Patchy hair loss on the scalp - Clinical Advisor

Patchy hair loss on the scalp

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Case #1

A 46-year-old woman presents with patchy hair loss around the circumference of her head in the frontal, temporal, and occipital regions for the previous 3 months. General and systemic examinations reveal no other abnormalities. The patient has a history of atopic dermatitis. Results of a complete blood count, thyroid panel, renal function tests, and liver function tests are within normal limits; the antinuclear antibody test result are positive at a 1:160 titer. Results of further rheumatic laboratory testing, such as double-stranded DNA antibodies, are negative. Cutaneous examination finds nonscarring, circumferential scalp alopecia. Trichoscopic findings show numerous yellow dots, a few black dots, and vellus hair. 

Case #2

A 40-year-old man presents with patchy hair loss of the scalp. The patient’s wife says the man’s acute-onset hair loss began 6 months earlier on the frontal scalp that later involved more temporal areas. His wife also states that she noticed recurrent hair-pulling behavior by the patient as stressful situations at his job increased in frequency. Review of symptoms and physical examination find no other abnormalities. Results of a complete blood count, thyroid panel, renal function tests, and liver function tests are within standard range. Dermatologic examination reveals patchy, nonscarring hair loss of the scalp with hairs of variable length distributed along the borders of the alopecia. The occipital scalp is largely spared. Trichoscopy demonstrates broken hairs of varying lengths, irregular coiled hairs, and black dots. Histopathology shows empty hair follicles. 

Case #1Alopecia areata (AA) is a cell-mediated autoimmune disease that targets hair follicles and is commonly seen by dermatologists, constituting 0.7% to 3.8% of all dermatologic visits.1 It typically presents as patchy, nonscarring hair loss in single, well-defined patches or...

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Case #1

Alopecia areata (AA) is a cell-mediated autoimmune disease that targets hair follicles and is commonly seen by dermatologists, constituting 0.7% to 3.8% of all dermatologic visits.1 It typically presents as patchy, nonscarring hair loss in single, well-defined patches or multiple patches, known as patchy AA.1-3

However, it can become a more progressive form, such as alopecia totalis, in which the entire scalp is involved, or alopecia universalis, in which there is a complete loss of hair on the scalp and body.2,3 More rare forms of AA include reticular patches of hair loss, band-like hair loss in the parietal, temporal, and occipital areas (ophiasis type), or a band-like hair loss in the frontal, parietal, and temporal scalp (ophiasis inversus).1

The exact cause of AA is still largely unknown, but it is thought to be a complex, multifactorial disease. With numerous studies, observations, and the formation of patient registries such as the National Alopecia Areata Registry (NAAR), genetics has increasingly been found to play a strong role in the pathogenesis of AA.3 For example, studies indicate a high incidence rate of AA, at 10% to 42%, among first-degree relatives of affected individuals.3 An earlier onset was correlated with an even greater incidence.3 One study showed that 7% of affected individuals had an affected parent, 3% had an affected sibling, and 2% had children with the disease; thus, an autosomal dominant inheritance pattern is suspected.3 Additionally, twin studies have shown a 55% concordance rate of AA in monozygotic twins, suggesting that possible genetic and environmental factors play a role in pathogenesis.3

Evidence also reveals that familial AA progresses more rapidly than sporadic cases, with more relapses and greater resistance to treatments.3 The human leukocyte antigen (HLA) class II alleles DQB1*03 and DRB1*1104 have been indicators of vulnerability to AA, and HLA-DR11 and HLA-DQ7 show possible susceptibility for alopecia totalis and universalis.1 Additionally, 139 single nucleotide polymorphisms are significantly associated with AA.1 Furthermore, studies have shown that emotional stress may play a role in AA pathogenesis due to alteration in the components of the hypothalamic-pituitary-adrenal axis, causing a diminished corticosterone response to acute physiologic stress.1 Patients with a history of atopic or autoimmune diseases have an increased risk of developing progressive types of AA.3 A significant association has also been noted between AA and developing vitiligo, systemic lupus erythematosus, psoriasis, atopic dermatitis, allergic rhinitis, and autoimmune thyroid diseases.3

On histologic examination, AA characteristically shows an accumulation of mononuclear cells surrounding the bulb of the affected hair follicles.1 The disease affects approximately 2% of the US population, with women and men being equally affected.1,4 The majority of affected individuals will achieve total remission within 1 year, with or without treatment, whereas typically 5% of these individuals will progress to chronic, more severe forms of AA.4

In AA, the most common trichoscopic findings are yellow dots, found in 63% to 94% of patients, exclamation-mark hairs that are thicker distally and thinner proximally, tapered hairs, broken hairs, and vellus hairs.5 Less commonly, trichorrhexis nodosa, monilethrix-like hairs, and Pohl-Pinkus constrictions are seen.5 In active AA, uniform black dots, broken hairs, and exclamation-mark hairs can indicate disease activity, whereas yellow dots and vellus hair indicate inactive AA.5 Trichoscopy can also be used to evaluate treatment progress, with pigmented, upright hairs and pigtail hairs demonstrating hair regrowth.5

The differential diagnosis of AA includes tinea capitis and trichotillomania. The lack of skin changes in AA differentiate it from tinea capitis. The patches of hair loss in AA are round compared to the geometric shape seen in trichotillomania. Pathology samples show peribulbar lymphocytic infiltrate around anagen hair follicles when CD4+ and CD8+ T cells become reactive to hair bulb autoantigens, inducing an inflammatory autoimmune response and causing hair loss.4

Treatment should be determined by disease severity and age of the patient.1 Most therapies are generally more successful in patchy AA than in alopecia totalis or universalis.1 First-line treatment includes corticosteroid injections such as triamcinolone acetonide injections into the deep dermis or upper subcutis, generally resulting in 71% of patients with subtotal alopecia showing hair regrowth.2 In addition, triamcinolone acetonide, at 2.5 to 10 mg/mL, can be used; 5 mg/mL is the preferred dosage for facial or scalp AA and is given in 4- to 6-week intervals.2 Topical corticosteroids, such as betamethasone valerate foam, can also be prescribed but are less effective against alopecia totalis or universalis, compared with injections.2 Second-line therapies include sulfasalazine, photochemotherapy, excimer laser, and fractional photothermolysis laser.2 Third-line therapies used are usually systemic corticosteroids and biologic agents.2 Treatment can also include psychologic support because patient self-esteem and body image may be altered due to the effects of the disease.2

In our case, the patient was diagnosed with AA and was prescribed injections of triamcinolone acetonide at 5 mg/mL each month. The patient began to see improvement in hair growth, texture, and density within 4 weeks of treatment, with full regrowth in 5 months.

 

Case #2

Trichotillomania is a self-inflicted skin disease that involves pulling out hair and is often associated with psychopathologic impulse control impairment.6 It commonly presents as solitary or multiple, patchy, irregularly bordered areas of alopecia of the scalp with varying lengths of the remaining hair.6 In more severe cases, a rare, extensive tonsure-pattern trichotillomania, in which hair is pulled from the vertex area of the scalp, may occur.7

The disorder typically begins during childhood or adolescence and can continue into adulthood, with girls and women being more affected than boys and men.8 Clinical presentation often consists of acute-onset hair loss, portions of scalp hair that are unaffected, and chaotic regrowth of hair in areas of alopecia.6 Eyebrows, eyelashes, and other body hair are usually not involved.6 Trichotillomania results in clinically significant social and occupational impairment, and patients usually feel embarrassed or ashamed of their pulling behavior.9

The pathogenesis of trichotillomania is complex and composed of many factors. Affected individuals may pull hair to cope with stress, anxiety, sadness, or other difficult emotions.7 Hormonal changes during pregnancy can improve or worsen trichotillomania by causing mood fluctuations.7 Patients feel a sense of relief after the hair is pulled and often do it during isolated time such as while in the bathroom, while driving, or before falling asleep.8 Most patients pull their hair without self-awareness, whereas others mindfully focus on pulling their hair.8,9 Many patients have psychiatric comorbidity; 65% have a mood disorder throughout their lifetimes, 57% have anxiety disorders, 22% have substance use disorders, and 20% have eating disorders.8 Not only can trichotillomania lead to psychiatric comorbidities, but it can also result in skin irritation and infection.8

Trichoscopic findings can vary depending on the frequency, force, and method of hair pulling. Generally, the examinations reveal numerous, disordered hair shaft deformities with no significant changes in the perifollicular area.7 The hair shafts often show broken hairs of differing lengths, short hairs with trichoptilosis, coiled hairs, exclamation-mark hairs, and black dots indicating hair shaft residues.7 Yellow dots that are characteristic of AA are usually not seen in trichotillomania, although they can occur infrequently.7 A very specific sign of trichotillomania are flame hairs, which occur in about a quarter of affected individuals.10 When more than two hairs emerge from a single follicular unit and are pulled out and break at the same length, a V-sign is created and also indicates trichotillomania.10 Diagonally broken hair shafts that result in dark, short hairs with flower-shaped ends are called tulip hairs, which can also help a clinician identify the condition in a patient.10 Hair shafts that have been continually damaged by the mechanical trauma of hair pulling may cause only hair residues to remain observable.10

The differential diagnosis of trichotillomania includes alopecia areata, androgenic alopecia, and tinea capitis.6 The geometric shape and irregular borders of trichotillomania differentiate it from other types of alopecia.

Treatment for trichotillomania can be psychologic or pharmacologic but will often only lessen existing symptoms without entirely eliminating the problem.9 The goal for some patients is complete self-restraint from hair pulling, whereas others strive for less frequent hair pulling.9 Selective serotonin reuptake inhibitors are commonly prescribed for the condition, but there is no evidence that these drugs perform better than placebo at improving the disease, according to a meta-analysis of pharmacologic treatment studies.9 However, there is strong empiric support that the amino acid N-acetylcysteine shows strong effectiveness over placebo.9

Nonpharmacologic treatments include habit reversal training: patients must become conscious of their hair pulling through awareness training.9 They also must acknowledge when their hands move toward the area of hair pulling through a process called competing response training.9 Social support is also important in order to keep the patient encouraged and motivated to eliminate the disease.9 Stimulus control can also be used as a treatment; this involves identifying situations that trigger hair pulling.9 The patient can learn to abolish or limit exposure to these situations.9 A combination of stimulus control and habit reversal training has proven to be very effective against trichotillomania.9

In this case, the patient was diagnosed with trichotillomania and referred to a psychiatrist for operationalized psychodynamic diagnosis and further cognitive behavioral management.7


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Kelly Wilmas is a medical student at McGovern Medical School of the University of Texas and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston.

References

  1. Ito T. Recent advances in the pathogenesis of autoimmune hair loss disease alopecia areata. Clin Dev Immunol. 2013;2013:348546.
  2. Alsantali A. Alopecia areata: a new treatment plan. Clin Cosmet Investig Dermatol. 2011;4:107-115.
  3. Biran R, Zlotogorski A, Ramot Y. The genetics of alopecia areata: new approaches, new findings, new treatments. J Dermatol Sci. 2015;78(1):11-20.
  4. Gorcey L, Spratt E, Leger MC. Alopecia universalis successfully treated with adalimumab. JAMA Dermatol. 2014;150(12):1341-1344.
  5. Mubki T, Rudnicka L, Olszewska M, Shapiro J. Evaluation and diagnosis of the hair loss patient: part II. Trichoscopic and laboratory evaluations. J Am Acad Dermatol. 2014;71(3):431.e1-431.e11.
  6. Harth W, Blume-Peytavi U. Psychotrichology: psychosomatic aspects of hair diseases. J Dtsch Dermatol Ges. 2013;11(2):125-135.
  7. Thakur BK, Verma S, Raphael V, Khonglah Y. Extensive tonsure pattern trichotillomania-trichoscopy and histopathology aid to the diagnosis. Int J Trichology. 2013;5(4):196-198.
  8. Franklin ME, Tolin DF. Treating Trichotillomania: Cognitive-behavioral Therapy for Hairpulling and Related Problems. New York, NY: Springer-Verlag; 2007.
  9. Woods DW, Houghton DC. Diagnosis, evaluation, and management of trichotillomania. Psychiatr Clin North Am. 2014;37(3):301-317.
  10. Yorulmaz A, Artuz F, Erden O. A case of trichotillomania with recently defined trichoscopic findings. Int J Trichology. 2014;6(2):77-79. 
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