to evaluate hair loss disorders (Figure). The hair pull test should be performed at the advancing edges of discrete areas of hair loss (i.e., alopecia areata), or if there are no discernible foci of hair loss, it can be performed diffusely over the scalp (i.e., telogen effluvium) (
      • McDonald K.A.
      • Shelley A.J.
      • Colantonio S.
      • Beecker J.
      Hair pull test: Evidence-based update and revision of guidelines.
      ). Trichoscopy (dermatoscopy of the hair and scalp) is a noninvasive tool that allows for magnification of skin structures (
      • Mubki T.
      • Rudnicka L.
      • Olszewska M.
      • Shapiro J.
      Evaluation and diagnosis of the hair loss patient: Part II. Trichoscopic and laboratory evaluations.
      ).
      The causes of hair loss can be categorized as acquired or congenital. Acquired causes of hair loss can be subdivided into scarring and nonscarring; however, some conditions may present as nonscarring and progress to scarring alopecia. The common causes of hair loss are reviewed in Table 1. In addition, there are uncommon or rare causes of alopecia in children, as listed in Table 2. These are usually diagnosed in a dermatology clinic and, if suspected, should be referred.
      TABLE 1Common causes of hair loss
      DiagnosisScarringHair pull testCommon presentationTreatment
      Acne keloidalis nuchae+Violaceous firm papules over the nuchal/occipital scalp that coalesce to form larger keloidsAvoidance of exacerbating factors ± corticosteroids, antibiotics, retinoids, surgery
      Alopecia areata+Hair loss in a well-defined, smooth round patch (or patches) on the scalpTopical/intralesional corticosteroids + minoxidil, topical immunotherapy
      Alopecia totalis+Total hair loss on the scalpMinoxidil + topical immunotherapy
      Alopecia universalis+Total body hair lossMinoxidil + topical immunotherapy
      Androgenetic alopeciaMales: Hair thinning at the vertex and bitemporal hairline recession Females: Diffuse hair thinning from frontal scalp to vertex with sparing of the frontal hairlineMinoxidil ± finasteride, spironolactone, laser therapy
      Aplasia cutis congenita+Solitary scalp patch with scarring alopecia present at birthConservative treatment ± surgery
      Bacterial folliculitis+Small pustules around the hair follicle with associated inflammationSpontaneous resolution ± topical or oral antibiotics
      Kerion (subtype tinea capitis)+Painful plaque or nodule with pustules, crusting, malodor, and purulent drainageSystemic antifungal treatment + systemic corticosteroids
      Telogen effluvium+Abrupt onset of diffuse hair shedding that affects the entire scalpTreatment of the underlying cause
      Tinea capitis+Diffuse scaling of the scalp without hair changes or a patch of hair loss with associated scaling, erythema, and pruritisSystemic antifungal treatment
      Traction alopeciaLate presentationGradual hair loss at the hairline in a patchy or symmetrical patternEarly: Discontinuation of triggering hairstyle. Late: Corticosteroids, antibiotics, minoxidil
      TrichotillomaniaLate presentationIncomplete, ill-defined area of hair loss with regrown hair of various lengthsStress management + cognitive-behavioral therapy
      TABLE 2Uncommon causes of hair loss
      DiagnosisScarringHair pull testCommon presentationTreatment
      Congenital triangular alopeciaUnilateral region of hair loss in the frontotemporal region that is triangular in shapeNo treatment
      Discoid lupus erythematosus+Indurated, smooth, shiny, and dyspigmented plaques that may have an atrophic appearance and associated scaleCorticosteroids ± hydroxychloroquine
      Dissecting cellulitis of the scalp+Pustules and abscesses that progress to draining sinus tractsOral isotretinoin ± antibiotics and steroids
      Hypotrichosis simplexNormal hair at birth with gradual hair loss by age 10 years old and progression to near-total hair loss by age 20 years oldNo treatment
      Keratosis follicularis spinulosa decalvans+Infancy: Keratosis pilaris of the face

      Childhood: Scarring alopecia
      Oral etretinate and isotretinoin Ophthalmological evaluation
      Loose anagen hair syndrome+Easily pulled anagen hairs and hair incapable of growing longNo treatment
      Marie Unna hypotrichosisInfancy: Few or no body hair

      Childhood: Development of twisted, bristly hair that is later lost after puberty
      No treatment
      Papular atrichiaNormal hair at birth followed by hair loss then papule formationNo treatment
      Pseudopelade of Brocq+Slowly progressive hair loss characterized by focal areas of irregular alopecia on the scalpNo treatment
      Short anagen hair syndrome+Short, fine hair present from birth that does not require cuttingNo treatment

      ACQUIRED NONSCARRING

      Alopecia Areata

      Alopecia areata (AA) is an autoimmune disorder resulting in nonscarring hair loss that generally presents in those aged between 3 and 16 years old (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). The lifetime risk of developing AA is 2.1%, and this risk is increased for those with a family history of AA (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). In addition, AA is strongly associated with atopic dermatitis, especially in prepubertal children. Coexisting autoimmune disorders are rare in children with AA; however, a family history of autoimmune disorders is common, with thyroiditis often being reported (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).
      There are variable clinical presentations of AA. However, the typical presentation is patch-type AA and is the sudden appearance of hair loss in a well-defined, smooth round patch (or patches) on the scalp. AA is nonscarring, and the surrounding skin is generally not affected. Pathognomonic “exclamation-mark” hairs may be present surrounding the patch of alopecia; these are hairs that increasingly narrow to the hair root, thus resembling an exclamation point best appreciated with trichoscopy. When hair growth resumes, hair will be at the same length and stage (as opposed to trichotillomania), and it is common for the regrown hair to be hypopigmented or depigmented; however, this will eventually be replaced by normally pigmented hair. Finally, like other autoimmune diseases, AA is associated with intermittent flares and remissions (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).
      Other presentations of AA are notable as they carry prognostic indicators and aid in treatment planning. Hair loss may occur in the ophiasis pattern, which occurs in a band-like distribution around the scalp. The hair loss begins on the posterior occiput and generally extends around the scalp above the ears (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). A less reported pattern is the sisaipho pattern, in which there is extensive alopecia everywhere except for the periphery of the scalp (
      • Beigi P.K.M
      Alopecia areata: A clinician's guide.
      ). Alopecia totalis is when there is progression to total hair loss on the scalp, and alopecia universalis is when there is progression to total hair loss over the entire body (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Approximately 5% of AA cases will progress to alopecia totalis or universalis, and these cases are more often associated with atopic dermatitis (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Patients with an earlier age at diagnosis, diffuse hair loss, or ophiasis-type AA have a worse prognosis (
      • Pratt C.H.
      • King Jr., L.E.
      • Messenger A.G.
      • Christiano A.M.
      • Sundberg J.P
      Alopecia areata.
      ).
      Evaluation of AA will show a positive hair pull test (Figure), and in patchy alopecia may be used at the border of hair loss to monitor the advancing edge. AA may also have associated nail changes with nail pitting commonly observed. The nail pits are smaller and shallower than those observed in psoriasis patients, and they characteristically form a grid-like stippling. Other nail changes include shedding, ridging, whitening, and dystrophy, with the latter most often occurring in alopecia totalis and universalis patients (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).
      AA has a strong psychosocial impact and can result in reduced patient quality of life. A systematic review of AA found that compared with age-matched controls, children with AA have a higher prevalence of anxiety and depression, and, in comparison with healthy siblings, children with AA experience more stressful life events (
      • Toussi A.
      • Barton V.R.
      • Le S.T.
      • Agbai O.N.
      • Kiuru M.
      Psychosocial and psychiatric comorbidities and health-related quality of life in alopecia areata: A systematic review.
      ). There is also a risk of social isolation for pediatric patients with AA, and deliberate hair styling, hats, and/or wigs may be useful to help cover the affected areas. In addition to the effect on the patient, AA can also be distressing for parents and caregivers, and the unpredictable course adds further duress. Counseling and psychological support for patients and family members are vital (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Toussi A.
      • Barton V.R.
      • Le S.T.
      • Agbai O.N.
      • Kiuru M.
      Psychosocial and psychiatric comorbidities and health-related quality of life in alopecia areata: A systematic review.
      ).
      There is no cure for AA, and the goal of treatment is to control the disorder. The therapy used is dependent on disease extent, and generally, at least 3–4 months of treatment is required. For limited patch-type alopecia (< 50% of the scalp is affected), superpotent topical corticosteroid ointments are the treatment of choice. Occlusion of the steroids on the scalp with a covering (i.e., swimming cap) may be beneficial, though impractical. Intralesional corticosteroids may also be beneficial if the patient is able to tolerate the treatment. Minoxidil (5%) has also demonstrated efficacy for hair regrowth in patients with AA and has a safeside effect profile. Minoxidil (5%) can be purchased over the counter and does not require a prescription. It is offered in a solution and foam vehicle, of which the latter is preferred. It has the greatest efficacy in limited patch-type alopecia when combined with topical steroid therapy (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Pratt C.H.
      • King Jr., L.E.
      • Messenger A.G.
      • Christiano A.M.
      • Sundberg J.P
      Alopecia areata.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Referral to pediatric dermatology is warranted for AA.
      AA affecting > 50% of the scalp, alopecia totalis, and alopecia universalis are more difficult to treat, and topical corticosteroids are generally ineffective. Topical immunotherapy, including squaric acid dibutyl ester or diphenylcyclopropenone, which is not an approved treatment, has been used in addition to anthralin cream. Oral therapies include methotrexate and systemic glucocorticoids for patients with more severe disease and heavy psychological burden. Pulse therapy with methylprednisolone has also been used. Although adult AA may be treated with systemic psoralen followed by ultraviolet A light or cyclosporine therapy, neither treatment is recommended in children because of side effects and unclear efficacy (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Strazzulla L.C.
      • Wang E.H.C.
      • Avila L.
      • Lo Sicco K.
      • Brinster N.
      • Christiano A.M.
      • Shapiro J
      Alopecia areata: An appraisal of new treatment approaches and overview of current therapies.
      ). There are new treatments for AA with Janus kinase inhibitors currently under investigation (
      • Strazzulla L.C.
      • Wang E.H.C.
      • Avila L.
      • Lo Sicco K.
      • Brinster N.
      • Christiano A.M.
      • Shapiro J
      Alopecia areata: An appraisal of new treatment approaches and overview of current therapies.
      ). In addition, sharing information with patients and families about advocacy groups such as the

      National Alopecia Areata Foundation. (n.d.). National Alopecia Areata Foundation. Retrieved from www.naaf.org

      and the

      Children's Alopecia Project. (n.d.). Children's Alopecia Project. Retrieved from www.childrensalopeciaproject.org

      can be beneficial.

      Androgenetic Alopecia

      Androgenetic alopecia (AGA) is the most common etiology of hair loss in adolescents and adults and is caused by circulating androgens (
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). It can occur in both males (more common) and females and typically presents after puberty. Early-onset is associated with more hair loss. In males, AGA can be either common balding or male-pattern hair loss, whereas, in females, it is typically hereditary thinning or female-pattern hair loss. The clinical presentation varies on the type, but in general, most patients notice hair thinning as opposed to hair shedding. Male-pattern hair loss is characterized by hair thinning at the vertex and concomitant bitemporal hairline recession. In females, there is generally diffuse hair thinning from the frontal scalp to the vertex with sparing of the frontal hairline (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).
      Clinical presentation is confirmatory for most AGA; however, dermoscopy and a scalp biopsy may be necessary for confirmation in some cases. In female patients, menstrual history and evaluation for other signs of hyperandrogenism should be obtained (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Concern for polycystic ovarian syndrome (PCOS) may warrant further hormonal evaluation and an endocrinology consult. PCOS is associated with insulin resistance, obesity, infertility, and malignancy. PCOS may also have other dermatologic manifestations of acne, hirsutism, and acanthosis nigricans (
      • Griggs J.
      • Burroway B.
      • Tosti A.
      Pediatric androgenetic alopecia: A review.
      ;
      • Schmidt T.H.
      • Khanijow K.
      • Cedars M.I.
      • Huddleston H.
      • Pasch L.
      • Wang E.T.
      • Shinkai K
      Cutaneous findings and systemic associations in women with polycystic ovary syndrome.
      ). Furthermore, males who have a female-pattern hair loss or abnormal pubertal development may also require further evaluation (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).
      AGA is progressive. The Food and Drug Administration has approved topical minoxidil and oral finasteride for AGA in patients aged ≥ 18 years; however, both may be used off-label in younger patients, with topical minoxidil being the initial treatment of choice (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Oral finasteride should be used judiciously in females, as it can cause feminization of a male fetus (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). There is some evidence of low-level laser therapy as a treatment in both sexes. Surgery is a potential option for adult patients but not for adolescents. Referral to a pediatric dermatologist is warranted for long-term management of AGA (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).

      Telogen Effluvium

      Telogen effluvium (TE) is a common cause of nonscarring hair loss in the pediatric population. TE is due to a rapid and simultaneous transition of multiple hair follicles from the anagen phase to the telogen phase with resultant hair shedding and diffuse hair loss. TE is associated with both physical and psychological stress, though an inciting event may not be determined. Pathological triggers may include illness, surgery, medications, trauma, nutritional deficiencies (i.e., iron and B12), metabolic disturbances, thyroid disorders, and metal poisoning. Psychological triggers include emotional stress. The clinical presentation of TE is a child with an abrupt onset of diffuse hair shedding that affects the entire scalp and typically occurs 3–4 months after the provoking event. The generalized hair thinning may not be apparent on physical examination, but the patient history of increased shedding warrants evaluation (
      • Malkud S.
      Telogen effluvium: A review.
      ;
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). A positive hair pull test over the full scalp (as opposed to a localized region) will be present. In addition, counting the number of hairs shed each day (i.e., collecting hairs on pillows and in the shower) and using this to determine the amount of hair in the telogen phase is also useful (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). The normal average daily hair loss is 100–200 strands per day (
      • Bolognia J.E.A.
      • Schaffer J.V.
      • Cerroni L
      Dermatology.
      ). Usually, 15% of scalp hair is in the telogen phase, and this can increase to more than 25% in TE. There is no treatment for TE itself, but treatment or resolution of the underlying cause typically results in improvement of the TE over 3 months. Persistent TE warrants a dermatology referral, although it is difficult to treat (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).

      Traction Alopecia

      Traction alopecia occurs secondarily to either continuous or repetitive stress on the hair root leading to hair follicle damage. Hairstyling practices are implicated in traction alopecia, including tight braids, tight buns/ponytails, heavy hair accessories, hair extensions, weaves, and cornrows (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Traction alopecia can occur in any patient, and it has been reported that 17.1% of school-aged African American girls developed traction alopecia because of styling preferences (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). The clinical presentation of traction alopecia is gradual hair loss at the hairline in a patchy and symmetrical pattern. Perifollicular erythema and pustules may occasionally be present (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). One potential clinical marker of traction alopecia is the “fringe sign,” which is when there are preserved hairs at the frontal and/or temporal rim of patients with hair thinning and/or loss immediately posterior to the anterior hairline. This sign has been demonstrated to be both sensitive and specific, but its absence does not efficiently rule out the diagnosis of traction alopecia (
      • Samrao A.
      • Price V.H.
      • Zedek D.
      • Mirmirani P.
      The “Fringe Sign” - A useful clinical finding in traction alopecia of the marginal hair line.
      ). Treatment of traction alopecia depends on the stage at diagnosis. When recognized early, discontinuation of contributory hairstyle practices can lead to a full recovery of hair loss. For longstanding traction alopecia, minoxidil may be used; furthermore, in the setting of inflammation, intralesional corticosteroids or oral/topical antibiotics may be helpful. However, for permanent hair loss, hair transplantation may be the sole therapeutic option (
      • Haskin A.
      • Aguh C.
      All hairstyles are not created equal: What the dermatologist needs to know about black hairstyling practices and the risk of traction alopecia (TA).
      ). Referral to pediatric dermatology is recommended when conservative management of traction alopecia proves to be ineffective.

      Trichotillomania

      Trichotillomania is a hair-pulling disorder resulting in noticeable, nonscarring hair loss (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). The exact incidence and prevalence of trichotillomania are not well defined, but the lifetime prevalence has been reported to be 3.5%, and studies of small cohorts of children have demonstrated an even greater prevalence (
      • Papadopoulos A.J.
      • Janniger C.K.
      • Chodynicki M.P.
      • Schwartz R.A.
      Trichotillomania.
      ; ). The hair-pulling may be performed consciously or subconsciously, and often patients attempt to keep this disorder hidden because of feelings of shame (
      • Noble C.M.
      • Gnilka P.B.
      • Ashby J.S.
      • McLaulin S.E.
      Perfectionism, shame, and trichotillomania symptoms in clinical and nonclinical Samples.
      ). Trichotillomania typically begins between early childhood and adolescence; before age 6 years old, it is more common in males, whereas after age 6 years old, it is more common in females (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). Trichotillomania is often associated with psychosocial stress, and it has been noted to occur in patients who place emphasis on “perfectionism” (
      • Noble C.M.
      • Gnilka P.B.
      • Ashby J.S.
      • McLaulin S.E.
      Perfectionism, shame, and trichotillomania symptoms in clinical and nonclinical Samples.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).
      The clinical presentation is an incomplete, ill-defined area of hair loss. Erythema may also be present if the patient picks at the skin surrounding the hair follicle. Differentiation of trichotillomania from other disorders is the presence of hairs of different lengths as opposed to the uniform regrowth of hair. The affected areas are generally contralateral to the side of the patient's dominant hand, with the occiput rarely involved. In addition to the scalp, eyebrows, eyelashes, facial, and pubic hair may be affected. Scalp excoriations and nail-biting may also be associated with trichotillomania, and some patients may ingest the hairs (bezoars), which have the potential to cause gastrointestinal obstruction. The hair pull test (Figure) is negative, and the regrown hairs will have normal pigmentation (in contrast to nonpigmented hairs in AA) (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).
      Because patients may keep hair pulling hidden, the interview should be conducted in a nonjudgmental manner when suggested by clinical presentation. It may be necessary to interview the patient alone to obtain the diagnosis. Treatment for trichotillomania varies by severity. In some cases, isolated stress management is beneficial, but often cognitive behavioral therapy (CBT) with a child psychologist is required (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). At 6 months follow-up evaluation, CBT with relapse prevention demonstrated a reduction in trichotillomania severity by 64% (
      • Tolin D.F.
      • Franklin M.E.
      • Diefenbach G.J.
      • Anderson E.
      • Meunier S.A.
      Pediatric trichotillomania: Descriptive psychopathology and an open trial of cognitive behavioral therapy.
      ). Furthermore, if there is a conscious urge associated with the hair pulling, habit reversal training can be effective; this involves methods such as having the child squeeze a ball when they have the desire to hair pull. For cases refractory to CBT, psychiatric intervention may be warranted with antidepressant and antipsychotic agents demonstrating some benefit. If management by the primary care provider and child psychology is unsuccessful, referral to child psychiatry or pediatric dermatology is appropriate (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).

      ACQUIRED SCARRING

      Acne Keloidalis Nuchae

      Acne keloidalis nuchae (AKN) is a scarring alopecia that can lead to permanent hair loss. It typically affects African American males aged 14–25 years old (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). It is associated with hair grooming practices and close shaving, leading to ingrown hairs and irritation. The clinical presentation is early lustrous violaceous firm papules over the nuchal and occipital scalp that, over time, coalesce and form larger keloids. There is scarring hair loss in the areas of keloids (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). The lesions are asymptomatic but may negatively impact patient quality of life (
      • Maranda E.L.
      • Simmons B.J.
      • Nguyen A.H.
      • Lim V.M.
      • Keri J.E.
      Treatment of acne keloidalis nuchae: A systematic review of the literature.
      ). The presence of pruritis and pain may indicate a secondary infection. AKN is often difficult to treat, and many common treatments demonstrate a lack of efficacy. Avoidance of exacerbating factors, such as scratching the affected area, close shaving, and wearing restrictive clothing, should be implemented. Topical or intralesional corticosteroids may be helpful and, although it is not an infectious process, there is evidence that topical or oral antibiotics can lead to lesion resolution because of their anti-inflammatory properties. Furthermore, there is evidence for treatment with retinoids, laser hair removal, and surgery. Referral to pediatric dermatology is warranted for suspected AKN because of the scarring nature and common mismanagement (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).

      Bacterial Folliculitis

      Bacterial folliculitis is an infectious process that occurs within a hair follicle. It is important to note that here we are discussing bacterial folliculitis though noninfectious folliculitis also exists; the two cannot be distinguished clinically as they both present as small pustules around the hair follicle with associated inflammation. A skin culture is needed to differentiate bacterial folliculitis from noninfectious folliculitis. Although bacterial folliculitis, in general, is not uncommon in children, untreated or undiagnosed bacterial folliculitis can rarely lead to scarring alopecia (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Immunosuppressed patients are especially predisposed to bacterial folliculitis. Bacterial folliculitis is often attributable to staphylococcal species or gram-negative organisms, such as pseudomonas; the exact incidence of this infection is unknown. Patients may have pruritis and diaphoresis. There may be a history of recent antibiotics or corticosteroid use, hot tub or swimming pool exposure, or frequent shaving. Simple cases of bacterial folliculitis will resolve spontaneously; however, topical or oral antibiotics with antistaphylococcal and gram-negative coverage may be necessary. A skin culture can be useful to diagnose bacterial folliculitis and decrease delays in diagnosis and treatment to lessen the potential progression to scarring alopecia. If there is no improvement with antibiotics, a fungal etiology should be considered with fungal culture and antifungal treatment when appropriate (see “Tinea Capitis”). Bacterial folliculitis of the scalp can be managed in the primary care setting (). Of note, the formation of a carbuncle (deep abscess of interconnected boils) from staphylococcal folliculitis coalescence may occur, which can lead to scarring alopecia. A carbuncle requires oral antistaphylococcal antibiotics and may require topical and/or oral corticosteroids; further, incision and drainage may be required when an abscess is present (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).

      Discoid Lupus Erythematosus

      Discoid lupus erythematosus (DLE) is a rare cause of hair loss in children seen equally in males and females (
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Less than 3% of patients develop DLE before 10 years old (
      • Arkin L.M.
      • Ansell L.
      • Rademaker A.
      • Curran M.L.
      • Miller M.L.
      • Wagner A.
      • Paller A.S.
      The natural history of pediatric-onset discoid lupus erythematosus.
      ). It can cause permanent hair loss. DLE presents clinically as indurated, smooth, shiny, and dyspigmented plaques that may have an atrophic appearance and associated scale. These plaques may involve any region of the body with the involvement of the scalp, potentially leading to permanent scarring alopecia. Scalp lesions may be mistaken for fungal or bacterial infections, and DLE should be considered if antimicrobial treatment of suspected infectious lesions is ineffective. Diagnostic confirmation typically requires biopsy for histopathology and direct immunofluorescence (
      • Gómez-Quispe H.
      • Elena de Las Heras-Alonso M.
      • Lobato-Berezo A.
      • Velasco-Tamariz V.
      • Pindado-Ortega C.
      • Moreno-Arrones O.M.
      • Saceda-Corralo D.
      Trichoscopic findings of discoid lupus erythematosus alopecia: A cross-sectional study.
      ;
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Antinuclear antibodies are typically absent in children and are not reliable for diagnosis. Patients should be counseled to avoid sun exposure, and treatment includes mid to high potency topical steroids, acitretin, and hydroxychloroquine (
      • Arkin L.M.
      • Ansell L.
      • Rademaker A.
      • Curran M.L.
      • Miller M.L.
      • Wagner A.
      • Paller A.S.
      The natural history of pediatric-onset discoid lupus erythematosus.
      ;
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Progression to systemic lupus erythematosus is common in children, with one study reporting 26% of pediatric patients progressing from DLE to systemic lupus erythematosus (
      • Arkin L.M.
      • Ansell L.
      • Rademaker A.
      • Curran M.L.
      • Miller M.L.
      • Wagner A.
      • Paller A.S.
      The natural history of pediatric-onset discoid lupus erythematosus.
      ). Careful monitoring of patients is required (
      • Arkin L.M.
      • Ansell L.
      • Rademaker A.
      • Curran M.L.
      • Miller M.L.
      • Wagner A.
      • Paller A.S.
      The natural history of pediatric-onset discoid lupus erythematosus.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Referral to pediatric dermatology for suspected DLE is necessary for possible biopsy and diagnosis confirmation.

      Dissecting Cellulitis of the Scalp

      Dissecting cellulitis of the scalp is a rare inflammatory cause of hair loss that is often associated with secondary infection (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). It is most often observed in adolescent and adult African American males (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). The clinical presentation is a series of pustules and abscesses that progress to draining sinus tracts. These tracts may be appreciated when pressure is placed on one lesion leading to drainage at another region of the scalp. This disorder results in scarring alopecia. When the patient also has concomitant hidradenitis suppurativa and acne conglobata, it is referred to as the follicular occlusion triad, and the addition of a pilonidal cyst results in the follicular occlusion tetrad (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). This disorder is often misdiagnosed as an infectious process such as folliculitis or kerion. For early disease, long-term antibiotics (3–6 months) and topical steroids may be effective. Oral isotretinoin has been demonstrated to be the most effective oral treatment, and delays in referral to dermatology for treatment with this medication may lead to permanent scarring. There have also been reports of laser therapy proving to be an effective treatment. Dissecting cellulitis of the scalp is a serious cause of hair loss and requires immediate dermatologic treatment (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).

      Tinea Capitis

      Tinea capitis is a fungal infection of the scalp and the most common dermatophytosis of childhood (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Rates of tinea capitis infection in school-aged children ranged from 0% to 19.4% (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). It primarily occurs in preadolescence, and African American children are particularly susceptible; however, it can appear in all ages and ethnicities (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). Trichophyton tonsurans and Microsporum canis are the most common pathogens isolated, but causative species vary depending on geographic location (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).
      Tinea infections are acquired from close human contact, animal contact, or direct contact with contaminated soil. Contact sports (i.e., wrestling) and mat sports (i.e., gymnastics) are common routes for tinea exposure. In addition, tinea may be spread from fomites such as hats, hairbrushes, and pillows. Pets in the home should be examined for excessive scratching and hair loss as a source of transmission (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ).
      The clinical presentation of tinea capitis varies. It can present with diffuse scaling of the scalp without hair changes or as an annular patch of hair loss with associated scaling, erythema, and pruritis. “Black dot” tinea capitis presents with small black dots in the area of alopecia, representing transverse breakage of the hair shaft. Posterior cervical lymphadenopathy is often associated with fungal causes of hair loss and may provide additional clues to the diagnosis (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).
      A potential complication of delays in treatment, untreated, or misdiagnosed tinea capitis is the development of a kerion. A kerion represents an inflammatory stage of tinea capitis that can mimic bacterial infections. It appears as a boggy suppurative indurated plaque or nodule with overlying pustules, crusting, malodor, and purulent drainage that can rapidly progress to scarring alopecia. Kerion occurs more commonly in children than adults and is often painful (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).
      A fungal culture is often necessary to confirm a diagnosis of tinea capitis and is easily collected in a primary care setting. The sample can be collected by taking a toothbrush or a cotton swab and firmly rubbing over the affected, scaly regions. The fungal culture needs to be transferred to specific fungal culture media (i.e., Sabouraud dextrose agar); however, the media may vary on the basis of institution. Fungal cultures grow slowly, and speciation may take weeks for results; therefore, treatment should be initiated when the index of suspicion is high for infection. False-negative fungal cultures can occur (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Early treatment for kerion is necessary, as a delay may lead to permanent scarring alopecia. In addition, if there is a concern for secondary bacterial infection, a bacterial culture should also be obtained, and empirical treatment should be initiated (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ).
      For children diagnosed with tinea capitis, systemic antifungal treatment is the standard of care; antifungal therapies include griseofulvin, terbinafine, and, less frequently, fluconazole and itraconazole (
      • Chen X.
      • Jiang X.
      • Yang M.
      • González U.
      • Lin X.
      • Hua X.
      • Bennett C
      Systemic antifungal therapy for tinea capitis in children.
      ;
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). In addition, because of the inflammatory nature of kerion, systemic corticosteroids for a short period are also used as an adjunctive therapy; the dosage is generally 0.5–2 mg/kg/day for 2–4 weeks with a 5–10 mg taper every 3–4 days (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). The use of oral steroids lowers the risk of permanent alopecia in these patients (
      • Chen X.
      • Jiang X.
      • Yang M.
      • González U.
      • Lin X.
      • Hua X.
      • Bennett C
      Systemic antifungal therapy for tinea capitis in children.
      ;
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ).
      Historically it was recommended that baseline laboratory tests for hepatic and hematologic evaluation be obtained before treatment and episodically throughout the treatment course. Evidence now suggests that routine testing of patients is unnecessary in asymptomatic patients (
      • Stolmeier D.A.
      • Stratman H.B.
      • McIntee T.J.
      • Stratman E.J.
      Utility of laboratory test result monitoring in patients taking oral terbinafine or griseofulvin for dermatophyte infections.
      ).

      CONGENITAL

      Aplasia Cutis Congenita

      Aplasia cutis congenita (ACC) is a rare, congenital condition caused by a failed closure of the skin with varying degrees of severity, including the epidermis, dermis, and subcutaneous tissue. In some cases, the underlying bone and dura may also be affected. Most ACC involves the scalp, especially the vertex (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). The incidence of ACC is estimated to be between 2 and 3 cases in 10,000 births (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). The clinical presentation of ACC is a solitary scalp patch with scarring alopecia present at birth that is typically between 0.5 cm and 3 cm (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). The “hair collar sign” may be seen and appears as a focal patch of coarse, long, darkly pigmented terminal hair encircling the ACC. This sign may represent an attenuated manifestation of a neural tube defect (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). The condition is generally isolated and sporadic; however, ACC can also be inherited and associated with other conditions. Associated conditions include midline defects, limb abnormalities, spinal dysraphism, and genetic disorders. Medications during gestation, such as methimazole, have also been correlated with development (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Treatment depends on the size of the lesion and the extent of involvement. Most ACC can be managed conservatively with monitoring for infection, as re-epithelization will occur, leaving an atrophic scar; however, larger lesions (> 3 cm) will most likely require more involved treatment, including surgery (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). Most ACC has an excellent prognosis, though the hair collar sign may be a marker of underlying abnormalities. Patients should be imaged if they have ACC that is midline or posterior to the vertex, there is suspicion for a bone defect, or if the hair collar sign is positive or a pit is present (
      • Kuemmet T.J.
      • Miller J.J.
      • Michalik D.
      • Lew S.M.
      • Maheshwari M.
      • Humphrey S.R.
      Low risk of clinically important central nervous system dysraphism in a cohort study of 69 patients with isolated aplasia cutis congenita of the head.
      ). For the larger lesions or lesions with associated malformations, a referral is recommended to an appropriate provider, including dermatology, otolaryngology, or neurology (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).

      Congenital Triangular Alopecia

      Congenital triangular alopecia (CTA) is a cause of localized hair loss that typically presents between the ages of 2–5 years old but may be noted at birth (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). It is sporadic but may be present in multiple family members suggesting an underlying heritable trait. The clinical presentation is most often a unilateral region of hair loss in the frontotemporal region that is triangular in shape. The area may have complete hair loss or may be partially covered and is usually between 3 and 5 cm (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Bilateral cases occur less commonly. It is both nonscarring and nonprogressive. The size of the involved area does not change and subjectively reduces as the patient's scalp grows. CTA is diagnosed clinically on the basis of its unique appearance, which helps differentiate it from androgenetic alopecia and AA. Currently, there are no treatments for CTA; surgical correction is possible but not necessary (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).

      Loose Anagen Hair Syndrome

      Loose anagen hair syndrome (LAS) is an infrequent etiology of hair loss that may be sporadic or inherited (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). It is present in 10% of pediatric patients with alopecia (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). LAS has a typical onset after 2 years of age with a mean age at diagnosis of 6 years old (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Patients tend to have blonde hair, and there is a female predominance, though this may be due to underreporting in males secondary to shorter hairstyle practices. There are variable clinical presentations of LAS, but it is overall characterized by anagen hairs that are easily pulled. The patient may have patches of disorderly, thin hair that is incapable of growing long or increased hair shedding; parents will often report the lack of a need for haircuts. The hair pull test is often positive (Figure), but a negative test does not rule out the diagnosis (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ). If a microscopic examination is available, the hair will show a ruffled cuticle and a distorted bulb (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). No treatment is available, and the condition improves with age. Patients should be counseled on avoiding trauma to the hair by using a mild hair care routine. It is important to rule out both TE and trichotillomania as these disorders have potential treatments or therapies that should be implemented. A clinical pattern can be used to exclude trichotillomania, whereas a pediatric dermatologist can differentiate between anagen hairs (LAS) and telogen hairs (TE, short anagen hair syndrome) on trichoscopy (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).

      Nevus Sebaceous

      Nevus sebaceous (NS) is a common congenital hamartoma that presents as an alopecic patch in children (
      • Baigrie D.
      • Troxell T.
      • Cook C.
      Nevus sebaceous.
      ). NS is seen in approximately 0.3% of newborns, and it occurs equally in males and females (
      • Baigrie D.
      • Troxell T.
      • Cook C.
      Nevus sebaceous.
      ). The clinical presentation of NS is an asymptomatic waxy, yellow, hairless patch or plaque, though, depending on the patient's skin color, the yellow patch may appear either tan, gray, or skin color. As children enter adolescence, the lesion tends to become thicker and more verrucous. There may be other lesions present independent of the scalp. Secondary benign adnexal neoplasms may occur within the NS though they generally arise in adults aged ≥ 40 years old (
      • Baigrie D.
      • Troxell T.
      • Cook C.
      Nevus sebaceous.
      ;
      • Eichenfield L.F.
      • Borok J.
      Nevus sebaceous.
      ;
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ). Basal cell carcinoma causes the greatest concern, though the incidence of basal cell carcinoma transformation is quite low (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Although surgery may not be recommended and NS can be safely followed, definitive treatment of NS is excision; if surgery is recommended, many factors may contribute to the timing of surgery (i.e., patient's age, size, and location, cosmesis, general vs. local anesthesia, etc.) (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ). Regardless of the patient situation, all new growths arising from the NS require evaluation (
      • Whiting D.A.
      • Trüeb R.M.
      • Blume-Peytavi U.
      Hair growth and disorders.
      ).

      Short Anagen Hair Syndrome

      Short anagen hair syndrome (SAS) is a rare, benign etiology of pediatric hair loss that is present from birth. It is similar to LAS. The clinical presentation is short, fine hair that does not require cutting. The hair pull test is positive, and it can be differentiated from LAS by trichoscopy; in SAS, the hair is shed in the telogen phase, whereas in LAS, they are shed in the anagen phase. Treatment is not required as SAS resolves spontaneously during puberty and adulthood (
      • Paller A.
      Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence.
      ;
      • Xu L.
      • Liu K.X.
      • Senna M.M.
      A practical approach to the diagnosis and management of hair loss in children and adolescents.
      ).

      CONCLUSIONS

      Hair loss is common in the pediatric population and is a source of significant concern for patients and parents. There are multiple etiologies for hair loss, and a broad differential is necessary; however, few are secondary to underlying systemic or neoplastic etiologies. Hair loss in pediatric patients is often first seen in the primary care office, and appropriate diagnosis and treatment may lead to decreased morbidity and better outcomes. If the examination is insufficient for diagnosis and trichoscopy is unavailable, referral to a dermatologist is recommended for accurate diagnosis. Furthermore, hair loss refractory to treatment, more nefarious in etiology, or causing concern for permanent hair loss also requires evaluation by a dermatologist.

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        The natural history of pediatric-onset discoid lupus erythematosus.
        Journal of the American Academy of Dermatology. 2015; 72: 628-633
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        Nevus sebaceous.
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      Biography

      Jenna E. Koblinski, MD, Medical Resident, University of Arizona College of Medicine - Phoenix, Phoenix, AZ.
      Judith A. O'Haver, PhD, RN, CPNP-PC, FAANP, FAAN, Assistant Professor of Pediatrics, Mayo Clinic College of Medicine and Science, Scottsdale, AZ, and Clinical Assistant Professor, Department of Child Health, University of Arizona College of Medicine - Phoenix, and Assistant Clinical Professor, Department of Pediatrics, Creighton University School of Medicine, Phoenix Regional Campus, Phoenix, AZ.
      Israel D. Andrews, MD, FAAD, Assistant Professor of Dermatology and Pediatrics, Mayo Clinic College of Medicine and Science, Scottsdale, AZ, and Associate Program Director, Pediatric Dermatology Fellowship, Department of Dermatology, Phoenix Children's Hospital, and Clinical Assistant Professor, University of Arizona College of Medicine - Phoenix, Phoenix, AZ.