Ixekizumab is a humanized monoclonal immunoglobulin G (IgG) 4 antibody generally tolerated well. Common side effects observed in patients using ixekizumab include: neutropenia, injection site reaction, hypersensitivity reactions. Also, fungal infections, nausea, thrombocytopenia are seen, and rarely Crohn's disease and ulcerative colitis are observed
2-3. In our case, the patient had no previous symptoms, no other medication use other than ixekizumab or no known disease, so we conclude that she developed LP potentially caused by ixekizumab. There are cases of oral lichen planus in the literature that occurred as a result of the use of secukinumab, another IL-17 inhibitor, but to our knowledge, this is the first case of oral lichen planus that developed with the use of ixekizumab
4-5.
We think that the exacerbation of LP lesions during the patient's use of guselkumab, an IL-23 inhibitor, may be due to the patient's lack of treatment at that time rather than a possible side effect of guselkumab. Because, a significant regression was observed in the lesions after intralesional steroid treatment administered without discontinuing the patient's guselkumab treatment.
Lichen planus (LP) is a chronic inflammatory disease characterized by violaceous papules and plaques. LP, which affetcs both skin and oral mucousa, is more commonly seen in women between the ages of 30 and 60. The prevalence of oral lesions varies between 0.1 and 2.2%. While lichen lesions on the skin respond well to treatment and tend to be self-limiting, oral mucosal lesions are chronic and often exhibit multiple remissions and exacebrations. Clinical types of oral LP include plaque-like, atrophic, papular, erosive and bullous type. Whickam's lines are a fine, asymptomatic, interwoven, lace-like pattern seen in the reticular type. The erosive type is painful due to erosions and rarely carries the risk of developing SCC. The etiology of oral LP has not been fully explained, and existing studies in the literature highlight its immunopathogenic basis with enhanced cytokine regulation 6-7.
It is known that biological treatments reduce the formation of pro-inflammatory cytokines by inhibiting the expression and differentiation of cytokines such as Th1 and Th17, which are involved in the pathogenesis of psoriasis 8.
However, IL-17 plays a critical role in mucocutaneous immunity by inducing antimicrobial peptides and chemokines that protect against fungal and bacterial infections. Inhibition of IL-17 may lead to reactivation of latent pathogens or new infections, triggering a T-cell-mediated immune response, particularly involving CD8+ T cells and dendritic cells. In patients with psoriasis, regulatory T cell (Treg) dysfunction is common; these dysfunctional Tregs, especially those producing IL-17, fail to suppress immune responses adequately, contributing to autoimmunity. This dysregulation, combined with IL-17 inhibition, may result in excessive activation of cytotoxic T cells and dendritic cells, provoking a lichenoid inflammatory response 9-10.
Based on these pathogenic mechanisms, we believe oral lichen planus in our case may have developed through a similar immunological process. Future studies are warranted to help deepen this issue.
Nowadays, biological agents are being used with increasing frequency in psoriasis. Although the selectivity of biological agents has increased, new adverse reactions may still occur. Clinicians who use ixekizumab in their patients should be careful about this side effect and follow up patients in terms of cutaneous-mucosal LP.
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