Remission of Alopecia Areata Post-colectomy in a Patient with Crohn’s Disease

J Clin Aesthet Dermatol. 2025;18(9):26–27.

by Caroline Sulich-Moore, DNP, FNP-C, and David Altman, MD, FAAD

Dr. Sulich-Moore and Dr. Altman are with the Midwest Center for Dermatology & Cosmetic Surgery in Warren, Michigan.

FUNDING: No funding was provided for this article.

DISCLOSURES: Dr. Altman reports speaking fees from AbbVie, Amgen, Arcutis, Bristol Myers Squibb, Dermavant, Incyte, Janssen, Lilly, and UCB. Dr. Sulich-Moore has no conflicts of interest to declare.

Abstract: Alopecia areata (AA) is an immune-mediated, nonscarring hair loss with established associations with various autoimmune conditions, including inflammatory bowel disease. The following case describes a 38-year-old White male patient with Crohn’s disease who developed rapidly-progressive alopecia areata during treatment with infliximab. Despite discontinuation of infliximab and aggressive treatment with corticosteroids and tofacitinib, the patient progressed to alopecia universalis within six months. Concurrently, the patient’s Crohn’s disease required escalation to colectomy with ostomy placement due to inadequate response to vedolizumab. Following his colectomy, the patient continued treatment with tofacitinib and demonstrated dramatic improvement in his AA, achieving complete hair regrowth within one year and maintaining remission two years after discontinuation of all immunosuppressive therapies. This case illustrates potential mechanistic connections between alopecia areata and Crohn’s disease through shared inflammatory pathways involving interferon-γ and JAK signaling. The temporal relationship between the patient’s colectomy and remission of his alopecia areata suggests a gut-immune axis mechanism, where addressing the primary intestinal inflammatory source may have influenced a remote autoimmune manifestation. This case highlights the potential for targeting primary inflammatory sources to achieve broader immunologic benefits in patients with concurrent autoimmune conditions. Keywords: alopecia areata, Crohn’s disease, autoimmune comorbidity, JAK inhibitors, gut-immune axis

Introduction

Alopecia areata (AA) is an immune-mediated, nonscarring hair loss involving chronic inflammation at the level of the hair follicle.¹ The disease is mediated by T-helper 1 (T_H1) lymphocytes and proinflammatory cytokines, and its etiology is multifactorial, involving genetic, environmental, and infectious components.² Loss of hair in AA commonly presents as localized, circumscribed patches in the scalp, but it may progress to involve the entire scalp (alopecia totalis) or the entire body (alopecia universalis).¹

A growing body of research suggests higher rates of comorbid autoimmune conditions, such as systemic lupus erythematosus, vitiligo, autoimmune hypothyroidism, and inflammatory bowel disease, among patients with AA than among the general population.³ In patients with inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease, hair loss consistent with AA is common, frequently attributed either to extraintestinal manifestations of the disease or to therapy with anti-tumor necrosis factor (TNF)-α agents.² The following case illustrates the disease course of AA in a patient with concomitant Crohn’s disease, perhaps suggesting related inflammatory pathways between these conditions.

Case Report

A 38-year-old White male patient presented with a rapidly progressive, patchy hair loss on the scalp of two weeks’ duration (Figure 1). The patient was undergoing treatment with infliximab for his Crohn’s disease at the time of presentation. A punch biopsy of the scalp revealed a dramatic shift to catagen and telogen phase hairs with miniaturization and peribulbar lymphocytic inflammation. The patient was diagnosed with AA, and treatment was initiated with oral prednisone, fexofenadine, intramuscular betamethasone, and intralesional triamcinolone. Following his AA diagnosis, the patient’s infliximab was discontinued.

At the time of diagnosis, no systemic agents were yet approved for the treatment of AA. Despite aggressive therapy with oral, intralesional, and systemic corticosteroids, his condition continued to progress, eventually leading to a near-complete loss of scalp, facial, and body hair within6 months of diagnosis (Figure 2 and Figure 3). In light of his disease severity, off-label treatment with oral tofacitinib was initiated.

During this time, the patient continued treatment for his Crohn’s disease. After discontinuation of infliximab, he was transitioned to vedolizumab; however, it did not sufficiently control escalating disease severity. The patient eventually underwent a colectomy with ostomy placement. Post-colectomy, the patient exhibited dramatic improvement of his AA on tofacitinib. After one year on therapy, the patient had demonstrated universal regrowth of hair, at which time a decision was made to taper his tofacitinib. Two years following discontinuation of all immunosuppressants, the patient has remained symptom-free with complete regrowth (Figure 4).

Discussion

The coexistence of multiple autoimmune conditions in a single patient highlights the complexity of immune-mediated pathologies in clinical practice. In this case, the concurrent presence of AA and Crohn’s disease offers an opportunity to examine potential mechanistic overlaps. In examining the immunologic cascades of both diseases, interferon-γ constitutes a common thread, as it is produced by T_H1 lymphocytes and CD8⁺ T cells.⁴ Interferon-γ activation is reliant upon Janus kinase (JAK) signal transduction, which explains the role of JAK inhibition in modulating both diseases.⁴

While it is possible that the patient’s AA was induced by infliximab therapy, his achievement of disease remission following colectomy and discontinuation of tofacitinib may support the gut-immune axis as a potential mediator in the pathogenesis of both conditions.⁴ Emerging evidence supports the potential for chronic inflammatory processes, particularly those of the large intestine, to trigger additional inflammation in remote areas throughout the body.^5,6 While the pathophysiology of this phenomenon has yet to be fully elucidated, it has been proposed that increased intestinal permeability can lead to abnormal lymphocyte homing, promotion of T-cell trafficking by chemokines and adhesion molecules, and molecular mimicry.^5,7

This case illustrates a potential relationship between two autoimmune conditions that may have previously been considered distinct. Furthermore, the patient’s remission of AA post-colectomy might suggest that addressing a primary inflammatory source may have downstream effects on remote autoimmune manifestations. Further research into the gut-immune axis and its role in various autoimmune pathologies may yield novel therapeutic strategies that target common inflammatory pathways, potentially reducing the need for multiple immunosuppressive agents in patients with concurrent autoimmune diseases.

References

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