Dr. Susan Taylor presented information about the pathogenesis, clinical features, diagnosis, and treatment of alopecia areata (AA). AA has a significant impact on patient quality of life, including low self-esteem, emotional distress, mood disturbances, and disrupted relationships. Thus, patients need timely diagnosis and appropriate treatment.
Susan Taylor, MD, Bernett Johnson Professor of Dermatology at the Perelman School of Medicine, University of Pennsylvania, in Philadelphia
First, Taylor discussed AA pathogenesis and clinical features. AA pathogenesis is multifactorial with genetic, environmental, emotional, and autoimmune components. It occurs when immune privilege collapse causes T-cell mediated destruction of the hair bulb, leading to hair loss. AA can be drug-induced, often due to monoclonal antibodies.
AA clinical features include coin-shaped areas of complete hair loss, generalized thinning of scalp hair (can be confused with androgenetic alopecia), ophiasis band, and sisaipho pattern. Alopecia totalis involves total loss of scalp hair; alopecia universalis involves hair loss on the entire body including eyebrows and eyelashes. AA nail manifestations include trachyonychia and nail pitting or ridging.
Second, Taylor discussed AA diagnosis and clinical course. AA is usually a clinical diagnosis. Features on dermatoscopy include exclamation point hairs, broken hair shafts, and black or yellow dots. A biopsy is indicated if patient history and physical exam are insufficient for diagnosis. The histopathology of areas of acute disease appears as inflammatory infiltrate surrounding anagen follicles known as a “swarm of bees.”
AA has a variable clinical course: 25% of patients have a single episode, and half of patients recover within one year without treatment. An estimated 5% of patients with AA have increased risk for alopecia totalis and 1% have higher risk for alopecia universalis. Forty percent of relapses occur within one year. Risk factors for poor prognosis include childhood onset, alopecia totalis or universalis on presentation, ophiasis pattern, nail involvement, atopy, and family history of AA.
AA severity is measured using the severity of alopecia tool (SALT), with scores ranging from 0 (no hair loss) to 100 (total hair loss). Mild AA involves <20% scalp hair loss; moderate AA involves 21–49% scalp hair loss; and severe AA involves >50% scalp hair loss. The severity of mild or moderate AA should be increased one level if any of the following are present: negative effect on psychosocial functioning, eyebrow or eyelash involvement, inadequate response after six months of treatment, or a multifocal positive hair pull test indicating rapidly progressing AA.
Comorbidities associated with AA include atopic diseases, inflammatory bowel disease, vitiligo, systemic lupus erythematosus, rheumatoid arthritis, and type 1 diabetes. Thyroid disease is highly associated with AA; AA patients should be screened for thyroid-related signs and symptoms.
Third, Taylor discussed AA treatments. Treatment options for mild-to-moderate AA include topical and intralesional corticosteroids. First-line treatment for severe AA is oral Janus kinase (JAK) inhibitors. FDA-approved JAK inhibitors for AA include baricitinib (JAK1/2 inhibitor), ritlecitinib (JAK3/tyrosine kinase expressed in hepatocellular carcinoma inhibitor), and deuruxolitinib (JAK1/2 inhibitor). Taylor reviewed the efficacy and safety results from the clinical trials of these agents.
Taylor receives many referrals from dermatologists who are uncomfortable prescribing JAK inhibitors due to the Black Box Warning for risk of major cardiovascular events, cancer, thrombosis, and death. The Black Box Warning was implemented based on data from patients with rheumatoid arthritis taking 5–10 mg tofacitinib twice daily. Taylor noted that most of these patients were older than 50 years and had more than one cardiovascular risk factor. By contrast, patients with AA are usually younger and healthier, without cardiovascular risk factors.
Taylor described patient selection and screening for JAK inhibitors. The European Medicines Association cautions against dermatologic use of JAK inhibitors in patients older than 65 years, with major cardiovascular risk, increased cancer risk, or smoking history. JAK inhibitor use should be avoided in patients with HIV, hepatitis, active tuberculosis, high infection risk, malignancy history, and thrombosis history; patients on oral contraceptives who fly frequently or hormone replace therapy; and pregnant patients. JAK inhibitors are contraindicated in patients with absolute neutrophil count <1000 cells/mm3, absolute lymphocyte count <500 cells/mm3, hemoglobin level <8g/dL, or severe hepatic or renal impairment.
Before starting a JAK inhibitor, patients should receive age-appropriate cancer screenings and vaccinations (e.g., herpes zoster, COVID-19, influenza, and RSV). Initial screening bloodwork includes complete blood count with differential, liver and kidney function, lipid panel, and testing for hepatitis B, hepatitis C, HIV, and tuberculosis. Bloodwork should be monitored one month after starting treatment and quarterly thereafter. JAK inhibitors are associated with frequent non–life-threatening side effects including acne, headache, fatigue, nausea, weight gain, and myalgia. Taylor emphasized the difference between safety and tolerability when using these agents.
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