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Can mannose-binding lectin explain the course and outcome of pregnancy in rheumatoid arthritis?
  1. F E van de Geijn,
  2. Y A de Man,
  3. M Wuhrer,
  4. S P Willemsen,
  5. A M Deelder,
  6. J M W Hazes,
  7. R J E M Dolhain
  1. Department of Rheumatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands

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Introduction

Rheumatoid arthritis (RA) improves during pregnancy and flares after delivery. It has been hypothesised that high levels of the complement factor mannose binding lectin (MBL) are associated with a favourable disease course of R A by facilitating the clearance of pathogenic immunoglobulin G (IgG) lacking galactose sugar moieties. During pregnancy, increased galactosylation of IgG is observed and MBL levels simultaneously increase, the latter being strictly related to maternal MBL genotypes. Increased MBL levels in concert with increased IgG galactosylation may therefore be associated with pregnancy-induced improvement of RA.

Objective

To investigate whether MBL genotypes are associated with changes in RA disease activity and with changes in IgG galactosylation during pregnancy and post partum and to study the association between MBL genotypes and pregnancy outcome in RA.

Methods

Serum from 216 patients with RA and 31 healthy controls in the Pregnancy-induced Amelioration of RA (PARA) study was collected before, during and after pregnancy. IgG galactosylation was determined by MALDI-TOF-MS. Disease activity was determined using DAS28. MBL genotypes were determined. Pregnancy outcome measures studied were gestational age, birth weight, spontaneous abortion and hypertensive disorders.

Results

No association was found between MBL genotype groups and changes in RA disease activity and changes in IgG galactosylation during pregnancy and post partum. Furthermore, MBL genotype groups were not related to the pregnancy outcome measures studied.

Conclusion

This study does not provide evidence for a role for MBL in the improvement of RA during pregnancy, nor for a role in pregnancy outcome.

This research was financed by the Dutch Arthritis Association (Reumafonds)

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