INTRODUCTION
Alopecia areata (AA) is an autoimmune disease characterized by nonscarring hair loss on the scalp and body, with periods of relapse and remission, or complete hair loss on the scalp (alopecia areata totalis [AT]) or whole body, including the eyebrows and eyelashes (alopecia areata universalis [AU]).1,2 Adults with AA seek outpatient primary and dermatological care more frequently than adults without AA, for both AA and comorbid conditions, negatively impacting mental health, social interactions, and employment.3 A model predicting demands for dermatological care in the US through the year 2030 suggests that nurse practitioners (NPs) and physician assistants (PAs) will become crucial providers in the dermatology workforce to avoid shortages in care; thus, continuing to educate NPs and PAs in dermatological conditions and treatments is critical.4
Alopecia areata affects 2% of the global population.1 Prevalence is higher in females than in males, which may be influenced by a greater tendency for females to seek medical care.5 Reported incidence is greatest in Black and Hispanic/Latino patients.6 While AA can develop at any time, the average age of diagnosis is 38.9 to 40.6 years; in a subgroup analysis, incidence is highest in adults 18 to 44 and children and adolescents 12 to 17 years of age.5 Occurrences of AA in identical twins and siblings support that AA is hereditary;7 genes associated with AA are involved in immune functions and Janus kinase (JAK) signaling pathways.7 Environmental factors, including traumatic events and acute stress, also influence the development and progression of AA.8 Pathologically, AA develops due to the loss of protection of hair follicles from immune cells (collapse in immune privilege), leading to the release of proinflammatory cytokines that activate JAK signaling pathways (Figure 1A).9,10
Comorbid Conditions and Psychosocial Burden
Based on a meta-analysis (n = 102 studies), autoimmune and inflammatory disorders are common comorbidities in patients with AA, including thyroid (autoimmune thyroiditis [prevalence, 41.4%] and autoimmune hypothyroidism [4.5%]), atopic (allergic rhinitis [26.5%] and allergic conjunctivitis [21.4%]), dermatological (skin infection [13.2%] and acne vulgaris [12.8%]), and rheumatic (rheumatoid arthritis [1.0%] and systemic lupus erythematous [0.3%]) diseases.11 Additional comorbidities include cardiovascular disease (13.4%), iron deficiency anemia (6.3%), and vitamin D deficiency (1.0%).11 A systematic review of 4 studies indicated that, globally, 66% to 74% of patients with AA suffer from psychiatric disorders, including anxiety and depression; an additional study reported that over half suffer from impaired quality of life (QoL).12
Clinical Presentation and Diagnosis
Alopecia areata presents as patchy hair loss without scarring or inflammation; besides minor itching and tingling, most patients are asymptomatic prior to and during AA episodes.1,2 Hair loss may visually differ between patients depending on the AA subtype, including patchy alopecia, ophiasis, AT, and AU.2
Alopecia areata is typically diagnosed through clinical examination and trichoscopy, although skin biopsy might be necessary when a diagnosis is uncertain.2,8 Clinical features of AA by trichoscopy include yellow dots, short vellus hairs, black dots, tapered hairs, broken hairs, exclamation mark hairs, upright regrown hairs, and pigtail hairs.2 As AA is hereditary and often comorbid with other conditions, family history and medical background should be considered when diagnosing AA.7, 8,11
Alopecia areata affects 2% of the global population.1 Prevalence is higher in females than in males, which may be influenced by a greater tendency for females to seek medical care.5 Reported incidence is greatest in Black and Hispanic/Latino patients.6 While AA can develop at any time, the average age of diagnosis is 38.9 to 40.6 years; in a subgroup analysis, incidence is highest in adults 18 to 44 and children and adolescents 12 to 17 years of age.5 Occurrences of AA in identical twins and siblings support that AA is hereditary;7 genes associated with AA are involved in immune functions and Janus kinase (JAK) signaling pathways.7 Environmental factors, including traumatic events and acute stress, also influence the development and progression of AA.8 Pathologically, AA develops due to the loss of protection of hair follicles from immune cells (collapse in immune privilege), leading to the release of proinflammatory cytokines that activate JAK signaling pathways (Figure 1A).9,10
Comorbid Conditions and Psychosocial Burden
Based on a meta-analysis (n = 102 studies), autoimmune and inflammatory disorders are common comorbidities in patients with AA, including thyroid (autoimmune thyroiditis [prevalence, 41.4%] and autoimmune hypothyroidism [4.5%]), atopic (allergic rhinitis [26.5%] and allergic conjunctivitis [21.4%]), dermatological (skin infection [13.2%] and acne vulgaris [12.8%]), and rheumatic (rheumatoid arthritis [1.0%] and systemic lupus erythematous [0.3%]) diseases.11 Additional comorbidities include cardiovascular disease (13.4%), iron deficiency anemia (6.3%), and vitamin D deficiency (1.0%).11 A systematic review of 4 studies indicated that, globally, 66% to 74% of patients with AA suffer from psychiatric disorders, including anxiety and depression; an additional study reported that over half suffer from impaired quality of life (QoL).12
Clinical Presentation and Diagnosis
Alopecia areata presents as patchy hair loss without scarring or inflammation; besides minor itching and tingling, most patients are asymptomatic prior to and during AA episodes.1,2 Hair loss may visually differ between patients depending on the AA subtype, including patchy alopecia, ophiasis, AT, and AU.2
Alopecia areata is typically diagnosed through clinical examination and trichoscopy, although skin biopsy might be necessary when a diagnosis is uncertain.2,8 Clinical features of AA by trichoscopy include yellow dots, short vellus hairs, black dots, tapered hairs, broken hairs, exclamation mark hairs, upright regrown hairs, and pigtail hairs.2 As AA is hereditary and often comorbid with other conditions, family history and medical background should be considered when diagnosing AA.7, 8,11
