[Thyroid status in anemic pregnant women under conditions of endemic goiter]. [Article in Russian] Zel'tser me



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Thyroid Function and Pregnancy

casey l. holley

Casey L. Holley, Yahoo! Contributor Network
Sep 1, 2010 "Share your voice on Yahoo! websites. Start Here."

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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.

Possible Complications

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.

Postpartum Thyroiditis

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.

Sources:
http://www.endo-society.org/guidelines/final/upload/Clinical-Guideline-Management-of-Thyroid-Dysfunction-during-Pregnancy-Postpartum.pdf
http://www.guidelines.gov/content.aspx?id=11283
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.

Conclusion

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



Casey Holley is a freelance writer specializing in Christian content and medical content. She has more than a decade of experience. She also enjoys writing about animals, beauty, fitness, weight loss, travel...  View profile

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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 ,
email: amuller@diakhuis.nl

Arie Berghout
Department of Internal Medicine, Medical Center Rijnmond Zuid - Zuiderziekenhuis, Groene Hilledijk 315 ,3075 EA, Rotterdam ,The Netherlands.

 

 

 

 

 

http://www.hotthyroidology.com/editorial_pics/print_editorial.gif  printed version

 

 

 

 










 

 

 

 

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).


Reference List

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