Otoimmün tiroid hastalıkları ve fetüse ait mikrokimerizm

Year 2004, Volume: 1 Issue: 3, 41 - 47, 01.04.2004

Azize Yasemin Göksu

Abstract

Gebelik esnasında, plasenta yoluyla, hematopoetik hücrelerin iki taraflı geçişi olmaktadır. Fetüse ait hücrelerin, anne kanına ulaştıkları ve annenin çeşitli dokularına nüfuz ettikleri iyi bilinmektedir fetüse ait mikrokimerizm . Bir bireyde, genetik olarak farklı bir bireyden alınmış az miktarda DNA ya da hücrenin var olma durumuna “mikrokimerizm” denmektedir. İnsanlarda, otoimmün tiroid hastalıklarının OTH seyir ve ciddiyetinin, gebelikten etkilendiği iyi bilinmektedir; gebelik esnasında OTH’nın baskılanıp, doğum sonrası dönemde ise başlaması ya da alevlenmesi buna bir kanıttır. Gebelik esnasında, tiroid otoantikorları ve Graves hastalığı, baskılanma eğiliminde iken; kadınların yüksek bir oranı , otoimmün Hashimoto’s tiroidite ya da Graves hastalığına doğumdan 3-12 hafta sonra yakalanmaktadırlar. Ek olarak, OTH, doğurganlığı ve gebeliğin akibetini de etkilemekte ve fetüs kayıplarına yol açabilmektedir. Ancak, OTH’nın bu etkilerinin mekanizması henüz tam olarak anlaşılamamıştır. Otoimmün hastalıklarla, kronik graft-versus-host reaksiyonu arasındaki bazı klinik benzerlikler, kadınlarda çocuk sahibi olma dönemini takiben otoimmün hastalıkların artmış insidansı ve mikrokimerizmin anne kanı ya da dokularında uzun dönem varlığını sürdürmesi, otoimmün hastalıkların patogenezinde mikrokimerizmin rol oynayabileceği hipotezini ortaya çıkarmıştır. Bu derlemede, OTH’nın üzerinde mikrokimerizmin muhtemel rolü hakkında en son bilgilere yer verilmiştir

Keywords

Gebelik, Graves hastalığı, Hashimoto tiroiditi, mikrokimerizm, otoimmün tiroid hastalıkları

Autoimmune thyroid diseases and fetal microchimerism

Abstract

During pregnancy, bi-directional trafficking of hematopoietic cells occurs through the placenta. Fetal cells are known to reach the maternal circulation and infiltrate a variety of tissues fetal microchimerism . The presence of a small population of cells or DNA in one individual that derives from another genetically distinct person is referred to as microchimerism. In humans, the course and severity of the autoimmune thyroid diseases AITD is well known to beaffected by pregnancy as evidenced by disease suppression during pregnancy and initiation / exacerbation in the postpartum period. Although thyroid autoantibodiesand Graves’ disease itself tend to be suppressed duringpregnancy, a high percentage 8–10 % of women developautoimmune Hashimoto’s thyroiditis or Graves’disease 3–12 months after delivery. Furthermore, AITD affect both fertility and pregnancy outcome and cause fetal loss. However, the mechanisms of this influence have not been fully understood. The clinical similarities between some features of autoimmune diseases and the chronic graft versus host disease, the increased incidence of autoimmune diseases in women after childbearing age, and the long-term persistence of microchimerism in maternal blood / tissues have raised the hypothesis that microchimerism could be involved in the pathogenesis of autoimmune diseases. Here we have reviewed recent information on the possible role of fetal microchimerism in autoimmune thyroid disease

Keywords

Autoimmune thyroid diseases, Hashimoto’s thyroiditis, Graves’ disease, microchimerism, pregnancy

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