PMID- 28225768
OWN - NLM
STAT- MEDLINE
DCOM- 20170821
LR  - 20190208
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 2
DP  - 2017
TI  - Anti-rheumatic treatment is not associated with reduction of pentraxin 3 in 
      rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis.
PG  - e0169830
LID - 10.1371/journal.pone.0169830 [doi]
LID - e0169830
AB  - BACKGROUND: Pentraxin 3 is proposed to be a marker of inflammation and 
      cardiovascular risk, but its role in inflammatory rheumatic diseases (IRDs) is 
      still uncertain. Therefore, we wanted to examine if anti-rheumatic treatment 
      reduced serum PTX3 (s-PTX3) levels in IRDs, and if s-PTX3 levels were related to 
      other markers of inflammation and to endothelial function (EF). METHODS: We 
      examined s-PTX3, EF and established inflammatory biomarkers in 114 IRD patients 
      from the PSARA study before and after 6 weeks and 6 months of treatment with 
      methotrexate (MTX) or anti-tumor necrosis factor alpha (anti-TNF) therapy with or 
      without MTX co-medication. RESULTS: s-PTX3 levels in all IRD diagnoses were above 
      the upper limit of the reference range. In contrast to established inflammatory 
      markers, in particular CRP and ESR, s-PTX3 levels did not change significantly 
      after 6 weeks and 6 months of anti-rheumatic therapy. There was no difference in 
      change in s-PTX3 levels from baseline to 6 weeks and 6 months between MTX 
      monotherapy and anti-TNF regimens. CRP, ESR and EF were not related to changes in 
      s-PTX3 neither in crude nor adjusted analyses. CONCLUSION: IRD patients have 
      increased s-PTX3 levels, which, in contrast to other inflammatory markers, do not 
      seem to improve within 6 months of therapy with MTX and/or anti-TNF. Thus, s-PTX3 
      might reflect a persisting immune process, even a causal factor of inflammation, 
      not inhibited by the standard anti-rheumatic treatment. Furthermore, even though 
      s-PTX3 is thought to be a strong predictor of cardiovascular prognosis, it was 
      not related to EF.
FAU - Deyab, Gia
AU  - Deyab G
AD  - Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, 
      Norway.
FAU - Hokstad, Ingrid
AU  - Hokstad I
AD  - Lillehammer Hospital for Rheumatic Diseases, Lillehammer, Norway.
FAU - Whist, Jon Elling
AU  - Whist JE
AD  - Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, 
      Norway.
AD  - Department of Research, Innlandet Hospital Trust, Brumunddal, Norway.
FAU - Smastuen, Milada Cvancarova
AU  - Smastuen MC
AD  - Institution of health care-Health science PhD programme, Oslo and Akershus 
      University College, Oslo, Norway.
FAU - Agewall, Stefan
AU  - Agewall S
AD  - Oslo University Hospital, Ulleval, Oslo, Norway.
AD  - Institute of Clinical Sciences, University of Oslo, Oslo, Norway.
FAU - Lyberg, Torstein
AU  - Lyberg T
AD  - Department of Medical Biochemistry, Oslo University Hospital, Ulleval, Oslo, 
      Norway.
FAU - Bottazzi, Barbara
AU  - Bottazzi B
AD  - Humanitas Research Hospital, Rozzano, Milan, Italy.
FAU - Meroni, Pier Luigi
AU  - Meroni PL
AD  - Department of Clinical Sciences and Community Health, University of Milan, Milan, 
      Italy.
AD  - IRCCS Istituto Auxologico Italiano, Milan, Italy.
AD  - ASST G Pini, Milan, Italy.
FAU - Leone, Roberto
AU  - Leone R
AD  - Humanitas Research Hospital, Rozzano, Milan, Italy.
FAU - Hjeltnes, Gunnbjorg
AU  - Hjeltnes G
AD  - Department of Medicine, Innlandet Hospital Trust, Lillehammer, Norway.
FAU - Hollan, Ivana
AU  - Hollan I
AD  - Lillehammer Hospital for Rheumatic Diseases, Lillehammer, Norway.
AD  - Department of Research, Innlandet Hospital Trust, Brumunddal, Norway.
AD  - Department of Medicine, Brigham and Women's Hospital, Boston, United States of 
      America.
AD  - Harvard Medical School, Boston, United States of America.
LA  - eng
PT  - Journal Article
DEP - 20170222
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biomarkers)
RN  - 0 (Serum Amyloid P-Component)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 148591-49-5 (PTX3 protein)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Psoriatic/*blood/drug therapy
MH  - Arthritis, Rheumatoid/*blood/drug therapy
MH  - Biomarkers/blood
MH  - C-Reactive Protein/*metabolism
MH  - Drug Therapy, Combination
MH  - Female
MH  - Humans
MH  - Inflammation/blood
MH  - Male
MH  - Methotrexate/*therapeutic use
MH  - Middle Aged
MH  - Serum Amyloid P-Component/*metabolism
MH  - Spondylitis, Ankylosing/*blood/drug therapy
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
PMC - PMC5321277
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2017/02/23 06:00
MHDA- 2017/08/22 06:00
PMCR- 2017/02/22
CRDT- 2017/02/23 06:00
PHST- 2016/09/21 00:00 [received]
PHST- 2016/11/24 00:00 [accepted]
PHST- 2017/02/23 06:00 [entrez]
PHST- 2017/02/23 06:00 [pubmed]
PHST- 2017/08/22 06:00 [medline]
PHST- 2017/02/22 00:00 [pmc-release]
AID - PONE-D-16-37905 [pii]
AID - 10.1371/journal.pone.0169830 [doi]
PST - epublish
SO  - PLoS One. 2017 Feb 22;12(2):e0169830. doi: 10.1371/journal.pone.0169830. 
      eCollection 2017.