Postpartum thyroiditis

Epp, Riley; Malcolm, Janine; Jolin-Dahel, Khiera; Clermont, Michaela; Keely, Erin

doi:10.1136/bmj.n495

“…However, thryotoxic or hypothyroid symptoms may be overlooked by patients and/or clinicians as "normal" responses in the postpartum setting. It is reasonable to measure serum TSH at 6-12-week postpartum in the absence of symptoms for high-risk populations, including patients with a previous episode of PPT, Graves' disease, women with Hashimoto's thyroiditis on thyroid hormone replacement, and those with known TPOAb positivity, type 1 diabetes mellitus, other nonthyroidal autoimmune disease, or chronic hepatitis C (Table 1) [13,14]. If the TSH is abnormal, peripheral thyroid hormone levels, thyroid antibodies, and/or thyroid ultrasound will aid in diagnosing thyroid disorders.…”

Section: Assessment Of the Thyroid Function In The Postpartum Periodmentioning

confidence: 99%

“…For women who have recovered from PPT and are euthyroid, periodic TSH measurement is recommended until 12-month postpartum and then annually. This recommendation is based on the high lifetime risk of developing permanent hypothyroidism and up to 70% recurrence following subsequent pregnancies [13,24,25].…”

Section: Managementmentioning

confidence: 99%

An update on thyroid disorders in the postpartum period

Peng

¹

,

Pearce

²

2022

J Endocrinol Invest

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Purpose To review the pathophysiology, diagnosis and management of postpartum thyroid dysfunction, and related management of thyroid disorders during lactation. Methods We reviewed the literature on postpartum thyroid dysfunction and management of thyroid disorders during lactation. ResultsThe postpartum period is characterized by a rebound from the immunotolerance induced by pregnancy. Routine thyroid function screening is not recommended for asymptomatic women in the postpartum period. Testing thyroid function should be considered at 6-12-week postpartum for high-risk populations, including women with a previous episode of postpartum thyroiditis, Graves' disease, or those with Hashimoto's thyroiditis on thyroid hormone replacement, known thyroid peroxidase antibody positivity, type 1 diabetes mellitus, other nonthyroidal autoimmune disease, or chronic hepatitis C. A serum TSH should also be checked in the setting of postpartum depression or difficulty lactating. If patients have thyrotoxicosis, new-onset or recurrent Graves' disease must be differentiated from postpartum thyroiditis, because the management differs. Periodic thyroid function testing is recommended following recovery from postpartum thyroiditis due to high lifetime risk of developing permanent hypothyroidism. Levothyroxine, and the lowest effective dose of antithyroid drugs, (propylthiouracil, methimazole, and carbimazole) can be safely used in lactating women. The use of radiopharmaceutical scanning is avoided during lactation and radioactive iodine treatment is contraindicated. Conclusions Diagnosing postpartum thyroid dysfunction is challenging, because symptoms may be subtle. A team approach involving primary care providers, endocrinologists, and obstetricians is essential for transitioning thyroid care from the gestational to the postpartum setting.

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“…Previous researches have shown that PPT is a thyroid dysfunction after delivery in women who were euthyroid prior to pregnancy as a result of an immune "rebound" as a result of an immune "rebound" affected by the relative immunosuppression of pregnancy, with the prevalence of 1-22 % [9]. Personal history of type 1 diabetes mellitus, systemic lupus erythematosus(SLE) or gestational diabetes mellitus, family history of thyroid disease, and the presence of TPOAb are reported to be risk factors for PPT [10]. In our study, 19.93 % of the women had PPT.…”

Section: Discussionmentioning

confidence: 99%

Effects of Thyroperoxidase Antibody and Thyroglobulin Antibody on Maternal and Neonatal Outcomes in Pregnant Women

Wang

¹

,

Tang

²

,

Yuan

³

et al. 2022

Horm Metab Res

2

0

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The aim of the study was to evaluate the effects of thyroperoxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) on maternal and neonatal adverse outcomes in pregnant women. A total of 296 singleton pregnant women were classified into four groups according to the thyroid auto-antibody in the first trimester. Finally, there were 97 women in TPOAb positive group (TPOAb+/TgAb–), 35 in TgAb positive group (TPOAb–/TgAb+), 85 in TPOAb and TgAb positive group (TPOAb+/TgAb+), and 79 in TPOAb and TgAb negative group (TPOAb–/TgAb–). Thyroid function, TPOAb, and TgAb were checked during pregnancy and followed up at 6 weeks, 3 months, 6 months, 9 months, and 12 months postpartum. Levothyroxine sodium tablets could be taken to maintain euthyroid antepartum. Thyroid function of women with postpartum thyroiditis (PPT) were followed up at 2 and 3 years postpartum. We observed the incidence of PPT, premature rupture of membranes (PROM), placental abruption, placenta previa, polyhydramnios, oligohydramnios, postpartum hemorrhage, preterm birth, and low birth Weight in the four groups. 19.93% of the women had PPT. The incidence of PPT in TPOAb+/TgAb–, TPOAb–/TgAb+, TPOAb+/TgAb+groups was significantly higher than that in TPOAb–/TgAb– group, respectively (16.49 vs. 6.33%, 22.86 vs. 6.33%, 35.29 vs. 6.33%, p <0.05). The incidence of PPT in TPOAb+/TgAb+group was significantly higher than that in TPOAb+/TgAb– group (35.29 vs. 16.49%, p <0.01). PPT occurred as early as 6 weeks postpartum, but mainly at 3 and 6 months postpartum in the four groups (62.50%, 75.00%, 70.00%, 80.00%). All PPT in TPOAb–/TgAb– group occurred within 6 months postpartum, while it was found at 9 months or 12 months postpartum in other three groups. There was no classical form of PPT in TPOAb–/TgAb– group, while in the other three groups, all three types (classical form, isolated thyrotoxicosis, isolated hypothyroidism) existed. At 2 years postpartum of the women with PPT, the rate of euthyroidism in TPOAb+/TgAb+group was significantly lower than that in TPOAb–/TgAb– group (p <0.05). At 3 years postpartum of the women with PPT, the rate of euthyroidism in TPOAb+/TgAb–, TPOAb–/TgAb+, and TPOAb+/TgAb+groups were significantly lower than that in TPOAb–/TgAb– group (p <0.05). The values of TPOAb and TgAb postpartum were significantly higher than those during pregnancy (p <0.05). The incidence of PROM in TPOAb+/TgAb– group was significantly higher than that in TPOAb–/TgAb– group (32.99 vs. 17.72%, p <0.05). The binary logistic regression for PPT showed that the OR value of TPOAb was 2.263 (95% CI 1.142–4.483, p=0.019). The OR value of TgAb was 3.112 (95% CI 1.700–5.697, p=0.000). In conclusion, pregnant women with positive thyroid auto-antibodies had an increased risk of PPT and a reduced rate of euthyroidism at 2 and 3 years postpartum. TPOAb is associated with the incidence of PROM. Both of TPOAb and TgAb were independent risk factors for PPT. TgAb deserves more attention when studying autoimmune thyroid disease (AITD) combined with pregnancy.

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“…2,14 Patients who have postpartum depression, diffi culties with milk production, or symptoms of thyroid disease, especially 3 to 6 months postpartum, should be tested for thyroid dysfunction. 1,2,14 Th e signs and symptoms of hypothyroidism or hyperthyroidism are oft en dismissed as part of the normal transition from pregnancy to the postpartum period, which can lead to delays in diagnosis and treatment of postpartum thyroiditis. [13][14][15] ■ Screening recommendations Universal screening of asymptomatic pregnant patients for thyroid dysfunction is not currently recommended based on the available evidence.…”

Section: ■ Hypothyroidism In Pregnancymentioning

confidence: 99%