Alopecia areata : Disease characteristics, clinical evaluation, and new perspectives on pathogenesis - 13/12/17

Doi : 10.1016/j.jaad.2017.04.1141

Lauren C. Strazzulla, BA ^a, Eddy Hsi Chun Wang, PhD ^b, Lorena Avila, MD ^a, Kristen Lo Sicco, MD ^a, Nooshin Brinster, MD ^a, Angela M. Christiano, PhD ^b, Jerry Shapiro, MD ^a,^⁎
^a The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York
^b Department of Dermatology, College of Physicians and Surgeons, Columbia University, New York, New York

^∗Correspondence to: Jerry Shapiro, MD, Department of Dermatology, New York University School of Medicine, 530 First Ave, Unit 7R, New York, NY 10016.Department of DermatologyNew York University School of Medicine530 First Ave, Unit 7RNew YorkNY10016

Abstract

Alopecia areata (AA) is a common, inflammatory, nonscarring type of hair loss. Significant variations in the clinical presentation of AA have been observed, ranging from small, well-circumscribed patches of hair loss to a complete absence of body and scalp hair. Patients affected by AA encompass all age groups, sexes, and ethnicities, and may experience frustration with the unpredictable nature of their disease for which there is currently no definitive treatment. The cause of AA remains incompletely understood, though it is believed to result—at least in part—from a loss of immune privilege in the hair follicle, autoimmune-mediated hair follicle destruction, and the upregulation of inflammatory pathways. Patients with AA frequently experience marked impairment in psychological well-being, self-esteem, and may be more likely to suffer from psychiatric comorbidities. Part one of this two-part continuing medical education series describes the epidemiology, clinical evaluation, prognosis, and recent advancements in the understanding of the pathogenesis of AA.

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Key words : alopecia areata, alopecia totalis, alopecia universalis, pathogenesis, prognosis, subtype

Abbreviations used : AA, AT, AU, CTL, CTLA-4, GWAS, HF, HLA, IFN, IL, JAK, MCH, MCHR2, MCHR2-AS1, MHC, NKG2D, PRDX5, SALT, STX17, Treg, ULBP

Plan

Epidemiology

Clinical evaluation

Differential diagnosis

Clinical subtypes

Prognosis

Pathogenesis

Autoimmune hypothesis

Animal models

Histologic findings

Genetic studies

The Janus kinase/signal transducers and activators of transcription signaling pathway

Comorbidities

Other factors contributing to alopecia areata

	Funding sources: None.
	Dr Shapiro is a consultant for Aclaris Therapeutics, Applied Biology, Incyte, Replicel Life Sciences, and Samumed. Dr Christiano is a consultant for Aclaris Therapeutics and a principal investigator for Pfizer. The other authors have no conflicts of interest to declare.
	Ms Strazzulla and Dr Wang contributed equally to this article.
	Date of release: January 2018
	Expiration date: January 2021