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.

Stable consumption of swordfish favors, whereas stable consumption of oily fish protects from, development of postpartum thyroiditis.

PURPOSE: In 236 pregnant women, we showed that selective or predominant consumption of swordfish (group A) was associated with high rates of positivity for serum thyroid autoantibodies (TPOAb and TgAb) throughout day 4 postpartum. In contrast, selective or predominant consumption of oily fish (group B) was associated with TPOAb and TgAb negativity. Rates were intermediate in group C (scanty consumption of swordfish) and group D (consumption of fish other than swordfish and oily fish). Gestational TPOAb positivity is a risk factor for postpartum thyroiditis (PPT), which evolves into permanent hypothyroidism (PH) in about 50% of cases. Purpose of this study was to verify that the different rates of thyroid autoantibodies in the four groups translated into different PPT rates. METHODS: We expanded our previous cohort (n = 412) and duration of follow-up (month 12 postpartum), and measured frequency of PPT and PH. RESULTS: At first timester of gestation, we confirmed the different Ab positivity rates in group A vs. group B (TPOAb = 21.7% vs. 4.7%, P < 0.0001; TgAb = 14.1% vs. 2.4%, P < 0.05). Overall, PPT prevalence was 63/412 (15.3%), but 22/92 in group A (23.9%), 4/85 in group B (4.7%; P < 0.0001 vs. group A), 17/108 (15.7%) in group C, and 16/117 (13.7%) in group D. Approximately half of the PPT women had PH, regardless of fish group. CONCLUSIONS: In conclusion, stable consumption of oily fish (which is enriched in polyunsaturated omega-3 fatty acids) protects from PPT, while stable consumption of swordfish (which is enriched in pollutants) favors PPT. Thus, a dietary prophylaxis of PPT is possible.

The effect of vitamin D on thyroid autoimmunity in non-lactating women with postpartum thyroiditis.

The study included 38 non-lactating l-thyroxine-treated women with postpartum thyroiditis (PPT) and 21 matched healthy postpartum women. Women with vitamin D deficiency were treated with oral vitamin D (4000 IU daily), whereas women with vitamin D insufficiency and women with normal 25-hydroxy vitamin levels were either treated with vitamin D (2000 IU daily) or left untreated. Serum hormone levels and thyroid antibody titers were measured at the beginning of the study and 3 months later. 25-hydroxy vitamin D levels were lower in women with PPT than in healthy women. Thyroid peroxidase and thyroglobulin antibody titers inversely correlated with vitamin D status. Apart from increasing serum levels of 25-hydroxy vitamin D and decreasing serum levels of parathyroid hormone, vitamin D reduced titers of thyroid peroxidase antibodies and this effect was stronger in women with vitamin D deficiency. The study's results suggest that vitamin D supplementation may bring benefits to l-thyroxine-treated women with PPT.

Lower Serum 25-Hydroxyvitamin D Level is Associated With 3 Types of Autoimmune Thyroid Diseases.

Autoimmune thyroid diseases (AITD) are common autoimmune disorders. A few studies have analyzed the association between serum vitamin D levels and AITD, and available data remain inconclusive. The aim of this study was to evaluate the association between serum vitamin D levels and 3 types of AITD, that is Graves' disease (GD), Hashimoto's thyroiditis (HT), and postpartum thyroiditis (PPT). Two independent case-control studies were designed. The first is a cross-sectional case-control study in which we examined the levels of 25(OH)D in patients with newly diagnosed GD or HT and in controls; the second is a nested case-control study in which we compared 25(OH)D levels in 610 women who developed PPT during the follow-up after delivery and those who did not. Compared with the controls, GD patients and HT patients had significantly lower 25(OH)D levels. PPT cases also had a lower serum 25(OH)D concentration than controls. Serum 25(OH)D levels were associated with neither antithyroid peroxidase antibody nor antithyroglobulin antibody in GD and HT. There was no significant relationship between thyroid-stimulating hormone and 25(OH)D levels. Every 5 nmol/L increase in serum 25(OH)D concentrations was associated with a 1.55-, 1.62-, and 1.51-fold reduction in GD, HT, and PPT risk, respectively. We observed a lower serum vitamin D levels in AITD patients compared with controls. The lower the vitamin D level is, not vitamin D deficiency per se, the higher the risk for developing AITD will be. However, vitamin D does not have strong association with the titers of thyroid antibodies or the levels of thyroid hormones.

Serum 25-Hydroxyvitamin D and Parathyroid Hormone Levels in Non-Lactating Women with Post-Partum Thyroiditis: The Effect of L-Thyroxine Treatment.

Vitamin D deficiency seems to be implicated in the onset and progression of some autoimmune disorders. No previous study has investigated vitamin D homeostasis in post-partum thyroiditis. We compared 25-hydroxyvitamin D and parathyroid hormone (PTH) levels between four groups of non-lactating women who gave birth within 12 months before the beginning of the study: hypothyroid women with post-partum thyroiditis (group A; n = 14), euthyroid females with post-partum thyroiditis (group B; n = 14), women with non-autoimmune hypothyroidism (group C; n = 16) and healthy euthyroid females without thyroid autoimmunity (group D; n = 15). In the second part of the study, groups A and C were treated for 6 months with L-thyroxine. Serum levels of 25-hydroxyvitamin D were lower, while PTH higher in patients with post-partum thyroiditis than in patients without thyroid autoimmunity. They were also lower (25-hydroxyvitamin D) or higher (PTH) in group A than in group B, as well as in group C in comparison with group D. L-thyroxine treatment increased 25-hydroxyvitamin D and reduced PTH levels only in hypothyroid women with post-partum thyroiditis. Baseline levels of 25-hydroxyvitamin D correlated with thyroid antibody titres, thyroid function and circulating PTH levels, while the effect of L-thyroxine on serum levels of this vitamin correlated with the changes in thyroid antibody titres and PTH levels. The results of our study suggest the association of vitamin D status with post-partum thyroiditis and L-thyroxine treatment of this disorder.

Sustained high levels of serum leptin rather than IL-6 observed in patients with postpartum thyroiditis during their first postpartum year.

The purpose of the study is to explore the roles of leptin and interleukin-6 (IL-6) during the first postpartum year in the occurrence and development of postpartum thyroiditis (PPT). We retrospectively collected serum samples from 57 PPT patients consisting of 34 overt PPT (O-PPT) and 23 subclinical PPT (S-PPT) in addition to 37 healthy postpartum women at four postpartum time points, i.e., 3-day and 3, 6, 12-month postpartum. Serum leptin and IL-6 levels were measured by radioimmunoassay and ELISA assay, respectively. Leptin level and leptin/BMI (LEP/BMI) ratio were higher in PPT patients than in control during the first postpartum year, but were not significantly different between O-PPT and S-PPT. However, a similar trend but did not reach significant difference in IL-6 level was observed during the postpartum period in PPT patients and control women. We conclude that a sustained high level of serum leptin after delivery may be involved in the pathogenesis of PPT. IL-6 does not contribute to the development of PPT.

The first case of association between postpartum thyroiditis and thyroid hormone resistance in an Italian patient showing a novel p.V283A THRB mutation.

BACKGROUND: Postpartum thyroiditis (PPT) is characterized by the development of postpartum thyroid dysfunction, which may occur up to 12 months after delivery. The syndrome usually presents with transient thyrotoxicosis, followed by transient hypothyroidism. The association of this condition with resistance to thyroid hormones (RTH) has never been described. PATIENT FINDINGS: In this report, we describe a 30-year-old patient affected by RTH due to a novel p.V283A thyroid hormone receptor-ß (THRB) heterozygous mutation in exon 8, which affects the ligand-binding domain, never before described in literature. A simple polymorphism was excluded through screening of 100 healthy controls. SUMMARY: The patient became pregnant twice (in 2008 and in 2009) and developed PPT after both deliveries. Two months after her first pregnancy and one month after her second pregnancy, she presented with severe endogenous thyrotoxicosis and concomitant suppressed thyrotropin (TSH) levels, which represents an unusual finding in patients affected by RTH. Other causes of hyperthyroidism were excluded. After the hyperthyroid phase, she became hypothyroid (TSH >75 mU/L and low free-thyroxine and free-tri-iodothyronine levels), and eventually returned to her usual euthyroid status. During the course of PPT, no specific treatment was required, except for ß-blockers used to treat tachycardia during the hyperthyroid phase. CONCLUSIONS: We report a unique case of a woman affected by RTH, due to a novel mutation V283A in THRB, who experienced PPT with a severe thyrotoxic phase after both her pregnancies. The association between RTH and PPT has never been reported in the literature. In particular, the marked suppression of TSH occurring when levels of TH are particularly elevated is not a frequent condition during RTH.

Prevalence of post-partum thyroiditis in Liguria (Italy): an observational study.

BACKGROUND: Post-partum thyroiditis (PPT) is an autoimmune disorder occurring within the first year following delivery. A variable prevalence has been reported in different surveys. We prospectively evaluated PPT prevalence and outcome in a cohort of pregnant women living in a well-defined geographic area. AIM: A subset from a group of healthy women consecutively evaluated for thyroid function and thyroid autoimmunity during pregnancy, referring to the same obstetric unit, were followed up at 4-6 months and 1 yr after delivery. MATERIALS/SUBJECTS AND METHODS: Follow-up for PPT was performed in 258 pregnant women. Control data were obtained in a comparable group of healthy non-pregnant women. Free T3 (fT3), free T4 (fT4), TSH thyroglobulin/thyroid peroxidase autoantibodies (TgAb/TPOAb), and urinary iodine excretion were measured. RESULTS: Autoantibody positivity was observed in 9.3% of pregnant, similar to control women. Forty-three out of 59 autoantibody-positive women were followed up; 23 showed PPT at the first control, 18 had hypothyroidism at 1 yr (5 had not shown PPT at the first control). Among 215 out of 584 autoantibody-negative women followed up, 27 developed PPT (15 of them without thyroid autoantibodies); 16 developed thyroid autoantibodies without PPT. After 1 yr, 9 women had hypothyroidism: only 1 of them was autoantibody-negative at the former control. Urinary iodine was increased in several pregnant women. CONCLUSIONS: An overall PPT prevalence of about 18% may be estimated. PPT was also observed in autoantibody- negative women. Differences with other surveys may be related to both study protocol and characteristics of the population studied.

[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.