INTRODUCTION
Alopecia areata (AA) is a nonscarring alopecia, characterized by patchy hair loss affecting the scalp, face, and body, with a smaller subset of patients progressing to alopecia totalis (AT) or universalis (AU). The pathogenesis of AA is widely accepted as an autoimmune condition involving lymphocytic infiltration around the hair bulb.1
Current AA therapies focus on hair regrowth in alopecic patches, and on minimizing progression of alopecia, with the mainstay of therapy centered around steroids or other immune-modulating medications. On histology, AA demonstrates a predominantly lymphocytic inflammatory infiltrate although mast cells adjacent to hair follicles are also seen. Interferon (IFN)-γ produced by T-cells induces expression of major histocompatibility classes I and II (MHC-I/-II), intercellular adhesion molecule-1 (ICAM-1), and human leukocyte antigen (HLA)-DR, implicated in the loss of immune privilege.2 Histamine enhances IFN-γ induced expression of ICAM-1 and MHC-I, thereby presenting a potential therapeutic target in AA.3
Atopy is common in AA patients, many presenting with concomitant atopic dermatitis (AD), allergic rhinitis, or asthma. AD is classically considered a Th2-mediated disease with elevated interleukin (IL)-4, IL-5, IL-13, and IL-31, a pathway classically not associated with AA.4 Dupilumab is a monoclonal antibody recently approved to treat moderate to severe AD, targeting IL-4 and IL-13 and thus downregulating Th2-mediated inflammation.5 Although the pathogenesis of AA is not fully understood, studies show an upregulation of Th1 and Th2 signaling cascades, as well as phosphodiesterase (PDE)-4, IL-23, and IL-9.6 With recent better understanding of the overlapping Th2 component of AA and AD, dupilumab and antihistamines may represent novel therapeutic options for AA. This systematic review aims to assess the use of antihistamines and dupilumab in AA.
Current AA therapies focus on hair regrowth in alopecic patches, and on minimizing progression of alopecia, with the mainstay of therapy centered around steroids or other immune-modulating medications. On histology, AA demonstrates a predominantly lymphocytic inflammatory infiltrate although mast cells adjacent to hair follicles are also seen. Interferon (IFN)-γ produced by T-cells induces expression of major histocompatibility classes I and II (MHC-I/-II), intercellular adhesion molecule-1 (ICAM-1), and human leukocyte antigen (HLA)-DR, implicated in the loss of immune privilege.2 Histamine enhances IFN-γ induced expression of ICAM-1 and MHC-I, thereby presenting a potential therapeutic target in AA.3
Atopy is common in AA patients, many presenting with concomitant atopic dermatitis (AD), allergic rhinitis, or asthma. AD is classically considered a Th2-mediated disease with elevated interleukin (IL)-4, IL-5, IL-13, and IL-31, a pathway classically not associated with AA.4 Dupilumab is a monoclonal antibody recently approved to treat moderate to severe AD, targeting IL-4 and IL-13 and thus downregulating Th2-mediated inflammation.5 Although the pathogenesis of AA is not fully understood, studies show an upregulation of Th1 and Th2 signaling cascades, as well as phosphodiesterase (PDE)-4, IL-23, and IL-9.6 With recent better understanding of the overlapping Th2 component of AA and AD, dupilumab and antihistamines may represent novel therapeutic options for AA. This systematic review aims to assess the use of antihistamines and dupilumab in AA.
