Differentiation of Postpartum Graves' Thyrotoxicosis from Postpartum Destructive Thyrotoxicosis Using Antithyrotropin Receptor Antibodies and Thyroid Blood Flow

Ide, Akane; Amino, Nobuyuki; Kang, Shino; Yoshioka, Waka; Kudo, Takumi; Nishihara, Eijun; M, Ito; Nakamura, Hirotoshi; Miyauchi, Akira

doi:10.1089/thy.2013.0585

Cited by 55 publications

(38 citation statements)

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“…Another consideration is the risk of GD relapse post-partum in women who experienced remission of GD in late pregnancy, and women who were in remission already before the pregnancy after previous ATD therapy. Post-partum relapse of GD has to be distinguished from thyrotoxicosis caused by post-partum thyroiditis (97). Severe thyrotoxicosis from post-partum thyroiditis tends to develop within the first 3 months post-partum (97), and the thyrotoxic condition tends to be soon replaced by hypothyroidism.…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

“…Post-partum relapse of GD has to be distinguished from thyrotoxicosis caused by post-partum thyroiditis (97). Severe thyrotoxicosis from post-partum thyroiditis tends to develop within the first 3 months post-partum (97), and the thyrotoxic condition tends to be soon replaced by hypothyroidism. GD most often develops more than 3 months after giving birth (Fig.…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

“…Moreover, TRAb is normally positive in GD and serum T 3 more elevated than serum T 4 (98). Measurement of thyroid blood flow by Doppler ultrasonography may assist to distinguish the two types of disease (97).…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

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ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

Laurberg

Andersen

2016

European Journal of Endocrinology

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Thyroid hormones are essential developmental factors, and Graves' disease (GD) may severely complicate a pregnancy. This review describes how pregnancy changes the risk of developing GD, how early pregnancy by several mechanisms leads to considerable changes in the results of the thyroid function tests used to diagnose hyperthyroidism, and how these changes may complicate the diagnosing of GD. Standard therapy of GD in pregnancy is anti-thyroid drugs. However, new studies have shown considerable risk of birth defects if these drugs are used in specific weeks of early pregnancy, and this should be taken into consideration when planning therapy and control of women who may in the future become pregnant. Early pregnancy is a period of major focus in GD, where pregnancy should be diagnosed as soon as possible, and where important and instant change in therapy may be warranted. Such change may be an immediate stop of anti-thyroid drug therapy in patients with a low risk of rapid relapse of hyperthyroidism, or it may be an immediate shift from methimazole/carbimazole (with risk of severe birth defects) to propylthiouracil (with less risk), or maybe to other types of therapy where no risk of birth defects have been observed. In the second half of pregnancy, an important concern is that not only the mother with GD but also her foetus should have normal thyroid function.Thyroid hormones are essential developmental factors as first shown by Gudernatsch when he, in 1912, fed tadpoles thyroid tissue and observed metamorphosis (1). In mammals, thyroid hormones are especially of importance for brain development (2, 3), and even a few months with lack of thyroid hormones in infant life may lead to irreversible brain damage. This is the background for the universal screening for congenital hypothyroidism performed in many countries. However, thyroid hormones are also important for normal pregnancy, and maternal thyroid disease may severely increase the risk of pregnancy complications, including Invited author's profile Peter Laurberg was Clinical Professor of Internal Medicine and Endocrinology, Department of Endocrinology, Aalborg University Hospital, Aalborg, Denmark. His research mainly focused on thyroid disease prevention, epidemiology, diagnosing and therapy, including studies on iodine and thyroid, and pregnancy and thyroid. He had special research interest on the risk from and optimal management of autoimmune hypo-and hyperthyroidism in pregnancy and post-partum, management of Graves' disease in general, and how the burden of thyroid disease can be minimized by adjusting the population's iodine intake. He has coauthored several international guidelines on thyroid disease management, including management of thyrotoxicosis, and thyroid disease in pregnancy. Peter Laurberg died June 20, 2016.

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Section: European Journal Of Endocrinologymentioning

confidence: 99%

Section: European Journal Of Endocrinologymentioning

confidence: 99%

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ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

Laurberg

Andersen

2016

European Journal of Endocrinology

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“…Cut off was 1.9 IU/L [10]. Thirty-eight TPOAbpositive samples were assayed for TSAb activity by sensitive bioassay [6].…”

Section: Methodsmentioning

confidence: 99%

Partial prediction of postpartum Graves’ thyrotoxicosis by sensitive bioassay for thyroid-stimulating antibody measured in early pregnancy

et al. 2016

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“…1) A strong correlation exists between the presence of thyroid peroxidase (TPO) antibodies and postpartum thyroid autoimmune dysfunction. Such thyroid dysfunction can manifest in various forms (hyperthyroid or hypothyroid, transient or persistent), each of which necessitates different treatment.…”

Section: Introductionmentioning

confidence: 99%

Recurrent Hyperthyroidism Following Postpartum Thyroiditis in a Woman with Hashimoto's Thyroiditis

2015

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Postpartum thyroid dysfunction occurs in 5-10% of women within one year after delivery. Women with hypothyroidism antedating pregnancy are at high risk for postpartum thyroiditis and should be closely monitored during the first year post-partum. Here, we report a case of recurrent hyperthyroidism between two episodes of postpartum thyroiditis in a woman diagnosed with subclinical hypothyroidism prior to pregnancy. It is of particular interest that spontaneously remitting hyperthyroidism as a sequela of postpartum thyroiditis can occur.

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Differentiation of Postpartum Graves' Thyrotoxicosis from Postpartum Destructive Thyrotoxicosis Using Antithyrotropin Receptor Antibodies and Thyroid Blood Flow

Abstract: Early onset of thyrotoxicosis postpartum was associated mainly with PPDT, and a late onset was suggestive of PPGr. Positive TRAb and high TBF >4.0% are indicators of postpartum onset of Graves' disease.

Cited by 55 publications

References 20 publications

ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

Partial prediction of postpartum Graves’ thyrotoxicosis by sensitive bioassay for thyroid-stimulating antibody measured in early pregnancy

Recurrent Hyperthyroidism Following Postpartum Thyroiditis in a Woman with Hashimoto's Thyroiditis

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Differentiation of Postpartum Graves' Thyrotoxicosis from Postpartum Destructive Thyrotoxicosis Using Antithyrotropin Receptor Antibodies and Thyroid Blood Flow

Abstract: Early onset of thyrotoxicosis postpartum was associated mainly with PPDT, and a late onset was suggestive of PPGr. Positive TRAb and high TBF >4.0% are indicators of postpartum onset of Graves' disease.

Cited by 55 publications

References 20 publications

ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

Partial prediction of postpartum Graves&rsquo; thyrotoxicosis by sensitive bioassay for thyroid-stimulating antibody measured in early pregnancy

Recurrent Hyperthyroidism Following Postpartum Thyroiditis in a Woman with Hashimoto's Thyroiditis

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Partial prediction of postpartum Graves’ thyrotoxicosis by sensitive bioassay for thyroid-stimulating antibody measured in early pregnancy