IL17 inhibition for psoriasis vulgaris and arthritis results in clinical and serological remission of coexistent pemphigus foliaceus

Pemphigus foliaceus (PF) is an autoimmune blistering disorder, mediated by autoantibodies against desmoglein 1 (Dsg1). It manifests with erosions and later on erythematous hyperkeratotic plaques/crusts without mucosal involvement.1 Few reports exist the coexistence of PF other diseases.2 Specifically, a higher prevalence plaque psoriasis (PP) has been reported among pemphigus patients.2 In psoriasis, besides genetic disposition epigenetic factors, stimulated dendritic cells produce IL-23, which promotes Th1 Th17 immune response. Continued exposure to IL-23 leads increased production IL-17A.3 The neutralization IL-17A secukinumab, IgG1κ monoclonal antibody, was shown be effective in treating PP psoriatic arthritis (PsA). Here we report 74-year-old patient, suffering from since 40, coexisting 28 years. Both diagnoses were confirmed histologically immunofluorescence diagnostics (direct indirect ELISA) (Figure S1). last years he presented overlapping clinical features generalized erythemato-squamous plaques 1a), as well progressive seronegative PsA fulfilled Caspar criteria. He suffered pronounced morning stiffness, intervertebral disc disease spondylarthritis, enthesitis nail psoriasis. His medical history included cardiovascular diseases, osteopenia depression, responding only lithium. Different treatments either for or PF, combined strategies clear improvement used over 25 1b). Treatment rituximab declined. had high-level Dsg1-antibodies, recorded 2005 We observed that aggravation his associated exacerbation PF. After diagnosis PsA, Dsg1-ELISA levels surprisingly decreased. Fumaric acid discontinued due lymphopenia low dose prednisolone given, while recurrent erosions, treated topical steroids. Due joint involvement, systemic treatment secukinumab initiated, therapy continued. This resulted quick both skin conditions 1c), followed long-term normalization titers now more than 3 considered Th2-mediated disease, play pivotal role. believe our case shift Th2 during active phase accounts decrease Dsg-1 autoantibodies, already before proven presence IL-17 lesions A similar pustular successfully although effect Dsg not prominent.4 Altogether, these data indicate possibly important role pathogenesis. Overexpression found patients, additionally sera levels.5 studied perilesional 20 patients no overexpression IL-17. Further studies estimate efficacy blockade are required. thank patient. Annegret Bedorf excellent technical assistance. study supported grant Berta-Ottenstein Advanced Clinician Scientist Program Medical Faculty, University Freiburg, DK, grants EB Research Partnership, Fritz-Thyssen Stiftung German Foundation DK. Open Access funding enabled organized ProjektDEAL. None declare. Please note: publisher responsible content functionality any supporting information supplied authors. Any queries (other missing content) should directed corresponding author article.