PS5:93 Marginal-zone-like b cells deficiency repeatedly detected in peripheral blood as a possible biomarker of hyposplenism/asplenia in sle

Objective SLE is a disease associated with a risk of serious infections, in case of hyposplenism/asplenia especially by encapsulated bacteria. For opsonization and phagocytosis of these agents are essential IgM natural Abs, produced only by B cells of the splenic marginal zone. Significant deficiency of marginal-zone-like B cell CD19 +CD27+IgM+ subpopulation absolute values x10–6/L in peripheral blood (PB) was demonstrated in a prospective, comparative, cross-over SLE study 1 ; goal of the present study is follow up persistence of this phenomenon. Design and method Sixty adult SLE (ACR/1982, update 1997) pts and 10 age-and sex-matched healthy controls (HC) were enrolled in month O’, and 56 SLE pts also repeatedly after twelve-month-period, i. e. month 12’; overlap syndromes, infection, monoclonal gammopathy and renal failure in SLE under study were excluded. The DuraClone IM panel (Beckman Coulter) was used to identify CD19 +CD27+IgM+B cell subpopulation in PB samples by flow cytometry Navios (Beckman Coulter) with software analysis using Kaluza version 1.2: data obtained were expressed in relative% of PB lymphocytes and absolute values x10–6/L. Parallel analysis of serological SLE biomarkers included C3, C4, ANA/IF (maximal titre), ANA/ELISA, anti-dsDNA/IFCL (maximal titre), andi-dsDNA/ELISA and antinucleosome Abs. Data obtained were statistically processed using Medcalc-Statistical Software programme. Results Significant differences (p 0.05); not significant differences were found in analysis using relative% of PB lymphocytes (p>0.05). In SLE month O’ was found a slight significant correlation between absolute values of CD19 +CD27+IgM+B cells and anti-dsDNA/ELISA Abs (rs=−0.28, p=0.034) without a confirmation in month 12’ control (rs=−0.09, p=0.491). Conclusions The data obtained demonstrated persistent character of marginal-zone-like B cells deficiency in peripheral blood, and are suggesting as possible biomarker of functional hyposplenism/asplenia in SLE. Reference . Hrncir Z, et al. Clin Exper Rheumatol 2016;34(S99):S-63. Acknowledgement Supported by the research project PROGRES Q40–15.