# Erosive Oral Lichen Planus Treated With Upadacitinib Amid Systemic Psoriatic Therapy

## TL;DR

A patient with severe mouth ulcers and psoriasis found relief using upadacitinib, a drug that targets immune system pathways.

## Contribution

Upadacitinib, a JAK1 inhibitor, successfully treated refractory erosive oral lichen planus in a patient with psoriatic arthritis.

## Key findings

- Upadacitinib resolved erosive oral lichen planus and improved psoriatic arthritis symptoms in a treatment-resistant patient.
- JAK1 inhibition may target shared inflammatory pathways in psoriatic arthritis and oral lichen planus.
- Systemic JAK inhibitors like upadacitinib could be a novel therapeutic option for refractory erosive oral lichen planus.

## Abstract

Oral lichen planus (OLP) is a rare immune-mediated mucocutaneous disorder with several subtypes, including erosive OLP, which is particularly challenging to manage. First-line therapies are topical corticosteroids or calcineurin inhibitors, while erosive OLP may require intralesional triamcinolone. Refractory OLP requires systemic immunosuppressants. JAK inhibitors are a new consideration for refractory disease. A 41-year-old female with psoriasis (PsO), psoriatic arthritis (PsA), and biopsy-confirmed OLP presented with worsening oral ulceration. Previous treatments, including prednisone, clobetasol gel, dexamethasone, chlorhexidine rinses, and mycophenolate, provided little relief. As her OLP remained unresponsive to treatment, her psoriasis also proved challenging, necessitating multiple therapeutic adjustments. She was started on apremilast for her PsO and PsA, which was ineffective. She transitioned to certolizumab pegol, which provided partial relief but led to recurrent infections. Bimekizumab was then initiated, clearing her PsO, but leaving her with persistent joint pain. Given her persistent PsA, she was started on upadacitinib 15 mg daily, which was later increased to 30 mg. At this dose, her joint pain improved, and her OLP erosions resolved. Upadacitinib, a JAK1 inhibitor approved for PsA, reduces STAT-dependent inflammatory signaling. Studies show JAK1 and JAK3 overexpression in lichen planus (LP) inflammatory infiltrates, implicating JAK signaling in its pathogenesis. Given the inflammatory pathway overlap between PsA and LP, JAK inhibition may mitigate the chronic inflammatory cascade that drives erosive OLP. Upadacitinib’s efficacy in this case of refractory erosive OLP warrants further clinical studies to establish its therapeutic role.