Iodinated contrast media (ICM)-induced thyroid dysfunction: a review of potential mechanisms and clinical management

Abstract

Iodinated contrast media (ICM) are extensively utilized in medical imaging to enhance tissue contrast, yet their impact on thyroid function has attracted increasing attention in recent years. ICM can induce thyroid dysfunction, with reported prevalence ranging from 1 to 15% and a higher incidence observed in individuals with pre-existing thyroid conditions or other risk factors like age, gender, underlying health issues, and repeated ICM exposure. This review summarized the classification of ICM and the potential mechanisms, risk assessment, and clinical management of ICM-induced thyroid dysfunction, especially in vulnerable populations such as pregnant women and elderly patients. Despite advancements that have enriched our understanding of the pathophysiology and treatment of ICM-induced thyroid dysfunction, critical knowledge gaps remain, such as the long-term effects of ICM on thyroid function, the dose–response relationship between ICM volume and thyroid dysfunction risk, and the ecological impacts of ICM. Therefore, further exploration of the underlying mechanisms of ICM-induced thyroid dysfunction and optimization of the management strategies will be crucial for the safe and effective use of ICM in clinical practice, and collaborative efforts between clinicians and researchers are essential to ensure that the risks of thyroid dysfunction do not outweigh the benefits of imaging.

Introduction

Iodine, a crucial element for thyroid hormone synthesis, can disrupt thyroid function when present in excess, causing iodine-induced hypothyroidism or hyperthyroidism [1]. Iodinated contrast media (ICM) are essential radiopaque agents widely used in modern radiology, particularly in computed tomography (CT) and angiography, for their ability to enhance tissue contrast. By improving diagnostic accuracy, ICM supports the detection and planning of treatment for various conditions, including vascular diseases, tumors, and other pathologies. Despite their significant role in clinical practice, ICM use carries inherent risks, particularly regarding thyroid function [2, 3]. Given the thyroid gland’s sensitivity to iodine, ICM can trigger thyroid dysfunctions, including hypothyroidism, hyperthyroidism, and autoimmune disorders such as Hashimoto’s thyroiditis and Graves’ disease [4–7]. Studies have reported the prevalence of ICM-induced thyroid dysfunction to range from 1 to 15% [8], with a higher incidence among individuals with pre-existing thyroid conditions or other risk factors like age, gender, underlying health issues, and repeated ICM exposure [9].

The potential impact of ICM on thyroid function emphasizes the need for clinicians to understand its effects and carefully monitor high-risk populations. ICM-induced thyroid dysfunction may present with various symptoms, such as fatigue, weight fluctuations, cardiovascular disturbances, and mood changes, that can severely affect both physical and mental health if untreated. For instance, untreated hypothyroidism may lead to metabolic deceleration, weight gain, and depression, while hyperthyroidism can cause weight loss, increased heart rate, anxiety, and heat intolerance [6, 7]. Pharmacovigilance studies have increasingly highlighted thyroid-related adverse events following ICM administration [5], stressing the importance of awareness among healthcare providers. However, the mechanisms underlying ICM-induced thyroid dysfunction are complex, including direct and indirect pathways, such as iodine metabolism alterations, inhibition of thyroid hormone synthesis, thyroid gland autoregulation, peripheral thyroid hormone metabolism, and potential autoimmune responses [4]. Specific populations, such as children and those with a thyroid disease history, are particularly vulnerable [10].

Therefore, understanding these mechanisms is crucial for developing strategies to minimize the impact of ICM on thyroid health and ensure proactive management in susceptible groups [1, 5, 11, 12]. This review aims to comprehensively examine the effects of ICM on thyroid function, offering insights into the underlying mechanisms, risk assessment, and clinical management strategies. By synthesizing the latest evidence, we seek to inform clinical decision-making, optimize patient management for those at risk, and contribute to the development of preventive and safe imaging practices.

Types of ICM and their mechanisms of action

ICM are primarily classified into ionic and non-ionic types, and the differences between the two types of ICM are shown in Table 1. Ionic ICM, such as diatrizoate and ioxaglate, have higher osmolality and dissociate into charged particles, thereby increasing the risk of adverse reactions, including contrast-induced nephropathy (CIN) and allergic responses. For instance, ioxaglate has been shown to induce more apoptosis in renal tubular cells, particularly in diabetic patients, compared to non-ionic counterparts [13]. Conversely, non-ionic agents like iohexol and iodixanol do not dissociate and exhibit lower osmolality, resulting in fewer side effects and improved patient tolerance during imaging procedures. This makes them the preferred choice in clinical practice. Some studies suggest that iodixanol may pose a slightly lower risk for CIN than low-osmolar ionic agents, although the clinical significance of this difference remains debated [14]. The selection of an appropriate ICM is influenced by multiple factors, including the patient’s renal function, the specific imaging modality or diagnostic requirements, and any history of allergic reactions [13–15]. For patients with compromised renal function, non-ionic ICM are generally preferred to mitigate the risk of CIN [13, 14]. Overall, non-ionic agents are preferentially recommended for patients with renal impairment or a history of iodine-related allergies due to their reduced immunogenic potential and maintained diagnostic efficacy [16–18]. Additionally, the pharmacokinetics of ICM, including their distribution, metabolism, and excretion, play a crucial role in their efficacy and safety [17]. Understanding these parameters helps clinicians select the most suitable agent for each patient, thereby minimizing risks while maximizing diagnostic yield.

Table 1.

Difference between the two types of ICM

Parameter	Ionic ICM	Non-ionic ICM
Representative drugs	e.g., diatrizoate, ioxaglate	e.g., iohexol, iodixanol
Chemical structure	Dissociate into charged particles in solution	Non-dissociating, more stable moleculr structure
Osmolality	Higher osmolality	Lower osmolality
Adverse reactions	Higher risk of adverse reactions, such as discomfort during injection, nephrotoxicity, and HSRs	Better patien tolerance, reduced risk of nephrotoxicity and HSRs
Renal safety	Avoid in renal impairment	Preferred in CKD patients
Cytotoxicity	Induces apoptosis in renal tubular cells	Reduced oxidative stress and cellular damage
Clinical preference	Limited use due to side effects	First-line for high-risk populations

ICM, iodinated contrast media; HSRs, hypersensitivity reactions; CKD, chronic kidney disease

ICM are essential in medical imaging, primarily due to their biochemical properties, particularly the high atomic number of iodine, which enhances X-ray absorption and radiopacity. Upon administration, ICM are rapidly distributed throughout the vascular system and predominantly excreted unchanged via the kidneys, highlighting the importance of assessing renal function to mitigate risks of nephrotoxicity, especially in patients with pre-existing kidney issues [17, 19–21]. The physicochemical properties of ICM, including solubility, viscosity, and osmolality, significantly influence their behavior in biological systems. High water solubility and viscosity can hinder renal clearance and exacerbate acute kidney injury by increasing cytotoxic retention [22, 23]. Furthermore, osmolality variations between iso-osmolar and low-osmolar formulations affect renal kinetics and can lead to cellular injury markers, such as vacuole formation in renal cells [23]. Cytotoxicity is another significant concern associated with ICM. In vitro studies have demonstrated that elevated concentrations of ICM can diminish endothelial cell viability and promote apoptosis, highlighting the necessity for careful consideration of the concentration and formulation of ICM used in clinical practice to minimize adverse effects [24]. Additionally, previous studies have indicated the potential for ICM to induce oxidative stress, which can lead to cellular damage and adverse reactions. For example, the contrast agent 2,3,5-triiodobenzoic acid (TIBA) has been shown to induce cell death in tumor cells by generating reactive oxygen species [25]. Emerging alternatives, such as nanosized triiodoaniline derivatives, show promise in reducing cytotoxicity while maintaining effective imaging capabilities [26]. Therefore, understanding these biochemical characteristics is critical for optimizing ICM use and ensuring patient safety during diagnostic procedures. Ongoing research is essential to optimize these properties and develop new formulations that enhance diagnostic capabilities while minimizing risks.

Iodine, an essential micronutrient, plays a pivotal role in synthesizing thyroid hormones, namely thyroxine (T4) and triiodothyronine (T3), which are crucial for regulating metabolism, growth, and development. The thyroid gland’s absorption of iodine directly influences hormone production. Insufficient iodine intake may lead to hypothyroidism and goiter, whereas excessive intake may lead to hyperthyroidism and an increased risk of thyroid cancer [27–30], particularly in populations with prior low iodine levels [29], highlighting the complex relationship between iodine levels and thyroid pathology. The use of ICM in imaging has raised concerns regarding their impact on thyroid function, especially in individuals with pre-existing thyroid conditions or those receiving high doses of contrast [31]. Studies indicate that excessive exposure to ICM can alter thyroid hormone levels and function, necessitating vigilance in monitoring thyroid health among at-risk populations. Genetic predispositions and environmental conditions also modulate the thyroid gland’s response to iodine. For example, single-nucleotide polymorphisms in the thyroid-stimulating hormone receptor (TSHR) gene may further modulate this response [32]. Additionally, the role of ion transporters in mediating iodine uptake and metabolic processes within thyroid cells further complicates the relationship between iodine and thyroid health [33]. Overall, the relationship between iodine and the thyroid gland is characterized by a delicate balance. While ICM are indispensable in imaging, their implications for thyroid health require careful patient assessment and monitoring to ensure safety and effective management of thyroid disorders, particularly in those with a history of thyroid disease [34].

Potential mechanisms of thyroid dysfunction induced by ICM

ICM may precipitate thyroid dysfunction, clinically presenting as hyperthyroidism or hypothyroidism (Table 2), with heightened susceptibility observed in individuals with pre-existing thyroid disorders and/or chronic exposure to iodine-deficient environments [8]. Hyperthyroidism is more common in patients with underlying conditions such as nodular goiter or latent Graves’ disease, especially in iodine-deficient areas. Conversely, hypothyroidism often occurs in patients with autoimmune thyroiditis, particularly in regions with adequate iodine supply. The mechanisms behind these dysfunctions include the perturbation of iodide uptake by the thyroid, occurring independently of free iodide levels in ICM [35]. Prophylactic measures, such as the administration of antithyroid drugs, may reduce the incidence of ICM-induced hyperthyroidism [36], and monitoring thyroid function before and after ICM exposure is crucial, especially in at-risk populations [37].

Table 2.

Comparison of the ICM-induced hyperthyroidism and hypothyroidism

Feature	Hyperthyroidism	Hypothyroidism
Mechanism	Jod-Basedow effect (iodine excess stimulates hormone release)	Wolff-Chaikoff effect (transient suppression of hormone synthesis)
Risk factors	Nodular goiter, latent Graves’ disease, high baseline FT4 level, iodine-deficient regions, age over 60, male gender, a family history of thyroid diseases	Autoimmune thyroiditis, iodine-sufficient regions, high dose of ICM, pre-existing thyroid dysfunction, a history of thyroid surgery
Key biomarkers	TSH↓, FT4/FT3↑	TSH↑, FT4↓
Clinical management	Antithyroid medications (e.g., methimazole or propylthiouracil), β-blockers, radioiodine therapy or surgical intervention	Levothyroxine replacement
Long-term outcomes	May persist even after one year	Mostly transient

ICM, iodinated contrast media; TSH, thyroid-stimulating hormone; FT4, free thyroxine; FT3, free triiodothyronine

Impact of iodine load on thyroid function

Iodine load from ICM significantly impacts thyroid function by influencing hormone synthesis. Iodine is essential for thyroid hormone production, and its excess can lead to both hyperthyroidism and hypothyroidism. Mechanisms include alterations in iodine uptake and metabolism by thyroid cells and potential cytotoxic effects of ICM [38, 39]. Acute iodine load may precipitate hyperthyroidism through the Jod-Basedow phenomenon, predominantly affecting individuals with autonomously functioning thyroid nodules or specific pre-existing thyroid pathologies, particularly Graves’ disease in remission and multinodular goiter with functional autonomy, wherein excessive iodine exposure bypasses normal regulatory mechanisms to drive unregulated hormone synthesis. Conversely, excessive iodine can trigger the Wolff-Chaikoff effect, temporarily inhibiting hormone synthesis, which may lead to subsequent hypothyroidism [38, 40, 41]. In patients with ischemic heart disease (IHD), ICM administration has been linked to increased hyperthyroidism prevalence, positively correlated with baseline free T4 levels, thyroid nodules, and family history of thyroid diseases [42]. Some patients continue to exhibit hyperthyroidism even one year post-ICM exposure [42], indicating a potential long-term effect of iodine load on thyroid function. Additionally, populations with WHO-recommended iodine intake (median urinary iodine concentration 100–199 μg/L for adults) and normal thyroid functionmay may still experience subtle thyroid function changes due to fluctuations in iodine levels [43], suggesting that the thyroid gland may be sensitive to iodine level variations, particularly relevant in ICM administration. The relationship between iodine load and thyroid dysfunction is complex, necessitating vigilant monitoring and individualized management strategies to mitigate potential adverse effects on thyroid health.

Direct toxicity of ICM on thyroid tissue

ICM can cause significant damage to thyroid tissue through direct cytotoxicity, apoptosis, and inflammation. Studies show that ICM disrupt iodide uptake by reducing the expression of the sodium-iodide symporter, impairing hormone synthesis and causing cellular stress [35]. This disruption triggers a cascade of oxidative stress and inflammatory responses, further exacerbating thyroid cell injury [44]. Apoptosis is a crucial mechanism, as ICM exposure has been associated with increased levels of reactive oxygen species and subsequent activation of apoptotic signaling cascades [3, 45]. In addition to direct cellular effects, ICM interaction with thyroid hormones and their regulatory pathways may exacerbate inflammatory responses, contributing to further tissue damage, including fibrosis [44]. These combined effects may lead to both acute and chronic thyroid dysfunction, potentially resulting in long-term consequences for patients undergoing imaging procedures utilizing ICM [35, 39, 45]. The evidence suggests that ICM not only disrupt iodide uptake but also induce apoptosis and inflammatory responses in thyroid tissue, highlighting the need for careful monitoring of thyroid function in patients undergoing ICM administration, particularly those with pre-existing thyroid conditions or at risk for thyroid dysfunction [35, 44]. Understanding these mechanisms can guide risk assessment and management strategies, helping to minimize adverse thyroid outcomes in clinical settings [1].

Autoimmune reactions and thyroid dysfunction induced by ICM

ICM have been implicated in the induction of autoimmune thyroid diseases, particularly in genetically predisposed individuals. The introduction of exogenous iodine can trigger an immune response, potentially leading to conditions such as Graves’ disease and Hashimoto’s thyroiditis [3]. This autoimmune response may be explained by molecular mimicry, where iodine-containing compounds resemble thyroid antigens, prompting the immune system to attack thyroid tissue [46, 47]. Clinical studies indicate an increase in thyroid autoantibodies following ICM exposure, suggesting a significant link between contrast administration and autoimmune thyroid dysfunction [3, 11, 46]. Moreover, ICM exposure can result in varying degrees of thyroid dysfunction, from transient hyperthyroidism to chronic hypothyroidism [39, 48, 49]. Notably, cases of thyrotoxicosis secondary to destructive thyroiditis have been reported after ICM administration, characterized by the rapid release of preformed thyroid hormones, which can result in significant clinical symptoms, especially in patients with unstable cardiac conditions [50]. Delayed hypersensitivity reactions to ICM can manifest as various cutaneous symptoms, which may be underdiagnosed due to misattribution to other medications [51]. A multicenter study involving over 196,000 patients revealed a prevalence of hypersensitivity reactions to ICM, with certain risk factors identified, including a history of drug allergies and previous hypersensitivity reactions [52]. Understanding these associations is crucial for developing preventive strategies and management protocols and ensuring optimal care for patients undergoing imaging procedures involving ICM. Continued research is essential to elucidate the mechanisms behind these reactions and to enhance patient safety in clinical practice.

Risk assessment and clinical management of ICM-induced thyroid dysfunction

Risk assessment strategies for patients receiving ICM

ICM use in radiographic procedures can lead to thyroid dysfunction, particularly in vulnerable populations, highlighting the need for thorough risk assessment strategies [53]. Studies have shown a significant link between ICM exposure and the onset of thyroid disorders, particularly hypothyroidism, even in individuals without prior thyroid issues. For example, a large-scale study in Taiwan reported an adjusted hazard ratio of 1.17 for developing thyroid disorders following ICM exposure [54], highlighting the importance of proactive monitoring. Although the prevalence of iodine-induced hyperthyroidism is generally low, it remains a clinically relevant concern [55], even in pediatric populations, where thyroid function monitoring is critical, especially for those with congenital heart disease who undergo multiple imaging studies. Additionally, research on children has identified transient decreases in thyroid-stimulating hormone (TSH) levels following ICM exposure [56]. A comprehensive risk assessment protocol should include pre-procedure screening to identify patients with a history of thyroid disorders, autoimmune conditions, or medications (such as amiodarone) known to affect thyroid function [11]. Baseline thyroid function tests, including serum TSH, free triiodothyronine (FT3), and free thyroxine (FT4) levels, are essential, particularly for high-risk groups such as the elderly or those with renal impairment [38]. Post-procedure follow-up should reassess thyroid function within weeks to detect any abnormalities early. Educating patients on recognizing potential symptoms of thyroid dysfunction, such as weight changes and fatigue, facilitates timely detection. In cases of abnormal test results, prompt referral to an endocrinologist for evaluation and management may be necessary [57]. By adopting these strategies, healthcare providers can mitigate the risks associated with ICM-induced thyroid dysfunction, improving patient outcomes in radiographic imaging.

Monitoring and management of ICM-induced thyroid dysfunction

Effective monitoring and management of ICM-induced thyroid dysfunction are essential for patient safety [57]. After ICM exposure, an iodine load can initiate the Wolff-Chaikoff effect, temporarily reducing thyroid hormone synthesis. Infants and patients with compromised thyroid function may experience prolonged hypothyroidism if they cannot adequately escape this effect [58]. For instance, a case involving a preterm infant demonstrated severe hypothyroidism after enteral ICM administration, highlighting the need for vigilant monitoring in vulnerable groups [58]. Thyroid function, especially TSH and free thyroid hormone levels, should be reassessed within the first three months following ICM exposure, as this period presents the highest incidence of dysfunction [5, 56]. Clinicians should monitor for symptoms of thyroid dysfunction, such as fatigue, weight fluctuations, and cognitive changes [5]. Management strategies should be tailored to the severity of the dysfunction. Mild cases may only require observation, while moderate to severe cases may necessitate treatment, including levothyroxine replacement for hypothyroidism or antithyroid drugs for hyperthyroidism [38, 53, 58]. Clinicians should also be aware of potential delayed allergic reactions to ICM, which may complicate thyroid management [59]. A multidisciplinary approach involving endocrinologists and allergists can enhance patient care in these cases. Systematic monitoring and timely interventions are crucial to minimizing risks associated with ICM and promoting better health outcomes.

Treatment options for ICM-induced thyroid dysfunction

Managing ICM-induced thyroid dysfunction requires an individualized approach based on the patient’s condition and overall health. For iodine-induced hyperthyroidism, antithyroid medications such as methimazole or propylthiouracil may be prescribed, along with beta-blockers to alleviate symptoms like tachycardia [60, 61]. In severe cases, radioactive iodine therapy or surgical intervention may be necessary. In severe cases, radioiodine therapy or surgical intervention may be necessary. However, radioiodine therapy may be precluded for several months by iodine excess from sources like ICM, as residual iodine competitively inhibits thyroid uptake and diminishes the efficacy of radioiodine therapy [62, 63]. In such cases, urinary iodine monitoring must confirm biochemical clearance before radioiodine therapy initiation, and alternative treatments may need to be considered temporarily, such as antithyroid drugs or even surgical options, until radioiodine therapy becomes viable [64, 65]. Hypothyroidism generally necessitates levothyroxine replacement, with dose adjustments guided by periodic TSH/FT4 monitoring [1, 61]. Patient education is crucial in recognizing thyroid dysfunction symptoms and is essential to support early detection and intervention [61, 66]. For high-risk individuals, alternative imaging methods such as MRI or ultrasound should be considered to avoid ICM exposure [67]. Regular follow-up and thyroid function testing are critical for those with prior thyroid dysfunction after ICM exposure, ensuring any persistent or emerging issues are promptly addressed [68]. By integrating monitoring, treatment, patient education, and alternative imaging options, healthcare providers can manage ICM-induced thyroid dysfunction effectively, leading to better patient outcomes [69].

Best practices for ICM use to avoid thyroid dysfunction

Adhering to best practices for ICM use is essential to minimize thyroid dysfunction risks in patients undergoing imaging (Fig. 1). Clinicians should follow established guidelines, using ICM judiciously and only when its diagnostic benefits outweigh potential risks [57, 70]. Pre-procedural thyroid screening should be standard for high-risk individuals, such as those with prior thyroid disease or renal impairment [1, 58, 71]. Using the lowest effective ICM dose and considering non-iodinated alternatives when feasible can also reduce risk. Proper hydration before and after ICM administration supports renal function and indirectly reduces thyroid complications [58, 72]. Prioritizing iso-osmolar contrast agents further mitigates risks [73, 74]. Educating patients on potential side effects and scheduling follow-up thyroid function tests, particularly for at-risk groups, are vital steps in patient care [55, 58]. Following updated clinical guidelines, such as those from the National Institute for Health and Care Excellence, can help providers implement best practices in ICM use. Continued research on the effects of ICM on thyroid function will aid in refining these guidelines and improve patient safety [55, 74].

Fig. 1.

The flow diagram of the clinical management algorithm for ICM-induced thyroid dysfunction

ICM-induced thyroid dysfunction in vulnerable populations

Patients with pre-existing thyroid disease

Patients with underlying thyroid conditions are particularly vulnerable to ICM-induced thyroid dysfunction. ICM can disrupt iodide uptake, exacerbating both hyperthyroidism and hypothyroidism [54]. In individuals with autoimmune thyroid diseases, particularly Graves’ disease, ICM exposure may transiently elevate thyroid hormone levels, worsening hyperthyroid symptoms [4, 75, 76]. Those with a history of thyroid disorders are at higher risk for developing thyroid dysfunction post-contrast exposure, highlighting the need for careful monitoring of thyroid function both before and after imaging procedures [5, 77]. The excessive iodine load from ICM can induce iodine-induced hyperthyroidism or exacerbate pre-existing hyperthyroidism, particularly in patients with autoimmune conditions like Hashimoto’s thyroiditis. Evidence suggests that repeated exposure to ICM may impair the thyroid gland’s auto-regulatory mechanisms, leading to significant hormonal fluctuations and long-term dysfunction [1, 4, 54]. For patients with known thyroid dysfunction, thorough thyroid function assessments pre- and post-ICM administration are critical. Adjustments in thyroid hormone replacement therapy may be necessary to maintain euthyroid status. A multidisciplinary approach, including endocrinology consultation, is essential to promptly address any thyroid abnormalities, ensuring optimal outcomes and minimizing complications.

Pregnant women

The use of ICM during pregnancy carries potential risks for both maternal and fetal thyroid function [11]. The fetal thyroid becomes active early in gestation, and excess iodine from ICM may impair normal hormone synthesis, increasing the risk of fetal hypothyroidism or congenital thyroid disorders [78]. Maternal thyroid dysfunction, compounded by ICM exposure, is associated with neurodevelopmental risks in offspring, including an increased likelihood of autism spectrum disorders [79]. Given these risks, clinicians must carefully evaluate the necessity of ICM-based imaging during pregnancy. Whenever possible, non-iodinated imaging modalities should be preferred [80]. If ICM use is unavoidable, close monitoring of thyroid function in both the mother and newborn is essential to detect and manage any dysfunction promptly. Special attention is warranted for first-trimester exposures, as the developing fetal thyroid is particularly sensitive during this period [11]. Long-term effects of in-utero ICM exposure remain unclear, further emphasizing the need for caution. A collaborative, multidisciplinary approach involving obstetricians and endocrinologists ensures comprehensive care. Informed decision-making and individualized management are crucial to balance diagnostic needs with the safety of both mother and fetus [80].

Elderly population

Elderly patients are particularly susceptible to ICM-induced thyroid dysfunction due to age-related physiological changes, a higher prevalence of thyroid disorders, and altered pharmacokinetics [5, 81, 82]. Thyroid dysfunction affects over 10% of older adults [83], and ICM exposure may exacerbate pre-existing thyroid abnormalities. This population is at increased risk for iodine-induced hypothyroidism or hyperthyroidism, particularly in those with baseline thyroid disorders. In clinical settings, procedures such as coronary angiography, commonly performed in elderly patients with IHD, are associated with elevated hyperthyroidism risks post-ICM exposure. A study of 810 IHD outpatients reported an increase in hyperthyroidism prevalence from 7.2 to 10% following ICM administration, and key predictors included baseline FT4 levels, thyroid nodules, and a family history of thyroid disorders [42]. The presence of comorbidities and polypharmacy further complicates thyroid management in older adults, as interactions between ICM and medications may necessitate individualized dose adjustments [84]. Pre-procedural thyroid screening and post-procedural monitoring are essential for early detection and timely intervention. Proactive strategies, including individualized hormone therapy adjustments and interdisciplinary collaboration, are critical to optimizing care and ensuring safe imaging practices in this vulnerable population [82, 85].

Pediatric populations

Children are particularly vulnerable to ICM-Induced thyroid dysfunction due to the developing nature of their endocrine systems. While the effects of ICM in adults, such as exacerbation of hyperthyroidism, are well-documented [42], the impact in infants and young children remains a crucial yet underexplored area. Infants born to mothers with thyroid disorders or iodine imbalance are especially susceptible, as maternal thyroid function directly influences fetal development and long-term neurocognitive outcomes [86]. Disruption in maternal thyroid hormone transfer during pregnancy can impair neurological development [86], emphasizing the importance of managing thyroid health in both mother and child. Maintaining appropriate iodine intake is critical for pediatric thyroid function. While iodine is essential for thyroid hormone synthesis, excessive iodine exposure, particularly in regions with routine iodine supplementation, can disrupt thyroid function, leading to conditions such as subclinical hypothyroidism [87, 88]. These disruptions highlight the delicate balance required in iodine management. Pediatric patients exposed to ICM, especially those with underlying thyroid issues or a maternal history of thyroid dysfunction, required close monitoring of thyroid hormone levels [89]. Early identification and intervention are vital to preventing adverse effects on growth, metabolism, and cognitive development. Given the variability in pediatric responses to iodine exposure, individualized follow-up protocols are essential. Further research is needed to elucidate the long-term effects of ICM exposure on pediatric thyroid function and development, and this will inform the creation of safer ICM usage guidelines, balancing the diagnostic value of imaging with the need to protect the thyroid health of children. A multidisciplinary approach, including pediatricians and endocrinologists, is also key to ensuring optimal outcomes for this population.

Future focus on ICM-induced thyroid dysfunction

While advancements have deepened our understanding of the pathophysiology and treatment of ICM-induced thyroid dysfunction, critical knowledge gaps remain. Future research should prioritize examining the long-term effects of ICM on thyroid function, especially in patients who undergo frequent imaging procedures [49]. Clarifying the dose–response relationship between ICM volume and thyroid dysfunction risk is essential, as recent studies suggest a correlation between higher doses and increased dysfunction risk [49, 66]. Additionally, as potential endocrine-disrupting chemicals, ICM raise concerns regarding environmental and public health impacts, particularly in aquatic ecosystems [90, 91]. Research on the ecological effects of ICM, including developing wastewater treatment to limit environmental contamination, is crucial. Future studies should investigate interactions between ICM and hormone receptors to understand the broader implications for human and ecological health. Moreover, the prophylactic use of agents like thiamazole or sodium perchlorate to prevent ICM-induced hyperthyroidism requires further investigation to assess their effectiveness and safety [36]. Enhancing patient education on the thyroid-related risks of ICM, exploring non-iodinated imaging alternatives, and implementing individualized monitoring protocols are also necessary. By advancing research in these areas, we can optimize clinical strategies, improve patient outcomes, and ensure that the diagnostic benefits of ICM are balanced against potential thyroid risks.

Conclusion

In conclusion, while ICM are invaluable in modern diagnostic imaging, their impact on thyroid function warrants careful consideration, particularly in at-risk populations. Further exploration of the underlying mechanisms of ICM-induced thyroid dysfunction and the development of improved management strategies will be crucial for the safe and effective use of ICM in clinical practice, and collaborative efforts between clinicians and researchers are essential to ensure that the risks of thyroid dysfunction do not overweigh the benefits of imaging.

Abbreviations

ICM

Iodinated contrast media

CT

Computed tomography

CIN

Contrast-induced nephropathy

T4

Thyroxine

FT4

Free thyroxine

T3

Triiodothyronine

FT3

Free triiodothyronine

IHD

Ischemic heart disease

Author contributions

Yaxi Hu and Lihong Zhao conceived this work; Yaxi Hu, Xia Zhong, and Dan Peng wrote the manuscript; and all the authors read and approved the final manuscript.

Funding

The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

Data availability

No datasets were generated or analyzed during the current study.

Declarations

Conflict of interests

The authors declare no competing interests.

Ethical approval

Not applicable.