Next Article in Journal
Skeletal Muscle Myofiber Development in Non-Human Primate Offspring Deprived of Estrogen in Utero
Previous Article in Journal
Diagnosis of Congenital and Acquired Generalized Lipodystrophies—Similarities and Differences
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Endocrines
Volume 6
Issue 4
10.3390/endocrines6040056
endocrines-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

The Impact of Chronic Autoimmune Thyroiditis During Pregnancy on Maternal and Fetal Outcomes

by
Olesea Scrinic
*,
Eduard Circo
and
Seila Musledin
Endocrinology Department, Faculty of Medicine, “Ovidius” University of Constanta, 900527 Constanța, Romania
*
Author to whom correspondence should be addressed.
Endocrines 2025, 6(4), 56; https://doi.org/10.3390/endocrines6040056
Submission received: 6 October 2025 / Revised: 11 November 2025 / Accepted: 17 November 2025 / Published: 20 November 2025
(This article belongs to the Section Female Reproductive System and Pregnancy Endocrinology)
Versions Notes

Abstract

Background/Objectives: Thyroid dysfunction during pregnancy is associated with a range of adverse perinatal outcomes. This study aims to evaluate the effect of maternal thyroid autoimmunity on selected gestational and perinatal outcomes of the newborn in a region with adequate iodine intake. Methods: This retrospective study included 74 full-term singleton pregnancies from women living in the coastal region of Romania. Participants were divided into two groups: group 1—women with chronic autoimmune thyroiditis and euthyroidism; group 2—women without thyroid disorders, serving as the control group. Maternal variables assessed included serum thyroid hormone levels and antithyroid autoantibodies. For newborns, parameters such as birth weight, neonatal TSH levels, and the incidence of gestational and perinatal events were evaluated. Results: The incidence of chronic autoimmune thyroiditis in the study population was 36.4%. Maternal thyroid autoimmunity was associated with an increased incidence of low birth weight, observed in 11% of the autoimmune group compared with 2.1% in the control group (p = 0.099). The incidence of preterm birth was significantly higher in the autoimmune group (18.5% vs. 4.2% in controls, p = 0.043), corresponding to a 4.3-fold increase in relative risk. The most frequent perinatal complication observed in pregnant women with thyroid autoimmunity was spontaneous abortion (11.1%). The median urinary iodine concentrations were within the adequate range in both study groups. Conclusions: Thyroid autoimmunity during pregnancy presents significant clinical challenges, even in areas with adequate iodine intake. Maternal autoimmune thyroiditis constitutes an established risk factor for impaired fetal development and adverse perinatal outcomes. Early assessment of thyroid function prior to conception or during the first trimester is recommended for both diagnostic and preventive purposes.

1. Introduction

Thyroid dysfunction during pregnancy affects about 2–3% of women [1] and can cause serious problems for a newborn if left undiagnosed or untreated [2]. The feto-placental unit is a complex system with its own endocrine activity, involving maternal adaptations that are crucial for healthy embryonic and fetal development. Changes in the thyroid during pregnancy are influenced by endogenous factors, such as autoimmunity and placental hormones, as well as environmental factors such as iodine intake and exposure to goitrogens [3]. Thyroid disorders are consistently cited as the second most common endocrine disorder (after diabetes mellitus) in women of reproductive age and during pregnancy [4].
Thyroid dysfunction during pregnancy affects approximately 0.3–0.5% of women with overt hypothyroidism, 2–2.5% with subclinical hypothyroidism, and 0.2–0.4% with overt hyperthyroidism [5]. Elevated levels of antithyroid antibodies, such as TPOAb (antithyroid peroxidase antibody) and TGAb (anti-thyroglobulin antibody), are common during pregnancy and indicate chronic autoimmune thyroiditis (Hashimoto’s disease). According to the 2017 American Thyroid Association guidelines, positive TPOAb and TGAb are found in 2% to 20% of pregnant women [3].
Chronic autoimmune thyroid disorders often cause hypothyroidism and are linked to risks such as recurrent pregnancy loss, miscarriage (doubling with positive TPOAb or TGAb), preterm birth, low birth weight, low APGAR scores, placental abruption, postpartum depression, neonatal respiratory distress, gestational hypertension, and ADHD in children of TPOAb-positive mothers. The prevalence of chronic autoimmune thyroiditis (CAT) during pregnancy varies by region, influenced by iodine intake, environmental factors, and genetics. According to the 2017 ATA guidelines, about 10–20% of pregnant women with thyroid autoimmunity remain euthyroid in the first trimester [3].
Due to the uncertain association between thyroid autoantibodies and maternal or fetal complications in euthyroid pregnant women, routine thyroid function screening is recommended. The guidelines recommend that euthyroid women with positive TPOAb/TGAb be checked upon confirmation of pregnancy and every 4 weeks until the second trimester for TSH level. Pregnant women with risk factors (e.g., age > 30, thyroid or autoimmune history, diabetes, multiple pregnancy, obesity, miscarriage history) should also have antithyroid antibodies assessed if TSH is between 2.5 and 10 mIU/L [3].
Although conducted in Romania’s coastal region—a geographical area with adequate iodine intake in the general population, some specific population groups, such as pregnant women, may experience moderate iodine deficiency, risking thyroid dysfunction and adverse maternal and fetal outcomes [6,7]. The study aimed to assess the impact of thyroid autoimmunity during pregnancy, its possible complications, and related risk factors in an iodine-sufficient area.

2. Materials and Methods

This retrospective study was conducted on a cohort of 74 singleton pregnancies originating from the Dobrogea region, Constanta city, between 2020 and 2021.
The levels of TPOAb and TGAb, along with trimester-specific TSH values, were measured using the electrochemiluminescence immunoassay (ECLIA) method. The diagnosis of chronic autoimmune thyroiditis was based on elevated antibody levels (TPOAb > 34 IU/mL and/or TGAb > 115 IU/mL), in conjunction with thyroid functional status according to trimester-specific laboratory TSH reference ranges. In the first trimester, the reference range for TSH was 0.33–4.59 µIU/mL.
Two study cohorts were established: group 1 (n = 27)—pregnant with chronic autoimmune thyroiditis and normal thyroid functionl; group 2 (control group, n = 47)—pregnant women without chronic autoimmune thyroiditis and normal thyroid function.
We assessed the median age of pregnant women, their nutritional and iodine status, smoking status (smoker or non-smoker), method of iodine intake, and gestational outcomes. In the neonatal evaluation, parameters such as birth weight (with low birth weight defined as less than 2500 g), gestational age at delivery (preterm birth defined as less than 37 weeks), mode of delivery, and the occurrence of perinatal events were analyzed.
Neonatal TSH levels, measured using FEIA (fluorimetric enzyme immunoassay), were utilized to evaluate iodine status. A TSH cutoff of 5 mIU/mL in whole blood defines the normal range. According to WHO/UNICEF/ICCIDD, a prevalence of 3–19.9% of newborns with TSH levels above this cutoff indicates mild iodine deficiency; 20–39.9% signifies moderate deficiency; and over 40% reflects severe iodine deficiency [8,9].
Iodine intake in pregnant women was evaluated following WHO guidelines by measuring the median urinary iodine concentration (mUIC) in spontaneous urine samples. The recommended range for adequate UIC is 150 to 249 mcg/L, with levels considered more than adequate between 250 and 499 mcg/L; insufficient intake is indicated by levels below 150 mcg/L; and excessive intake is above 500 mcg/L [9].
Although the study included a limited number of cases, which may have restricted its statistical power, it provided data from a geographic region with few prior population-based studies on pregnant women.
The study was approved by the Institutional Ethics Committee of University Ovidius Constanta, Romania.

Statistical Data Analysis

Data analysis was performed using the SPSS statistical software, version 25. Continuous variables were summarized as medians with interquartile ranges (IQRs), while categorical variables were presented as counts and percentages (%). Non-parametric tests (Mann–Whitney U test and median test) were applied for ordinal data and non-normally distributed numerical variables. Logistic regression analysis was used to evaluate the association between two categorial variables. A p-value of less than 0.05 was considered statistical significance.

3. Results

As shown in Table 1, among the 74 pregnant women, a positive TPOAb/TGAb was found in 27 of cases (36.4%), and negative antithyroid antibodies were present in 47 cases (63.6%) considered the control group.
Additionally, the mean age of pregnant women with chronic autoimmune thyroiditis (31 years) was significantly higher than that of women with negative TPOAb/TGAb (28.7 years) (p = 0.004).
The association test indicated that there was no significant relationship between positive TPOAb/TGAb and iodized salt consumption (p = 0.090).
Significant differences in TSH levels were observed between TPOAb/TGAb-positive pregnant women and the control group, with median (IQR) values of 2.52 mIU/L (1.55–4.50) versus 1.69 mIU/L (0.79–2.87), respectively (p = 0.030). Nonetheless, TSH levels in both groups remained within the normal trimester-specific reference range.
Less than 3% of newborns have a neonatal TSH value greater than 5 mUI/L, excluding iodine deficiency in our study groups, and there were no statistical differences between the neonatal TSH of the pregnant with or without chronic autoimmune thyroiditis (p = 0.896).
Additionally, we observed an adequate iodine status in pregnant women, as indicated by urinary iodine concentration (UIC) levels within the sufficient range, with median values exceeding 150 mcg/L (group 1: median UIC = 159.4 mcg/L; group 2: median UIC = 155 mcg/L).
Other variables, including nutritional status, smoking status, type of delivery, and FT4 level, showed no significant differences between the two groups (p > 0.05).
In Table 2, we present an evaluation of gestational outcomes such as preeclampsia, gestational diabetes, spontaneous abortion, and thrombophilia, showed no significant statistical differences in study and control group of pregnant (p > 0.05).
Even though the incidence of LWB was higher in newborns from mothers with thyroid autoimmunity, we did not find significant differences between the study and control groups (p = 0.099).
There was a statistically significant increase in preterm birth rates at 18.5% in the TPOAb-positive group compared to 4.3% in the TPOAb-negative group (difference of 14.3%, p = 0.043). The odds ratio (OR) was 5.11 (95% CI 0.92–28.48).
We used logistic regression to evaluate whether a positive TPOAb/TGAb serves as an independent risk factor for preterm birth. The analysis revealed a relative risk of 4.3 in pregnant women with Hashimoto’s thyroiditis; however, this result was not statistically significant (p = 0.06).
There were no statistically significant differences in fetal distress, intrauterine growth restriction (IUGR), umbilical cord abnormalities, or prolonged jaundice between pregnant women with and without autoimmune thyroiditis (all p > 0.05).

4. Discussion

Chronic autoimmune thyroiditis during pregnancy is frequently recognized as a potential contributor to immune dysregulation, which may interfere with materno–fetal tolerance and predispose the patient to adverse pregnancy outcomes.
According to current guidelines, the prevalence of CAT during pregnancy ranges from 2 to 17% (3). In our study, however, the incidence of chronic autoimmune thyroiditis was 36.4%, notably higher than these reported values. This discrepancy may be related to the relatively small sample size and/or to variations in exogenous iodine intake—whether excessive or insufficient—which can act as a trigger for thyroid autoimmunity. Although iodine supplementation is essential for preventing goiter and hypothyroidism, epidemiological studies indicate that adequate or excessive iodine intake may paradoxically increase the prevalence of chronic autoimmune thyroiditis. This effect is believed to result from increased thyroglobulin iodination, oxidative stress that mediates thyroid injury, and a possible underlying genetic predisposition [10,11,12].
In our study, 15% of pregnant women with chronic autoimmune thyroiditis (representing slightly over half of those with thyroid autoimmunity) reported using iodine supplements. However, no association was found between the presence of positive thyroid autoantibodies and iodine supplement use, even though some studies have claimed the opposite [13]. Importantly, iodine supplementation in patients with thyroid autoimmunity may potentially worsen or accelerate disease progression toward subclinical or clinical hypothyroidism, thereby negatively affecting fetal morpho-functional development [13,14]. The present study was conducted in a non-endemic area for iodine deficiency dysfunctions; therefore, increased attention should be paid to pregnant women with thyroid autoimmunity in terms of iodine supplements that can be considered triggers for maternal morpho-functional autoimmune thyroid dysfunction with a series of repercussions in the perinatal period. Thus, we consider it necessary to evaluate maternal iodine status through urinary iodine (in large population studies) in order to assess whether iodine supplements are needed.
During pregnancy, women affected by chronic autoimmune thyroiditis appear to be at particularly high risk. Antithyroid antibodies are considered surrogate markers of a generalized autoimmune imbalance, and several mechanisms have been proposed to explain this association. Pregnancy is an inflammatory process that involves a change in the regulation of the cytokine network at the placental-decidual level, and an imbalance at this level can be associated with miscarriage and premature birth [15]. Several mechanisms have been proposed to be responsible for immune disbalance in pregnant women with autoimmune thyroiditis: Th1/Th2 balance shift—pregnancy typically shifts immune response towards a Th2 dominant profile to tolerate the fetus, but in autoimmune thyroiditis, an imbalance may occur, with increased Th1 activity promoting inflammation and autoantibody production [16]; dysfunction of regulatory T Cell (Treg) that plays a crucial role in maintaining immune tolerance and an impaired Treg function or reduced numbers can lead to a loss of tolerance to thyroid antigens, exacerbating autoimmunity [17]; cytokine dysregulation, where elevated pro-inflammatory cytokines such as IFN-γ, IL-17, and TNF-α can promote autoimmune responses and thyroid tissue destruction [18]; dysregulated B cell responses lead to increased production of pathogenic autoantibodies, such as TPOAb and TGAb, which are important to the pathogenesis of autoimmune thyroiditis [19]; aberrant antigen presentation by dendritic cells can promote activation of autoreactive T cells via MHC class II pathways, further fueling thyroid autoimmunity [20].
Furthermore, women with autoimmune thyroiditis prior to conception are at higher risk of developing subclinical or overt hypothyroidism during pregnancy, conditions that are known to affect both maternal and fetal health [3]. Additionally, autoimmune thyroiditis has been linked to infertility, and the common occurrence of advanced maternal age among antibody-positive women may partly explain the increased risk of pregnancy loss observed in this population [21].
The assessment of gestational complications in this study did not reveal a statistically significant difference between pregnant women with or without thyroid autoimmunity. Although more than half of the pregnancy losses occurred in women diagnosed with chronic autoimmune thyroiditis (4.1% with CAT out of the 6.8% of incomplete pregnancies reported in the total sample), we did not observe a significant association between positive autoantibodies and the number of pregnancy losses, unlike other similar studies [22,23]. However, numerous specialized investigations have documented that women with thyroid autoantibodies present a 2–4 times higher risk of spontaneous or recurrent miscarriage, even when euthyroid [23,24]. Although the exact mechanism of this adverse outcome is not clearly identified, some researchers sustain that in euthyroid women, the presence of thyroid autoantibodies may be associated with a slight reduction in thyroid hormone levels or an impaired ability of the thyroid gland to appropriately adapt to the increased physiological demands of pregnancy. Additionally, thyroid autoantibodies reflect systemic immune activation and, specifically, enhanced reactivity toward the feto-placental unit, suggesting a generalized autoimmune imbalance in affected women [23].
In the studied pregnant women, the most common perinatal pathology was preterm birth, with an incidence of 18.5% in women with thyroid autoimmunity. This group had a 4.3-fold higher relative risk of preterm birth compared to the control group. Numerous studies have also reported a higher prevalence of preterm births among pregnant women with positive autoantibodies and normal TSH levels, findings that are consistent with the results of this study [25,26].
A potential mechanism underlying this complication is that premature birth in euthyroid women with autoimmune thyroiditis is thought to arise from a combination of immune-mediated placental dysfunction, subtle thyroid hormone insufficiency and maternal factors such as advanced age and infertility treatments, rather than overt hypothyroidism [27,28]. The results of a recent meta-analysis in 2025 support that maternal autoimmunity increases the risk of preterm birth by 2 times and of spontaneous/recurrent abortion by 3 times in pregnant women with normal thyroid function [29].
Although low birth weight (LBW) is a well-recognized adverse perinatal outcome associated with autoimmune thyroiditis—even in euthyroid women—this risk may be attributed to a gradual increase in TSH levels from the first to the third trimester, potentially leading to overt or subclinical hypothyroidism complications that manifest later in pregnancy. Additionally, the presence of autoimmunity may contribute to placental immune dysregulation, which can impair nutrient transfer to the fetus via the placenta [13,29]. While positive TPOAb has been identified as an independent risk factor for LBW, our study did not find a statistically significant association between this adverse outcome and TPOAb positivity, which contrasts with findings from other studies [30].
Avoiding gestational and perinatal complications in pregnant women with antithyroid antibodies requires regular monitoring and prompt intervention in cases of thyroid dysfunction in pregnant women diagnosed with thyroid autoimmunity. There are rather controversial data among various international societies regarding the adoption of universal screening versus high risk-based screening for pregnant women, with no consensus reached among the major professional forums.
The 2014 ETA guidelines recommend universal screening, highlighting the benefits of early treatment for overt hypothyroidism and the risk of underdiagnosing subclinical cases [3,31]. In contrast, the 2017 ATA guidelines state that most pregnant women have TSH levels between 2.5 and 5 mIU/L, for which the benefits of treatment are uncertain. Therefore, the ATA advises early identification of women at high risk for developing thyroid disorders during pregnancy [3].
Universal screening enables the identification and treatment of all pregnant women with overt hypothyroidism, as well as those who are asymptomatic. Several studies have demonstrated that interpreting maternal thyroid functional status using only risk-based screening may result in the underdiagnosis of approximately 30–40% of thyroid dysfunctions [32,33]. The cost-effectiveness of universal versus risk-based screening has been debated. In 2012, Dosiou et al. demonstrated that first-trimester universal screening for TSH and TPOAb is more cost-effective than risk-based screening, as early detection and treatment of TPOAb-positive women with subclinical hypothyroidism reduced rates of miscarriage and preterm birth [34]. Furthermore, universal screening facilitates earlier diagnosis of postpartum thyroiditis (PPT) and hypothyroidism in the years following delivery [35].
We recognize that the limited sample size, retrospective nature of the study, and lack of multivariate analysis may impact the generalizability and strength of our conclusions.
We will consider conducting future studies with larger prospective cohorts and using multivariate analyses to confirm and expand our results. Additional data collection and collaboration with obstetricians and family doctors are necessary, as extensive longitudinal studies are essential to develop effective preventive measures against the adverse effects of autoimmune thyroid disease on both mother and child.

5. Conclusions

Pregnancy induces significant physiological and immunological changes that promote the production of thyroid autoantibodies that are associated with modifications in pregnancy progression and are important clinical markers for predicting thyroid dysfunction in the mother, fetus, and neonate.
The most significant finding in our study is that autoantibodies are valuable predictors of thyroid-related pregnancy complications such as miscarriage, preterm birth, and low birth weight.
To prevent adverse perinatal outcomes related to autoimmune thyroiditis, a comprehensive management strategy is essential. This should include preconception TSH optimization, regular monitoring of thyroid function throughout pregnancy, and early initiation of levothyroxine when TSH levels rise, ensuring iodine sufficiency, close obstetric surveillance, and postpartum thyroid screening.
Early assessment of thyroid function, ideally before conception or during the first weeks of gestation, is highly recommended as both a diagnostic tool and preventive approach to minimize maternal and fetal complications associated with thyroid dysfunction.
Future studies should focus on elucidating the immunological mechanisms leading to thyroid autoantibody development during pregnancy, including identification of the genetic, environmental and hormonal factors involved and clarification of the causal relationships between autoantibody presence and pregnancy outcomes, which may enable the development of targeted interventions.

Author Contributions

Conceptualization, O.S. and E.C.; methodology, O.S. and S.M.; software, O.S.; validation, O.S. and E.C.; formal analysis, E.C.; investigation, O.S. and S.M.; resources, O.S.; data curation, S.M.; writing—original draft preparation, O.S.; writing—review and editing, O.S. and S.M.; visualization, O.S. and E.C.; supervision, E.C.; project administration, O.S.; funding acquisition, O.S. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Ethics Committee of University Ovidius Constanta, Romania for studies involving humans (approval code: 14758; 1 October 2019).

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study.

Data Availability Statement

All original data and findings discussed in this study are contained within the article. For additional information please contact the corresponding author.

Acknowledgments

The authors acknowledge the cooperation of all the participants in this study.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
ATAAmerican Thyroid Association
ADHDAttention-deficit/Hyperactivity disorder
ETAEuropean Thyroid Association
PPTPostpartum Thyroiditis
LT4Levothyroxine

References

  1. Dong, A.C.; Stagnaro-Green, A. Differences in diagnostic criteria mask the true prevalence of thyroid disease in pregnancy: A systematic review and meta-analysis. Thyroid 2019, 29, 278–289. [Google Scholar] [CrossRef]
  2. Männistö, T.; Vääräsmäki, M.; Pouta, A.; Hartikainen, A.-L.; Ruokonen, A.; Surcel, H.-M.; Bloigu, A.; JärVelin, M.-R.; Suvanto-Luukkonen, E. Perinatal outcome of children born to mothers with thyroid dysfunction or antibodies: A prospective population-based cohort study. J. Clin. Endocrinol. Metab. 2009, 94, 772–779. [Google Scholar] [CrossRef] [PubMed]
  3. Alexander, E.K.; Pearce, E.N.; Brent, G.A.; Brown, R.S.; Chen, H.; Dosiou, C.; Grobman, W.A.; Laurberg, P.; Lazarus, J.H.; Mandel, S.J.; et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid 2017, 27, 315–389. [Google Scholar] [CrossRef] [PubMed]
  4. Puthiyachirakal, M.A.; Hopkins, M.; AlNatsheh, T.; Das, A. Overview of thyroid disorders in pregnancy. Matern. Health Neonatol. Perinatol. 2025, 11, 9. [Google Scholar] [CrossRef]
  5. Singh, S.; Haq, N.; Sandhu, S. Thyroid Disease and Pregnancy. Available online: https://www.ncbi.nlm.nih.gov/books/NBK538485/ (accessed on 15 August 2025).
  6. Zimmermann, M.B.; Gizak, M.; Abbott, K.; Andersson, M.; Lazarus, J.H. Iodine deficiency in pregnant women in Europe. Lancet Diabetes Endocrinol. 2015, 3, 672–674. [Google Scholar] [CrossRef] [PubMed]
  7. Scrinic, O.; Circo, E.; Corina, D.; Musledin, S. Suboptimal Urinary Iodine Level in Pregnant Women from Perimarine Area of Romania. J. Clin. Med. 2025, 14, 3666. [Google Scholar] [CrossRef]
  8. Institutul Pentru Ocrotirea Mamei şi Copilului “Alfred Rusescu”; UNICEF România. Statusul Nutriţional al Femeii Gravide: România—2005; MarLink: București, Romania, 2006; pp. 238–258. Available online: https://www.insmc.ro/wp-content/uploads/2021/01/statusul-nutritional-al-femeii-gravide_1.pdf (accessed on 1 September 2021)ISBN 973-8411-47-5.
  9. World Health Organisation. Assessment of Iodine Deficiency Disorders and Monitoring Their Elimination: A Guide for Programme Managers, 3rd ed.; World Health Organization: Geneva, Switzerland, 2007; Available online: https://apps.who.int/iris/handle/10665/43781 (accessed on 1 September 2021).
  10. Liu, J.; Mao, C.; Dong, L.; Kang, P.; Ding, C.; Zheng, T.; Wang, X.; Xiao, Y. Excessive Iodine Promotes Pyroptosis of Thyroid Follicular Epithelial Cells in Hashimoto’s Thyroiditis Through the ROS-NF-κB-NLRP3 Pathway. Front. Endocrinol. 2019, 10, 778. [Google Scholar] [CrossRef]
  11. Burek, C.L.; Talor, M.V. Environmental triggers of autoimmune thyroiditis. J. Autoimmun. 2009, 33, 183–189. [Google Scholar] [CrossRef]
  12. Cai, T.; Du, P.; Suo, L.; Jiang, X.; Qin, Q.; Song, R.; Yang, X.; Jiang, Y.; Zhang, J.-A. High iodine promotes autoimmune thyroid disease by activating hexokinase 3 and inducing polarization of macrophages towards M1. Front. Immunol. 2022, 13, 1009932. [Google Scholar] [CrossRef]
  13. Sun, X.; Shan, Z.; Teng, W. Effects of Increased Iodine Intake on Thyroid Disorders. Endocrinol. Metab. 2014, 29, 240–247. [Google Scholar] [CrossRef]
  14. Nishiyama, S.; Mikeda, T.; Okada, T.; Nakamura, K.; Kotani, T.; Hishinuma, A. Transient hypothyroidism or persistent hyperthyrotropinemia in neonates born to mothers with excessive iodine intake. Thyroid 2004, 14, 1077–1083. [Google Scholar] [CrossRef]
  15. Challis, J.R.; Lockwood, C.J.; Myatt, L.; Norman, J.E.; Strauss, J.F., 3rd; Petraglia, F. Inflammation and pregnancy. Reprod. Sci. 2009, 16, 206–215. [Google Scholar] [CrossRef] [PubMed]
  16. Świątkowska-Stodulska, R.; Berlińska, A.; Stefańska, K.; Zieliński, M.; Kwiatkowski, S.; Połom, J.; Andrysiak-Mamos, E.; Wydra, P.; Sworczak, K. Endocrine Autoimmunity in Pregnancy. Front. Immunol. 2022, 13, 907561. [Google Scholar] [CrossRef] [PubMed]
  17. Marazuela, M.; García-López, M.A.; Figueroa-Vega, N.; de la Fuente, H.; Alvarado-Sánchez, B.; Monsiváis-Urenda, A.; Sánchez-Madrid, F.; González-Amaro, R. Regulatory T cells in human autoimmune thyroid disease. J. Clin. Endocrinol. Metab. 2006, 91, 3639–3646. [Google Scholar] [CrossRef] [PubMed]
  18. Antonelli, A.; Ferrari, S.M.; Corrado, A.; Di Domenicantonio, A.; Fallahi, P. Autoimmune thyroid disorders. Autoimmun. Rev. 2015, 14, 174–180. [Google Scholar] [CrossRef]
  19. Iddah, M.A.; Macharia, B.N. Autoimmune thyroid disorders. ISRN Endocrinol. 2013, 2013, 509764. [Google Scholar] [CrossRef]
  20. Bogusławska, J.; Godlewska, M.; Gajda, E.; Piekiełko-Witkowska, A. Cellular and molecular basis of thyroid autoimmunity. Eur. Thyroid. J. 2022, 11, e210024. [Google Scholar] [CrossRef]
  21. Kaprara, A.; Krassas, G.E. Thyroid autoimmunity and miscarriage. Hormones 2008, 7, 294–302. [Google Scholar] [CrossRef]
  22. van Dijk, M.M.; Vissenberg, R.; Fliers, E.; Post, J.A.M.v.d.; van der Hoorn, M.-L.P.; de Weerd, S.; Kuchenbecker, W.K.; Hoek, A.; Sikkema, J.M.; Verhoeve, H.R.; et al. Levothyroxine in euthyroid thyroid peroxidase antibody positive women with recurrent pregnancy loss (T4LIFE trial): A multicentre, randomised, double-blind, placebo-controlled, phase3 trial. Lancet Diabetes Endocrinol. 2022, 10, 322–329. [Google Scholar] [CrossRef]
  23. Thangaratinam, S.; Tan, A.; Knox, E.; Kilby, M.D.; Franklyn, J.; Coomarasamy, A. Association between thyroid autoantibodies and miscarriage and preterm birth: Meta-analysis of evidence. BMJ 2011, 342, d2616. [Google Scholar] [CrossRef]
  24. Chen, L.; Hu, R. Thyroid autoimmunity and miscarriage: A meta-analysis. Clin. Endocrinol. 2011, 74, 513–519. [Google Scholar] [CrossRef]
  25. Nazarpour, S.; Tehrani, F.R.; Simbar, M.; Azizi, F. Thyroid dysfunction and pregnancy outcomes. Iran. J. Reprod. Med. 2015, 13, 387–396. [Google Scholar] [PubMed]
  26. Korevaar, T.I.M. Euthyroid Thyroperoxidase Antibody Positivity during Pregnancy, to Treat or Not to Treat? Endocrinol. Metab. 2022, 37, 387–391. [Google Scholar] [CrossRef] [PubMed]
  27. Karakosta, P.; Alegakis, D.; Georgiou, V.; Roumeliotaki, T.; Fthenou, E.; Vassilaki, M.; Boumpas, D.; Castanas, E.; Kogevinas, M.; Chatzi, L. Thyroid dysfunction and autoantibodies in early pregnancy are associated with increased risk of gestational diabetes and adverse birth outcomes. J. Clin. Endocrinol. Metab. 2012, 97, 4464–4472. [Google Scholar] [CrossRef] [PubMed]
  28. Wu, J.N.; Peng, T.; Xie, F.; Li, M.-Q. Association of thyroid dysfunction and autoantibody positivity with the risk of preterm birth: A hospital-based cohort study. BMC Pregnancy Childbirth 2022, 22, 473. [Google Scholar] [CrossRef]
  29. Yang, S.; Huang, Z.; Zhang, Y.; Li, Y.; Zhou, Y.; Guan, H.; Fan, J. Association of Maternal Thyroglobulin Antibody With Preterm Birth in Euthyroid Women. J. Clin. Endocrinol. Metab. 2025, 110, dgaf118. [Google Scholar] [CrossRef]
  30. Chen, L.; Lin, D.; Lin, Z.; Ye, E.; Sun, M.; Lu, X. Maternal thyroid peroxidase antibody positivity and its association with incidence of low birth weight in infants. Front. Endocrinol. 2023, 14, 1285504. [Google Scholar] [CrossRef]
  31. Lazarus, J.; Brown, R.S.; Daumerie, C.; Hubalewska-Dydejczyk, A.; Negro, R.; Vaidya, B. 2014 European thyroid association guidelines for the management of subclinical hypothyroidism in pregnancy and in children. Eur. Thyroid J. 2014, 3, 76–94. [Google Scholar] [CrossRef]
  32. Altomare, M.; La Vignera, S.; Asero, P. High prevalence of thyroid dysfunction in pregnant women. J. Endocrinol. Investig. 2013, 36, 407–411. [Google Scholar] [CrossRef]
  33. Vaidya, B.; Anthony, S.; Bilous, M.; Shields, B.; Drury, J.; Hutchison, S.; Bilous, R. Detection of thyroid dysfunction in early pregnancy: Universal screening or targeted high-risk case finding? J. Clin. Endocrinol. Metab. 2007, 92, 203–207. [Google Scholar] [CrossRef]
  34. Dosiou, C.; Barnes, J.; Schwartz, A.; Negro, R.; Crapo, L.; Stagnaro-Green, A. Cost-effectiveness of universal and risk-based screening for autoimmune thyroid disease in pregnant women. J. Clin. Endocrinol. Metab. 2012, 97, 1536–1546. [Google Scholar] [CrossRef]
  35. Lazarus, J.H.; Bestwick, J.P.; Channon, S.; Paradice, R.; Maina, A.; Rees, R.; Chiusano, E.; John, R.; Guaraldo, V.; George, L.M.; et al. Antenatal thyroid screening and childhood cognitive function. N. Engl. J. Med. 2012, 366, 493–501, Correction in N. Engl. J. Med. 2012, 366, 1650.. [Google Scholar] [CrossRef]
Table 1. Maternal variables of pregnant women with CAT and the control group.
Table 1. Maternal variables of pregnant women with CAT and the control group.
VariableTPOAb/TGAb
Positive, n = 27		TPOAb/TGAb
Negative, n = 47		p
Median age (years), (IQR)31.0 (24–40)28.7 (21–42)0.004
Nutritional status, n (%) 0.242
  Normal weight18 (24.3)27 (36.5)
  Overweight6 (8.1)13 (17.6)
  Obesity class I2 (2.7)4 (5.4)
  Obesity class II1 (1.7)3 (4.1)
Smoker, n (%) 0.312
  Yes13 (17.6)17 (23.0)
  No14 (18.9)30 (40.5)
Mode of iodine consumption, n (%) 0.090
  I salt12 (16.2)32 (43.2)
  I supplements4 (5.4)4 (5.4)
  I salt + supplements7 (9.5)10 (13.5)
  Non-iodized salt4 (5.4)1 (1.4)
TSH (mUI/L), median, IQR2.52 (1.55–4.50)1.69 (0.79–2.87)0.030
FT4 (pmol/L), median, IQR13.56 (11.67–16.10)15.19 (13.51–17.40)0.334
Neonatal TSH (mUI/L), median, IQR4.145 (3.17–4.90) 4.230 (3.70–4.82)0.896
UIC, mcg/dl, median, IQR159.4 (110–232)155 (90–200)1.000
Type of delivery, n (%) 0.735
  Natural12 (44.4)19 (40.4)
  Cesarian section15 (55.5)28 (59.6)
Table 2. Comparative gestational and perinatal outcomes between pregnant with/without CAT.
Table 2. Comparative gestational and perinatal outcomes between pregnant with/without CAT.
Gestational Outcomes, n (%)TPOAb/TGAb
Positive
n = 27		TPOAb/TGAb
Negative
n = 47		Total
n = 74		p
Preeclampsia 1 (3.7)3 (6.3)4 (5.4)0.623
Gestational diabetes1 (3.7)2 (4.2)3 (4.1)0.907
Spontaneous abortion3 (11.1)2 (4.2)5 (6.7)0.258
Thrombophilia 2 (7.4)79 (12.1)0.342
Perinatal outcomes, n (%)
LWB3 (11.1)1 (2.1)4 (5.4)0.099
Premature birth5 (18.5)2 (4.2)7 (9.5)0.043
Fetal distress with IUGR2 (7.4)5 (10.6)7 (9.5)0.647
Umbilical cordon pathology2 (7.4)1 (2.1)3 (4.3)0.267
Prolonged jaundice 1 (3.7)2 (4.2)3 (4.3)0.907
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Scrinic, O.; Circo, E.; Musledin, S. The Impact of Chronic Autoimmune Thyroiditis During Pregnancy on Maternal and Fetal Outcomes. Endocrines 2025, 6, 56. https://doi.org/10.3390/endocrines6040056

AMA Style

Scrinic O, Circo E, Musledin S. The Impact of Chronic Autoimmune Thyroiditis During Pregnancy on Maternal and Fetal Outcomes. Endocrines. 2025; 6(4):56. https://doi.org/10.3390/endocrines6040056

Chicago/Turabian Style

Scrinic, Olesea, Eduard Circo, and Seila Musledin. 2025. "The Impact of Chronic Autoimmune Thyroiditis During Pregnancy on Maternal and Fetal Outcomes" Endocrines 6, no. 4: 56. https://doi.org/10.3390/endocrines6040056

APA Style

Scrinic, O., Circo, E., & Musledin, S. (2025). The Impact of Chronic Autoimmune Thyroiditis During Pregnancy on Maternal and Fetal Outcomes. Endocrines, 6(4), 56. https://doi.org/10.3390/endocrines6040056

Article Metrics

Back to TopTop