PMID- 28336519
OWN - NLM
STAT- MEDLINE
DCOM- 20170821
LR  - 20220317
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 76
IP  - 9
DP  - 2017 Sep
TI  - Anticollagen type II antibodies are associated with an acute onset rheumatoid 
      arthritis phenotype and prognosticate lower degree of inflammation during 5 years 
      follow-up.
PG  - 1529-1536
LID - 10.1136/annrheumdis-2016-210873 [doi]
AB  - OBJECTIVE: Antifibrillar collagen type II (anti-CII) antibody-positive patients 
      with rheumatoid arthritis (RA) have early but not late signs of increased 
      inflammation and joint erosions. We wanted to replicate this in a large RA 
      cohort, and to relate to human leukocyte antigen (HLA)-DRB1* alleles. METHODS: 
      Anti-CII and anti-cyclic citrullinated peptide (CCP)2 were measured at baseline 
      in 773 patients with RA from the Swedish Epidemiological Investigation in 
      Rheumatoid Arthritis (EIRA) study with clinical follow-up data from the Swedish 
      Rheumatology Quality Register (SRQ) registry, and 1476 with HLA-DRB1* 
      information. Comparisons were done concerning C reactive protein (CRP), 
      erythrocyte sedimentation rate (ESR), tender joint count (TJC), swollen joint 
      count (SJC), Disease Activity Score encompassing 28 joints based on ESR (DAS28), 
      DAS28CRP, pain-Visual Analogue Scale (VAS), global-VAS and Health Assessment 
      Questionnaire Score (HAQ) at eight occasions during 5 years, and association with 
      HLA-DRB1* alleles. RESULTS: Anti-CII associated with elevated CRP, ESR, SJC, 
      DAS28 and DAS28CRP at diagnosis and up to 6 months, whereas anti-CCP2 associated 
      with SJC and DAS28 from 6 months to 5 years, but not earlier. The 
      anti-CII-associated phenotype was strong, and predominated in anti-CII/anti-CCP2 
      double-positive patients. Anti-CII was associated with improvements in CRP, ESR, 
      SJC, TJC and DAS28, whereas anti-CCP2 was associated with deteriorations in SJC 
      and DAS28 over time. Anti-CII-positive patients achieved European League Against 
      Rheumatism good or moderate response more often than negative patients. Anti-CII 
      was positively associated with HLA-DRB1*01 and HLA-DRB1*03, with significant 
      interaction, and double-positive individuals had >14 times higher mean anti-CII 
      levels than HLA double negatives. Whereas smoking was associated with elevated 
      anti-CCP2 levels, smokers had lower anti-CII levels. CONCLUSIONS: Anti-CII 
      seropositive RA represents a distinct phenotype, in many respects representing 
      the converse to the clinical, genetic and smoking associations described for 
      anticitrullinated protein peptide autoantibodies. Although not diagnostically 
      useful, early anti-CII determinations predict favourable inflammatory outcome in 
      RA.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://www.bmj.com/company/products-services/rights-and-licensing/.
FAU - Manivel, Vivek Anand
AU  - Manivel VA
AD  - Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala 
      Sweden.
FAU - Mullazehi, Mohammed
AU  - Mullazehi M
AD  - Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala 
      Sweden.
FAU - Padyukov, Leonid
AU  - Padyukov L
AD  - Rheumatology Unit, Department of Medicine, Karolinska University Hospital and 
      Karolinska Institutet, Stockholm, Sweden.
FAU - Westerlind, Helga
AU  - Westerlind H
AD  - Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
FAU - Klareskog, Lars
AU  - Klareskog L
AD  - Rheumatology Unit, Department of Medicine, Karolinska University Hospital and 
      Karolinska Institutet, Stockholm, Sweden.
FAU - Alfredsson, Lars
AU  - Alfredsson L
AD  - Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
FAU - Saevarsdottir, Saedis
AU  - Saevarsdottir S
AD  - Rheumatology Unit, Department of Medicine, Karolinska University Hospital and 
      Karolinska Institutet, Stockholm, Sweden.
FAU - Ronnelid, Johan
AU  - Ronnelid J
AD  - Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala 
      Sweden.
LA  - eng
PT  - Journal Article
DEP - 20170323
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Autoantibodies)
RN  - 0 (Collagen Type II)
RN  - 0 (HLA-DRB1 Chains)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (cyclic citrullinated peptide)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Acute Disease
MH  - Arthritis, Rheumatoid/genetics/*immunology/physiopathology
MH  - Autoantibodies/*immunology
MH  - Blood Sedimentation
MH  - C-Reactive Protein/immunology
MH  - Case-Control Studies
MH  - Collagen Type II/*immunology
MH  - Female
MH  - Follow-Up Studies
MH  - HLA-DRB1 Chains/genetics
MH  - Humans
MH  - Inflammation/immunology
MH  - Logistic Models
MH  - Male
MH  - Odds Ratio
MH  - Peptides, Cyclic/*immunology
MH  - Phenotype
MH  - *Registries
MH  - Severity of Illness Index
MH  - Smoking/immunology
MH  - Sweden
PMC - PMC5561381
OTO - NOTNLM
OT  - DAS28
OT  - Outcomes research
OT  - Rheumatoid Arthritis
COIS- Competing interests: None declared.
EDAT- 2017/03/25 06:00
MHDA- 2017/08/22 06:00
PMCR- 2017/08/18
CRDT- 2017/03/25 06:00
PHST- 2016/11/25 00:00 [received]
PHST- 2017/02/26 00:00 [revised]
PHST- 2017/03/02 00:00 [accepted]
PHST- 2017/03/25 06:00 [pubmed]
PHST- 2017/08/22 06:00 [medline]
PHST- 2017/03/25 06:00 [entrez]
PHST- 2017/08/18 00:00 [pmc-release]
AID - annrheumdis-2016-210873 [pii]
AID - 10.1136/annrheumdis-2016-210873 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2017 Sep;76(9):1529-1536. doi: 10.1136/annrheumdis-2016-210873. 
      Epub 2017 Mar 23.