Practical Update on Treatment of Oral Candidiasis

Many commonly administered, older biologics for psoriasis target interleukin (IL)-17 and IL-23, which are essential to neutrophil recruitment for fungal defense, predisposing patients to mostly oral candidiasis.^1–3 Such drugs are less likely to result in vulvovaginal candidiasis, which relies less on IL-17 and more on S100A8 alarmin and IL-1β.4,5 With the advent of new, more potent psoriasis agents like bimekizumab that block both IL-17A and IL-17B, there is an increased risk of candidiasis, estimated between 8 and 18%.⁶ Bimekizumab achieves over 90% reduction in Psoriasis Area and Severity Index (PASI) scores more frequently than other agents, and it is expected to be widely used given its recent approval.^7–9 As such, dermatologists must prepare to treat oral candidiasis (though unlikely esophagitis) that may result from broad-spectrum IL-17 blocking agents.^6,7

Presentation and Diagnosis of Oral Candidiasis
Oral candidiasis can present as white or red.¹⁰ The two major forms of white candidiasis include the pseudomembranous variant, which is the most common, classical form of white, cottage cheese consistency plaques that can be scraped off, revealing an erythematous surface underneath.^10–12 The plaques can cover the soft and hard palates, buccal mucosa, and extend into the oral segment of the pharynx.^10,13 The other type of white candidiasis is hyperplastic, which also presents with white plaques on the buccal mucosa, except these plaques may also be found at the labial commissures.^10–12 Lesions can be speckled, nodular, small, large, translucent, or opaque, and cannot be scraped off.¹⁰ Therefore, the challenge lies in differentiating these lesions from oral leukoplakia and lichen planus.^10,11,14 Erythematous candidiasis affects the buccal mucosa, tongue, or