Acta Dermato-Venereologica 98-4CompleteContent | Page 23

SHORT COMMUNICATION 465 Abatacept Improves Skin-score and Reduces Lesions in Patients with Localized Scleroderma: A Case Series Simon WEHNER FAGE, Kristian Bakke ARVESEN and Anne Braae OLESEN Department of Dermatology, University Hospital of Aarhus, Marselisborg Centret, P.P. Orumsgade 11, DK-8000 Aarhus C, Denmark. E-mail: [email protected] Accepted Jan 8, 2018; Epub ahead of print Jan 9, 2018 In 2011 we reported 2 cases of patients with treatment- resistant, diffuse, deep, localized scleroderma (LoS), who showed significant improvement of both active disease and old fibrotic lesions on treatment with abatacept (1). Since then we have offered abatacept to adult patients with therapy-resistant, moderate-to-severe, active LoS. Abatacept is a fusion protein that acts as a T-cell co- stimulation blocker to inhibits tumour necrosis factor alpha (TNF-α) and prevent T-cell activation. Another group has also reported a good effect of abatacept in 3 patients with LoS (2), and there is an ongoing study of subcutaneous abatacept to treat diffuse cutaneous sys- temic sclerosis (SSc) (ASSET; https://clinicaltrials.gov/ ct2/show/NCT02161406). The LoS diseases are a group of sclerosing skin di- seases of rare occurrence. They mainly affect females and young adults (3, 4). Adjacent tissue (fascia, muscle, bone) may also be affected in LoS, but, in contrast to SSc, there is no involvement of the internal organs (3). In the subtype called “en coup de sabre” involvement of the underlying central nervous system (e.g. seizures, migraine, headache) and abnormal ophthalmological findings (e.g. uveitis) can occur (5). Untreated LoS , especially the linear deep form, may result in joint cont- ractures, muscle atrophy and growth limitations (5, 6). Although causing significant morbidity, plaque-type LoS typically has a benign self-limiting course of 3–5 years duration of disease activity of each lesion. In general, the course of the disease can vary, with improvement and reactivation over some years. Currently, there is no evidence-based causal (antifibrotic) treatment for LoS, and there is a lack of clinical trials with regard to other treatment options (7). The aim of this study is to further determine whether abatacept may have a positive effect on disease activity in otherwise treatment-resistant LoS. MATERIALS AND METHODS The scleroderma clinic at the Department of Dermato-Venereology of Aarhus University Hospital manages approximately 650 patients with scleroderma and scleroderma-like diseases. Each week a total of 2–4 new patients are admitted and 25–45 patients attend for regular control of disease and treatments. Through 2009 to 2016 we followed up on all adult treatment-resistant LoS patients who were treated experimentally with abatacept. The patients were treated with either 500 mg (patients weighing < 60 kg) or 750 mg (> 60 kg) abatacept intravenously on days 1, 15, 30, and thereafter every 4–6 weeks. Some patients switched to subcutaneous injection of 125 mg abatacept/week during treatment. Evaluations, including either modified Rodnan Skin Score (MRSS) or Localized Sclero- derma Cutaneous Assessment Tool (LoSCAT) (8), were performed by well-trained doctors. Medical records review were conducted to extract data at two time points: At the beginning of abatacept treatment (the day the first abatacept treatment was injected) 1 st assessment and either the latest follow up during treatment (the patient is still treated with abatacept) or at the determination (2 nd assessment) of abatacept treatment. Regarding patients with generalized LoS, MRSS and LoSCAT, data were collected at any time, prior to, during, and after abatacept treatment. Primary endpoints were changes in MRSS, LoSCAT, and/or change of size of lesions. Secondary endpoints were changes in CRP, C3c, C4, and/or PIIINP. RESU