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Postpartum thyroiditis is believed to result from the modifications to the immune system necessary in pregnancy, and histologically is a subacute lymphocytic thyroiditis. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism.
Hypothyroidism is common in pregnancy with an estimated prevalence of 2-3% and 0.3-0.5% for subclinical and overt hypothyroidism respectively. [8] Endemic iodine deficiency accounts for most hypothyroidism in pregnant women worldwide while chronic autoimmune thyroiditis is the most common cause of hypothyroidism in iodine sufficient parts of the world.
When subacute lymphocytic thyroiditis occurs up to 12 months postpartum, it is called postpartum thyroiditis. It has an increased incidence in women with presence of thyroid peroxidase (TPO) antibodies prior to pregnancy and in women with preexisting Type 1 diabetes. Postpartum thyroiditis can recur in subsequent pregnancies. [2] [4] [5]
Symptoms of normal pregnancy, like fatigue, can make it easy to overlook thyroid problems in pregnancy. [1] Thyroid hormone is vital during pregnancy. The unborn baby's brain and nervous system need thyroid hormone to develop. During the first trimester, the baby depends on the mother's supply of thyroid hormone. At 10 to 12 weeks of pregnancy ...
Women are 4-5 times more likely to develop a clot during pregnancy and in the postpartum period than when they are not pregnant. [25] Hypercoagulability in pregnancy likely evolved to protect women from hemorrhage at the time of miscarriage or childbirth. In developing countries, the leading cause of maternal death is still hemorrhage. [25]
It takes place in normal pregnancies as well as when there are obstetric or trauma related complications to pregnancy. Normally the maternal circulation and the fetal circulation are kept from direct contact with each other, with gas and nutrient exchange taking place across a membrane in the placenta made of two layers, the syncytiotrophoblast ...
Higher secretion of IFN-γ and IL-4, and lower plasma cortisol concentration during pregnancy has been reported in females with postpartum thyroiditis than in healthy females. It indicates that weaker immunosuppression during pregnancy could contribute to the postpartum thyroid dysfunction. [138]
Thyroiditis is generally caused by an immune system attack on the thyroid, resulting in inflammation and damage to the thyroid cells. This disease is often considered a malfunction of the immune system and can be associated with IgG4-related systemic disease, in which symptoms of autoimmune pancreatitis, retroperitoneal fibrosis and noninfectious aortitis also occur.