FRI0140 The clinical utility of CD64 expression on neutrophil in acute-onset interstitial lung damage complicated in patients with rheumatoid arthritis. (23rd January 2014)

• Record Type: Journal Article
• Authors: Arinuma, Y.; Matsui, T.; Komiya, A.; Nogi, S.; Iwata, K.; Futami, H.; Takaoka, H.; Hashimoto, A.; Nakayama, H.; Tohma, S.
• Is Part Of: Annals of the rheumatic diseases. Volume 71(2012)Supplement 3
• Page Start: 357
• Page End: 358
• Publication Date: 2014-01-23
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2012-eular.2597
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Acute-onset interstitial lung damage (AILD) is one of the most cumbersome involvements complicated during the therapy for rheumatoid arthritis (RA). Especially, discrimination of the cause developing AILD is very important because that could have a great affect on choice of subsequent RA therapy. We have reported the up-regulation of CD64 molecule expression on neutrophil, which was a useful biomarker for detecting infection in patients with RA and can distinguish infection from RA flare, was also shown in interstitial lung damage (ILD) in RA. However, it is still unclear whether neutrophil CD64 could distinguish the cause of ILD. Objectives: To assess the relationship between clinical causes developing AILD in patients with RA and the number of neutrophil CD64 molecule expression Methods: Thirty-eight patients with RA who had admitted to our hospital due to AILD from 2005 to 2011 were enrolled in this study. Clinical diagnoses for AILD were retrospectively reviewed based on the medical records, laboratory data and the chest CT scan images. The number of neutrophill CD64 molecule expression before treatments of AILD were statistically compared among the groups classified according to the primary disease developing AILD. The cut-off of neutrophil CD64 was set at 2000 molecules/cell which had been reported to discriminate infection from a flare of arthritis in RA. Results: Of 38 cases, 23 cases were classified into Pneumocystis jiroveci pneumonia (PCP) group, 8 cases were into methotrexate-induced pneumonia (MTX-IP) group and 7 cases were into extra-articular pulmonary involvement of RA (RA-IP) group. The number of CD64 molecule expression was 11077±7380 (mean ± SD) in PCP group, 4478±4834 in MTX-IP group and 5228±4507 in RA-IP group, respectively. The level of CD64 expression was significantly higher in PCP group compared with MTX-IP or RA-IP group, but there was no difference between MTX-IP and RA-IP group. The positive rate of CD64 expression (>2000 molecules/cell) was 95.7% in PCP group, 50.0% in MTX-IP group and 85.7% in RA-IP group, respectively. Conclusions: Our data indicates that neutrophil CD64 molecule expression up-regulates not only on infection but also on AILD in RA patients. However, the absolute elevation of neutrophil CD64 molecule expression level was different for respective cause developing AIDL. References: Matsui T, et al. CD64 on neutrophils is a sensitive and specific marker for detection of infection in patients with rheumatoid arthritis. J Rheumatol. 2006 Dec;33(12):2416-24. Disclosure of Interest: None Declared