Subject(s)
Langerhans Cell Sarcoma , Humans , Antigens, CD , Lectins, C-Type , Mannose-Binding LectinsABSTRACT
Lichen planus is a chronic T-cell-mediated disorder in which lymphocytes, including Th17 cells, react toward the dermo-epidermal junction, which shows interface changes. Recently, IL-17-mediated changes in the oral mycobiome, including the proliferation of Candida and Aspergillus fungi, have been proposed as a possible pathomechanism of oral lichen planus (OLP). We treated a 54-year-old male who had been suffering from psoriatic arthritis. Secukinumab rapidly improved the skin and joint symptoms, but a painful erosion on the lip and thrush on the buccal mucosa appeared within 4 weeks. The erosion was histopathologically diagnosed as OLP. Although the candidiasis was successfully treated with topical miconazole nitrate, the labial OLP worsened during the secukinumab administration, despite the application of various topical agents. We finally switched from secukinumab to risankizumab, an anti-IL-23p19 agent, which dramatically improved the patient's OLP lesion in 4 weeks without candidiasis recurrence. Anti-IL-23p19 agents do not affect the oral mycobiome, and they are a potential therapeutic option for refractory OLP, including OLP induced by biologics.
Subject(s)
Arthritis, Psoriatic , Candidiasis, Oral , Lichen Planus, Oral , Male , Humans , Middle Aged , Lichen Planus, Oral/chemically induced , Lichen Planus, Oral/drug therapy , Arthritis, Psoriatic/drug therapy , Th17 CellsABSTRACT
During biologic treatments, attention should be paid to adverse reactions, particularly infectious diseases. Furthermore, drug-induced interstitial lung disease is also known to be associated with biologic therapies. We retrospectively reviewed serum Krebs von den Lungen-6 (KL-6) levels in psoriatic patients who underwent treatment with seven different biologics. A total of 67 patients who received 80 biologic treatments were evaluated. The 31 anti-tumor necrosis factor (TNF)-α treatments consisted of 17 infliximab (IFX) and 14 adalimumab. The 23 anti-interleukin (IL)-23 treatments consisted of 14 ustekinumab and nine guselkumab. The 26 anti-IL-17 treatments consisted of nine secukinumab, six ixekizumab and 11 brodalumab. The IFX showed significantly increased mean serum KL-6 (170.9%), but none of the other treatments showed significant increases. Thirteen of the 17 (75.6%) patients in the IFX and 17 of the 31 (54.8%) patients in the total anti-TNF-α group demonstrated at least a 25% increase in serum KL-6. Levels exceeding the cut-off (500 U/mL) were detected in three patients before treatment and in seven patients after treatment. This study showed that anti-IL-17 and anti-IL-23 treatments have no significant impact on serum KL-6 level. In addition to the influence of IFX, a significantly large number of patients in the IFX group had a history of methotrexate administration associated with psoriatic arthritis, which might have influenced the KL-6 level. None of the patients with elevated serum KL-6 showed pulmonary changes by computed tomography and/or X ray.
