Breastfeeding and thyroid disease: a literature review.
Article Type: Report
Subject: Thyroid hormones (Physiological aspects)
Thyroid hormones (Health aspects)
Pregnancy (Physiological aspects)
Pregnancy (Health aspects)
Lactation (Physiological aspects)
Lactation (Health aspects)
Authors: Speller, Elisabeth
Brodribb, Wendy
McGuire, Elizabeth
Pub Date: 07/01/2012
Publication: Name: Breastfeeding Review Publisher: Australian Breastfeeding Association Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2012 Australian Breastfeeding Association ISSN: 0729-2759
Issue: Date: July, 2012 Source Volume: 20 Source Issue: 2
Product: Product Code: 2834135 Thyroid & Antithyroid Prep NAICS Code: 325412 Pharmaceutical Preparation Manufacturing SIC Code: 2834 Pharmaceutical preparations
Geographic: Geographic Scope: Australia Geographic Code: 8AUST Australia
Accession Number: 299258847
Full Text: INTRODUCTION

The thyroid and thyroid hormones are intimately connected with the maintenance of pregnancy and lactation. As such, any disorders of the thyroid can have an impact on women's ability to breastfeed. In addition, some thyroid disorders that occur in the postnatal period can be misinterpreted as postnatal depression or other illnesses. In the past, the need to take certain thyroid medications meant that mothers were instructed not to breastfeed for fear of disrupting the thyroid function of their babies. Newer and safer drugs to treat thyroid disorders now mean that mothers can safely continue to breastfeed.

This paper outlines the development of knowledge about thyroid disorders and their treatment in relation to mothers who wish to breastfeed their children. It looks at the historical basis on which early recommendations were made and the subsequent development of knowledge on this topic. It also addresses the development of postpartum thyroiditis, its effects on milk supply, and the forms of treatment available for it. Normal thyroid function during pregnancy is essential for normal foetal development, but thyroid function in pregnancy is beyond the scope of this paper.

Thyroid gland

The main function of the thyroid gland is to produce thyroxine (T4) and triiodothyronine (T3), hormones that regulate the body's metabolism and energy production, as well as growth and cognitive development in children. Thyroid hormones have essential roles in the growth, differentiation and normal function of all tissues.

The thyroid gland is made up of follicles full of a proteinaceous material (thyroglobulin). Iodine combines with thyroglobulin to produce T4 and T3. While T4 can only be produced in the thyroid gland, only 20% of T3 is manufactured in the thyroid, the remainder being produced by the removal of one iodine atom from T4 in extra thyroidal tissues. Nearly all the thyroid hormones in the bloodstream are bound to protein, mainly to thyroid binding globulin (TBG) and albumin (Jameson & Weetman 2012). Only the non-bound (or free) hormone is metabolically active, therefore changes in the amount and ratio of the binding proteins (such as occurs during pregnancy) may affect the total amount of thyroid hormone necessary to maintain a euthyroid (normal) state, and in the past have made test interpretation difficult.

Of particular relevance to breastfeeding, animal studies have shown that thyroid hormones are involved in establishing and maintaining lactation. In hypothyroid mice, administering prolactin and T4 increases milk production to normal levels, whereas giving prolactin alone does not (Capuco et al 1999). In the transition to lactation the mammary gland increases its number of thyroid hormone receptors and also increases its production of the enzyme that converts T4 to T3. Hence during lactation the mammary gland can activate and use more thyroid hormone and thus up-regulate its metabolic priority (Capuco et al 2008).

Regulation of thyroid function

Thyroid hormone production is regulated by a feedback mechanism involving the hypothalamus and the anterior pituitary. Thyrotropin-releasing hormone (TRH), produced in the hypothalamus, stimulates the production of thyroid-stimulating hormone (TSH) by the pituitary, while thyroid hormones themselves inhibit the production of TSH (Jameson & Weetman 2012). Thus TSH levels rise in response to low T3 or T4 levels (hypothyroidism) and stimulate the thyroid to produce more hormone, whereas high levels of T3 or T4 (hyperthyroidism) inhibit production of TSH and so T3 and T4 production is slowed.

TSH is a very sensitive marker of the activity of the thyroid gland. Even very slight changes in T3 and T4 levels bring about much greater opposite change in the TSH level. The unbound portion of T4 and T3 (free T4 and free T3) can also be measured.

Individuals maintain thyroid hormone levels within a rather narrow range compared to the population reference range. Although a TSH between 0.3 and 5.0 mlU/L falls within the reference range for the population, a given healthy individual usually maintains a 'personal set point' or personal range about half as wide as the population reference range. This means that an individual may have altered thyroid activity, with altered TSH levels and yet not have T3 or T4 levels outside the population reference range. Because TSH changes dramatically in response to changes in T4 and T3 levels, TSH may fall outside the population reference range while T3 and T4 do not. This is usually called subclinical thyroid disease, but it may represent significant dysfunction in an individual (Andersen et al 2002).

Thyroid disorders

Thyroid disease is common with around 7.5% of women and 1.5% of men experiencing thyroid disease (Stevens 2000).

Thyroid disease takes several forms including hypothyroidism, hyperthyroidism, and thyroid carcinoma. During the first year after a woman has given birth, regulation of thyroid function can be disrupted by postpartum thyroiditis. Because thyroid hormones affect general metabolism, the onset of symptoms of both hypo and hyperthyroidism are usually gradual and subtle, and are often attributed to other disease or lifestyle. Many symptoms are common in the postpartum period in 'normal' women so the diagnosis can be missed or not considered by the woman or her medical adviser.

During pregnancy the thyroid gland has to adapt to physiological changes. Renal iodine loss increases and the amount of thyroid binding globulin increases (so the bound thyroid hormone increases). The thyroid needs to produce more thyroid hormones to maintain levels of free T3 and T4 and to supply the foetus in the first half of pregnancy. Thyroid size increases by about 10% in a normal, iodine-replete pregnancy (Stagnaro-Green et al 2011). In 2011 the American Thyroid Association recommended recognising altered reference ranges for thyroid hormones during pregnancy but these reference ranges may not be widely accepted as yet (Stagnaro-Green et al 2011).

Women who have thyroid disease prior to becoming pregnant need to have their thyroid levels monitored regularly throughout their pregnancy and lactation. It is often necessary to adjust medication doses to maintain normal thyroid hormone levels.

Hyperthyroidism

Hyperthyroidism, an overactive thyroid, can cause fatigue, tremors, anxiety, palpitations, intolerance of heat, sweating, weight loss, increased pulse rate, diarrhoea, and light or no menstrual flow (Jameson & Weetman 2012). It is usually treated with anti-thyroid drugs during pregnancy and lactation. These are thioamide compounds that inhibit thyroid hormone synthesis. Radioactive iodine or surgery are alternative treatments for thyrotoxicosis (hyperthyroidism), particularly if it is long standing or difficult to control with medication.

In the 12 months after delivery, hyperthyroidism due to Graves' disease should be distinguished from the hyperthyroid phase of postpartum thyroiditis. The two conditions have different aetiologies and different treatments so the distinction is clinically important (Stagnaro-Green 2002).

Hyperthyroidism in animals has been associated with early onset of secretory activation (lactogenesis II), and lower levels of oxytocin and prolactin at milk ejection, lower volume of milk released at milk ejection, lower weight gain in the pups and milk stasis leading to inappropriate/ early involution (Varas et al 2002). Some women report abundant milk production while hyperthyroid, but others seem to have no functional milk ejection reflex and consequently lactation fails (West & Marasco 2009). The reason for the difference is not yet understood.

Hypothyroidism

Hypothyroidism, an underactive thyroid, can cause symptoms of fatigue, weight gain, intolerance to cold, difficulty concentrating and poor memory, menorrhagia, or amenorrhoea, galactorrhoea, constipation, dry scaly skin and hair loss (Jameson & Weetman 2012). The signs may be subtle and in women who have recently given birth these symptoms may be confused with those of postnatal depression. Women with untreated hypothyroidism often experience relative infertility. In addition they are at greater risk of miscarriage, stillbirth and congenital abnormality, as thyroid hormones are necessary for the continuation of pregnancy (Buckshee et al 1992; Moody 1994; Ramsay 1995). In fact menstrual irregularities and low milk supply may precede the diagnosis of hypothyroidism (Joshi et al 1993). Thyroid hormones are necessary for normal breast development and initiation of lactation. There is a significant relationship between the levels of the hormones T4 and T3 and milk production in women (Motil et al 1994). When these hormones are not being produced in adequate quantities by the thyroid, then the milk supply may be adversely affected (Miyake et al 1989). A study in rats showed a diminished oxytocin response to suckling in hypothyroid mothers and accordingly, less milk given to their pups (Hapon et al 2003). The milk of hypothyroid rats was also low in triglycerides compared to euthyroid rats' milk (Hapon et al 2005). The authors suggested that both factors might be significant in the decreased growth observed in the pups.

Case studies written by mothers who have experienced low supply associated with hypothyroidism are available [Breastfeeding Review 1995; Nursing Mothers' Association of Australia (NMAA) members 1995). Thyroid replacement therapy may be required to maintain lactation in such cases as well as being necessary for the mother's well being (Lawrence & Lawrence 2011; Motil et al 1994: Kaiser 1996). Hypothyroidism is treated with thyroxine to replace the thyroid hormone that the body is not itself producing, in order to bring the levels back to normal. Women who have been adequately treated for hypothyroidism, report that they have experienced no adverse effect on milk supply (NMAA members 1995). Some women report that their milk supply is sensitive to the level of thyroid hormone achieved in their bloodstream. That is, some women report that having thyroid hormones within the population reference range was not enough to support full milk production but they have a full milk supply when their thyroid hormone level is within the upper part of the reference range, possibly reflecting their own personal set point referred to above.

Postpartum thyroiditis

Postpartum thyroiditis is an autoimmune disease that occurs in the postpartum period due to immune rebound after the immune suppression that is integral to pregnancy. It may represent the uncovering of thyroid autoimmunity that was silent before pregnancy. Studies have reported prevalences of postpartum thyroiditis of between 1 and 17% of women. Women with type 1 diabetes have a higher rate than the general population (Stagnaro-Green 2002). Postpartum thyroiditis may manifest as hypothyroidism alone (43% of cases), hyperthyroidism alone (32% of cases), or hyperthyroidism followed by hypothyroidism (25% of cases) (Stagnaro-Green 2002). The symptoms of hyperthyroidism most commonly occur 2-10 months after delivery and are usually mild, mainly causing fatigue, irritability and palpitations, but the diagnosis can be missed by the health professional because of normal fatigue associated with caring for a new baby (Stagnaro-Green 2002). Some women advise that their milk supply is more than adequate at this time.

During the hypothyroid phase the symptoms of a slowed metabolism occur--impaired memory and concentration, lethargy and fatigue, and symptoms of depression. Again these may be confused with either postnatal depression or the normal reactions to dealing with life with a new baby. Some women have no recognisable hyperthyroid phase and first become concerned when they show signs of being hypothyroid. Most women recover, although some (approx 3.5%) will remain hypothyroid, and many more are at risk of developing permanent thyroid disease later in life. While some women experience milk supply problems, others breastfeed without difficulty (Kaiser 1996; NMAA members).

Postpartum thyroiditis has a high recurrence rate; 70% of women who have it following one pregnancy will have it again after the next pregnancy (Stagnaro-Green 2002).

Cancer of the thyroid

Cancer of the thyroid usually presents as a solitary nodule in the thyroid gland. It carries risks to the breastfeeding mother and her baby in both diagnosis and treatment, as both require the use of radioactive drugs including radioactive iodine. As these drugs can be concentrated in the breastmilk, they are readily transferred to the breastfeeding baby (Bakheet & Hammami 1994; Grunwald et al 1995).

TREATMENT

Hyperthyroidism

Anti-thyroid drugs act on the overactive thyroid by inhibiting the production of T3 and T4. They include methimazole, carbimazole (a derivative of methimazole) and propylthiouracil (Abalovich et al 2007). Propylthiouracil is ionised at physiologic pH and is heavily protein-bound, thus limiting its diffusion across membranes. For this reason it is not present in significant concentrations in breastmilk (Cooper 1987). Carbimazole is metabolised to methimazole after ingestion and, as methimazole is neither ionised nor bound to serum proteins, it readily enters breastmilk (Cooper 1987; Hansen 1990; Lambergetal 1984). The milk:plasma ratio of methimazole is approximately 1, that is methimazole reaches about the same concentration in milk as it does in maternal plasma, compared to propylthiouracil which has a milk:plasma ratio of approximately 0.1 (Glatstein et al 2009).

An early study on the effects of anti-thyroid hormones on human milk took place in 1944. This study, using a fairly basic nonspecific colorimetric assay, examined two milk samples and detected three times the amount of thiouracil, an anti-thyroid drug, in the breastmilk as in the serum of the mothers (Williams 1944). On the strength of this one small study, breastfeeding while taking thiouracil was deemed dangerous to the breastfed baby. Even though the use of thiouracil was discontinued in 1946, the results of this study were extrapolated to include propylthiouracil and methimazole, and breastfeeding was subsequentiy contraindicated for mothers using these treatments for fear of causing hypothyroidism in their babies (Hansen 1990).

This dictum was challenged in 1979 and the early 1980s when further research provided evidence that propylthiouracil was safe to use while breastfeeding (Kampmann et al 1980; Low et al 1979). In the study by Low and others, the level of propylthiouracil in breastmilk was measured and found to be only 0.077% of the administered dose over 24 hours. The study by Kampmann measured propylthiouracil concentrations in the breastmilk of nine women after the ingestion of one 400 mg dose of the drug. The finding was that only 0.025% was excreted in the breastmilk over 4 hours. This study also monitored the thyroid function of an infant whose mother was on a daily dose of 200-300 mg propylthiouracil and found no adverse effects to the infant's thyroid function.

Results from studies on methimazole and carbimazole were less definitive, with one study estimating that it is possible to transfer 7-16% of the dose of methimazole to the infant [Hull 1982). Three other studies in the early 1980s indicated that methimazole freely enters breastmilk [Cooper et al 1984; Johansen et al 1982; Tegler & Lindstrom 1980; all cited in Cooper 1987). In another study carbimazole was administered to 11 breastfeeding mothers. One woman in the study took propylthiouracil. The dose of carbimazole was from 5-15 mg daily, and propylthiouracil 125 mg per day. The study was conducted over a period of 4 months. All the babies had normal thyroid function at 4, 14 and 21 days. The two babies who were monitored at 3 and 4 months of age both maintained normal thyroid function. The authors concluded that where daily doses of carbimazole do not exceed 15 mg, and doses of propylthiouracil do not exceed 159 mg per day, it is safe to breastfeed. They also recommended having facilities available for monitoring the thyroid hormone levels of the babies [Lamberg et al 1984).

Momotani and others (1989) studied 8 mothers with hyperthyroidism and their babies. The doses of propylthiouracil were between 50-300 mg daily. The study verified the safety of propylthiouracil while breastfeeding, but the authors suggested that the medication be taken just after a breastfeed and to wait another 3-4 hours to feed again. If this can be managed then the babies may not need their thyroid function monitored.

Azizi (1996) followed two groups of women. The first took methimazole during pregnancy for hyperthyroidism and continued on the maintenance treatment of 5 mg daily after the birth of their babies. Breastfeeding was not restricted. Another group developed hyperthyroidism between 2 and 8 months postpartum and were prescribed methimazole, 5 mg to be taken twice daily, and breastfeeding continued. All infants had normal thyroid function. This study demonstrated that the treatment of hyperthyroidism with a daily dose of methimazole between 5-20 mg does not harm the babies of lactating mothers and has no effect on their thyroid function.

In 2000, 2002 and 2003 Azizi and others published further studies of women breastfeeding while taking methimazole. In 2000 they assessed the effects of breastfeeding while taking 20 mg methimazole. Of 139 mothers, 51 had been treated with methimazole both during pregnancy and breastfeeding, which on average lasted 11 months. All the infants had thyroid function tests monthly to 6 months and all were normal. Eighty-eight mothers took methimazole only during breastfeeding (they breastfed an average of 13 months) and their infants showed normal thyroid function for the 12 months they were monitored. Fourteen of the children were followed up at 48-74 months of age. Weight, height, IQ, thyroid function, thyroid antibodies and urinary iodine concentration were all normal in the studied children (Azizi et al 2000).

To investigate the safety of higher doses of methimazole, Azizi and Hedayati (2002) assessed the thyroid function of 42 infants of mothers taking 30 mg methimazole daily. All infants maintained normal thyroid function throughout 12 months.

A follow-up study was published in 2003 assessing 42 children who were breastfed by hyperthyroid mothers treated with 20-30 mg methimazole and compared to children breastfed by mothers with normal thyroid function (Azizi et al 2003). There were no differences in the physical or intellectual development of the children, or their thyroid function at follow-up at 48 to 86 months of age.

In the light of these studies, moderate doses of antithyroid drugs (<300 mg/d propylthiouracil or 20-30 mg/d methimazole) during lactation are regarded as safe. Propylthiouracil is the second-line agent because it has been associated with more severe hepatotoxic side effects than methimazole (Stagnaro-Green et al 2011). The American Thyroid Association recommends that breastfed infants of mothers treated with ATD should have their thyroid function monitored and that antithyroid drugs should be taken in divided doses immediately after breastfeeding to avoid breastfeeding at the time of peak plasma levels (Stagnaro-Green et al 2011). According to Hale, peak plasma levels occur approximately 1 hour after taking methimazole and 1-1.5 hours after taking propylthiouracil (Hale 2010).

Hypothyroidism

Hypothyroidism is treated with thyroid hormones. The result of taking thyroid hormones is to raise the serum thyroid hormone levels to normal, so there is little concern when these are prescribed to mothers who are breastfeeding. Some concern has been expressed about babies of women who are extremely hypothyroid due to partial or full removal of the thyroid and are inadequately treated. The concern centres around the theory that significant amounts of thyroid stimulating hormone, produced by the maternal pituitary, may be present in the mother's milk. This seems, from a study reported in 1994, not to be the case (Robinson & Hoad 1994).

Animal studies can be useful in providing some indications of how certain drugs will act in humans. The studies in rats referred to above suggest that thyroid hormone replacement is likely to restore normal milk production (Hapon et al 2003), and women's personal accounts support this [NMAA members 1995).

Postpartum thyroiditis

For women experiencing the early, hyperthyroid phase of postpartum thyroiditis, treatment of the symptoms with R-blockers is all that is appropriate. High levels of thyroid hormone are due to the release of preformed thyroid hormones and so thioamide drugs that inhibit the formation of thyroid hormones are not useful (Stagnaro-Green et al 2011). In those women who go on to develop symptoms of hypothyroidism, or if these are the first symptoms they have developed, replacement thyroid hormones are prescribed. Thyroxine is used as treatment when required (Ramsay 1995; Terry & Hague 1998). If the symptoms of hypothyroidism are mild, many women are not actively treated. The American Thyroid Association (ATA) guidelines (Stagnaro-Green 2011) recommend that if symptoms require treatment with thyroxine, that treatment should be maintained to sustain normal thyroid status while the woman is breastfeeding, pregnant or attempting pregnancy.

Thyroid carcinoma

Both the diagnosis and treatment of thyroid carcinoma require the use of radioactive isotopes. These drugs are administered intravenously for imaging of the brain and thyroid, and orally for the treatment of hyperthyroidism and thyroid carcinoma (Herman & O'Neill 1995). Studies of X-rays of women recently treated with radioactive compounds have demonstrated that lactating breasts take up these compounds (Bakheet & Hammami 1994; Grunwald, Palmedo & Biersack 1995; Robinson et al 1994). In addition, the compounds are rapidly transferred to the breastmilk of lactating mothers and therefore to their babies. However, the transfer from mother to baby is highly individual (Herman & O'Neill 1995).

The radioactive half life of these compounds varies: iodine-131 has a half life of 8.0 days, for iodine-125 it is 60.1 days, and for iodine-123 it is 13.2 hours. For most of the radioactive iodines used in medicine Hale (2010) recommends weaning because they are concentrated in the breast and breastmilk. It may be possible to resume breastfeeding several days after a scan using iodine-123.

Iodine

Iodine is an essential component of T3 and T4, so of course, adequate dietary iodine intake is essential to healthy thyroid function. Australia is classed as mildly to moderately iodine-deficient on the basis of urinary iodine measurements. Urinary iodine concentration (UIC) is not a reliable measure of an individual's iodine status because wide variations occur across the day and from day to day. However it is useful as a measure of a population's iodine status. To increase Australians' iodine intake, since 2009 Food Standards of Australia and New Zealand (FSANZ) require manufacturers to use iodised salt in bread making. (Specialist breads such as organic or gluten-free breads do not have to comply.) A pilot study in Tasmania reported in 2007 showed that the program successfully improved the population's iodine status, but it does not provide sufficient daily iodine to match the World Health Organization's recommended daily iodine intake for pregnant and lactating women, which is 250 [micro]g (Azizi & Smyth 2009). Pregnant and lactating women have increased iodine needs in order to supply the foetus and neonate and, during pregnancy, increased renal iodine loss. Iodine is concentrated in breastmilk compared to maternal plasma, which in evolutionary terms ensures the best outcome for the infant during the essential first years of brain development (Azizi & Smyth 2009). Hence Gallego, Goodall and Eastman (2010) recommended that Australian women who are pregnant, breastfeeding or planning pregnancy should take an iodine supplement unless they have pre-existing thyroid disease. The National Health & Medical Research Council (NHMRC) also recommends that all pregnant and lactating women take a supplement of 150 [micro]g of iodine daily (National Health & Medical Research Council).

Inadequate iodine intake effectively results in hypothyroidism, with the attendant cognitive and physical developmental damage to the foetus, infant or young child. Excessive iodine intake can also be dangerous. Crawford and others (2010) reported a number of Australian cases of iodine toxicity as a result of drinking soy milk, or seaweed soup. The particular brand of soy milk involved no longer has dangerously high levels of iodine in the Australian product, Japanese and Korean women commonly drink seaweed soup during pregnancy and postpartum, and this can be a source of excessive iodine. The two infants reported in the case series showed hypothyroid effects. Iodine excess can cause a range of thyroid effects, from hyperthyroid to hypothyroidism (Crawford et al 2010).

Iodine skin antiseptic used before caesarean delivery or epidural anaesthetic has also been associated with iodine overload (Chanonine et al 1988). As a result skin disinfection with povidone-iodine is contraindicated for pregnant women, obstetric surgery and young infants (Smerdely et al 1989).

CONCLUSION

Thyroid disease has an impact on breastfeeding mothers. While women with hypothyroidism may have a low milk supply, adequate treatment with thyroxine is not contraindicated during lactation. If a woman's milk supply does not adequately respond to thyroxine treatment it may be necessary to increase the thyroxine dose to bring the TSH into the lower part of the reference range. It may be that the individual's TSH would normally be at the lower end of the range.

On the other hand, women with hyperthyroidism may or may not have a problem breastfeeding but in historical terms thyroid medications have been problematic. There seems to have been some suggestion that the early medication thiouracil was contraindicated. However, later studies have provided evidence that moderate doses of antithyroid drugs are safe.

Studies have indicated that the concentration of propylthiouracil secreted in breastmilk is too low to affect the thyroid function of breastfed babies. However, propylthiouracil has been associated with severe liver disease as a rare side effect. Mothers taking methimazole have been followed and their children have shown no ill effects of the treatment. As methimazole is not available in Australia, carbimazole is therefore regarded as the antithyroid drug of choice in breastfeeding women. It is also recommended that the baby's thyroid function be monitored.

Breastfeeding should be suspended for the duration of the diagnosis and treatment of cancers that require radioactive compounds. Diagnostic use of radioactive compounds may require weaning, or it may be possible to return to breastfeeding after some time, depending on the radioactive compound used. Mothers should discuss with their medical practitioners whether their treatments are compatible with breastfeeding. Iodine is contraindicated for use in (pregnant or) breastfeeding women for any reason, including skin preparation for surgery.

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Keywords: breastfeeding, postpartum thyroiditis, hyperthyroid, hypothyroid, iodine, antithyroid drugs

Elisabeth Speller BA (Hons) IBCLC Wendy Brodribb AM MBBS IBCLC PhD FABM Updated by Elizabeth McGwire BSc IBCLC
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