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Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring lifelong treatment. Postpartum thyroiditis is believed to result from the modifications to the immune system necessary in pregnancy, and histologically is a subacute lymphocytic thyroiditis.
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.
This is a shortened version of the eleventh chapter of the ICD-9: Complications of Pregnancy, Childbirth, and the Puerperium. It covers ICD codes 630 to 679 . The full chapter can be found on pages 355 to 378 of Volume 1, which contains all (sub)categories of the ICD-9.
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 ...
Subacute lymphocytic thyroiditis, also called painless or silent thyroiditis, occurs in individuals with underlying autoimmune disease or after pregnancy. [2] [4] [5] It is considered to be a variant of Hashimoto's thyroiditis. When subacute lymphocytic thyroiditis occurs up to 12 months postpartum, it is called postpartum thyroiditis.
Many treatment options are available based on symptom severity. Non-invasive treatment options include activity modification, pelvic support garments, analgesia with or without short periods of bed rest, and physiotherapy to increase strength of gluteal and adductor muscles reducing stress on the lumbar spine.
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]
Pregnancy itself is a factor of hypercoagulability (pregnancy-induced hypercoaguability), as a physiologically adaptive mechanism to prevent post partum bleeding. [7] The pregnancy associated hypercoaguability is attributed to an increased synthesis of coagulation factors, such as fibrinogen, by the liver through the effects of estrogen.