INTRODUCTION — Postpartum thyroiditis is a destructive thyroiditis induced by an autoimmune mechanism within one year after parturition. Postpartum thyroiditis can also occur after spontaneous or induced abortion [1]. It usually presents in one of three ways (figure 1):
●Transient hyperthyroidism alone
●Transient hypothyroidism alone
●Transient hyperthyroidism followed by hypothyroidism and then recovery
The clinical manifestations, diagnosis, and treatment of postpartum thyroiditis are reviewed here. Other forms of thyroiditis and the diagnosis and management of thyroid dysfunction during pregnancy are discussed separately. (See "Overview of thyroiditis" and "Overview of thyroid disease in pregnancy" and "Hyperthyroidism during pregnancy: Treatment" and "Hypothyroidism during pregnancy: Clinical manifestations, diagnosis, and treatment".)
PREVALENCE AND NATURAL HISTORY — The reported prevalence of postpartum thyroiditis varies globally and ranges from 1 to 17 percent [2-5]. In systematic reviews of prospective studies, the mean prevalence in the general population of women was approximately 7 to 8 percent [2,3]. Higher rates, up to 25 percent, have been reported in women with type 1 diabetes mellitus [2,3], and the highest rates occur among women with a prior history of postpartum thyroiditis (pooled prevalence 42 percent) and in women with positive antithyroid peroxidase antibodies who had normal thyroid function during pregnancy (40 to 60 percent compared with 0 to 5 percent of women without antibodies) [2]. Postpartum thyroid dysfunction can occur in women already taking thyroid hormone replacement for hypothyroidism antedating pregnancy (eg, goitrous Hashimoto's thyroiditis), if they have some remaining thyroid tissue capable of producing thyroid hormone [6].
Most women recover and are euthyroid within one year postpartum. However, some women never recover from the initial hypothyroid phase and have permanent hypothyroidism or goiter [7-10]. In addition, women with reversible hypothyroidism are at increased risk for developing permanent hypothyroidism in the future [4,11,12]. Studies evaluating the likelihood of a woman developing permanent hypothyroidism report a wide incidence (4 to 54 percent), but the best estimate is approximately 20 to 40 percent within 3 to 12 years [4]. As an example, in a study of 45 patients followed for eight years, 14 (31 percent) developed permanent hypothyroidism [13]. Although there are no definitive characteristics that can assist in predicting which patients will develop hypothyroidism, progression to permanent hypothyroidism may be related to higher initial TSH concentrations and the antithyroid peroxidase antibody titer [4,9,12,13], maternal age, and female sex of the infant [13].
PATHOGENESIS — Postpartum thyroiditis, like painless thyroiditis, is considered a variant form of chronic autoimmune thyroiditis (Hashimoto's thyroiditis). The pathologic findings in the two disorders are similar (see 'Pathology' below), and both are associated with particular HLA-B and HLA-D haplotypes, suggesting that inherited risk factors are important [14].
Women destined to develop postpartum thyroiditis usually have high serum antithyroid peroxidase antibody concentrations early in pregnancy, which decline later (as immunologic tolerance increases during pregnancy) and then rise again after delivery [15]. Thus, women destined to develop postpartum thyroiditis have subclinical thyroid autoimmune disease early in pregnancy and soon after it.
Whatever factors initiate postpartum thyroiditis, the resulting thyroid inflammation damages thyroid follicles and activates proteolysis of the thyroglobulin stored within the follicles. The result is unregulated release of large amounts of thyroxine (T4) and triiodothyronine (T3) into the circulation, and subsequent hyperthyroidism. This state lasts only until the stores of thyroglobulin are exhausted, because new hormone synthesis ceases, not only because of damage to the thyroid follicular cells but also because of inhibition of thyroid-stimulating hormone (TSH) secretion by the increased serum T4 and T3 concentrations. As the inflammation subsides, the thyroid follicles regenerate and thyroid hormone synthesis and secretion resume (figure 1). There may be a transient period of hypothyroidism and increased TSH secretion before thyroid secretion becomes normal again.
CLINICAL FEATURES
Clinical manifestations — The presentation of postpartum thyroiditis can be identical to painless thyroiditis, but the course of postpartum thyroiditis may be more variable. This apparent difference may reflect the greater ease of studying postpartum women prospectively than women in the general population. (See "Painless thyroiditis".)
Approximately 20 to 30 percent of women with postpartum thyroiditis have the characteristic sequence of hyperthyroidism, which usually begins one to four months after delivery and lasts two to eight weeks, followed by hypothyroidism, which lasts from about two weeks to six months, and then recovery (figure 1) [4,16]. However, 20 to 40 percent have only hyperthyroidism, and the remaining 40 to 50 percent have only hypothyroidism, which begins two to six months after delivery. Some women do not restore normal endogenous thyroid function after the initial episode of hypothyroidism [7,8].
The symptoms and signs of hyperthyroidism, when present, are typically mild and consist mainly of fatigue, weight loss, palpitations, heat intolerance, anxiety, irritability, tachycardia, and tremor. Similarly, hypothyroidism is also usually mild, leading to lack of energy, cold intolerance, constipation, sluggishness, and dry skin [4] (see "Overview of the clinical manifestations of hyperthyroidism in adults" and "Clinical manifestations of hypothyroidism"). The symptoms that occur during the hyperthyroid phase are often only apparent retrospectively when the hypothyroid phase is diagnosed. Many of the symptoms of postpartum thyroiditis are inadvertently attributed to breastfeeding or the stresses of having a newborn child, as many postpartum women with normal thyroid function tests have fatigue, loss of energy, and anxiety, making the recognition of thyroid dysfunction difficult.
While it has been suggested that hypothyroidism may be associated with or aggravate postpartum depression [17,18], in subsequent prospective studies there was no association despite a high prevalence of postpartum thyroid dysfunction (11 to 12 percent) and postpartum depression (2 to 9 percent) [19,20].
Most women with postpartum thyroiditis have a mildly enlarged, diffuse, nontender thyroid gland when their thyroid function is abnormal, which disappears with recovery. In some women, however, goiter is the presenting complaint.
In addition to the usual clinical consequences of thyroid dysfunction, postpartum hypothyroidism may decrease milk volume [21].
Laboratory findings — The biochemical findings in patients with postpartum thyroiditis are similar to those of painless thyroiditis: high or high-normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations and low serum thyroid-stimulating hormone (TSH) concentrations during the hyperthyroid phase, which may be overt or subclinical. During the hypothyroid phase, serum free T4 concentrations are low or low-normal, and serum TSH concentrations are high, consistent with either overt or subclinical hypothyroidism (see "Subclinical hyperthyroidism" and "Subclinical hypothyroidism in nonpregnant adults"). In those women with hyperthyroidism followed by hypothyroidism, serum T4 concentrations may be low for several days to weeks before serum TSH concentrations rise above the normal range, because of prolonged TSH suppression that had occurred during the hyperthyroid phase.
Serum antithyroid peroxidase antibody concentrations are high in 60 to 85 percent of women with postpartum thyroiditis [10,16,22], and are highest during the hypothyroid phase or soon thereafter. Routine laboratory studies (eg, complete blood count [CBC], comprehensive metabolic panel [CMP]) are usually normal, but some women have a slightly increased erythrocyte sedimentation rate and/or C-reactive protein. No consistent abnormalities in numbers or types of peripheral blood (or intrathyroidal) T lymphocytes have been reported.
Pathology — Thyroid biopsies in women with postpartum thyroiditis show lymphocytic infiltration, with occasional germinal centers, and disruption and collapse of thyroid follicles (lymphocytic thyroiditis) [10,23]. Fine needle aspiration biopsies reveal lymphocytes, thyroid follicular cells, and masses of colloid. During recovery, lymphocytic infiltration is still seen, and there may be some fibrosis, but the thyroid follicles are more normal. Thyroid aspirations are not typically required unless there is a specific indication, such as detection of a thyroid nodule.
Radioiodine uptake — During the hyperthyroid phase of postpartum thyroiditis, values for thyroid radioiodine uptake are low, usually less than 1 percent, compared with high values in Graves’ hyperthyroidism. However, breastfeeding is a strong relative contraindication to radioiodine (or technetium) administration, and must be suspended for at least several days until the breast milk is no longer radioactive. Because the hyperthyroid phase of postpartum thyroiditis is often only apparent retrospectively when the hypothyroid phase is diagnosed, radioiodine scanning is not usually necessary. (See 'Differential diagnosis' below and "Hyperthyroidism during pregnancy: Clinical manifestations, diagnosis, and causes", section on 'Diagnosis'.)
DIAGNOSIS — The diagnosis of postpartum thyroiditis is based upon clinical manifestations and thyroid function tests (thyroid-stimulating hormone [TSH], free thyroxine [T4]). Clinicians caring for women after pregnancy should be alert to the possibility of postpartum thyroid dysfunction as a cause of many symptoms during this period.
Thyroid function tests — Routine measurement of thyroid function tests in the postpartum period in patients without relevant specific signs or symptoms is not usually required. However, laboratory assessment of thyroid function should be performed at three and six months postpartum in women at high risk for developing postpartum thyroiditis (see 'Screening' below), including women with:
●Type 1 diabetes mellitus
●A history of postpartum thyroiditis after a previous pregnancy
●A history of high serum antithyroid peroxidase antibody concentrations prior to pregnancy
And at the time of symptoms, in women with:
●Clinical manifestations of postpartum thyroiditis
●Postpartum depression (because of the potential association between postpartum depression and postpartum hypothyroidism, and because hypothyroidism is a reversible cause of depression)
We typically measure TSH and free T4, rather than TSH alone, because thyroid function tests may fluctuate during the course of postpartum thyroiditis, and changes in TSH concentrations lag behind changes in serum free T4. If the TSH is low, triiodothyronine (T3) should also be measured.
Additional evaluation — Additional evaluation depends upon whether a women presents with hypothyroidism or hyperthyroidism.
●Postpartum hypothyroidism – For women presenting with postpartum hypothyroidism, assessment of antithyroid peroxidase antibodies may be helpful in confirming postpartum thyroiditis and also in helping to predict the future course of the disease. (See 'Prevalence and natural history' above and 'Duration of thyroid hormone therapy' below.)
When antithyroid peroxidase antibodies are not measured, the diagnosis of postpartum thyroiditis can be confirmed if hypothyroidism resolves within several weeks without thyroid hormone replacement.
●Postpartum hyperthyroidism – For women presenting with hyperthyroidism, further evaluation may be needed to differentiate postpartum thyroiditis from Graves’ disease. We obtain radioiodine uptake (if not contraindicated) and/or serum thyrotropin receptor antibodies (TRAb, also called TSI) levels in women with clinical manifestations of Graves’ disease (ophthalmopathy), women with persistent hyperthyroidism (>1 month), or severe hyperthyroidism (markedly elevated T3 > T4).
For women without these findings, we do not obtain additional tests, but we repeat thyroid function tests (TSH, free T4, T3) in three to four weeks. By that time, most women with postpartum thyroiditis will have improved, whereas those with Graves' hyperthyroidism will usually be unchanged or worse.
Radionuclide imaging is contraindicated in pregnant women and in women who are actively or recently breast feeding. When radionuclide imaging is contraindicated, thyroid ultrasound with Doppler flow may also be useful to distinguish Graves’ disease (high blood flow) from the hyperthyroid phase of painless or postpartum thyroiditis (low blood flow) [24]. (See "Diagnosis of hyperthyroidism", section on 'Determining the etiology'.)
DIFFERENTIAL DIAGNOSIS
Hyperthyroid phase — For women who present with clinical and/or laboratory (high or high-normal serum free thyroxine [T4] and triiodothyronine [T3] and low serum thyroid-stimulating hormone [TSH]) manifestations of hyperthyroidism, it may be difficult to distinguish the hyperthyroid phase of postpartum thyroiditis from Graves' hyperthyroidism, which can also begin during the postpartum period, either as recurrent or new-onset hyperthyroidism [3]. (See "Diagnosis of hyperthyroidism", section on 'Determining the etiology'.)
The timing of onset, severity of symptoms, and pattern of thyroid function tests may suggest one etiology over the other, but there is significant overlap [24,25].
●In general, onset of hyperthyroidism within three months of delivery is more suggestive of postpartum thyroiditis, whereas onset after six months is more likely Graves’ disease.
●The primary clinical differences between women with postpartum thyroiditis and those with Graves' hyperthyroidism are that hyperthyroidism in women with postpartum thyroiditis is usually mild (both clinically and biochemically), thyroid enlargement is minimal, and Graves' ophthalmopathy is absent. In contrast, women with Graves' hyperthyroidism are usually more symptomatic, have more thyroid enlargement, and may have ophthalmopathy or pretibial myxedema.
●Women with Graves’ hyperthyroidism have higher serum thyroid hormone concentrations. In Graves’ disease, the serum T3 is typically elevated (in comparison with the upper limits of normal) to a greater degree than is the free T4, whereas the opposite is true in postpartum thyroiditis. Thus, a high T3 to T4 ratio (the value of which is assay and unit dependent) suggests Graves’ disease, while a ratio close to that of euthyroid patients suggests a destructive thyroiditis.
●Serum thyrotropin receptor antibody (TRAb, also called TSI) levels are typically elevated in Graves’ hyperthyroidism but not in postpartum thyroiditis.
In some women, particularly those without new-onset ophthalmopathy, the distinction may nevertheless be difficult. In such cases, further evaluation may be needed. (See 'Additional evaluation' above.)
Hypothyroid phase — For women who present with clinical manifestations of hypothyroidism, the hypothyroid phase of postpartum thyroiditis (low or low-normal serum free T4 and high TSH) must be differentiated from lymphocytic hypophysitis, which also may occur during late pregnancy or the postpartum period. Lymphocytic hypophysitis may cause deficiency of TSH as well as one or more additional pituitary hormones including adrenocorticotropic hormone (ACTH) [26,27]. Spontaneous recovery of pituitary gland function or, alternatively, persistent and chronic hypopituitarism may occur [28]. In lymphocytic hypophysitis, the serum TSH is expected to be inappropriately normal or low in the context of a low free T4, whereas in hypothyroidism with postpartum thyroiditis, the TSH should be elevated in conjunction with a decreased FT4. (See "Causes of hypopituitarism", section on 'Hypophysitis'.)
Postpartum thyroiditis is considered a variant form of chronic autoimmune thyroiditis (Hashimoto's thyroiditis) (see 'Pathogenesis' above). It is not necessary to routinely measure antithyroid peroxidase antibodies in women with postpartum hypothyroidism. Women who do not recover from the initial hypothyroid phase within one year postpartum likely have chronic autoimmune thyroiditis and permanent hypothyroidism, and in these individuals measurement of antithyroid peroxidase antibodies should be considered.
SCREENING — The frequency of postpartum thyroiditis raises the question of whether screening is indicated [29]. This could be done by periodic clinical evaluation or serum thyroid-stimulating hormone (TSH) assay after delivery. Alternatively, serum antithyroid peroxidase antibodies could be measured, either early in pregnancy or soon after delivery. High antibody concentrations at these times predict (but not with certainty) the later development of postpartum thyroiditis, and low concentrations make it very unlikely [11,15,16,30].
We agree with the Endocrine Society clinical guidelines that there is insufficient evidence to support a recommendation for screening all pregnant women for postpartum thyroiditis [3]. However, women at highest risk for developing postpartum thyroiditis (eg, antithyroid peroxidase antibody positive, type 1 diabetes, previous episode of postpartum thyroiditis) should have a serum TSH measurement at three and six months postpartum [3]. If the TSH level is abnormal, it should be repeated soon thereafter along with a free thyroxine (T4) level and triiodothyronine (T3) (T3 measurement indicated if TSH is low), within one to two weeks.
PREVENTION — There are no established therapies to prevent the occurrence of postpartum thyroiditis in patients with antithyroid peroxidase antibodies. Administration of T4 (levothyroxine) or iodine to pregnant women with high serum antithyroid antibody concentrations did not prevent postpartum thyroiditis [31,32]. In contrast, selenium supplementation may decrease inflammatory activity in pregnant women with autoimmune hypothyroidism [33], and may reduce the risk of postpartum thyroiditis in women who are positive for thyroid peroxidase (TPO) antibodies. This was illustrated in a trial of 151 TPO-positive women randomly assigned to receive selenium (200 mcg daily) or placebo (beginning at about the 12th week of gestation). The prevalence of postpartum thyroiditis was significantly lower in the selenium group (22 of 77 women [29 percent] versus 36 of 74 [49 percent]) [34]. The routine clinical application of this supplementation requires further study, especially since selenium deficiency may have existed in this cohort from Italy.
TREATMENT — In the absence of randomized trials comparing different treatment strategies, treatment recommendations are based upon observational studies and clinical experience [3,7-9,13].
Our approach — Our approach, which is similar to that of the Endocrine Society [3] and the American Thyroid Association (ATA) [5], is outlined below:
●Asymptomatic with mild thyroid function test abnormalities – The majority of women with postpartum thyroiditis need no treatment during either the hyperthyroid or the hypothyroid phases of their illness. However, thyroid function tests (thyroid-stimulating hormone [TSH], free thyroxine [T4], and if hyperthyroid, triiodothyronine [T3]) should be monitored every four to eight weeks to confirm resolution of biochemical abnormalities or to detect the development of more severe hypothyroidism, indicating possible permanent hypothyroidism.
Asymptomatic women who have a mildly elevated serum TSH (between the upper limit of the normal range and 10 mU/L), and who are not planning another pregnancy, do not necessarily require intervention, although individual decisions should be made in the clinical and laboratory context.
●Symptomatic hyperthyroidism – Women who have bothersome symptoms of hyperthyroidism can be treated with 40 to 120 mg propranolol or 25 to 50 mg atenolol daily until their serum T3 and serum free T4 concentrations are normal. For women who are breastfeeding, propranolol is preferred because, due to high plasma protein binding, it is not concentrated in breast milk as much as other beta blockers [35]. In the hyperthyroid phase, radioiodine treatment and antithyroid drugs (ie, methimazole) are of no value because the synthesis of T4 and T3 is decreased, not increased as in most other disorders causing hyperthyroidism.
●Symptomatic hypothyroidism or TSH above 10 mU/L – Women with symptomatic hypothyroidism should be treated with T4 (levothyroxine) (typically about 50 to 100 mcg/day, although requirements may vary), irrespective of the degree of TSH elevation.
In asymptomatic women, we prefer to treat when the TSH exceeds 10 mU/L.
When T4 is instituted in these circumstances, the goal is a normal TSH.
Duration of thyroid hormone therapy — The duration of thyroid hormone therapy, once initiated, is uncertain. Since postpartum thyroid dysfunction is often transient, many experts favor weaning T4 after 6 to 12 months, unless the woman is pregnant, attempting pregnancy, or breastfeeding [4]. Because there are no prospective, controlled data confirming the best approach, the decision to withdraw thyroid hormone therapy should be based upon individual patient characteristics and preferences.
We favor withdrawing thyroid hormone as a clinical trial in most women, except as noted above, after 6 to 12 months of therapy. Thyroid hormone can be completely stopped with assessment of thyroid function (TSH, free T4) six weeks later. In patients at high risk for permanent hypothyroidism or patients who are reluctant to stop hormone fearing a return of hypothyroid symptoms, the dose could he halved for six weeks, and if the TSH does not rise, stopped with reassessment of thyroid function after an additional six weeks.
Up to 30 percent of women never recover from the initial hypothyroid phase, and a rising TSH level during T4 weaning is indicative of persistent hypothyroidism, requiring long-term T4. In some reports, high titers of antithyroid peroxidase antibodies and the severity of the initial hypothyroid phase predicted the development of permanent hypothyroidism [7,12,13,36]. Thus, in women with very elevated initial TSH values (>50 or 100 mU/L), an alternative approach is to continue thyroid hormone indefinitely.
Long-term follow-up — Any woman who has had postpartum thyroiditis should be told that recurrence is likely after future pregnancies and that she is at substantial risk for the later development of hypothyroidism or goiter, and she should be educated regarding the possible development of symptoms. For women who have fully recovered from postpartum thyroiditis, we measure serum TSH levels annually, particularly within 5 to 10 years after the initial diagnosis [3].
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●Basics topics (see "Patient information: Thyroiditis after pregnancy (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Postpartum thyroiditis is a destructive thyroiditis induced by an autoimmune mechanism within one year after parturition. It occurs more often in women with a previous history of postpartum thyroiditis, positive antithyroid peroxidase antibody titers, and type 1 diabetes. (See 'Prevalence and natural history' above.)
●Approximately 20 to 30 percent of women with postpartum thyroiditis have the characteristic sequence of hyperthyroidism, which usually begins one to four months after delivery and lasts two to eight weeks, followed by hypothyroidism, which also lasts from about two weeks to six months, and then recovery (figure 1). However, other women have only hyperthyroidism or only hypothyroidism. The symptoms and signs of hyperthyroidism, when present, are typically mild and consist mainly of fatigue, weight loss, palpitations, heat intolerance, anxiety, irritability, tachycardia, and tremor. Similarly, hypothyroidism is also usually mild, leading to lack of energy, cold intolerance, constipation, sluggishness, and dry skin.
The biochemical findings depend upon the phase of postpartum thyroiditis: high or high-normal serum free thyroxine (T4) and triiodothyronine (T3) and low serum thyroid-stimulating hormone (TSH) during the hyperthyroid phase, and low or low-normal serum free T4 concentrations and high serum TSH during the hypothyroid phase. (See 'Clinical manifestations' above.)
●The diagnosis of postpartum thyroiditis is based upon clinical manifestations and thyroid function tests. In women with symptoms or signs of hyperthyroidism or hypothyroidism in the postpartum period, we measure TSH and free T4, rather than TSH alone. Thyroid function tests may fluctuate during the course of postpartum thyroiditis, and changes in TSH concentrations lag behind changes in serum free T4. If the TSH is low, T3 should also be measured. (See 'Diagnosis' above and 'Thyroid function tests' above.)
●For women presenting with postpartum hypothyroidism, assessment of antithyroid peroxidase antibodies may be helpful in confirming postpartum thyroiditis and also in helping to predict the future course of the disease. (See 'Additional evaluation' above.)
●For women presenting with postpartum hyperthyroidism, further evaluation may be needed to differentiate postpartum thyroiditis from Graves’ disease. We obtain radioiodine uptake (if not contraindicated due to recent or active breastfeeding or the patient being pregnant) and/or serum thyrotropin receptor antibodies (TRAb, also called TSI) levels in women with clinical manifestations of Graves’ disease (ophthalmopathy), persistent hyperthyroidism (>1 month), or severe hyperthyroidism (markedly elevated T3 > T4). (See 'Additional evaluation' above.)
For women without these findings, we do not obtain additional tests, but we repeat thyroid function tests (TSH, free T4, T3) in three to four weeks. By that time, most women with postpartum thyroiditis will have improved, whereas those with Graves' hyperthyroidism will usually be unchanged or worse.
●For women at high risk for developing postpartum thyroiditis (eg, previously known to be thyroid peroxidase antibody positive, type 1 diabetes, prior history of postpartum thyroiditis), we suggest screening for postpartum thyroiditis (Grade 2C). We typically measure a TSH level three and six months postpartum. If the TSH level is abnormal, it should be repeated along with a free T4 level and T3 (if TSH is low), within one to two weeks. (See 'Screening' above.)
●Most women with postpartum thyroiditis have only mild symptoms during the hyperthyroid phase and do not require any treatment. Such women should have repeat thyroid tests in four to eight weeks to confirm resolution of hyperthyroidism. Beta blockers may be useful to relieve bothersome palpitations or tremulousness in symptomatic women. In breastfeeding women, we prefer propranolol because it has the lowest transfer into milk. There is no role for antithyroid drugs (ie, methimazole) or radioiodine in the treatment of the hyperthyroid phase of postpartum thyroiditis. (See 'Treatment' above and "Hyperthyroidism during pregnancy: Treatment", section on 'Beta blockers'.)
●During the hypothyroid phase of postpartum thyroiditis, symptomatic women with an elevated TSH above the normal range require treatment with T4 (levothyroxine). For asymptomatic women with a TSH level ≥10 mU/L, we also suggest T4 replacement (Grade 2C). We do not routinely treat asymptomatic women with TSH levels below 10 mU/L. (See 'Treatment' above.)
●Most women recover and are euthyroid within one year postpartum. Thus, we typically continue thyroid hormone for six to twelve months before attempting withdrawal. However, up to 30 percent of women never recover from the initial hypothyroid phase and have permanent hypothyroidism. Thus, monitoring for persistent hypothyroidism is required after thyroid hormone withdrawal.
Thyroid hormone can be completely stopped with assessment of thyroid function (TSH, free T4) six weeks later. In patients at high risk for permanent hypothyroidism or patients who are reluctant to stop hormone fearing a return of hypothyroid symptoms, the dose could be halved for six weeks, and if the TSH does not rise, stopped with reassessment of thyroid function after an additional six weeks.
(See 'Duration of thyroid hormone therapy' above.)
●Women with reversible hypothyroidism are also at increased risk for developing permanent hypothyroidism in the future and, therefore, require yearly monitoring of TSH. (See 'Long-term follow-up' above.)
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