Pregnancy has variable effects on thyroid hormone concentrations throughout pregnancy as well as being associated with goitre. T he latter is largely preventable by ensuring optimal iodine intake of at least 200 µg per day. Hypothyroidism in pregnancy usually characterized by a high serum TSH value has been found to occur in around 2– 3% of otherwise normal pregnancies with the prevalence of overt hypothyroidism estimated to be up to 0.5% [26]. On a worldwide basis the most important cause of thyroid insufficiency remains iodine deficiency, while in iodine- replete communities the cause is usually chronic autoimmune thyroiditis. Untreated hypothyroidism may lead to obstetric complications, such as preterm de livery and fetal loss. Epidemiological data suggest that the children of women with hypothyroxinaemia may have psychoneurological deficits. In classic areas of iodine deficiency, a similar range of deficits in children has been described where maternal hypothyroxinaemia rather than high serum TSH is the main biochemical abnormality. In these areas, maternal iodine intake is often substantially less than the 200 µg per day currently recommended. Even in areas previously thought to be iodine sufficient, there is now evidence of substantial gestational iodine deficiency, which may lead to low ma ternal circulating thyroxine concentrations.

Hyperthyroidism is found in 0.1– 0.4% of all pregnancies and is usually caused by Graves’ disease characterized by TSH receptor (TSHR) antibodies, which usually decrease in titre throughout pregnancy. Maternal complications include miscarriage, placenta abruption, pre- eclampsia, and preterm delivery. High titres of TSHR antibodies predict a high risk of neonatal thyrotoxicosis.

Antithyroid antibodies, particularly TPOAb, occur in 10% of women at 14 weeks of gestation, which is compatible with the prevalence of antithyroid antibodies in community surveys [1, 13]. A proportion of these women will have subclinical hypothyroidism with a high serum TSH, but most will be euthyroid. However, after delivery a transient, destructive autoimmune thyroiditis that occurs between the twelfth and sixteenth week postpartum will develop in 50% of TPOAb positive women, as ascertained in early gestation, clinically apparent as postpartum thyroiditis (PPT). It presents as a temporary, usually painless, episode of hypothyroidism, occasionally preceded by a short episode of hyperthyroidism. Up to 25% of women progress to permanent hypothyroidism within approximately five years following an episode of PPT, particularly those with high antibody titres.

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عرض شائع في الفم قد يكون مرتبطا بخطر الإصابة بأمراض خطيرة

نصائح عامة لاستخدام سماعات الرأس بأمان

تأثير اللياقة البدنية على الدماغ

المزيد

الآخبار التكنلوجية

ديدان الأرض تكشف تلوث التربة بالمعادن الثقيلة

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المزيد

مواضيع ذات صلة

Hypothyroidism

Hyperthyroidism

Clinical Manifestations of Iron Deficiency

Thyroid Imaging: nuclear Medicine Techniques - Thyroiditis

Thyroid Imaging: nuclear Medicine Techniques - Thyrotoxicosis

Pathobiology of Iron Deficiency

Outcome and Prevention of Infectious Diseases

Serum and Tissue Thyroid Hormone concentrations in NTI

Microorganism Entry, Invasion, and Dissemination: The Host’s Perspective

Microorganism Colonization of Host Surfaces

The Encounter Between Host and Microorganism

Systemic Approach to Anemia