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Owing to the great vascularity incident to pregnancy, the various pelvic joints always show a somewhat increased motility. In rare instances, particularly when the pelvis is contracted in the lower portion, spontaneous rupture of the symphysis pubis or one or both sacro-iliac joints has been observed.

—J. Whitridge Williams (1903)

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INTRODUCTION

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The principal concerns in the 1st edition of Williams Obstetrics with disorders of the joints were the obstructed pelvis caused by rickets. There is no mention of the arthritides complicating pregnancy. And of course, immune-mediated disease had not yet been elucidated.

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Connective tissue disorders, which are also termed collagen vascular disorders, have two basic underlying causes. First are the immune-complex diseases in which connective tissue damage is caused by deposition of immune complexes. Because these are manifest by sterile inflammation—predominately of the skin, joints, blood vessels, and kidneys—they are referred to as rheumatic diseases. Many of these immune-complex diseases are more prevalent in women, for example, systemic lupus erythematosus (SLE) and rheumatoid arthritis. Second are the inherited disorders of bone, skin, cartilage, blood vessels, and basement membranes. Some examples include Marfan syndrome, osteogenesis imperfecta, and Ehlers-Danlos syndrome.

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IMMUNE-MEDIATED CONNECTIVE TISSUE DISEASES

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These disorders can be separated into those associated with and those without autoantibody formation. The rheumatoid factor (RF) is an autoantibody found in many autoimmune inflammatory conditions such as SLE, rheumatoid arthritis, systemic sclerosis (scleroderma), mixed connective tissue disease, dermatomyositis, polymyositis, and various vasculitis syndromes. The RF-seronegative spondyloarthropathies are strongly associated with expression of the human leukocyte antigen B27 (HLA-B27) antigen and include ankylosing spondylitis, psoriatic arthritis, Reiter disease, and other arthritis syndromes.

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Pregnancy may mitigate activity in some of these syndromes as a result of the immunosuppression that also allows successful engraftment of fetal and placental tissues. These changes are discussed in detail in Chapters 4 and 5. One example is pregnancy-induced predominance of T2 helper cells compared with cytokine-producing T1 helper cells (Keeling, 2009). Pregnancy hormones also alter immune cells. Namely, estrogens upregulate and androgens downregulate T-cell response, and progesterone is immunosuppressive (Cutolo, 2006; Häupl, 2008a; Robinson, 2012).

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In contrast, immune-mediated disease may contribute to obstetrical complications. One longitudinal cohort study found that unrecognized autoimmune systemic rheumatic disorders are associated with significant risk for preeclampsia and fetal-growth restriction (Spinillo, 2016). In this study, the prevalence of unrecognized rheumatic arthritis was 0.4 percent, and was 0.3 percent each for SLE, Sjögren syndrome, and antiphospholipid syndrome.

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Last, some immune-mediated diseases may either be caused or activated as a result of prior pregnancies. To explain, fetal cells and free fetal DNA are detectable in maternal blood beginning early in pregnancy (Simpson, 2013; Sitar, 2005; Waldorf, 2008). Fetal cell microchimerism is the persistence of fetal cells in the maternal circulation and in organs following pregnancy. These fetal cells may become engrafted in maternal tissues and stimulate ...

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