PMID- 21281477
OWN - NLM
STAT- MEDLINE
DCOM- 20120210
LR  - 20211020
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 13
IP  - 1
DP  - 2011 Jan 31
TI  - Mannose-binding lectin does not explain the course and outcome of pregnancy in 
      rheumatoid arthritis.
PG  - R10
LID - 10.1186/ar3231 [doi]
AB  - INTRODUCTION: Rheumatoid arthritis (RA) improves during pregnancy and flares 
      after delivery. It has been hypothesized that high levels of the complement 
      factor mannose-binding lectin (MBL) are associated with a favourable disease 
      course of RA by facilitating the clearance of pathogenic immunoglobulin G (IgG) 
      lacking galactose sugar moieties. During pregnancy, increased galactosylation of 
      IgG and simultaneously increased MBL levels can be observed, with the latter 
      being strictly related to maternal MBL genotypes. Therefore, increased MBL levels 
      in concert with increased IgG galactosylation may be associated with 
      pregnancy-induced improvement of RA. The objective of this study was to 
      investigate whether MBL genotypes are associated with changes in RA disease 
      activity and with changes in IgG galactosylation during pregnancy and in the 
      postpartum period. We also studied the association between MBL genotypes and 
      pregnancy outcomes in RA. METHODS: Serum from 216 patients with RA and 31 healthy 
      controls participating in the Pregnancy-induced Amelioration of Rheumatoid 
      Arthritis (PARA) Study was collected before, during and after pregnancy. IgG 
      galactosylation was determined by performing matrix-assisted laser 
      desorption/ionization time of flight mass spectrometry. Disease activity was 
      determined using the internationally recognized Disease Activity Score 28 
      (DAS28). MBL genotypes were determined. The pregnancy outcome measures studied 
      were gestational age, birth weight, miscarriage and hypertensive disorders. 
      RESULTS: No association was found between the MBL genotype groups and changes in 
      RA disease activity (P = 0.89) or changes in IgG galactosylation (patients, P = 
      0.75, and controls, P = 0.54) during pregnancy and in the postpartum period. 
      Furthermore, MBL genotype groups were not related to the studied pregnancy 
      outcome measures. CONCLUSIONS: This study does not provide evidence for a role 
      for MBL in the improvement of RA during pregnancy or for a role for MBL in 
      pregnancy outcome.
FAU - van de Geijn, Fleur E
AU  - van de Geijn FE
AD  - Department of Rheumatology, Erasmus University Medical Center Rotterdam, Dr. 
      Molewaterplein 50, NL-3015 GE, Rotterdam, The Netherlands. 
      f.vandegeijn@erasmusmc.nl
FAU - de Man, Yael A
AU  - de Man YA
FAU - Wuhrer, Manfred
AU  - Wuhrer M
FAU - Willemsen, Sten P
AU  - Willemsen SP
FAU - Deelder, Andre M
AU  - Deelder AM
FAU - Hazes, Johanna M W
AU  - Hazes JM
FAU - Dolhain, Radboud J E M
AU  - Dolhain RJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110131
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Immunoglobulin G)
RN  - 0 (Mannose-Binding Lectin)
SB  - IM
MH  - Adult
MH  - Arthritis, Rheumatoid/*genetics/immunology
MH  - Female
MH  - Genotype
MH  - Humans
MH  - Immunoglobulin G/immunology/metabolism
MH  - Mannose-Binding Lectin/*genetics/immunology
MH  - Pregnancy
MH  - Pregnancy Complications/*genetics/immunology
MH  - Real-Time Polymerase Chain Reaction
MH  - Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
PMC - PMC3241354
EDAT- 2011/02/02 06:00
MHDA- 2012/02/11 06:00
PMCR- 2011/01/31
CRDT- 2011/02/02 06:00
PHST- 2010/09/01 00:00 [received]
PHST- 2010/12/23 00:00 [revised]
PHST- 2011/01/31 00:00 [accepted]
PHST- 2011/02/02 06:00 [entrez]
PHST- 2011/02/02 06:00 [pubmed]
PHST- 2012/02/11 06:00 [medline]
PHST- 2011/01/31 00:00 [pmc-release]
AID - ar3231 [pii]
AID - 10.1186/ar3231 [doi]
PST - epublish
SO  - Arthritis Res Ther. 2011 Jan 31;13(1):R10. doi: 10.1186/ar3231.