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Iodine and the Body

 

Pregnancy

 

Lazarus

 

Screening for thyroid disease in pregnancy.

Lazarus JH, Premawardhana LD.

J Clin Pathol. 2005 May;58(5):449-52. Review.

 

"Although gestational hyperthyroidism is uncommon (0.2%), hypothyroidism (autoimmune disease or suboptimal iodine intake) occurs in 2.5% of women and is predictive of reduced neonatal and child neuropsychological development and maternal obstetric complications. Postpartum thyroid dysfunction (PPTD) occurs in 5-9% of women and is associated with antithyroid peroxidase antibodies (antiTPOAb) in 10% of women in early pregnancy. Therefore, screening for thyroid dysfunction in pregnancy should be considered. T4 and thyroid stimulating hormone measurements could be used to screen for hypothyroidism, which would require levothyroxine intervention treatment. T4 supply is crucial to fetal nervous system maturation; currently, the recommended daily iodine intake is 200 microg, and this is not always achieved, even in the UK. At present, a randomised prospective trial is ongoing to provide the evidence base for this screening strategy. Meanwhile, it is reasonable to (a) optimise iodine nutrition during pregnancy; (b) ascertain women with known thyroid disease; (c) identify women at increased risk of thyroid disease-for example, those with other autoimmune diseases. PPTD can be predicted by measurement of antiTPOAb in early gestation."

 

 

Thyroid disorders associated with pregnancy: etiology, diagnosis, and management.

Lazarus JH.

Treat Endocrinol. 2005;4(1):31-41. Review.

[abstract only]

 

"Pregnancy has an effect on thyroid economy with significant changes in iodine metabolism, serum thyroid binding proteins, and the development of maternal goiter especially in iodine-deficient areas. Pregnancy is also accompanied by immunologic changes, mainly characterized by a shift from a T helper-1 (Th1) lymphocyte to a Th2 lymphocyte state. Thyroid peroxidase antibodies are present in 10% of women at 14 weeks' gestation, and are associated with (i) an increased pregnancy failure (i.e. abortion), (ii) an increased incidence of gestational thyroid dysfunction, and (iii) a predisposition to postpartum thyroiditis. Thyroid function should be measured in women with severe hyperemesis gravidarum but not in every patient with nausea and vomiting during pregnancy. Graves hyperthyroidism during pregnancy is best managed with propylthiouracil administered throughout gestation. Thyroid-stimulating hormone-receptor antibody measurements at 36 weeks' gestation are predictive of transient neonatal hyperthyroidism, and should be checked even in previously treated patients receiving thyroxine. Postpartum exacerbation of hyperthyroidism is common, and should be evaluated in women with Graves disease not on treatment. Radioiodine therapy in pregnancy is absolutely contraindicated. Hypothyroidism (including subclinical hypothyroidism) occurs in about 2.5% of pregnancies, and may lead to obstetric and neonatal complications as well as being a cause of infertility. During the last few decades, evidence has been presented to underpin the critical importance of adequate fetal thyroid hormone levels in order to ensure normal central and peripheral nervous system maturation. In iodine-deficient and iodine-sufficient areas, low maternal circulating thyroxine levels have been associated with a significant decrement in child IQ and development. These data suggest the advisability of further evaluation for a screening program early in pregnancy to identify women with hypothyroxinemia, and the initiation of prompt treatment for its correction. Hypothyroidism in pregnancy is treated with a larger dose of thyroxine than in the nonpregnant state. Postpartum thyroid dysfunction (PPTD) occurs in 50% of women found to have thyroid peroxidase antibodies in early pregnancy. The hypothyroid phase of PPTD is symptomatic and requires thyroxine therapy. A high incidence (25-30%) of permanent hypothyroidism has been noted in these women. Women having transient PPTD with hypothyroidism should be monitored frequently, as there is a 50% chance of these patients developing hypothyroidism during the next 7 years."
 

 

Thyroid disease in pregnancy and childhood.

Lazarus JH.

Minerva Endocrinol. 2005 Jun;30(2):71-87. Review.

[abstract only]

 

"The subject of thyroid disease in pregnancy is receiving increasing attention from many scientific disciplines. Thyroid function in pregnancy is characterised by a T4 surge at 12 weeks declining thereafter. Serum thyroid hormone concentrations fall in the second half of pregnancy but there are few data on normal reference ranges. Fetal brain development depends on T4 transport into the fetus which in turn depends on sufficient maternal iodine supply. There is current concern that adequate iodisation is not present in large parts of Europe. There is increasing evidence that thyroid autoimmunity is associated with fetal loss but the mechanism is unclear and therapy requires carefully conducted studies. While hyperthyroidism in pregnancy is uncommon, effects on both mother and child are critical if untreated. The use of propylthiouracil is recommended together with measurement of TSH receptor antibodies at 36 weeks gestation. Women receiving thyroxine therapy for hypothyroidism or as suppressive therapy should have their dose increased by up to 50% during pregnancy. There are now substantial data to show deleterious effects on child IQ resulting from low maternal T4 (or high TSH) during gestation. Major advances in molecular biology have contributed to elucidation of many genetic causes of congenital hypothyroidism. However, the aetiology of the majority of cases is still unclear and further research is required. The presence of TPO antibodies in about 10% of pregnant women in early gestation is a predictor of an increased incidence of subclinical hypothyroidism during pregnancy and also of postpartum thyroid dysfunction. The latter condition occurs in 5-9% of women and 25-30% progress to permanent hypothyroidism. This review suggests that screening for thyroid function in early pregnancy and levothyroxine intervention therapy for maternal subclinical hypothyroidism should be considered but evidence is awaited. Screening for both thyroid dysfunction and thyroid antibodies ideally at a preconception clinic but certainly in early gestation is recommended."
 

 

Sequential studies on thyroid antibodies during pregnancy.

Smyth PP, Wijeyaratne CN, Kaluarachi WN, Smith DF, Premawardhana LD, Parkes AB, Jayasinghe A, de Silva DG, Lazarus JH.

Thyroid. 2005 May;15(5):474-7.

[abstract only]

 

"Thyroid antibodies were measured sequentially in 25 pregnant women from a Sri Lankan population. A high prevalence of antithyroid antibodies, particularly antithyroglobulin antibodies (TgAb) had previously been demonstrated in female schoolchildren drawn from this population. In the present study TgAb were detected in 36.8% of nonpregnant controls while thyroid peroxidase antibody (TPOAb) positivity was present in 26.3%. The prevalence of both antibodies in the pregnancy study group showed a progressive decline compared to nonpregnant controls throughout gestation becoming undetectable in the third trimester. The results are consistent with an immunosuppressive effect of pregnancy in a population in whom high thyroid autoantibody titers may have resulted from a recent salt iodization program."

 

 

Epidemiology and prevention of thyroid disease in pregnancy.

Lazarus JH.

Thyroid. 2002 Oct;12(10):861-5. Erratum in: Thyroid. 2003 Apr;13(4):415.

[abstract only]

 

"Pregnancy has variable effects on thyroid hormone concentrations throughout pregnancy as well as being associated with goiter. The latter is largely preventable by ensuring optimal iodine intake of at least 200 microg/d. Immunologic changes in pregnancy include a so-called T(H)2 shift that reverts to T(H)1 status around birth or early in the postpartum period. Hyperthyroidism during gestation, usually caused by Graves' disease, is rare (0.2%) and is best managed medically with propylthiouracil; thyroid-stimulating antibodies should be measured. Prevention of the deleterious effects of Graves' disease includes adequate preconception advice, adequate monitoring during pregnancy, and total avoidance of (131)I therapy during pregnancy. Hypothyroidism during pregnancy has an incidence of 2.5% although there is a 10% incidence of thyroid peroxidase (TPO)-antibody positivity in early gestation. There are convincing epidemiologic data to show that suboptimal thyroid function in pregnancy is associated with impaired neurointellectual development (e.g., 19% with IQ < 85 compared to 5% in one study). Therefore, there is a case for screening for thyroid function in early pregnancy with thyroxine (T(4)) intervention therapy. Maintenance of optimal iodine intake is critical to prevent nonautoimmune gestational maternal hypothyroxinaemia. Postpartum thyroid dysfunction (PPTD) occurs in 5%-9% of women and in up to 50% of TPO-antibody positive women (as ascertained in early pregnancy). Prevention of PPTD at this time could only be achieved by pregestational ablation of the thyroid. Another approach is to at least improve the prediction of postpartum thyroid disease (PPT) because the TPO antibody has a sensitivity of only 50%."

 

 

Epidemiology and prevention of thyroid disease in pregnancy.

Lazarus JH.

Thyroid. 2002 Oct;12(10):861-5. Erratum in: Thyroid. 2003 Apr;13(4):415.

[abstract only]

 

"Pregnancy has variable effects on thyroid hormone concentrations throughout pregnancy as well as being associated with goiter. The latter is largely preventable by ensuring optimal iodine intake of at least 200 microg/d. Immunologic changes in pregnancy include a so-called T(H)2 shift that reverts to T(H)1 status around birth or early in the postpartum period. Hyperthyroidism during gestation, usually caused by Graves' disease, is rare (0.2%) and is best managed medically with propylthiouracil; thyroid-stimulating antibodies should be measured. Prevention of the deleterious effects of Graves' disease includes adequate preconception advice, adequate monitoring during pregnancy, and total avoidance of (131)I therapy during pregnancy. Hypothyroidism during pregnancy has an incidence of 2.5% although there is a 10% incidence of thyroid peroxidase (TPO)-antibody positivity in early gestation. There are convincing epidemiologic data to show that suboptimal thyroid function in pregnancy is associated with impaired neurointellectual development (e.g., 19% with IQ < 85 compared to 5% in one study). Therefore, there is a case for screening for thyroid function in early pregnancy with thyroxine (T(4)) intervention therapy. Maintenance of optimal iodine intake is critical to prevent nonautoimmune gestational maternal hypothyroxinaemia. Postpartum thyroid dysfunction (PPTD) occurs in 5%-9% of women and in up to 50% of TPO-antibody positive women (as ascertained in early pregnancy). Prevention of PPTD at this time could only be achieved by pregestational ablation of the thyroid. Another approach is to at least improve the prediction of postpartum thyroid disease (PPT) because the TPO antibody has a sensitivity of only 50%."
 

 

 
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