Study of Anti-Carbamylated Protein Antibody in the Rheumatoid Patients Who Were Clinically Active and Under Treatment with Biological Dmards

Kazuko Shiozawa¹ and Shunichi Shiozawa², ¹Rheumatic Diseases Center, Konan Kakogawa Hospital, Kakogawa, Japan, ²Department of Medicine, Rheumatic Diseases Unit, Kyushu University Beppu Hospital, Beppu, Japan

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: anti-CCP antibodies, antibodies and rheumatoid arthritis (RA)

Session Information

Date: Tuesday, November 10, 2015

Title: Rheumatoid Arthritis - Clinical Aspects Poster Session III

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: A newly discovered anti-carbamylated protein antibody (anti-CarP) is found prior to disease-onset, associates with the conversion towards arthralgia and with a more severe disease course in patients negative for ACPA. We here studied anti-CarP in 141 rheumatoid patients who were clinically active and under treatment with biological DMARDs with reference to anti-CCP2 protein antibody2 (ACPA2) and ACPA3.

Methods: ACPA2, ACPA3, anti-CarP-Fetal Calf Serum (aCarPFCS) and anti-CarP-Fibrinogen (aCarPFib) were measured by using ELISA in sera of 141 Japanese patients with RA who were clinically active (fulfilling either DAS-CRP > 4.0 or DAS-ESR > 4.2 and either CDAI > 22 or SDAI >26) and under treatment with biological DMARDs (53 with ETN, 40 with IFX, 19 with TCX, 15 with ADA, 8 with ABA, and 6 with GLM). Data were compared by classifying into ACPA2b (0~0.6 U/mL; below assay limit), ACPA2n (0.7~4.4; negative) or ACPA2p (4.5~20; low positive) subgroups.

Results: Among ACPA2b group (n=41), ACPA3, aCarPFCS and aCarPFib were positive in 8 (19.5%), 0 (0%) and 4 (9.8%), respectively. Likewise, among ACPA2n group (n=31), they were positive in 16 (51.6%), 3 (9.7%) and 6 (19.4%). Among ACPA2p group (n=69), they were 64 (92.8%), 26 (37.7%) and 18 (26.1%). Within ACPA2b and ACPA3-positive groups (n=8), aCarPFCS and aCarPFib were 0 and 3 (37.5%). Within ACPA2n and ACPA3-positive groups (n=17), they were 3 (17.6%) and 2 (11.8%). Within ACPA2p and ACPA3-positive groups (n=64), they were 24 (37.5%) and 17 (26.6%). It was noted that among ACPA2b and ACPA3-negative groups (n=1) and ACPA2n and ACPA3-negative groups (n=2), aCarPFCS was all negative, however, aCarPFib was positive in 1/1 (100%) and 2/2 (100%), respectively. These 3 anti-CarP sole positive patients were with DAS28-ESR3: 5.1, 7.0, and 5.4, and ΔTSS: 4, 0, 4.


ACPA3	aCarPFCS	aCarPFib	ACPA2below	ACPA2negative	ACPA2positive
–	–	–	32	12	3
+	–	–	5	12	31
+	+	–	0	1	16
+	+	+	0	2	8
+	–	+	3	2	9
–	+	–	0	0	1
–	+	+	0	0	1
–	–	+	1	2	0
Total			41	31	69

Conclusion: Anti-CarP was positive in a substantial fraction of ACPA2 negative subset, in which most of them were also ACPA3 positive. There existed 3 patients who were sole positive for anti-CarP whose disease was clinically active despite treatment with biological DMARDs.

This study is a co-work with Drs. Verheul MK and Trouw LA, Department of Rheumatology, Leiden University, Netherlands.

Disclosure: K. Shiozawa, None; S. Shiozawa, None.

To cite this abstract in AMA style:

Shiozawa K, Shiozawa S. Study of Anti-Carbamylated Protein Antibody in the Rheumatoid Patients Who Were Clinically Active and Under Treatment with Biological Dmards [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/study-of-anti-carbamylated-protein-antibody-in-the-rheumatoid-patients-who-were-clinically-active-and-under-treatment-with-biological-dmards/. Accessed .

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