Lymphadenopathy in systemic lupus erythematosus: no microbial trigger found by shotgun metagenomics in a retrospective study on 38 patients

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Papo, Matthias | Cappy, Pierre | Degachi, Alexandre | Woerther, Paul-Louis | Saal, Caroline | Charlotte, Frédéric | Brocheriou, Isabelle | Lhote, Raphaël | Trefond, Ludovic | Hié, Miguel | Haroche, Julien | Pha, Micheline | Cohen-Aubart, Fleur | Mathian, Alexis | Rodriguez, Christophe | Amoura, Zahir

Edité par CCSD ; Oxford University Press (OUP) -

International audience. Abstract Objectives Lymphadenopathy is a classical manifestation of SLE flare, occurring in approximately half of patients during the course of the disease. Lymphadenopathy in SLE is frequently associated with fever. Microbial infection may play a role in SLE onset and flares. The objectives of this study were to describe lymphadenopathy in the course of SLE and identify potential infectious triggers using microbial metagenomic analysis. Methods We performed a retrospective monocentric study of 38 patients with SLE who had lymph node biopsy at baseline or during follow-up. Shotgun metagenomics were performed in the patient’s lymph node biopsy to look for microbial RNA and/or DNA. Results Lymph node pathological analyses revealed follicular and/or paracortical hyperplasia in 73.7% of patients and histiocytic necrotizing lymphadenitis in 23.7%. At the time of biopsy, SLE patients exhibited fever in 29%, splenomegaly in 10%, cutaneous manifestations in 47%, polyarthritis in 32%, seritis in 13% and LN in 18%. Half of the patients (50%) had an increased CRP level, 35% had low C3, 65% had hypergammaglobulinemia. Microbial metagenomic analysis of lymph node biopsy revealed an absence of microbial DNA in 92% of patients, the presence of CMV in very small quantities in 2 patients, and the presence of HHV-7 in low quantities in a single patient. Conclusion Despite suggestion that certain microorganisms may play a role in the pathogenesis and flares of SLE, our microbial metagenomic analysis study did not highlight possible infectious triggering factors. Further and better-designed studies are needed to confirm these results.

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