Scandinavian journal of rheumatology. Supplement最新文献

The various therapeutic modalities which are found to be beneficial in experimental antiphospholipid syndrome include: bone marrow transplantation, anti-CD4 monoclonal antibodies, bromocriptine, intravenous immunoglobulins and anti-idiotypes, interleukin-3, and various anti-coagulant and anti-aggregate agents. The advantage of animal models is the ability to evaluate experimental treatments that cannot be tested directly on patients. In this paper, we review the effect of these agents on animal models of antiphospholipid syndrome, their mechanisms of action, and their clinical implications.

The antiphospholipid (APS) syndrome frequently includes severe pregnancy complications such as fetal wastage and recurrent spontaneous abortions. Animal models for APS in pregnancy can provide both an understanding of the pathogenic mechanisms of anti-phospholipid antibodies (aPL), and aid in the evaluation of various therapeutic modalities in APS. Animal models for APS include both spontaneously developed diseases, as is the case for secondary APS in mice with another autoimmune disease, and induced models of APS. The latter includes either passive induction of disease by antibodies infusion, or active induction via manipulation of the idiotypic network. This article summarizes the literature reports of animal models of APS in pregnancy, deal with the various possible mechanisms of action of aPL in pregnancy, and discuss the treatment options of women having pregnancy complications of APS.

Osteoporosis leading to fracture can occur during pregnancy. Bone density may be low before pregnancy due to recognised causes such as coeliac disease, osteogenesis imperfecta and previous anorexia nervosa (secondary osteoporosis). In some patients there is no identifiable cause. This condition is referred to as "pregnancy associated or pregnancy related osteoporosis"; it is not known whether pregnancy causes the osteoporosis or merely coincides with it. Typically the loss of bone leads to vertebral fracture with loss of height or pain in the hips also sometimes with fracture. Symptoms most often begin in the third trimester of the first pregnancy and improve after delivery; they do not usually recur in subsequent pregnancies. The cause is unknown and there is no specific treatment; follow up bone density measurements show that the osteoporosis slowly improves post partum. Recent research in non osteoporotic women shows that breast feeding maintains a low bone density; it is therefore contraindicated in pregnancy associated osteoporosis.

This review addresses on various methods used in the detection of human teratogenic effects of drug use in early pregnancy. Data are presented from the new Swedish ongoing recording of drug use in early pregnancy. These data do not indicate a teratogenic effect of the main antirheumatic drugs used in Sweden.

The application of molecular techniques to the study of human pregnancy has resulted in the recognition that there is bi-directional cell traffic during pregnancy. Recent studies indicate fetal progenitor cells can persist in the maternal peripheral blood for decades after childbirth. Scleroderma is increased in women, has a peak incidence following childbearing years, and has clinical similarities to chronic graft-versus-host disease that occurs after allogeneic stem cell transplantation. This paper explores the idea that microchimerism is involved in scleroderma and considers insights gained from transplantation biology in seeking to understand how microchimerism might contribute to the pathogenesis of scleroderma. Chimerism means that a body contains cell populations derived from different individuals and microchimerism low levels of chimerism. Although highlighted in the study of scleroderma, microchimerism is also implicated in selected other autoimmune disorders.