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Benefit of pregnancy in inflammatory arthritis
  1. R H Straub1,
  2. F Buttgereit2,
  3. M Cutolo3
  1. 1Laboratory of Experimental Rheumatology and Neuroendocrinoimmunology, Division of Rheumatology, Department of Internal Medicine I, University Hospital Regensburg, Germany
  2. 2Department of Rheumatology and Clinical Immunology, Charité University Hospital, Berlin, Germany
  3. 3Division of Rheumatology, Department of Internal Medicine and Medical Specialties, San Martino University Hospital, Genova, Italy
  1. Correspondence to:
    Professor R H Straub
    Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I, University Hospital, 93042 Regensburg;

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Pregnancy related hormones provide an anti-inflammatory milieu

Observations in the 19th century (Trousseau 1871, Charcot 1881, Bannatyne 1896) indicated that pregnancy is favourable in rheumatoid arthritis (RA). This was summarised in the Nobel Prize lecture of the rheumatologist Philip S Hench, 11 December 1950 (, accessed 5 April 2005). This intriguing finding stimulated clinical and basic research into endocrine immune interactions and gender studies in rheumatic diseases, particularly in RA and systemic lupus erythematosus (SLE).

Philip S Hench wrote: “…after 1931, records of these cases (of cases with RA) were more carefully made and assembled … because of my growing belief that this phenomenon of relief (from arthritic disability) was analogous to, if not identical with, that which may occur during jaundice, and that the same agent might be responsible for the relief both during pregnancy and jaundice, although the mechanism … might be different.”1

Until today, the sole and only factor during pregnancy responsible for the relief from arthritic disability is not known. However, the collection of important data, which might explain the positive effects of pregnancy in these diseases, has helped us to understand this interesting phenomenon. Østensen et al in this issue of the Annals make another important contribution to the field.2


RA, psoriatic arthritis, and, to a lesser degree, ankylosing spondylitis are viewed as T helper type 1 (Th1) lymphocyte dominated inflammatory diseases, in which the balance between Th1 and Th2 responses is shifted towards Th1 pathways.3 This paradigm was complemented by the finding that aggressive fibroblasts/macrophages/osteoclasts are important in destroying bone and cartilage in arthritis.4,5 In addition, B lymphocytes were recently found to participate in the inflammatory process in RA; this finding was supported by the disease ameliorating effects of the B cell depleting antibody, rituximab.6 In collagen …

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