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Thyroid function, autoimmunity, thyroid volume, and metabolic profile in people with Hashimoto thyroiditis

BMC Endocrine Disorders volume 24, Article number: 281 (2024) Cite this article

Abstract

Background

Hashimoto’s thyroiditis (HT) is associated with high cardiovascular risk. Thyroid volume has a notable dispersion of values in these patients. This study aims to clarify the association between thyroid antibodies, thyroid morphology, insulin resistance, and lipid profile in patients with HT.

Methods

Cross-sectional study that includes 409 subjects diagnosed with HT. We assessed thyroid function, markers of autoimmunity, and markers of cardiovascular risk. We also evaluated thyroid ultrasound and studied the correlation between all factors.

Results

Among the study population, 9.8% were male, the mean age was 56.4 ± 17.4 years, 63.7% had dyslipidemia, and 29.5% had diabetes. Patients with hypothyroidism had higher levels of anti-thyroperoxidase antibodies (TPOab), and the decreased thyroid dimensions subgroup had a higher percentage of patients taking levothyroxine (98.7%). Positive correlations were found between TPOab and volume, and negative correlations were observed between thyroid-stimulating hormone (TSH) and volume.

Conclusion

The current study reveals a complex interrelationship between cardiovascular disease risk factors, thyroid function, autoimmunity, and thyroid volume in HT. These associations may be of clinical relevance, and further studies are needed to elucidate how these findings may be used clinically to reduce the cardiovascular risk in patients with HT.

Peer Review reports

Introduction

The thyroid gland is the most affected organ by autoimmune diseases [1]. Hashimoto’s thyroiditis (HT) represents the foremost prevalent endocrine disorder and the principal cause of hypothyroidism [2]. The diagnosis of HT requires an evaluation including clinical features, serological detection of antibodies against thyroid antigens, such as thyroperoxidase and thyroglobulin, and characteristic findings on thyroid ultrasound [2]. Anti-thyroperoxidase antibodies (TPOab) emerge as the best serologic hallmark for establishing an HT diagnosis due to their specificity and sensitivity [2, 3]. TPOab are detectable in nearly 95% of HT patients while rare in healthy controls [2], in contrast to anti-thyroglobulin antibodies (Tgab), antibodies against the most abundant protein on the thyroid gland, which are positive in approximately 60 − 70% of patients (less sensitive) and are also present in a higher number and proportion of healthy controls (less specific) [2, 3].

Hypothyroidism from Hashimoto’s disease becomes more common with advancing age, with a predilection for women and individuals with concomitant autoimmune conditions [1,2,3,4]. Clinical hypothyroidism is defined as thyroid-stimulating hormone (TSH) concentrations surpassing the reference range alongside decreased free thyroxine (FT4) concentrations, while subclinical hypothyroidism delineates TSH concentrations above the reference range despite normal FT4 concentrations [4, 5].

Thyroid glands affected by autoimmune diseases can show a hypoechogenic pattern. These structural changes usually precede autoantibodies detection and other laboratory alterations [6]. Although about 50% of HT patients demonstrate normal thyroid volume, there is a notable dispersion in volume values when compared to healthy controls [7]. Patients with smaller thyroid volume have more pronounced hypothyroidism, while those with subclinical hypothyroidism predominantly have goiter [7]. In the initial phase, there is lymphocytic infiltration, culminating in thyroid volume augmentation. After that, subsequent atrophy precipitates progressive volume reduction [8].

Studies have shown that thyroid hormones play a relevant role, especially if abnormal, in cardiovascular disease, given the presence of thyroid hormone receptors in both myocardial and vascular tissue [9, 10]. Thyroid hormones are involved in lipid metabolism [9, 11], and clinical hypothyroidism is accompanied by marked changes in modifiable atherosclerotic risk factors, such as hyperlipidemia [10, 11]. Hypothyroidism is associated with increased lipid markers, particularly an elevation of serum low-density lipoproteins (LDL) and increased LDL oxidation, which is associated with atherogenesis [10], a decrease in serum high-density lipoproteins (HDL) and an increase in triglycerides [12]. Given that TPOab levels are correlated with pro-inflammatory cytokines levels, autoimmunity in HT may be associated with the progression of atherosclerosis [13]. Hypothyroidism is also associated with decreased insulin sensitivity [14,15,16].

Although several studies have established a relationship between a greater cardiac risk, evaluating lipid profile and insulin resistance, and the presence of thyroid antibodies, particularly TPOab [17,18,19,20,21], the results are not consistent. While in some analyses elevated TPOab levels are associated with a worse lipid profile [19], in other studies the presence of TPOab is not related to lipid profile [17].

Given the high prevalence of HT and the need for more evidence in this field, this study aims to clarify the association between thyroid antibodies, thyroid morphology, insulin resistance, and lipid profile in patients with HT, and, specifically, we evaluated the association between all those parameters in patients with HT comparing patients with different thyroid function between themselves, as well as patient with different thyroid dimensions. We also evaluated how thyroid dimensions are associated with all those factors. Additionally, we evaluated the correlation between the studied variables.

Methods

This study was conducted at the Endocrinology Department of São João Hospital University Center, Porto, Portugal. It represents a cross-sectional study that includes 409 subjects diagnosed with HT and followed between 2008 and 2023. All data was collected from electronic registers. HT diagnosis was established based on TPOab or Tgab levels above the reference range (5.6 UI/ml and 4.1 UI/ml, respectively) and/or ultrasound evidence of thyroiditis [2]. The study protocol, conducted according to Declaration of Helsinki, was reviewed and approved by the Ethic Commission for Health of São João Hospital University Center (411/2023). The need for informed consent was waived by the Institutional Review Board (IRB) due to the retrospective nature of the study.

The study analyzed the following parameters: thyroid function markers [TSH, FT4 and free triiodothyronine (FT3)], indices of autoimmunity (TPOab and Tgab), body mass index (BMI), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides, hemoglobin A1c, fasting glucose, C-reactive protein (CRP), folic acid, thyroid ultrasound-derived parameters (dimensions and nodules) and thyroid volume calculated using the formula: volume = maximum length x width x depth x 0,524 for each lobe and then the addiction of both lobes [22]. Drugs potentially affecting thyroid function or metabolic parameters, such as levothyroxine and medication for dyslipidemia and diabetes, were also evaluated.

Dyslipidemia was defined as TC > 240 mg/dL, LDL > 130 mg/dL, HDL < 40 mg/dL, triglycerides > 150 mg/dL, or medication usage [23]. Diabetes was characterized by fasting glucose ≥ 126 mg/dL, hemoglobin A1c ≥ 6.5%, or antidiabetic agents administration [24]. Three subgroups were created based on TSH levels at the moment of the evaluation, regardless of whether participants were receiving treatment with levothyroxine or not (hypothyroidism (n = 26), normal thyroid function (n = 346), and thyrotoxicosis(n = 37)). Three subgroups based on thyroid dimensions (decreased (n = 90), normal (n = 231), and increased (n = 49)) were also evaluated.

Statistical analyses were performed using Stata/SE 18.0. Categoric variables were described using absolute and relative frequencies and continuous variables through mean and standard deviation, if normally distributed, or median and percentiles, if not normally distributed. Continuous variables were compared using t-tests (for normally distributed data) or Wilcoxon rank sum tests (for nonnormally distributed data). Spearman correlation coefficients were used to assess the strength of association between analyzed variables, with p-values < 0.05 deemed statistically significant. Missing data were excluded from the analysis.

Results

Characteristics of the population

In the current study, we analyzed 409 subjects diagnosed with HT. Among them, 9.8% (40 subjects) were male, and the remaining 90.2% (369 individuals) were female. The mean age was 56.4 ± 17.4 years. Out of the total population, 252 subjects (63.7%) had dyslipidemia, and 119 subjects (29.5%) had diabetes. Among all the subjects, 81.6% (266 subjects) were taking levothyroxine. Regarding thyroid function, 26 (6.4%) had hypothyroidism and 37 (9.0%) had hyperthyroidism. In the hypothyroidism subgroup, only one participant had clinical hypothyroidism, while in the thyrotoxicosis subgroup, there were nine subjects with clinical hyperthyroidism. All the analyzed parameters are summarized in Table 1. Concerning the differences between BMI, being normal < 25 kg/m², overweight between 25 and 30 kg/m², and obesity ≥ 30 kg/m², they are shown in supplementary Table 1, revealing more patients with dyslipidemia, diabetes, and worse lipid profile when higher BMI. For the main variables of interest, the numbers of missing data were the following: 0 TSH, 1 FT4, 25 FT3, 18 TPOab, 19 Tgab, 202 BMI, 39 thyroid dimensions, and 34 nodules.

Table 1 Baseline characteristics of the population, such as demographic features and analyzed parameters
Full size table

Thyroid function subgroups

Regarding the differences between subgroups of thyroid function, patients with hypothyroidism had significantly higher levels of TPOab (258.5 [21.6, 756.0] UI/mL in the hypothyroidism subgroup vs. 33.3 [1.1, 208.0] in the normal thyroid function subgroup and 18.1 [1.4, 172.3] in the thyrotoxicosis subgroup, p = 0.013). There were differences in the prevalence of thyroid nodules on ultrasound, with 82.6% in the hypothyroidism subgroup without thyroid nodules. In comparison, only 45.3% in the normal thyroid function subgroup and 62.5% in the thyrotoxicosis subgroup had no thyroid nodules. The thyrotoxicosis subgroup had more subjects with decreased thyroid glands (50.0% in the thyrotoxicosis subgroup vs. 21.6% in the normal thyroid function subgroup and 26.1% in the hypothyroidism subgroup, p = 0.003). These results are shown in Table 2.

Table 2 Statistical differences between thyroid function subgroups (hypothyroidism, normal thyroid function, and thyrotoxicosis)
Full size table

Thyroid dimensions subgroups

Regarding the analysis based on the subgroups of thyroid dimensions, the normal dimensions subgroup had a lower mean age (54.2 ± 17.1 years) when compared to the decreased thyroid gland subgroup (63.7 ± 14.1 years) and the increased subgroup (61.4 ± 17.7 years, p < 0.001). The decreased thyroid gland subgroup had a higher percentage of patients taking levothyroxine (98.7%) compared to the other two subgroups (77.4% in the normal subgroup and 68.4% in the increased, p < 0.001). They also presented greater levels of FT4 when compared to the normal and increased subgroups (1.2 ± 0.3 ng/dL vs. 1.1 ± 0.2 ng/dL vs. 1.1 ± 0.3 ng/dL, p = 0.013). The increased thyroid gland subgroup had higher levels of FT3 (2.9 ± 0.4 pg/mL), greater thyroid volume (27.3 ± 13.8 mL), and multinodular pattern [35 (71.4%)] compared to the other two subgroups. This subgroup also had higher levels of Tgab (36.8 [3.0, 151.6] UI/mL). These results are shown in Table 3.

Table 3 Statistical differences between thyroid dimensions subgroups (decreased, normal, and increased)
Full size table

Study population correlations

In the entire study population, positive correlations were observed between TSH and TPOab (r = 0.1643, p = 0.0011), Tgab (r = 0.2740, p = 0.0000), TC (r = 0.1128, p = 0.0246) and triglycerides (r = 0.1927, p = 0.0001). FT4 positively correlated with hemoglobin A1c (r = 0.1289, p = 0.0174) and FT3 positively correlated with TC (r = 0.1032, p = 0.0455) and thyroid volume (r = 0.1833, p = 0.0016). Positive correlations were found between TPOab and thyroid volume (r = 0.1833, p = 0.0016). Negative correlations were observed between age and FT3 (r= -0.4749, p = 0.0000) and TPOab (r=-0.1898, p = 0.0002). FT3 negatively correlated with hemoglobin A1c (r=-0.1489, p = 0.0071). Negative correlations were also demonstrated between TPOab and fasting glucose (r=-0.1041, p = 0.0410), and Tgab negatively correlated with HDL (r=-0.1041, p = 0.0412). All these results are shown in the supplementary table 2 A. Scatterplots of the significant associations between variables are represented in supplementary Fig. 1.

Thyroid function subgroups correlations

In the hypothyroidism subgroup, there were positive correlations between TSH and Tgab (r = 0.6003, p = 0.0015) and triglycerides (r = 0.4967, p = 0.0136). TPOab positively correlated with thyroid volume (r = 0.7750, p = 0.0000). Negative correlations were observed between age and FT3 (r=-0.5090, p = 0.0079) and thyroid volume (r=-0.4929, p = 0.0198). FT3 negatively correlated with folic acid (r=-0.4722, p = 0.0307). These results are shown in the supplementary table 2B.

In the normal thyroid function subgroup, TSH positively correlated with fasting glucose (r = 0.1128, p = 0.0374). A positive correlation was found between FT4 and hemoglobin A1c (r = 0.1255, p = 0.0342). Positive correlations were demonstrated between FT3 and TC (r = 0.1965, p = 0.0004), LDL (r = 0.1615, p = 0.0040) and thyroid volume (r = 0.1611, p = 0.0114). TPOab positively correlated with LDL (r = 0.1333, p = 0.0170) and thyroid volume (r = 0.1355, p = 0.0325). Age negatively correlated with FT3 (r=-0.4815, p = 0.0000) and TPOab (r=-0.1462, p = 0.0078). A negative correlation was demonstrated between TSH and thyroid volume (r=-0.1950, p = 0.0015). FT3 negatively correlated with hemoglobin A1c (r=-0.1997, p = 0.0009), CRP (r=-0.1996, p = 0.0393), and folic acid (r=-0.1481, p = 0.0209), as well as Tgab negatively correlated with TC (r=-0.1213, p = 0.0298), and HDL (r=-0.1309, p = 0.0182). These results are shown in the supplementary Table 2 C.

In the thyrotoxicosis subgroup, a positive correlation was demonstrated between age and TSH (r = 0.4140, p = 0.0109). BMI and TPOab were also positively correlated (r = 0.5581, p = 0.0306). Positive correlations were found between TSH and fasting glucose (r = 0.3364, p = 0.0418). FT4 positively correlated with hemoglobin A1c (r = 0.4502, p = 0.0111) and CRP (r = 0.6138, p = 0.0149). A positive correlation was demonstrated between FT3 and TPOab (r = 0.3963, p = 0.0184). A negative correlation was observed between age and FT3 (r=-0.5462, p = 0.0007) and TPOab (r=-0.3382, p = 0.0469). FT3 negatively correlated with TC (r=-0.3601, p = 0.0364) and LDL (r=-0.3611, p = 0.0359). These results are shown in the supplementary table 2D. Scatterplots of the significant associations between variables are represented in supplementary Fig. 1.

Discussion

In the current study, we observed a predominance of female subjects, consistent with existing literature indicating a higher prevalence of thyroid disorders in women compared to men [2]. A considerable proportion of the current study population had dyslipidemia, aligning with previous research linking thyroid dysfunction to alterations in lipid metabolism [9,10,11,12, 25].

Hyperthyroidism was present in 9.0% of the total population, a proportion that may be influenced by overtreatment, given that 81,6% of the subjects were taking levothyroxine.

HT comprises a spectrum of thyroid volume, ranging from goiter on one end to an atrophic thyroid gland on the other [7, 26]. Previous studies have shown that smaller thyroid volumes may be associated with clinical hypothyroidism, whereas increased thyroid gland may be often correlated with subclinical hypothyroidism [26]. The higher prevalence of decreased thyroid gland volume observed in the thyrotoxicosis subgroup may be attributed to the more advanced stage of the disease [27], with the need for supplementation. Furthermore, it is plausible that a significant portion of this population was overtreated, leading to a further reduction in thyroid gland volume [7]. Our results regarding overtreatment in chronic treatment with levothyroxine are in line with those described in previous cohorts of patients with HT and hypothyroidism [28].

Our investigation revealed positive correlations between TSH and TC and triglycerides, consistent with previous research [16, 29,30,31,32]. Additionally, FT3 positively correlated with TC, consistent with findings reported in other studies [12]. This association was also observed within the normal thyroid function subgroup. However, negative correlations were found in the thyrotoxicosis subgroup between FT3 and TC and LDL, as observed by other studies [30, 32, 33].

Interestingly, there was also found a positive correlation within the normal thyroid function subgroup between FT3 and LDL, which contradicts previous findings showing a negative correlation between those two parameters [32].

FT3 exhibited a negative correlation with folic acid levels within the hypothyroidism subgroup and the normal thyroid function subgroup, a relevant finding given the lack of clear data in the literature. FT3 also exhibited a negative correlation with CRP within the normal thyroid function subgroup, also demonstrated by Christ-Crain M et al. [34].

FT4 exhibited a positive correlation with hemoglobin A1c, observed not only in the total population but also within the normal thyroid function subgroup and in the thyrotoxicosis subgroup, suggesting an increase in hemoglobin A1c levels with rising FT4 levels. Previous studies have found opposing conclusions showing higher hemoglobin A1c levels in patients with clinical hypothyroidism compared to control subjects [35, 36]. FT3 demonstrated a negative correlation with hemoglobin A1c, both in the total population and the normal thyroid function subgroup, which is relevant as most previous studies typically rely solely on fasting glucose levels to assess cardiovascular risk and diabetes.

The association between thyroid volume and other parameters remains understudied. In the current study, both in the total subgroup and the normal thyroid function subgroup, FT3 positively correlated with thyroid volume. Additionally, positive correlations were discerned between TPOab and thyroid volume, observed both in the total population and within the hypothyroidism subgroup, as well as the normal thyroid function subgroup. These findings, which are also shown by Carle et al. [37], were expected since higher TPOab values indicate a more active disease, with inflammation and lymphocytic infiltration. TSH showed a negative correlation with thyroid volume in the normal thyroid function subgroup, consistent with the findings of Giusti M. et al. [7].

Furthermore, within the normal thyroid function subgroup, a negative correlation was identified between age and thyroid volume. Interestingly, a separate study reported no relationship between age and thyroid volume in patients with HT [37].

Additionally, few studies have examined the correlation between autoimmunity and parameters such as those analyzed in the current study. Negative correlations were observed between TPOab and fasting glucose levels. This finding holds significance, as previous investigations have not identified any significant correlation between blood glucose levels and thyroid autoantibodies [19]. In the normal thyroid function subgroup, a negative correlation was observed between age and TPOab levels. In the thyrotoxicosis subgroup, there was a positive correlation between BMI and TPOab levels, suggesting an association wherein higher levels of TPOab correspond to higher BMI values, as also demonstrated by Wu Y et al. [19].

Furthermore, a negative correlation was noted between Tgab and HDL levels in the total population and within the normal thyroid function subgroup. Prior research has shown higher LDL levels in individuals positive for Tgab compared to controls [19], a relationship also corroborated by Cunha C et al. [3]. In the normal thyroid function subgroup, we observed a negative correlation between Tgab and TC, a correlation also documented by Cunha C et al. [3], but that contrasts with previous studies indicating positive correlations between these parameters [38]. In the hypothyroidism subgroup, positive correlations were noted between TSH and Tgab, suggesting an elevation in Tgab levels with higher TSH levels. However, a previous study reported no association between TSH and Tgab levels [39]. Moreover, TPOab also exhibited positive correlations with LDL in the normal thyroid function subgroup, as documented in other studies [38]. Kumar M et al. similarly concluded that patients with elevated TPOab levels have an increased incidence of dyslipidemia [40].

Additionally, in the normal thyroid function subgroup, TSH displayed a positive correlation with fasting glucose levels, a noteworthy observation given a prior study that reported no association between these two parameters [41]. This correlation was also evident within the thyrotoxicosis subgroup.

Therefore, the current study complements the already existing information about the relationship between HT and autoimmunity, as well as cardiovascular risk factors [19, 30, 38].

We acknowledged relevant limitations in the current study. In the first place, it is a cross-sectional study, which limits the directionality interpretation of the associations found. Second, the study had more than 90% female patients among participants, which may limit the generalizability of these results to male patients but reflects the higher prevalence of HT among women. Finally, this was a single-center study, which may also limit the generalizability for other contexts. Despite these limitations, the sample size of the current study was larger than most previous studies, which reinforces its relevance.

In conclusion, the current study shows a complex interrelationship between cardiovascular disease risk factors, thyroid function, autoimmunity, and thyroid volume in HT. These associations may be of clinical relevance, and further studies are needed to elucidate how these findings may be clinically used to reduce the cardiovascular risk in patients with HT.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Funding

The authors did not receive support from any organization for the submitted work.

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Author notes

  1. Bruna Couto and Celestino Neves are equally contributing first authors of this paper.

Authors and Affiliations

  1. Faculty of Medicine, University of Porto, Porto, Portugal

    Bruna Couto & Celestino Neves

  2. Department of Endocrinology, Diabetes and Metabolism, ULS São João, Porto, Portugal

    Celestino Neves & João Sérgio Neves

  3. Instituto de Investigação e Inovação da Saúde, University of Porto, Porto, Portugal

    Celestino Neves

  4. Departament of Surgery and Physiology, Cardiovascular Investigation Unit, Faculty of Medicine, University of Porto, Porto, Portugal

    João Sérgio Neves

  5. Basic and Clinical Immunology, Department of Pathology, Faculty of Medicine, University of Porto, Porto, Portugal

    Luís Delgado

  6. Laboratory of Immunology, Department of Clinical Pathology, ULS São João, Porto, Portugal

    Luís Delgado

  7. CINTESIS@RISE, Faculdade Medicina da U. Porto, Porto, Portugal

    Luís Delgado

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  1. Bruna Couto
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  3. João Sérgio Neves
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  4. Luís Delgado
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Contributions

The study was designed by BC, JSN, and CN. Data collection was performed by BC. Statistical analysis was performed by JSN and BC, as well as the interpretation of results. The draft of the manuscript was prepared by BC and CN, and all authors read and reviewed the final version. All authors approved the final version of the manuscript.

Corresponding author

Correspondence to Bruna Couto.

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Ethical approval

The study protocol, conducted according to Declaration of Helsinki, was reviewed and approved by the Ethic Commission for Health of São João Hospital University Center. The need for informed consent was waived by Institutional Review Board (IRB) due to the retrospective nature of the study.

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Not applicable.

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Couto, B., Neves, C., Neves, J.S. et al. Thyroid function, autoimmunity, thyroid volume, and metabolic profile in people with Hashimoto thyroiditis. BMC Endocr Disord 24, 281 (2024). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12902-024-01765-4

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Keywords

BMC Endocrine Disorders

ISSN: 1472-6823

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