Hair Disorders




Abstract


The evaluation of a patient with hair loss requires a detailed history, physical examination, and, in some cases, laboratory tests and biopsy ( Table 20.1 ). Important elements of the history include the time of onset, medications taken, recent emotional or physical stress, diet, grooming techniques, and family history of baldness or hair disorders.


The physical examination is helpful in making an accurate diagnosis by observing the pattern (patchy or diffuse) of hair loss and whether scarring is present as evidenced by loss of follicular openings. Patchy hair loss is readily apparent. However, diffuse hair loss may not be noticeable until the patient has more than 50% hair loss. The presence or absence of scarring is important diagnostically and prognostically. In nonscarring alopecia, the diagnosis is usually made without biopsy. In scarring alopecia, a biopsy is useful in establishing a prognosis and diagnosis and should be performed. Nonscarring alopecia may be a temporary phenomenon, whereas scarring indicates permanent hair loss. Except for discoid lupus, the main disorders discussed in this chapter are nonscarring.






Key Points




  • 1.

    Diagnosis requires a detailed history


  • 2.

    Diagnose pattern as patchy or diffuse


  • 3.

    Determine whether hair loss is scarring or nonscarring






Observe the pattern of hair loss and whether scarring is present.





Alopecia Areata




Key Points




  • 1.

    Autoimmune disorder


  • 2.

    Acute onset of well-circumscribed, oval patches of nonscarring alopecia


  • 3.

    No cure




Table 20.1

Alopecia



































































Incidence (%) a History Physical Examination Scarring Pattern Differential Diagnosis Laboratory Test (Biopsy)
Alopecia areata 0.9 Acute onset Exclamation point hairs Absent Circular patches Trichotillomania
Secondary syphilis
Fungal infection
None
Discoid lupus erythematosus < 0.1 Photosensitivity
Other symptoms of lupus
Erythema
Follicular plugs
Present Patchy Fungal infection
Lichen planopilaris
Neoplasm
Biopsy
Androgenetic (Male & female pattern hair loss) 0.6 Family history of thinning Normal scalp Absent Patterned Androgen excess in women None
Telogen effluvium 1.0 Physical or emotional stress 2–3 months previously Positive hair pull > 25% telogen hair Absent Diffuse Female pattern hair loss
Identify trigger or cause
None
Trichotillomania 0.1 Emotional problems Broken hair Absent Patchy Alopecia areata
Tinea capitis
None
Tinea capitis 0.1 Schoolmates with hair loss Scaling, erythema, pustules Absent Patchy Seborrheic dermatitis
Alopecia areata
Bacterial infection
Trichotillomania
KOH preparation, culture

KOH , Potassium hydroxide.

a Percentage of new dermatology patients with this diagnosis seen at the Hershey Medical Center Dermatology Clinic, Hershey, PA.



Definition


Alopecia areata is an idiopathic disorder characterized by well-circumscribed, round or oval patches of nonscarring hair loss ( Fig. 20.1 ).




Figure 20.1


Alopecia areata – characteristic round patch of nonscarring alopecia.


Incidence


Alopecia areata affects both sexes equally, with onset occurring most often in early adulthood. Almost 1% of the authors’ new patients had this diagnosis. The incidence in Olmsted County, Minnesota, was 20.2 per 100,000 person-years. Alopecia areata occurs in 1.7% of Americans by the age of 50 years.


History


Alopecia areata has an acute onset. It is sometimes associated with emotional stress, but in most patients the emotional stress seems to be caused by the hair loss. Approximately 25% of patients have other autoimmune disorders, such as type 1 diabetes mellitus, thyroid disease, and vitiligo. Atopic dermatitis is especially common in alopecia areata. Patients are generally healthy otherwise. Some 20% to 25% of patients have a family history of alopecia areata.


Physical Examination


The disorder is characterized by well-circumscribed, round or oval patches of hair loss, leaving a smooth, normal- appearing scalp. Erythema and slight tenderness may be present early in the course. Characteristically, the periphery of the patches of hair loss is studded with exclamation point hairs , which are so named because of their resemblance to a punctuation mark ( Fig. 20.2 ). These fractured hairs are 2 to 3 mm long and tapered at the base.




Alopecia areata is characterized by nonscarring circular patches of alopecia with exclamation point hairs.




Figure 20.2


Alopecia areata – note exclamation point hairs at periphery of alopecia.


Alopecia areata most often affects the scalp, frequently with several 2- to 3-cm patches of hair loss. The eyebrows, eyelashes, and beard may also be affected, as may hair elsewhere on the body ( Fig. 20.3 ). Approximately 1% to 2% of patients develop loss of all scalp hair ( alopecia totalis ) or loss of all body hair ( alopecia universalis ) ( Fig. 20.4 ). Fine stippling and pitting of the nails are infrequent associated findings.




Figure 20.3


Alopecia areata in beard area – patch of nonscarring alopecia extending from chin to cheek.



Figure 20.4


Alopecia universalis – complete absence of hair on scalp, eyebrows, and eyelashes.


Differential Diagnosis


Other nonscarring forms of alopecia need to be considered in the differential diagnosis. Secondary syphilis can be ruled out by appropriate serologic examination. Trichotillomania and tinea capitis should also be considered. Ill-marginated, irregular patches of alopecia containing the stubble of broken hairs are typical of trichotillomania ( Fig. 20.5 ). If doubt exists, a biopsy helps to differentiate trichotillomania from alopecia areata. A potassium hydroxide (KOH) preparation and culture, and clinical evidence of redness and scale, enable the diagnosis of a fungal infection ( Fig. 20.6 ).



Differential Diagnosis for Alopecia Areata





  • Secondary syphilis



  • Trichotillomania



  • Tinea capitis





Figure 20.5


Trichotillomania. Note hairs of uneven length and “black dots” which represent snapped off anagen hairs. This child was mistakenly diagnosed as having alopecia areata.



Figure 20.6


Tinea capitis – circular patch of alopecia with typical scale and “black dot” hairs due to breakage of weakened hair shafts from fungal invasion.


Laboratory and Biopsy


Histopathologic examination of alopecia areata reveals the presence of small, dystrophic hair structures. A lymphocytic infiltrate surrounds the early anagen hair bulbs like a “swarm of bees” ( Fig. 20.7 ).




Figure 20.7


Dystrophic follicle without a hair shaft. Dermis – lymphocytes surrounding the hair bulb.


Therapy


The treatment of alopecia areata depends on the extent of involvement and the patienťs emotional need for regrowth of hair. There is no cure for alopecia areata. In localized disease, topical potent steroids such as clobetasol (Temovate) gel or intralesional injections of triamcinolone (Kenalog-10) are sometimes effective. In widespread disease, systemic steroids are sometimes used, but their hazards must be considered before starting treatment. Prompt hair loss after discontinuation of oral steroids is discouraging. Other modes of therapy include immunotherapy by induction of allergic contact dermatitis (aka contact sensitization), phototherapy, topical minoxidil, and oral cyclosporine. Janus kinase (JAK) inhibitors, both orally and topically administered, are under investigation. Patients with alopecia areata need psychologic support, and all patients should visit the National Alopecia Areata Foundation’s website ( http://www.naaf.org ) or Children’s Alopecia Project ( www.childrensalopeciaproject.org ). A wig is recommended when the hair loss is extensive.



Therapy for Alopecia Areata


Initial





  • Steroids



  • Topical – clobetasol b.i.d.



  • Intralesional – triamcinolone 5 mg/mL every 4–6 weeks



  • Topical minoxidil



Alternative





  • Contact sensitization



  • Systemic – prednisone (short course only)




Course and Complications


Alopecia areata has a variable, unpredictable course. Most patients with localized disease have spontaneous recovery. However, relapses are not uncommon. Duration of more than 1 year and extensive hair loss are poor prognostic signs. Spontaneous regrowth of hair in alopecia totalis (scalp) and alopecia universalis (total body) may occur but is uncommon; fewer than 5% of patients show any tendency toward hair regrowth.




Poor prognosis:



  • 1.

    Long duration


  • 2.

    Large areas of alopecia




Pathogenesis


The pathogenesis of alopecia areata remains poorly understood, although an immunologic process is favored. Recent research shows the common initiation of the autoimmune response in alopecia areata, celiac disease, rheumatoid arthritis, and diabetes. A lymphocytic inflammatory infiltrate surrounds the affected bulbs and presumably has a role in the disease. In response to this autoimmune process, the hair matrices become arrested, but retain the capacity for normal hair regrowth after months or years.




Lupus Erythematosus




Key Points




  • 1.

    Alopecia can be scarring or nonscarring


  • 2.

    Biopsy confirms diagnosis


  • 3.

    Treat aggressively to prevent permanent hair loss




Definition


Lupus erythematosus is an autoimmune disorder that often affects the scalp and causes alopecia. Hair loss may be diffuse and nonscarring (systemic lupus erythematosus; SLE) or patchy and scarring (discoid lupus erythematosus; DLE). A general discussion of lupus erythematosus is found in Chapters 9 and 14 .


Physical Examination


Diffuse nonscarring alopecia of the scalp in the form of a telogen effluvium accompanies the acute phases of SLE in more than 20% of patients. In addition, short, broken hairs (“lupus hair”) may be present, particularly in the frontal margin.




SLE – nonscarring


DLE – scarring



Discoid lupus erythematosus is characterized by oval, scarring areas of alopecia. A typical plaque has an active erythematous margin and a white, atrophic, inactive center ( Fig. 20.8 ). Within the plaques, telangiectasia and dilated keratin-filled follicles are present. Similar discoid lesions may be found on the ears, face, trunk, and extremities.


Mar 20, 2019 | Posted by in Dermatology | Comments Off on Hair Disorders

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