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Clinical significance of plasma presepsin levels in patients with systemic lupus erythematosus

Objectives: Presepsin (PSEP: soluble CD14 subtype) is produced from bacteria-stimulated monocytes or neutrophils, thus recognized as a biomarker of sepsis. Aberrant functions in monocyte or neutrophils are increasingly recognized in systemic lupus erythematosus (SLE). We investigated whether plasma...

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Published in:Modern rheumatology 2018-09, Vol.28 (5), p.865-871
Main Authors: Tanimura, Shun, Fujieda, Yuichiro, Kono, Michihiro, Shibata, Yuhei, Hisada, Ryo, Sugawara, Eri, Nakamura, Hiroyuki, Ohmura, Kazumasa, Shimamura, Sanae, Mitani, Asako, Shida, Haruki, Watanabe, Toshiyuki, Kato, Masaru, Oku, Kenji, Bohgaki, Toshiyuki, Amengual, Olga, Yasuda, Shinsuke, Shimizu, Chikara, Atsumi, Tatsuya
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Language:English
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Summary:Objectives: Presepsin (PSEP: soluble CD14 subtype) is produced from bacteria-stimulated monocytes or neutrophils, thus recognized as a biomarker of sepsis. Aberrant functions in monocyte or neutrophils are increasingly recognized in systemic lupus erythematosus (SLE). We investigated whether plasma PSEP reflects disease activity in patients with SLE. Methods: This retrospective study comprised 35 patients with SLE and 72 with non-SLE autoimmune diseases who visited our facility during the period from August 2012 to September 2015. Plasma PSEP levels and laboratory data were compared between SLE and non-SLE. Clinical markers of SLE disease activity, including SLE disease activity index 2000 (SLEDAI-2K), serum complement concentrations and serum anti-ds-DNA antibodies were assessed in correlation with plasma PSEP levels. Results: Plasma PSEP levels in SLE were higher than those in non-SLE. This phenomenon holds true when comparing SLE and non-SLE patients in the absence of infection (p = .0008). Plasma PSEP levels in SLE patients negatively correlated with C3 (r = -0.4454, p = .0430), CH50 (r = -0.4502, p = .0406) and positively with SLEDAI-2K (r = 0.4801, p = .0237). Conclusion: Elevated plasma PSEP levels were correlated with disease activity of SLE, suggesting inappropriate monocyte or neutrophil activation in the pathophysiology of SLE exacerbation.
ISSN:1439-7595
1439-7609
DOI:10.1080/14397595.2017.1408755