A case of postpartum thyroiditis following SARS-CoV-2 infection.

Postpartum thyroiditis (PPT) is characterized by mild thyrotoxicosis occurring within one year of parturition commonly followed by transient hypothyroidism. Having genetic background of autoimmune thyroid disorders is a risk factor for it because the immune reactivation during postpartum period is a trigger for PPT. Pandemic of COVID-19: caused by SARS-CoV-2 infection is a global health problem, and occurrence of Graves' disease and Hashimoto's thyroiditis after the viral infection have been reported but occurrence of PPT with COVID-19 has never been reported. A 29-year-old woman developed general fatigue four and a half months after parturition, and was diagnosed as having PPT: one month before, she had COVID-19. Hereafter, we define the date of delivery as Day 0 to make timeline clear. SARS-CoV-2 infection was diagnosed by PCR on Day 103, its disappearance from the upper airway confirmed on Day 124, and the thyroiditis diagnosed on Day 136. She had been euthyroid on Day 0 and 95, but thyrotoxic on Day 136. Serum thyroglobulin (Tg) concentration was normal in the presence of anti-Tg antibody, other thyroid-related autoantibodies were negative, and by ultrasonography, the thyroid gland was normal in size and no evidence of increased vascularity. Thyroid function returned to normal by Day 172 without any specific drug therapy. In conclusion, although a clear causal relationship could not be found, we documented the world's first case of PPT developed following COVID-19.

Thyroid physiology and autoimmunity in pregnancy and after delivery.

During pregnancy and after delivery, the maternal thyroid gland faces several metabolic, hemodynamic and immunologic changes. In this article we first summarize the current knowledge on the physiologic adaptation of the healthy thyroid to pregnancy, including variations of thyroid-stimulating hormone and free thyroid hormones, as well as variations of thyroid volume. Our second aim is to illustrate the background of thyroid autoimmunity in this period, which characteristically ameliorates during pregnancy and aggravates after delivery. Although rare during pregnancy, Graves' disease is the most frequent cause of hyperthyroidism, while Hashimoto's thyroiditis is the most frequent cause for hypothyroidism. Both types of thyroid dysfunction may lead to detrimental complications in mother and child and therefore timely recognition and treatment is essential. Postpartum autoimmunity most frequently exacerbates in the form of postpartum thyroiditis, which presents with diverse clinical presentations and may lead to permanent hypothyroidism.

[Thyroid disorders in pregnancy and after delivery]. / Choroby tarczycy w ciazy i po porodzie.

During pregnancy, normal thyroid activity undergoes significant changes. Endocrine adaptation to pregnancy involves changes in iodine metabolism, serum thyroxine binding globulin, chorionic gonadotropin, suppressed immune activity and the small enlargement of the thyroid gland, particularly in iodine-deficient areas. Consequently, pregnancy and the postpartum period often influence on the course of pre-existing thyroid diseases, which are encountered frequently in pregnant women and after delivery. In addition, some thyroid diseases occurring exclusively during these periods may develop. Most of the thyroid disorders in pregnancy and postpartum period are treatable but may affect mother and foetus adversely if they are not evaluated and managed appropriately. In this paper, the pathophysiology, clinical presentation, diagnosis and management of different thyroid diseases during pregnancy and postpartum period are reviewed. Particular attention is devoted to the results of recently published studies.

[Postparum thyroiditis]. / Poporodowe zapalenie tarczycy.

Postpartum thyroiditis is one of the most common endocrinological disorders annually affecting millions of women world-wide. It is is defined as a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery. A thyrotoxic phase of postpartum thyroiditis may be brief and unnoticed before a more long-lasting (permanent in up to 30%) hypothyroid phase occurs. The disease, found in approximately 5-10% of mothers in the general population, is an autoimmune disorder, and thyroid antibody-positive women in the first trimester have a 33% to 50% chance of developing thyroiditis in the postpartum period. Women suffering from other autoimmune conditions, or having a previous or family history of thyroid disease are at increased risk of its development. In this paper we present an overview of the pathogenesis, clinical aspects, diagnosis, and treatment options for postpartum thyroiditis with putting special emphasis on the results of recently published studies.

High iodine intake is a risk factor of post-partum thyroiditis: result of a survey from Shenyang, China.

The aim of the present study is to obtain the epidemiological data on post-partum thyroiditis (PPT) firstly in Chinese women, and to tryto evaluate whether excessive intake of iodine in post-partum women imposes any danger of occurring PPT. Sixty hundred and ten pregnant women were involved in the cohort just before delivery. Four hundred and eighty-eight (80%) of them accepted taking part in follow-ups more than 6 months post-partum. A blood sample was taken from participants before delivery and every 3 months post-partum for testing of serum TSH, thyroid autoantibodies. Free T3 (FT3), free T4 (FT4) and TSH receptor antibody (TRAb) were detected if TSH was abnormal. The iodine nutrition was evaluated according to the mean level of the fasting urinary iodine excretions at different times during the studying period, and participants were subgrouped into 3 categories with low, adequate and high iodine intake. For those participants who had thyroid dysfunction within 6 months post-partum, the follow-up persisted for 1 yr. Of 488 pregnant women, PPT developed in 11.9% (58/488). Given overt and subclinical PPT, the prevalence was 7.17% (no.=35) and 4.71% (no.=23), respectively. There was a strong association between the presence of thyroid peroxidase antibody (TPOAb) at delivery and the risk of developing PPT [RR=6.76, 95% (CI) 4.42-10.34]. Overt cases had much higher titers of TPOAb than subclinical patients (all p<0.05). The median urinary iodine (MUI) of patients with PPT was significantly higher than that of healthy women (231.93 vs 199.88 microg/l p=0.00153). Both the prevalence of PPT and positive TPOAb rise with the increment of iodine intakes. Pregnant women with high iodine intake had more risk of developing PPT when compared with those with low iodine intake (RR=2.92, 95%CI 1.31-6.50). We concluded that positive TPOAb was of value for predicting the occurrence and severity of PPT, and a high iodine intake was a risk factor triggering PPT.