The exact cause of AA is still unknown, though the current body of evidence supports an autoimmune origin with a strong genetic contribution, further modified by unknown environmental influences. A positive family history is evident in approximately 10–25% of cases.^1–3 

Abbreviation

AA, alopecia areata.

References

1. Spano F, Donovan JC. Can Fam Physician. 2015;61:751–5.
2. Wang S, et al. Dermatol Online J. 2018;24:14.
3. American Academy of Dermatology Association. Alopecia areata causes. Available at: www.aad.org/public/diseases/hair-loss/types/alopecia/causes (accessed 1 September 2022).

AA has been shown to impair patients’ emotional and psychological wellbeing, relationships, and lifestyles.¹ Furthermore, patients’ perception of their current AA as moderate to severe consistently predicts scores on QoL (Skindex-16) and daily impairment (WPAI).² A framework for understanding disease severity has been proposed, whereby disease severity is anchored in the amount of scalp hair loss and then modified depending on the presence of either non-scalp hair loss (eyebrows, eyelashes), inadequate treatment response, multifocal diffuse positive hair pull test (indicating poor prognosis), and negative impact on psychosocial functioning.³ 

Abbreviations

AA, alopecia areata; QoL, quality of life; WPAI, Work Productivity and Activity Impairment.

References

1. Aldhouse NVJ, et al. J Patient Rep Outcomes. 2020;4:76.
2. Senna M, et al. J Invest Dermatol. 2022;doi.org/10.1016/j.jid.2022.02.019.
3. King BA, et al. Dermatol Ther (Heidelb). 2022;12:825–34.

AA is caused by the destruction of immune privilege in healthy hair follicles. Substance P is a stress-associated neuropeptide believed to play a significant role in the expression of proinflammatory signals associated with AA. Recent evidence supports the hypothesis that interaction between perifollicular mast cells and substance P activation induces neurogenic inflammation, resulting in immune privilege collapse. Additionally, substance P has also been shown to prevent hair growth and induce keratinocyte apoptosis. 

Abbreviation

AA, alopecia areata. 

Reference

Kim C, et al. Ann Dermatol. 2022;34:270–7.

Currently, there is no consensus on the optimal duration of maintenance of treatment with JAK inhibitors in AA, although several studies suggest that to maintain hair regrowth, continuous treatment should be considered where it is effective and well tolerated.^1–3 

Patients with nearly complete or complete scalp hair loss, with or without substantial eyelash or eyebrow hair loss, can be treated with baricitinib 4 mg once daily.⁴ Dosing should be reduced to the recommended dose of 2 mg daily when an adequate response has been achieved.⁴ This recommendation reflects findings from a randomized down-titration period in the BRAVE-AA2 trial, where 75% of patients who achieved an adequate response (SALT ≤20) to baricitinib 4 mg once daily were shown to maintain that response following an additional 24 weeks’ treatment with baricitinib 2 mg once daily versus 98% of patients remaining on baricitinib 4 mg once daily.⁴ 

Abbreviations

AA, alopecia areata; JAK, Janus kinase; SALT, Severity of Alopecia Tool.

References

1. Kennedy Crispin M, et al. JCI Insight. 2016;1:e89776.
2. Almutairi N, et al. Dermatology. 2019;235:130–6.
3. Peeva E, et al. J Am Acad Dermatol. 2021;87:390–3.
4. FDA. Baricitinib PI. Available at: www.accessdata.fda.gov/drugsatfda_docs/label/2022/207924s007lbl.pdf (accessed 30 August 2022).

Baricitinib lowers the ability of the immune system to fight infection. Patients with evidence of active hepatitis B or C infection were excluded from clinical trials and the risk of chronic viral hepatitis reactivation during treatment with baricitinib is unknown. It is, therefore, recommended that patients be screened for viral hepatitis in accordance with clinical guidelines, before starting treatment; if positive for hepatitis antibody but negative for active disease, they should be monitored during treatment for evidence of reactivation. 

Reference

FDA. Baricitinib PI. Available at: www.accessdata.fda.gov/drugsatfda_docs/label/2022/207924s007lbl.pdf (accessed 30 August 2022).