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Purpose. – Anti-SSA/Ro and anti-SSB/La autoantibodies are frequently encountered in SLE or SGS where anti-SSA subtypes 52 and 60 kDa seems to be differently found in connection with the disease type: anti-SSA/Ro 60 kDa more frequently found in SLE and anti-SSA/Ro 52 kDa in SGS. We try to find if it was interesting in identifying these specificities for all anti-ENA screening.Method. – The study included 162 patients’ sera found anti-SSA 52 and/or anti-SSA 60 and/or anti-SSB positive among 1600 screening tests from the different hospital’s services. We used two assays: first, dotblot (Innolia-Ana Update INGEN) as a screening test and second, an Elisa (ENA-LISA BMD) as confirmation. Thirty-eight control sera were found negative with dotblot.Results. – Only one subtype of anti-SSA (52 or 60 kD) or anti-SSB was found for 55 sera (44 anti-SSA 52, 10 anti-SSA 60, 1 anti-SSB) and 107 sera were found positive for two or more (73 anti-SSA 52 + 60 and 34 anti-SSA 52 or 60 with another anti-ENA). While anti-SSA 60kDa alone or not was always positive with the Elisa test, neither anti-SSA 52 alone was anti-SSA Elisa’s positive. Diseases associations results show a greater linking of anti-SSA 60 kDa with SLE, a frequent linking of combined reactivity anti-SSA 52/60 in SLE and SGS and a greater spreading of anti-SSA 52 kDa alone among pathological groups, showing an autoimmune disease’s linking in 68%. Among SGS, 29% had only anti-SSA 52 kDa.Conclusion. – We suggest screening specific tests for identifying anti-SSA/Ro 52kDa reactivity which are missed by routine testing (tests using animal’s antigens) and could represent an additional serum marker in Connective Tissue Diseases. [Copyright &y& Elsevier]

Background: The detection of additional autoantibodies is of great concern in systemic sclerosis (SSc) when those included in the ACR/EULAR classification are negative. In this context, the interest of antifibrillarin (anti-U3RNP) autoantibodies (AFAs) in the routine evaluation of SSc remains unclear. We aimed to assess the relevance of AFAs and their clinical association in SSc patients., Methods: In a multicenter observational retrospective study, we collected immunological and clinical data associated with AFA positivity in SSc ( n = 42) and non-SSc patients ( n = 13). Patients with SSc negative for AFAs ( n = 83) were considered as a control group. AFAs were detected by indirect immunofluorescence (IIF) using HEp-2 cells, EliA or immunoblot techniques., Results: We confirmed a typical nuclear IIF pattern and showed that AFAs are mostly exclusive towards SSc conventional autoantibodies. Although also observed in non-SSc patients, high levels of AFAs with the ELiA technique allowed the diagnosis of SSc. Compared to AFA-negative SSc patients, AFA-positive SSc patients more frequently exhibited visceral involvements. They more frequently suffered from the diffuse cutaneous form and had a higher global severity of the disease., Conclusions: We demonstrate the usefulness of quantifying AFAs in the immunological exploration of SSc, especially when patients are seronegative for SSc conventional autoantibodies and display a typical IIF pattern. AFAs might constitute an interesting marker of SSc severity.

Monoclonal IgM anti-MAG associated peripheral neuropathies are part of demyelinating dysimmune peripheral neuropathies. The hematological disease probably does not influence the outcome of the neuropathy. Neuropathies associated with IgM anti-MAG antibodies are predominantly sensory and distal polyneuropathies associated with ataxia, unsteadiness and tremor. The neurophysiological features include a symmetric sensorimotor demyelinating neuropathy with more slowing of conduction in the distal than in the proximal nerve segments, a length-dependence, and a variable degree of denervation. High titers of IgM anti-MAG antibodies confirm the diagnosis. The natural history is mostly slow with mild to moderate functional impairment. However, some patients have a faster evolution associated with a more severe handicap. Immunotherapies studies have failed to demonstrate significant efficacy of these treatments. Furthermore, severe adverse effects are not uncommon with any of these therapies. Thus, the risk of possible severe adverse effects must be balanced against any possible benefits. More research is needed to improve the management of anti-MAG neuropathies: research on treatment, on prognostic factors, and development of specific assessment scales adapted to the particularities of anti-MAG neuropathies., (Copyright © 2012 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.)