A Practical Guide to the Management of Oral Candidiasis in Patients with Plaque Psoriasis Receiving Treatments That Target Interleukin-17

Abstract

Plaque psoriasis is an immune-mediated inflammatory skin disease associated with the dysregulation of cytokines, especially those involved in the interleukin (IL)-23/IL-17 pathways. In recent years, there has been growing interest in developing biologic therapies that target these pathways. However, inhibition of the cytokines of the IL-23/IL-17 pathways may increase patients' risk of developing fungal infections, particularly oral candidiasis. Therefore, it is important that dermatology practitioners can effectively diagnose and treat oral candidiasis. In this review, we examine the role of the IL-23/IL-17 pathways in antifungal host defense, and provide a practical guide to the diagnosis and treatment of oral candidiasis in patients with psoriasis. Overall, while treatment with anti-IL-17 medications leads to an increased incidence of oral candidiasis in patients with psoriasis, these cases are typically mild or moderate in severity and can be managed with standard antifungal therapy without discontinuing treatment for psoriasis. If applicable, patients with psoriasis should also be advised to practice good oral hygiene and manage or control co-existing diabetes, and should be provided with information on smoking cessation to prevent oral candidiasis.

Keywords: Candida; Interleukin-17; Oral candidiasis; Plaque psoriasis.

Fig. 1

Simplified model of host defense against oral candidiasis. Colonization of the oral mucosal epithelium by Candida results in the activation of macrophages and DCs, either directly or indirectly, via alarmins such as IL-1α, IL-1β, and IL-36, which are released in response to tissue damage by the peptide candidalysin. This then triggers the expression and secretion of IL-6, IL-1β, and IL-23, which induce the differentiation and proliferation of Th17 cells from naïve CD4⁺ T cells. These Th17 cells produce the cytokines IL-17A, IL-17F, and IL-22, which recruit neutrophils to the site of infection and act on epithelial cells to induce the release of antifungal β-defensins. Through the inhibition of IL-17 or its receptors, anti-IL-17 medications prescribed for psoriasis can increase the risk of oral candidiasis through inhibition of Th17 cell-mediated antifungal pathways. DC dendritic cells, IL interleukin, R receptor, Th17 T-helper cell type 17

Fig. 2

Algorithm for the diagnosis and management of oral candidiasis in patients with plaque psoriasis. ^aIn the case that administration of anti-IL-17 treatment falls on the same day in which the antifungal treatment for oral candidiasis is initiated, administration of anti-IL-17 can be postponed for 3–4 days to prioritize resolution of oral candidiasis

Fig. 3

Clinical presentations of oral candidiasis. A Pseudomembranous candidiasis in a male patient receiving anti-IL-17A treatment for plaque psoriasis; this patient was also a smoker. Patient image was provided courtesy of Dr Gisondi. B Acute erythematous candidiasis of the tongue. Patient image was borrowed from the Mount Sinai collection