Hyperthyroidism occurs in 1 to 2 of every 1,000 pregnancies (Inoue 2009), with Graves' disease being the most frequent cause (85%: Marx 2008). It often improves in the third trimester of pregnancy by reducing or suppressing the medication and usually worsens after childbirth, requiring reinstatement or reinforcement of treatment, which is safe for the infant whether it is continued from gestation or if it is instituted during breastfeeding and it does not require monitoring of the thyroid function of the infant, it is enough to monitor adequate physical and psychomotor development (Alexander 2017, Inoue 2009, Marx 2008, Mandel 2001). There is no data which suggests that hyperthyroidism can affect milk production or breastfeeding in general (Alexander 2017). Postpartum thyroiditis, with its clinical phases of hyperthyroidism and hypothyroidism, is an autoimmune inflammation that occurs in the first year after birth, with an incidence of 3 to 16% (Serrano 2014, Muller 2001). There is no data to recommend universal screening, but there is in women with type 1 diabetes mellitus or associated depression (Abalovich 2007). There is controversy over its association with hyperprolactinemia (Sanjari 2016, Onal 2014). Anti-TSH receptor antibodies (TRAb) can be found in the milk of mothers treated with thyrotoxicosis during the first two months, and may cause transient thyroid disease in the infant (Törnhage 2006), usually hyperthyroidism that may require treatment (Azizi 2011). During pregnancy and breastfeeding iodine needs are increased, from around 250 micrograms (μg) daily and not exceeding 500 μg daily (Alexander 2017, Serrano 2014, Stagnaro 2011, Abalovich 2007). In areas with severe iodine deficiency and without iodized salt, post-partum administration of a single oral dose of 400 mg of iodized oil ensures an adequate amount of iodine in breast milk for 6 months (Bouhouch 2014). There is widespread consensus among societies specialized in giving treatment without interrupting breastfeeding (Alexander 2017, Poppe 2012, Lazarus 2012, Mestman 2012). Medication should be administered immediately after breastfeeding (Hudzik 2016). Propylthiouracil at doses of up to 750 mg daily does not alter thyroid function or normal infant development (Inoue 2009, Glatstein 2009, Marx 2008, Azizi 2006, Bartalena 2005, Momotani 2000 and 1989, Cooper 1987, McDougall 1986, Kampmann 1980). Other authors limit the safe dose to 300-450 mg / day (Alexander 2017, Stagnaro 2011, Mandel 2001). Methimazole at doses up to 20-30 mg daily does not alter the infant's thyroid function or psychomotor development (Alexander 2017, Serrano 2014, Stagnaro 2011, Inoue 2009, Glatstein 2009, Marx 2008, Azizi 2006, 2003, 2002, 2000 and 1996, Bartalena 2005, Cooper 1987). Given the risk of hepatic toxicity from propylthiouracil, methimazole is considered to be the preferred treatment for hyperthyroidism, especially during breastfeeding (Hudzik 2016, Serrano 2014, Karras 2012, 2010 and 2009, Azizi 2011). 50 mg of Carbimazol weekly also does not alter the thyroid function nor the normal development of the infant (Bartalena 2005, Verd 1998). The radioactivity of iodine 131 is concentrated in breast milk and its long half-life necessitates interruption of breastfeeding in both diagnostic and treatment doses (Alexander 2017, Prunty 2016, Serrano 2014, Am.Thyr.Ass 2011, Stagnaro 2011, Abalovich 2007, Azizi 2006, Dydek 1988) and the radioactivity can be measured weekly in milk samples in order to resume it (Saenz 2000). If required, for diagnostic or control purposes, iodine 123 can be used with a half-life of 13 hours, suspending breastfeeding for about 4 days or Technetium 99m can be used, which requires an interruption of only one day. Beta-blockers are necessary to control thyrotoxicosis status; propranolol or metoprolol at a sufficient minimum dose are compatible with breastfeeding (Alexander 2017). See below the information of these related products: