INTRODUCTION — Neonatal Graves disease refers to the hyperthyroidism that is seen in a small percentage of infants born to mothers with Graves disease. Although neonatal Graves disease is usually self-limited, it can be severe, even life-threatening, and have deleterious effects on neural development. Maternal Graves disease is by far the most common cause of neonatal hyperthyroidism. Active Graves disease in a pregnant woman can lead to either hyper- or hypothyroidism in the fetus and neonate, depending on the balance of the maternal stimulatory and inhibitory antibody and antithyroid drug effect [1]. Babies destined to develop neonatal Graves disease, however, are almost always hyperthyroid at or within one week of birth. (See "Hyperthyroidism during pregnancy: Treatment".)
INCIDENCE — Graves hyperthyroidism occurs in approximately 0.2 percent of women, and it occurs in approximately 1 to 5 percent of infants born to these mothers [2-4]. Thus, neonatal Graves hyperthyroidism would be expected to occur in approximately 1:25,000 neonates and affects males and females equally.
Why only 1 to 5 percent of infants of mothers with Graves hyperthyroidism are affected is explained by the level of the maternal serum stimulatory thyrotropin (thyroid-stimulating hormone [TSH]) receptor antibody (TSHR-Ab). The higher the maternal stimulatory TSHR-Ab concentration is during the third trimester, the greater is the likelihood of neonatal Graves hyperthyroidism. Given the pathogenesis, one would expect twins to be equally affected. However, in a single case report, one twin was hyperthyroid and the other was hypothyroid [5]. Both eventually recovered to a euthyroid state. (See 'Pathogenesis and risk factors' below.)
PATHOGENESIS AND RISK FACTORS
●Maternal stimulatory thyrotropin (thyroid-stimulating hormone [TSH]) receptor antibodies (TSHR-Ab) – Neonatal (and fetal) Graves hyperthyroidism is caused by the transplacental passage of TSHR-Ab [3,6,7].
In a systematic review, the lowest level of maternal TSHR-Ab leading to neonatal Graves disease was 4.4 U/L, which corresponded to 3.7 times the upper limit of normal [8]. In practice, neonatal hyperthyroidism is most likely when the TSHR-Ab activity of maternal serum is above 500 percent of the upper limit of the assay reference range [9-11]. (See "Hyperthyroidism during pregnancy: Treatment".)
●Maternal thyroid disease – Most neonatal Graves disease occurs in the setting of active Graves hyperthyroidism in the mother. Importantly, the disorder also can occur in infants of women with a history of Graves hyperthyroidism treated with thyroidectomy or radioactive iodine in the past [12]. After a woman with Graves disease undergoes one of these treatments, the risk of having an infant affected by neonatal Graves disease falls over time, in conjunction with decreases in TSHR-Ab levels. In one study, the incidence of neonatal Graves disease was 8.8 percent for newborns who were conceived between 6 to 12 months after maternal radioactive iodine treatment, compared with 5.5 percent for those conceived between 12 and 18 months and 3.6 percent for those conceived between 18 and 24 months after maternal radioactive iodine [13]. The risk of neonatal Graves disease is low five years after radioactive iodine, but some mothers still have persistent TSHR-Ab elevation and will deliver babies with neonatal Graves disease [14]. A study of the time course of decrease in TSHR-Ab after total thyroidectomy reported that the median TSHR-Ab half-life was 93.5 days, though it was longer in patients with Graves ophthalmopathy and/or those who smoked (162.5 days for those with one of these risk factors and 357.4 days for those with both) [15]. Neonatal Graves disease has also been reported in a baby born to a woman with a stimulatory TSHR-Ab associated with Hashimoto thyroiditis [16].
As described above, measurement of maternal serum TSHR-Ab in the third trimester may be helpful in predicting whether a newborn will be affected.
CLINICAL MANIFESTATIONS
Symptoms of hyperthyroidism — The clinical manifestations of hyperthyroidism in neonates are those of hyperthyroidism in general plus some features unique to neonates. The characteristic abnormalities are (picture 1):
●Low birth weight for gestational age (intrauterine growth restriction) [17]
●Premature birth
●Microcephaly (may be a manifestation of accelerated brain development with premature completion of neuronal morphogenesis)
●Frontal bossing and triangular facies
●Warm, moist skin
●Irritability, hyperactivity, restlessness, and poor sleep
●Tachycardia with a bounding pulse and, sometimes, cardiomegaly, cardiac arrhythmias, or heart failure
●Persistent pulmonary hypertension (rare)
●Fetal hydrops (uncommon)
●Hyperphagia, but poor weight gain, and increased frequency of bowel movements
●Hepatosplenomegaly
●Diffuse goiter, usually small, but occasionally large enough to cause compression of the airway
●Stare and, occasionally, exophthalmos (presumably true Graves ophthalmopathy)
Timing of symptoms — The time of onset and severity of symptoms are variable, depending upon whether the mother is taking an antithyroid drug at the time of delivery:
●Without maternal antithyroid drug treatment – Infants born to mothers not receiving an antithyroid drug, including mothers who are euthyroid as a result of previous ablative treatment for Graves hyperthyroidism, are hyperthyroid at the time of birth.
●With maternal antithyroid drug treatment – Infants of mothers taking an antithyroid drug may be euthyroid or even hypothyroid at birth and become hyperthyroid as the antithyroid drug is metabolized and excreted by 7 to 10 days after birth [18]. In a report of six infants born to mothers with Graves disease treated with antithyroid drugs during pregnancy, symptoms and signs of congenital hyperthyroidism developed between days 10 and 20 of life [19]. In a larger study of 96 neonates born to mothers with Graves disease, most had a "subclinical" course with high serum free thyroxine (T4) levels peaking at five days of age; after 14 days of age, free T4 levels normalized, although serum TSH remained suppressed for up to three months [20].
Neonatal Graves hyperthyroidism resolves spontaneously in 3 to 12 weeks as the maternal TSHR-Ab is metabolized and disappears from the infant's circulation.
DIAGNOSIS — Neonatal Graves disease is diagnosed in a newborn infant with elevated free thyroxine (T4) and total triiodothyronine (T3) and low thyroid-stimulating hormone (TSH), typically measured in a baby born to a mother with Graves disease. These values should be interpreted in the context of the infant's age because the normal range for these values is higher during the first few days and weeks of life compared with values in older infants (table 1). (See "Thyroid physiology and screening in preterm infants".)
Once the diagnosis of neonatal Graves disease is made, treatment should be initiated, as outlined below. (See 'Neonatal Graves disease' below.)
A summary of the pathways to diagnosis is presented in the algorithm (algorithm 1), which reflects recommendations in a literature-based review [21]. The steps in diagnosing neonatal Graves disease depend on how the infant comes to medical attention:
Maternal Graves disease during pregnancy — Many cases of neonatal Graves disease are suspected based on a history of maternal Graves disease and are recognized during pregnancy. In such cases, we suggest the following sequence of laboratory tests:
Prenatal testing — Measurement of maternal serum thyrotropin receptor antibody (TSHR-Ab) during the third trimester helps to predict which infants are at higher risk for development of fetal and neonatal Graves hyperthyroidism.
●Interpretation – The fetus or infant is more likely to have Graves hyperthyroidism when the maternal TSHR-Ab value is more than 500 percent of the upper limit of the assay reference range [9,22]. (See 'Pathogenesis and risk factors' above.)
•If the maternal TSHR-Ab is positive, the infant is at risk for developing neonatal Graves disease, particularly if the value is greater than 500 percent of the upper limit of the assay reference range. In this case, the infant should be evaluated at birth and monitored during the first few weeks of life, as outlined below.
•If a mother with positive TSHR-Ab has active Graves disease and is treated with an antithyroid drug during pregnancy, the newborn will be either euthyroid or have transient hypothyroidism after birth, then becomes euthyroid or hyperthyroid as the antithyroid drug is metabolized and excreted during the first week or life.
•If the maternal TSHR-Ab is negative, neonatal Graves disease is unlikely; these cases can be followed clinically, with measurement of thyroid function only if symptoms or signs of hyperthyroidism develop.
The most accurate TSHR-Ab test is a measurement of thyroid-stimulating immunoglobulin (TSI). TSI is a functional bioassay, measuring production of cyclic adenosine monophosphate (cAMP) in cultured thyroid follicular cells, confirming the presence of a stimulating antibody. Alternative TSHR-Ab tests use competitive protein binding methodology, abbreviated as "TR-Ab" or "TBII" (thyrotropin-binding inhibitory immunoglobulin). This test shows that there is an antibody that competes with thyroid-stimulating hormone (TSH) binding to its receptor, but it does not provide information about whether it is a stimulating or blocking antibody. Although TR-Ab assays do not indicate biologic activity, women with Graves disease usually have stimulatory antibodies.
●Fetal ultrasonography – Serial in utero ultrasonography with measurement of fetal thyroid size has also been reported to help determine which neonates are likely to manifest neonatal hyperthyroidism [23]. In a report of 20 pregnant women with Graves disease treated with an antithyroid drug, the fetal thyroid gland was enlarged in five pregnancies. In these five patients, the maternal antithyroid medication dose was decreased, resulting in a reduction of the fetal thyroid gland to a normal size in three cases, but in the other two cases, the gland remained enlarged. These latter two infants both developed neonatal Graves disease [23]. Thus, care must be taken because fetal goiter may be a feature of in utero hypothyroidism or hyperthyroidism. Another study using ultrasonography reported that a hyperthyroid fetus was more likely to have a goiter with central vascularization, along with other findings including fetal tachycardia, increased fetal movement, and advanced bone maturity [24].
Fetal thyroid dysfunction — High maternal serum thyrotropin receptor antibody (TSHR-Ab) concentrations may cause fetal hyperthyroidism, which is characterized by fetal hyperactivity, tachycardia (>160 beats/min) after 22 weeks gestation, advanced bone maturation, and a goiter. If these abnormalities are present, corrective therapy (eg, cautious administration of an antithyroid drug to the mother) may be indicated [25]. In addition to the adverse hypermetabolic effects, fetal hyperthyroidism may accelerate fetal central nervous system maturation, causing disorganization of brain development and related intellectual disability. The diagnosis and treatment of fetal hyperthyroidism are discussed elsewhere. (See "Hyperthyroidism during pregnancy: Treatment", section on 'Fetal or neonatal hyperthyroidism'.)
Maternal antithyroid drug treatment may also result in fetal goiter and hypothyroidism. Such cases may be managed by decreasing the maternal antithyroid dose (if this can be done safely) or by intraamniotic injections of thyroid hormone [26,27]. (See "Hyperthyroidism during pregnancy: Treatment", section on 'Fetal or neonatal hyperthyroidism'.)
Cord blood — Measurement of TSHR-Ab in cord blood is not essential for the diagnosis but helps to predict the risk of neonatal Graves disease in the infant. In a report of 68 pregnant women with a history of Graves disease, 33 had positive TSHR-Ab. Of those with positive TSHR-Ab, 73 percent (27 of 33) had infants with positive TSHR-Ab on cord blood assays and 26 percent (7 of 27) of those infants went on to develop neonatal Graves disease [28]. None of the 35 babies born to mothers with negative TSHR-Ab developed Graves disease. If the mother is known to have positive TSHR-Ab and is or was recently treated with an antithyroid drug, thyroid function tests (free thyroxine [T4] and TSH) in cord blood will show the effects on balance of the stimulating antibody and antithyroid drug in utero but do not predict the risk of neonatal hyperthyroidism [21]. For these reasons, in this situation, we recommend measurement of free T4 and TSH starting at two to three days of life rather than in cord blood.
Testing of the neonate — For infants born to mothers with a history of Graves disease but in whom the maternal TSHR-Ab status is unknown, thyroid function should be assessed by measuring serum free T4, total triiodothyronine (T3), and TSH at birth or soon thereafter. If the mother has a significantly elevated stimulatory TSHR-Ab level and was not treated with an antithyroid drug during pregnancy, hyperthyroidism will be present in the infant on initial testing. In cases where the mother was treated with an antithyroid drug up to delivery, thyroid function tests in the first day of life are normal or may even show hypothyroidism.
Thyroid function tests should be repeated at three to five days of life and again at 10 to 14 days of life. The results are interpreted as follows (algorithm 1):
●Hyperthyroidism – Infants with biochemical evidence of hyperthyroidism (elevated free T4 and total T3, with low TSH) at any of these time points have neonatal Graves disease and should be treated until the disease resolves. (See 'Differential diagnosis' below and 'Treatment' below.)
In the report cited above, a rising free T4 and free T3 during the first postnatal week predicted the development of hyperthyroidism [28]. Another study showed that a serum TSH less than 0.90 mU/L between three and seven days of age predicted the development of hyperthyroidism in most cases [29].
●Hypothyroidism – Infants with biochemical evidence of hypothyroidism (low free T4 and total T3, with high TSH) should be reevaluated one week later and then serially until thyroid function is stably normal or to determine if hypothyroidism will persist.
•In the majority of cases, the hypothyroidism is due to maternal antithyroid drug treatment and will resolve by two weeks of age; no treatment is necessary in these cases. Hypothyroidism persisting longer than two weeks likely is caused by maternal TSHR-Ab, now a blocking antibody. (See "Clinical features and detection of congenital hypothyroidism", section on 'Transient congenital hypothyroidism'.)
•In a minority of cases, infants born to mothers with a high TSHR-Ab titer will become hyperthyroid around one to two weeks of age as the maternal antithyroid drug is metabolized and excreted. A rare infant may evolve from hypothyroidism to hyperthyroidism as the balance of TSHR-Ab switches from a blocking to a stimulating antibody.
Some infants may develop central hypothyroidism (manifested by low free T4 and low TSH) as neonatal Graves disease resolves, typically between 3 and 12 weeks of age. This type of hypothyroidism also may be transient.
Treatment depends on the duration and type of the hypothyroidism. (See 'Hypothyroidism (transient)' below.)
●Normal results – Infants with normal results at all of these time points should be followed clinically, with repeat measurements of thyroid function tests if symptoms develop.
Infants coming to attention after birth — Some infants come to medical attention after birth for one of the following reasons:
●Maternal Graves disease was not recognized until after birth (mother not previously diagnosed or her diagnosis was not known during labor and delivery).
●An infant comes to medical attention because of symptoms suggesting neonatal Graves disease, which may include low birth weight, microcephaly, irritability, and tachycardia. (See 'Clinical manifestations' above.)
●Routine newborn screening identifies elevated T4 in an infant [30]. This scenario is uncommon because most newborn screening programs in the United States and worldwide undertake an initial TSH test and so would not identify a baby with an elevated T4. Some programs employ a T4-reflex TSH test approach, or combined T4 and TSH test approach, and have the potential to identify a baby with an elevated T4, but only a few programs actually follow-up such cases.
In any of these scenarios, thyroid function tests should be performed in the infant as soon as this issue is recognized, repeated at three to five days of age, and repeated again at 10 to 14 days of age (algorithm 1) [21]. Results of the maternal TSHR-Ab tests, if available, are not critical to management but may be helpful to estimate the infant's risk of developing neonatal Graves disease. (See 'Testing of the neonate' above.)
DIFFERENTIAL DIAGNOSIS — Rarely, neonatal hyperthyroidism may be caused by genetic defects of the thyroid-stimulating hormone (TSH) receptor or its mediators; these forms are not associated with maternal Graves disease, and TSHR-Ab tests are negative.
●Thyrotropin-receptor activating mutations – Activating germline mutations of the TSH receptor are a rare cause of neonatal hyperthyroidism [31-33]. Neither the infant nor the mother has circulating TSHR-Ab or evidence for autoimmune thyroid disease. This condition is inherited as an autosomal dominant trait, and there may be a family history of hyperthyroidism.
In contrast with neonatal Graves hyperthyroidism, this form of hyperthyroidism persists indefinitely [34] and will recur whenever antithyroid drug treatment is discontinued. Thus, treatment with either surgery or radioactive iodine (in children >10 years of age) is indicated eventually.
●McCune-Albright syndrome – Another rare cause of neonatal hyperthyroidism is an activating mutation of the alpha subunit of the G protein that stimulates adenylate cyclase [35-37]. This typically occurs as part of McCune-Albright syndrome. As with thyrotropin receptor-activating mutations, neither mother nor infant has TSHR-Ab. In contrast with thyrotropin receptor-activating mutations, however, these are somatic cell mutations, so this is a sporadic disorder.
This form of hyperthyroidism will persist indefinitely, so surgery or radioactive iodine treatment (in children >10 years of age) is indicated eventually.
TREATMENT
Neonatal Graves disease — Once neonatal Graves disease is confirmed by clinical and biochemical evaluation, treatment should be initiated promptly. Before beginning treatment, we recommend measuring total triiodothyronine (T3) concentration in addition to free thyroxine (T4) and thyroid-stimulating hormone (TSH) to use as a "baseline" when monitoring treatment with methimazole. With methimazole treatment, often the free T4 is low-normal and the total T3 is high-normal, such that both are needed for accurate dose adjustments.
Therapy consists of:
●Methimazole and a beta adrenergic blocker
•The antithyroid drug, methimazole (0.25 to 1.0 mg/kg per day), should be administered every 12 hours (see "Thionamides in the treatment of Graves' disease"). Propylthiouracil is also effective but has more frequent and severe side effects, including a risk of hepatotoxicity [38]. Because of these safety concerns, the Endocrine Society, American Thyroid Association, and US Food and Drug Administration recommend against the use of propylthiouracil as first-line treatment for Graves disease throughout childhood [39-41].
•A beta adrenergic blocker, such as propranolol (2 mg/kg per day every eight hours), is an important adjunct in controlling neuromuscular and cardiovascular hyperactivity. A potential advantage of propranolol is inhibition of T4 conversion to T3. If a more cardio-specific beta blocker is preferred, atenolol (1 mg/kg daily) can be used. (See "Beta blockers in the treatment of hyperthyroidism".)
In most cases, the above combination will control the hyperthyroidism within a few weeks and is sufficient treatment.
●Iodine – Iodine may be added for neonates whose hyperthyroidism is not controlled with methimazole and a beta adrenergic blocker. This is given to inhibit thyroid hormone release. Some clinicians prefer to routinely use iodine instead of the methimazole/beta adrenergic blocker combination.
The dose is one drop (8 mg) of Lugol's solution (126 mg iodine/mL) given every eight hours orally or potassium iodide solution one to two drops daily. If iodine is used, it is generally given for only one to two weeks. (See "Iodine in the treatment of hyperthyroidism".)
●Other – Glucocorticoids can also be given in extremely ill infants. In addition to their antiinflammatory actions, glucocorticoids inhibit thyroid hormone secretion and decrease peripheral conversion of T4 to T3. Digoxin may be helpful if heart failure is present.
Once improvement is evident, treatment should be gradually decreased and then discontinued. This may require frequent (ie, weekly) monitoring of thyroid function tests to allow adjustment of the antithyroid drug dose to maintain normal serum free T4 and T3 levels. As noted above, neonatal Graves hyperthyroidism usually resolves spontaneously between 3 and 12 weeks of life, although it can persist for six months or even longer.
Hypothyroidism (transient)
●Primary hypothyroidism – For infants with primary hypothyroidism (indicated by low free T4 and total T3 and elevated TSH), this is usually due to maternal antithyroid drug treatment and will resolve by two weeks of age; no treatment is necessary in these cases. If the hypothyroidism persists beyond two weeks of age, as occurs with a thyrotropin receptor (TSHR)-blocking antibody, then levothyroxine treatment should be started. In these cases, we recommend following the management guidelines as for infants with congenital hypothyroidism (see "Treatment and prognosis of congenital hypothyroidism"). Such cases are usually transient; measurement of the infant's TSHR-blocking antibody will provide guidance as to when it is safe to discontinue levothyroxine. If it is unclear whether the infant has recovered to euthyroidism, we recommend treating until age two years, followed by a trial off of treatment and measurement of serum free T4 and TSH four weeks later.
●Central hypothyroidism – Infants who develop central hypothyroidism (manifested by low free T4 and low [or "inappropriately normal"] TSH) as neonatal Graves disease resolves (typically between 3 and 12 weeks of age) should be treated with levothyroxine until it resolves. (See "Clinical features and detection of congenital hypothyroidism", section on 'Transient congenital hypothyroidism' and "Treatment and prognosis of congenital hypothyroidism".)
PROGNOSIS — With adequate therapy, initiated promptly, most neonates with hyperthyroidism improve rapidly. Nevertheless, some of these patients have intelligence quotients (IQs) in the 80s when measured at school age, even if they were treated promptly for hyperthyroidism during the neonatal period. These observations suggest that fetal or neonatal hyperthyroidism has adverse effects on the developing nervous system. Growth retardation, craniosynostosis, hyperactivity, and developmental and behavioral problems have been described as long-term sequelae of neonatal Graves hyperthyroidism; the relationship between these findings and the adequacy of treatment is uncertain [42].
A few infants with neonatal Graves hyperthyroidism later have diminished thyroid-stimulating hormone (TSH) secretion, which may result in central hypothyroidism. This is thought to be secondary to prenatal exposure of the hypothalamus and pituitary to high serum thyroid hormone concentrations during a critical stage of development. Although the neonatal Graves disease usually is transient, there is evidence that insufficient antithyroid drug treatment during pregnancy increases the risk of permanent central hypothyroidism, drawing attention to the importance of careful monitoring of maternal thyroid function and appropriate antithyroid drug dosing during pregnancy [43]. There is also evidence that decreased TSH secretion might impair normal fetal thyroid gland development, in a process described as thyroid "disintegration" [44].
SUMMARY AND RECOMMENDATIONS
●Incidence and pathogenesis – Neonatal Graves disease develops in approximately 1 to 5 percent of infants born to mothers with Graves disease, regardless of maternal medication use or level of control of hyperthyroidism, and is caused by the transplacental passage of maternal stimulatory thyrotropin-receptor antibodies (TSHR-Ab). (See 'Incidence' above and 'Pathogenesis and risk factors' above.)
●Clinical manifestations
•Neonatal hyperthyroidism – The clinical manifestations of hyperthyroidism in neonates include premature birth and/or low birth weight for gestational age, microcephaly, irritability, hyperactivity, tachycardia and arrhythmias, hyperphagia, increased frequency of bowel movements, hepatosplenomegaly, goiter, and stare (picture 1). The time of onset and severity of symptoms are variable, depending upon whether the mother is taking an antithyroid drug during pregnancy through delivery. Neonatal Graves hyperthyroidism resolves spontaneously within 3 to 12 weeks after birth as the maternal TSHR-Ab disappears from the infant's circulation. (See 'Clinical manifestations' above.)
•Other patterns – The clinical manifestations and timing depend upon the balance of the maternal stimulatory TSHR-Ab and maternal antithyroid drug (if given). Infants of mothers who are not receiving an antithyroid drug, including mothers who are euthyroid as a result of previous ablative treatment for Graves hyperthyroidism, are hyperthyroid at the time of birth. Infants of mothers who are taking an antithyroid drug may be euthyroid or even hypothyroid at birth and become hyperthyroid as the antithyroid drug is metabolized and excreted during the first week after birth. Other infants develop central hypothyroidism as neonatal Graves disease resolves. (See 'Timing of symptoms' above.)
●Monitoring during pregnancy – Pregnancies complicated by maternal Graves disease should be monitored as follows (algorithm 1):
•Maternal TSHR-Ab and risk for neonatal Graves disease – Measure maternal serum TSHR-Ab during the third trimester to estimate the risk of neonatal Graves disease in the offspring. Neonatal hyperthyroidism is most likely when the TSHR-Ab activity of maternal serum is above 500 percent of the upper limit of the assay reference range. (See 'Prenatal testing' above.)
•Fetal hyperthyroidism – Monitor the fetus for symptoms of fetal hyperthyroidism, including fetal hyperactivity, tachycardia after 22 weeks gestation, advanced bone maturation, and a goiter. If these abnormalities are present, corrective therapy (administration of an antithyroid drug to the mother) may be indicated. (See 'Fetal thyroid dysfunction' above.)
●Diagnosis
•Cord blood – At birth, measure TSHR-Ab in the cord blood to predict the risk of neonatal Graves disease. A negative TSHR-Ab in cord blood suggests low risk for neonatal Graves disease; these infants can be followed clinically, with a check of thyroid function tests only if symptoms or signs of hyperthyroidism develop. (See 'Cord blood' above.)
•Serum tests – For all infants born to mothers with a history of Graves disease and whose cord blood TSHR-Ab status is unknown, measure serum free thyroxine (T4), total triiodothyronine (T3), and thyroid-stimulating hormone (TSH) at birth (or soon thereafter) and again at three to five days of age and 10 to 14 days of age (algorithm 1). The normal range for both serum free T4, total T3, and TSH concentrations is higher in the first few days and weeks of life than in older children and adults. (See 'Testing of the neonate' above and "Thyroid physiology and screening in preterm infants".)
●Treatment
•Hyperthyroidism – If neonatal hyperthyroidism is confirmed by clinical and biochemical evaluation, treatment should be initiated promptly. We recommend that these infants be treated with a combination of the antithyroid drug methimazole and a beta adrenergic blocker such as propranolol or atenolol, rather than no treatment or monotherapy (Grade 1B). Most neonates improve rapidly and can be weaned from medication by 3 to 12 weeks of age. (See 'Treatment' above.)
•Hypothyroidism – For infants with hypothyroidism related to maternal Graves disease, treatment depends on the type (primary versus central) and duration of the hypothyroidism. (See 'Hypothyroidism (transient)' above.)
