Session Title: Miscellaneous Rheumatic Diseases
Session Type: Abstract Submissions (ACR)
Making the diagnosis of adult-onset Still’s disease (AOSD) is mainly based on the exclusion of inflammatory, infectious and malignant diseases. There are no specific clinical or laboratory findings for AOSD. Therefore, we aimed to identify new autoantibodies as diagnostic tools for AOSD.
As a screening procedure, we studied sera of 3 patients with AOSD using a protein array loaded with more than 28000 human recombinant proteins (imagenes biolifesciences, Berlin). Sera of patients with spondyloarthritis (SpA), rheumatoid arthritis (RA), eosinophilic granulomatosis with polyangiitis, granulomatosis with polyangiitis (GPA), HIV infection, B-NHL, chronic regional pain syndrome, giant cell arteritis (GCA), polymyalgia rheumatica (PMR), multiple sclerosis, osteoarthritis, Takayasu arteritis and sarcoidosis served as controls.
In the next step, we next established ELISAs in order to measure the respective autoantibodies in larger patient numbers.
Using the protein array, we detected IgG antibodies against the two new autoantigens Macropain subunit C2 and DRP-4 in 2/3 AOSD patients, respectively, but in none of the 50 controls.
Using the ELISA, we measured autoantibodies binding to peptides of Macropain subunit C2 and Dihydropyrimidinase-related protein 4 (DRP-4) in the sera of patients with AOSD and other inflammatory disorders. The results are summarized in the table (AOSD* = patients with active AOSD before the onset of treatment, systemic JIA = systemic juvenile idiopathic arthritis, PsoA = psoriatic arthritis, BD = blood donors):
|AOSD (n=78)||AOSD* (n=39)||systemic JIA (n=50)||SpA/ PsoA (n=58)||RA (n=66)||GPA (n=29)|
|MP + DRP-4||43%||56%||0%||19%||5%||10%|
|PMR/ GCA (n=60)||Sjögren’s syndrome (n=29)||SLE (n=38)||febrile infections (n=63)||Malignant Disease (n=37)||BD (n=147)|
|MP + DRP-4||15%||0%||5%||18%||3%||1%|
The new autoantibodies against Macropain subunit C2 and DRP-4 are associated with AOSD and may be useful as a diagnostic tool of AOSD. In addition, these markers clearly differentiate AOSD from systemic juvenile idiopathic arthritis.
N. T. Baerlecken,
R. E. Schmidt,
W. L. Gross,
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