PO:18:271 | Managing concomitant sle and psoriasis: the role of anifrolumab in a clinical case

Background. Systemic Lupus Erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the interaction of genetic, environmental, and immunological factors. The type I interferon (IFN-I) pathway, particularly IFN-alpha, represents a central element in its pathogenesis. IFN-I is produced by pDCs and other cells in response to exposure to immune complexes containing DNA or RNA, and it promotes the activation and differentiation of B and T cells, the maturation of DCs, and the expression of pro-inflammatory cytokines. Anifrolumab is a human monoclonal antibody that binds to the type I interferon receptor (IFNAR1), inhibiting the activity of all type I interferons. Interferons, particularly IFN-gamma and type I IFN, also play a crucial role in the pathogenesis of psoriasis: pDCs can be activated by nucleic acids released from damaged keratinocytes or by immune complexes, producing IFN and contributing to the inflammation.   Methods and Results. A 57-year-old woman presented with a diagnosis of inverse psoriasis and undifferentiated connective tissue disease, previously treated with Hydroxychloroquine (discontinued due to an allergic reaction) and then with Methotrexate and Cyclosporine. Laboratory tests showed ANA positivity (1/640 speckled pattern), anti-dsDNA and anti-SSA/Ro60 positivity, ESR 44 mm/h, CRP 18.1 mg/L. On physical examination, she presented with erythematous, desquamative, and infiltrated lesions in the intergluteal fold, buttocks, submammary and retroauricular regions, alopecia and a malar rash. A diagnosis of Systemic Lupus Erythematosus was made, and initially treatment with Cyclosporine 300 mg/day was maintained. One year later, blood tests showed an increase in ESR and CRP, mild anemia, and 24-hour proteinuria of 884 mg/24h. The patient also presented with a painful swelling of the right sternoclavicular joint, and ultrasound documented inflammatory involvement (consistent with Tietze's syndrome). Cyclosporine therapy was suspended, and treatment with Methotrexate and Prednisone was initiated. One month later, at the follow-up visit, tests showed a reduction in proteinuria (168 mg/24h) and inflammatory markers, as well as the resolution of the sternoclavicular swelling, so prednisone taper was started. At subsequent follow-ups, the patient showed clinical stability in laboratory tests; however, a strong psoriatic component persisted with erythema in the submammary, inguinal, retroauricular, elbow, intergluteal fold, and left calf regions. An erythematous lesion also appeared on the V of the chest. Therefore, after screening to initiate biotechnological drug therapy, treatment with Anifrolumab 300 mg/month was scheduled.   Conclusions. Type I interferon is a common pathogenetic driver in both SLE and psoriasis. Anifrolumab, by blocking the type I IFN receptor, has demonstrated clear efficacy in SLE, reducing disease activity and improving clinical outcomes. Its targeted action on the IFN-I pathway suggests a potential benefit for psoriasis as well, by acting on a shared inflammatory mechanism. The introduction of Anifrolumab in this patient could offer a potential benefit for both conditions.