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During pregnancy, estrogen and human chorionic gonadotropin (hCG) are produced. These increase the thyroid hormones in the blood. When the mother's thyroid function is abnormal, there is a chance that the baby will get too much or not enough of the thyroid hormone. This affects the way the baby's brain and nervous system develop.
The baby needs thyroid hormone so its nervous system and brain develop properly. Up until the 10th to 12th week of pregnancy, the baby gets all of the thyroid hormone it needs from the mother. After that time, the baby's own thyroid begins to function, but the baby still needs the mother to get enough iodine to support proper thyroid function.
Congestive heart failure, low birth weight, developmental disabilities, premature birth, miscarriage and still birth are all possible during a pregnancy when the mother's thyroid function is abnormal. Preeclampsia, or high blood pressure during pregnancy, and anemia, or low levels of iron in the blood that affect the way oxygen is carried to the organs, are both possible. Delivery complications, such as stalled labor or prolonged labor are also possible.
Some women may experience thyroid storms, or worsened thyroid function and symptoms, during the first trimester when the baby relies on her thyroid hormones. During the second and third trimesters, however, the woman may experience a period of remission because of the body's natural immune system suppression that occurs during that period. The remission phase usually ends at delivery, when the thyroid storms begin again. These storms usually last two to three months and begin to stabilize as the mother's hormones return to normal.
Approximately 8 percent of women who have delivered a baby will suffer from an inflammation of the thyroid called postpartum thyroiditis. This condition may go undiagnosed because the symptoms often mimic postpartum blues. These symptoms include lethargy, exhaustion, fatigue and moodiness.
A woman who is suffering from postpartum thyroiditis will go through a cycle of symptoms. One to eight months after delivery, the woman will go through a mild phase of hyperthyroidism lasting one to two months. From there, a period of approximately six months to a year, the woman will suffer from hypothyroidism. In most cases, after the period of hyperthyroidism, the thyroid will begin to function properly. However, in a small number of women, the thyroid is severely damaged by the inflammation and function never returns to normal. In that case, the woman will have to take synthetic hormones.
Because of the effects of thyroid dysfunction on the baby and the mother, it is necessary for a obstetrician to treat the mother, sometimes with synthetic hormones, during pregnancy and in the postpartum period.
Published by Casey L. Holley
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THYROID AUTOIMMUNITY AND PREGNANCY OUTCOME
Alex F. Muller Department of Internal Medicine, Diakonessenhuis Utrecht, Bosboomstraat 1 ,3582 KE, Utrecht ,The Netherlands ,
Arie Berghout Department of Internal Medicine, Medical Center Rijnmond Zuid - Zuiderziekenhuis, Groene Hilledijk 315 ,3075 EA, Rotterdam ,The Netherlands.
Introduction Several, disorders that are historically associated with pregnancy loss - such as collagen vascular diseases (most notably systemic lupus erythematosus), chronic active hepatitis, inflammatory bowel disease, diabetes mellitus and thyroid disease - are autoimmune disorders (1). A number of studies have specifically addressed the relationship between thyroid autoimmunity and spontaneous pregnancy loss.
Autoimmune hypo- and hyperthyroidism also increase the risk for obstetrical complications. It appears that low birth weight; prematurity and eclampsia are associated with the severity of the thyroid dysfunction (2-5).
Thyroid failure (6) - and even low normal free thyroxine (fT4) levels! (7) - in early pregnancy are associated with impaired neuropsychological development. Considering the fact that thyroid autoimmunity often leads to the gradual development of permanent thyroid failure it becomes clear that the presence of thyroid autoimmunity has important repercussions on clinical practice in women of childbearing age (8).
In conclusion, there is accumulating evidence that thyroid autoimmunity is associated - causally or as an epiphenomenon - with adverse pregnancy outcomes. In this comment we will discuss some aspects of thyroid autoimmunity and pregnancy outcome. For an oversight of the factors that are involved in the pathogenesis of autoimmune thyroiditis, especially in relation to pregnancy the reader is referred a recent review (9).
Thyroid autoimmunity and pregnancy loss Spontaneous pregnancy loss is common. It has been shown that the total rate of spontaneous pregnancy loss is 31% (10). An increasingly recognized factor in the aetiology of pregnancy loss is the presence of autoantibodies (11).
How might autoimmunity influence miscarriage? An extensive discussion of this issue is beyond the scope of this comment, for this the reader is referred to some excellent reviews (12;13). However, several points are worth mentioning at this point. Since the fetus expresses paternal MHC molecules adaptation of the maternal immune system is essential for a successful pregnancy. Such adaptation is accomplished through an increased production of cytokines that have immunosuppressive capacities. These cytokines are produced by so-called (CD4+) T-helper 2 (TH2) lymphocytes. Another subset of T cells exists that is also CD4+, these so-called T-helper 1 (TH1) lymphocytes are - unlike TH2 cells - well equipped to stimulate the cytotoxic and cytolytic arm of the cell mediated immune system (e.g. to activate macrophages and Natural Killer cells) via TH1 cytokines to kill target cells. During successful pregnancy there is a TH1 to TH2 shift characterized by down-regulation of the TH1 mediated effector arms of the immune system, concomitantly there is increased immunoglobulin production (9). Interestingly, experimentally induced changes in the TH1 / TH2 balance during pregnancy can induce increased rates of miscarriage (14). From these data it is clear that an adequate adaptation of the immune system is of paramount importance for a successful pregnancy to occur.
Stagnaro-Green et al. studied 552 consecutive women in the first trimester of pregnancy and found that the presence of thyroid peroxidase (TPO) and/or thyroglobulin (Tg) antibodies in the first trimester of pregnancy is a risk factor for spontaneous fetal loss (17% vs. 8.4% in controls) (15). These results were confirmed by Glinoer et al. who found a higher rate of spontaneous abortion in 45 women with thyroid autoantibodies compared to 603 controls: 13.3% vs. 3.3% (16).
In a prospective study of 54 women who conceived after in vitro fertilization (IVF) we were unable to find a significant association between the spontaneous abortion rate and the presence of TPO antibodies before pregnancy. Although miscarriages occurred in 33% of TPO antibody positive women and in only 19% of the TPO antibody negative women, the difference was not statistically significant (17). Our results thus contradict those of the two studies mentioned above and several biases can be proposed to explain this discrepancy (18). Firstly, the prevalence of thyroid autoimmunity was low in our pregnant women and if present the severity of the thyroid autoimmune process was mild. Secondly, we determined TPO antibodies before pregnancy, while in the other studies antibodies were determined during pregnancy. In view of the immunologic changes that occur during pregnancy (see ref. 7 for review) these differences in study design have probably led to inclusion of women with less severe forms of thyroid autoimmunity which might - at least in part - explain the discrepancy.
In women with a history of habitual abortion the presence of non-organ specific autoantibodies, notably of antiphospholipid and anticardiolipin antibodies, has been associated with fetal loss (19). Data on the relationship between thyroid autoantibodies and habitual abortion are conflicting. Several studies found an association between TPO antibodies and recurrent first-trimester fetal loss (20-24). However, others could not confirm this observation (25;26). Interestingly, Vaquero et al. have recently investigated the role of mild thyroid abnormalities in women with thyroid antibodies and recurrent first trimester abortions (27). In this small study the authors showed that treatment with thyroid hormone was more effective than treatment with intravenous immunoglobulins. These data might be taken to suggest that mild degrees of thyroid insufficiency and not thyroid autoimmunity per se - is causal in the association between the presence of thyroid antibodies and recurrent abortion (27;28).
In conclusion there are presently sufficient data showing an association of thyroid autoimmunity in early pregnancy and subsequent 'incidental' miscarriage. However, the data on the presence of thyroid antibodies and recurrent abortion are conflicting. Most likely, 'incidental' and recurrent abortion represent distinctive entities.
Autoimmune thyroid dysfunction and obstetrical complications Despite the association between decreased fertility and hypothyroidism 2-2.5% of pregnant women have elevated TSH levels (29-31). Hyperthyroidism in pregnancy is less often encountered: approximately only in 1 of 1000-2000 pregnancies (2;3;32)
When women with hypothyroidism do become pregnant it appears that the most prevalent disorder is pregnancy induced hypertension (33-36). Other complications that have been described in some but not all studies are placenta abruptio, postpartum haemorrhage, stillbirths, low birth weight and significant anaemia (33;35;36). Considering treatment it is important to note that thyroid hormone replacement with T4 significantly improves - but not diminishes - the excess risk of obstetrical complications (33).
Hyperthyroidism during gestation is also associated with obstetrical complications such as low birth weight, prematurity and eclampsia (2). It is outside the scope of this editorial to discuss the treatment of hyperthyroidism during pregnancy, for this purpose the reader is referred to some excellent recent overviews (2;33).
Thyroid autoimmunity and offspring Several studies have shown that the presence of thyroid antibodies is a powerful risk marker for the transition from subclinical to overt hypothyroidism (8;37). Indeed, women with thyroid antibodies are at risk of becoming hypothyroid during pregnancy with its increased demand for thyroid hormones (34).
In a recent study by Pop et al. it has been shown that children born to women with maternal serum fT4 levels below the 10th percentile at 12 weeks gestation (irrespective of elevation of TSH and/or presence of TPO antibodies), had significantly lower neurodevelopmental scores compared to children of mothers with higher fT4 values. It is important to note that women with low fT4 levels at 12 weeks gestation were largely affected by autoimmune thyroiditis. However, there was no correlation between neurodevelopmental scores of the infants and maternal fT4 at 32 weeks gestation which is a puzzling finding in view of the expected deterioration in thyroid function during pregnancy in women with autoimmune thyroiditis (7;34). Whatever the explanation for this unexpected finding the fact remains that after appropriate statistical analysis fT4 levels below the 10th percentile at 12 weeks gestation represented a significant risk factor for impaired psychomotor development.
Haddow et al. have extended the findings of Pop et al. by (6). These investigators provided evidence that children born to mothers with hypothyroidism during the second trimester of pregnancy, as determined by an elevated TSH, have lower IQ-scores and more educational difficulties at age 7-9 than children born to mothers with normal TSH levels during pregnancy. In their study 25,216 serum samples were prospectively collected and 47 women with TSH-levels at or above the 99th percentile of the values for all pregnant women were identified. Additionally 15 women with TSH values between the 98th and 99.6th percentiles, and low thyroxine levels were also included, as were 124 matched controls. The children of the 62 women with elevated TSH levels during pregnancy performed less well on all 15 neuropsychological tests carried out (in 2 of these the difference was significant), and children had more school difficulties and learning problems (p=0.06). In this study 77% of the women with hypothyroidism had high titres of TPO antibodies (6). These data further underline the notion that chronic autoimmune thyroiditis is the most frequent cause of low normal fT4 levels and raised TSH levels in these women. Taken together, the studies by Pop et al. and Haddow et al. provide evidence that not only overt but also relatively mild and hitherto unrecognised states of thyroid failure are associated with persistent and significant impairment in neuropsychological performance of the offspring.
Concluding remarks and consequences for clinical practice
Thyroid autoimmunity with its impaired thyroid reserve has important consequences on pregnancy outcome (table 1).
Table: key messages
Thyroid autoimmunity and recurrent pregnancy loss
--> consider treatment with L-thyroxine
Thyroid autoimmune dysfunction during pregnancy
--> hypothyroidism should be treated with full replacement dose immediately
--> hyperthyroidism should be treated according to fT4 levels
Thyroid autoimmunity and offspring
--> check for overt hypothyroidism and act accordingly. No data are available on the effects of LT4 in cases of mild/subclinical thyroid failure.
Thyroid autoimmunity and pregnancy loss: As there are now data to suggest that recurrent miscarriage in women with thyroid antibodies can be prevented by thyroxine administration (27), we are of the opinion that in women with recurrent miscarriage and thyroid antibodies treatment with L-thyroxine should be considered, though further controlled studies are essential.
Autoimmune thyroid dysfunction and obstetrical complications: As the risk to mother and child seems to be correlated with the severity of the thyroid dysfunction it is clear that - depending on the fT4 level at presentation - treatment should be instituted immediately. Thus, when a woman is diagnosed with hypothyroidism during pregnancy full replacement with thyroxine (1.6µg/kg ideal body weight) should be started immediately. In view of the expected increase in thyroxine requirement during gestation regular clinical and laboratory follow-up is essential, with periodic determinations of TSH and free T4 concentrations (30). Women diagnosed with hyperthyroidism during pregnancy should be treated with antithyroid drugs exclusively, aiming at a fT4 at - or slightly above - the upper limit of normal (33)
Thyroid autoimmunity and offspring: In a recent publication Morreale de Escobar et al. have summarized and discussed epidemiological and experimental evidence and - convincingly - argued that conditions resulting in first trimester hypothyroxinaemia (defined as a low for gestational age circulating maternal free T4, whether or not TSH is increased) pose an increased risk for poor neuropsychological development of the fetus (38). It is at present unknown if thyroxine replacement therapy will effectively prevent detrimental effects on the offspring in these cases. Clearly, double blind randomised trails are needed to clarify this issue (39).
(1) Gleicher N. Autoantibodies and pregnancy loss. Lancet 1994; 343(8900):747-748.
(2) Mandel SJ, Cooper DS. The use of antithyroid drugs in pregnancy and lactation. J Clin Endocrinol Metab 2001; 86(6):2354-2359.
(3) Millar LK, Wing DA, Leung AS, Koonings PP, Montoro MN, Mestman JH. Low birth weight and preeclampsia in pregnancies complicated by hyperthyroidism. Obstet Gynecol 1994; 84(6):946-949.
(4) Davis LE, Leveno KJ, Cunningham FG. Hypothyroidism complicating pregnancy. Obstet Gynecol 1988; 72(1):108-112.
(5) Leung AS, Millar LK, Koonings PP, Montoro M, Mestman JH. Perinatal outcome in hypothyroid pregnancies. Obstet Gynecol 1993; 81(3):349-353.
(6) Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999; 341(8):549-555.
(7) Pop VJ, Kuijpens JL, van Baar AL, Verkerk G, van Son MM, de Vijlder JJ et al. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy. Clin Endocrinol (Oxf) 1999; 50(2):149-155.
(8) Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F et al. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clin Endocrinol (Oxf) 1995; 43(1):55-68.
(9) Muller AF, Drexhage HA, Berghout A. Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care. Endocr Rev 2001; 22(5):605-630.
(10) Wilcox AJ, Weinberg CR, O'Connor JF, Baird DD, Schlatterer JP, Canfield RE et al. Incidence of early loss of pregnancy. N Engl J Med 1988; 319(4):189-194.
(11) Gleicher N, Pratt D, Dudkiewicz A. What do we really know about autoantibody abnormalities and reproductive infertility? A critical review. Contracept Fertil Sex 1995; 23(4):239-254.
(12) Formby B. Immunologic response in pregnancy. Its role in endocrine disorders of pregnancy and influence on the course of maternal autoimmune diseases. Endocrinol Metab Clin North Am 1995; 24(1):187-205.
(13) Wegmann TG, Lin H, Guilbert L, Mosmann TR. Bidirectional cytokine interactions in the maternal-fetal relationship: is successful pregnancy a TH2 phenomenon?. Immunol Today 1993; 14(7):353-356.
(14) Szekeres-Bartho J, Par G, Szereday L, Smart CY, Achatz I. Progesterone and non-specific immunologic mechanisms in pregnancy. Am J Reprod Immunol 1997; 38(3):176-182.
(15) Stagnaro-Green A, Roman SH, Cobin RH, el Harazy E, Alvarez-Marfany M, Davies TF. Detection of at-risk pregnancy by means of highly sensitive assays for thyroid autoantibodies. JAMA 1990; 264(11):1422-1425.
(16) Glinoer D, Soto MF, Bourdoux P, Lejeune B, Delange F, Lemone M et al. Pregnancy in patients with mild thyroid abnormalities: maternal and neonatal repercussions. J Clin Endocrinol Metab 1991; 73(2):421-427.
(17) Muller AF, Verhoeff A, Mantel MJ, Berghout A. Thyroid autoimmunity and abortion: a prospective study in women undergoing in vitro fertilization. Fertil Steril 1999; 71(1):30-34.
(18) Glinoer D. Thyroid autoimmunity and spontaneous abortion [letter]. Fertil Steril 1999; 72(2):373-374.
(19) Cowchock S, Smith JB, Gocial B. Antibodies to phospholipids and nuclear antigens in patients with repeated abortions. Am J Obstet Gynecol 1986; 155(5):1002-1010.
(20) Roberts J, Jenkins C, Wilson R, Pearson C, Franklin IA, MacLean MA et al. Recurrent miscarriage is associated with increased numbers of CD5/20 positive lymphocytes and an increased incidence of thyroid antibodies. Eur J Endocrinol 1996; 134(1):84-86.
(21) Pratt DE, Kaberlein G, Dudkiewicz A, Karande V, Gleicher N. The association of antithyroid antibodies in euthyroid nonpregnant women with recurrent first trimester abortions in the next pregnancy. Fertil Steril 1993; 60(6):1001-1005.
(22) Kutteh WH, Yetman DL, Carr AC, Beck LA, Scott RT, Jr. Increased prevalence of antithyroid antibodies identified in women with recurrent pregnancy loss but not in women undergoing assisted reproduction. Fertil Steril 1999; 71(5):843-848.
(23) Mecacci F, Parretti E, Cioni R, Lucchetti R, Magrini A, La Torre P et al. Thyroid autoimmunity and its association with non-organ-specific antibodies and subclinical alterations of thyroid function in women with a history of pregnancy loss or preeclampsia. J Reprod Immunol 2000; 46(1):39-50.
(24) Bussen SS, Steck T. Thyroid antibodies and their relation to antithrombin antibodies, anticardiolipin antibodies and lupus anticoagulant in women with recurrent spontaneous abortions (antithyroid, anticardiolipin and antithrombin autoantibodies and lupus anticoagulant in habitual aborters). Eur J Obstet Gynecol Reprod Biol 1997; 74(2):139-143.
(25) Esplin MS, Branch DW, Silver R, Stagnaro-Green A. Thyroid autoantibodies are not associated with recurrent pregnancy loss. Am J Obstet Gynecol 1998; 179(6):1583-1586.
(26) Rushworth FH, Backos M, Rai R, Chilcott IT, Baxter N, Regan L. Prospective pregnancy outcome in untreated recurrent miscarriers with thyroid autoantibodies. Hum Reprod 2000; 15(7):1637-1639.
(27) Vaquero E, Lazzarin N, De Carolis C, Valensise H, Moretti C, Ramanini C. Mild thyroid abnormalities and recurrent spontaneous abortion: diagnostic and therapeutical approach. Am J Reprod Immunol 2000; 43(4):204-208.
(28) Glinoer D. Thyroid immunity, thyroid dysfunction, and the risk of miscarriage: a propos article by Vaquero et al. Mild thyroid abnormalities and recurrent spontaneous abortion: diagnostic and therapeutical approach. Am J Reprod Immunol 2000; 43(4):202-203.
(29) Glinoer D, Riahi M, Grun JP, Kinthaert J. Risk of subclinical hypothyroidism in pregnant women with asymptomatic autoimmune thyroid disorders. J Clin Endocrinol Metab 1994; 79(1):197-204.
(30) Glinoer D. Potential repercussions for the progeny of maternal hypothyroxinemia during pregnancy. Thyroid 2000; 10(1):59-62.
(31) Klein RZ, Haddow JE, Faix JD, Brown RS, Hermos RJ, Pulkkinen A et al. Prevalence of thyroid deficiency in pregnant women. Clin Endocrinol (Oxf) 1991; 35(1):41-46.
(32) Davis LE, Lucas MJ, Hankins GD, Roark ML, Cunningham FG. Thyrotoxicosis complicating pregnancy. Am J Obstet Gynecol 1989; 160(1):63-70.
(33) Glinoer D. The regulation of thyroid function in pregnancy: pathways of endocrine adaptation from physiology to pathology. Endocr Rev 1997; 18(3):404-433.
(34) Glinoer D, Delange F. The potential repercussions of maternal, fetal, and neonatal hypothyroxinemia on the progeny. Thyroid 2000; 10(10):871-887.
(35) Mestman JH, Goodwin TM, Montoro MM. Thyroid disorders of pregnancy. Endocrinol Metab Clin North Am 1995; 24(1):41-71.
(36) Brent GA. Maternal hypothyroidism: recognition and management. Thyroid 1999; 9(7):661-665.
(37) Geul KW, van Sluisveld IL, Grobbee DE, Docter R, de Bruyn AM, Hooykaas H et al. The importance of thyroid microsomal antibodies in the development of elevated serum TSH in middle-aged women: associations with serum lipids. Clin Endocrinol (Oxf) 1993; 39(3):275-280.
(38) Morreale dE, Obregon MJ, Escobar dR. Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia?. J Clin Endocrinol Metab 2000; 85(11):3975-3987.
(39) Smallridge RC, Ladenson PW. Hypothyroidism in pregnancy: consequences to neonatal health. J Clin Endocrinol Metab 2001; 86(6):2349-2353.
THYROID AUTOIMMUNITY AND PREGNANCY OUTCOME