Beyond levothyroxine: a narrative review of adjunctive management strategies for Hashimoto’s thyroiditis

Introduction

Hashimoto’s thyroiditis (HT) is an autoimmune disorder that has been well documented as the leading cause of hypothyroidism and the most common form of thyroiditis (1). It is characterized by lymphocytic infiltration of the thyroid tissue, primarily T-cell mediated, with B-cell autoantibody production and resultant follicular destruction of the thyroid parenchyma (2). The exact pathogenesis of HT remains largely unclear but is thought to be a combination of genetic susceptibility, environmental triggers, and epigenetic factors (3). It is associated with elevated anti-thyroid peroxidase antibodies (TPOAb) and often anti-thyroglobulin antibodies (TgAb) (4). Laboratory findings commonly reveal hypothyroidism, characterized by low free thyroxine (fT4) and triiodothyronine (T3) with elevated thyroid-stimulating hormone (TSH). However, patients may initially present with subclinical hypothyroidism or, rarely, a transient thyrotoxic phase. Patients may be euthyroid at different time points during the course of the disease. The diagnosis of HT is established based on a combination of clinical symptoms, elevated anti-thyroid antibodies, characteristic sonographic features on ultrasound, and, when available, histological confirmation.

Common clinical features of HT include fatigue, weight gain, cold intolerance, mood disturbances, constipation, and goiter. The Wickham survey [1977] estimated the mean incidence of hypothyroidism secondary to HT to be 3.5 per 1,000 in women and 0.6 per 1,000 in men (5). Although the Whickham survey remains a historic reference, more contemporary studies demonstrate that HT remains highly prevalent worldwide, with substantial geographic and demographic variability. The incidence of HT has increased over recent decades and is higher with advancing age, in women, and in iodine-sufficient populations (1,6). A meta-analysis [2022] estimated the global prevalence of HT in adults to be 7.5% (7). Collectively, these data indicate a significant and potentially increasing burden of autoimmune thyroid disease in contemporary populations.

The current management of HT is primarily supportive and centers on thyroid hormone replacement therapy. The most common thyroid hormone replacement therapy used is synthetic thyroxine (T4), while combination therapy with T4 and T3 may be considered in select patients (8). Most patients require lifelong thyroid hormone replacement therapy at varying doses, representing a significant long-term burden in terms of cost, lab monitoring, and adherence. Thyroid hormone replacement with levothyroxine effectively normalizes TSH but does not modify the underlying autoimmune process. A subset of patients remains symptomatic despite achieving biochemical euthyroidism. Surgical intervention with partial or total thyroidectomy is a current treatment option for patients presenting with neck discomfort, compressive symptoms, or presence of thyroid malignancy (9). Thyroidectomy can be more challenging in patients with HT due to chronic inflammation and fibrosis, which complicate dissection. Complications of thyroidectomy are slightly higher in patients with HT, including postoperative bleeding, injury to the recurrent laryngeal nerve, and permanent hypoparathyroidism (10). Patients will also remain on lifelong thyroid hormone replacement therapy postoperatively.

Even with current treatments, including thyroid hormone replacement therapy and surgical intervention when indicated, many patients continue to experience HT symptoms such as fatigue, weight changes, and constipation (11). In recent years, there has been growing interest in adjuvant therapies for HT. This review aims to provide a comprehensive assessment of non-surgical and integrative approaches in the management of HT. We present this article in accordance with the Narrative Review reporting checklist (available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-554/rc).

Methods

A narrative review was conducted through systematic searches of PubMed (National Library of Medicine) and Embase (Elsevier) to identify articles on adjunctive treatments for HT. Two authors (L.P. and T.A.) independently performed the literature searches, screened the retrieved references for relevance and applicability, and resolved any discrepancies by consensus. The final search was completed on July 20, 2025. Search terms included “Hashimoto’s thyroiditis”, “adjunct”, “diet”, “wet cupping”, “acupuncture”, and “micronutrients” (Table 1). Articles that were not peer-reviewed or not written in English were excluded.

Interventions

Cupping therapy

There has been a growing body of literature on the use of wet cupping therapy, al-hijamah, for various conditions, such as lower back pain and migraines (12,13). Wet cupping involves making superficial skin incisions, applying a cup over the site, and using suction to draw out small amounts of blood and interstitial fluid (14). It has been proposed that wet cupping may be effective in treating autoimmune disorders by reducing auto-antibodies and inflammatory cytokines (15,16). One proposed mechanism is that superficial incisions under negative pressure facilitate the clearance of potential pathological substances from the blood and interstitial fluid (17). Additionally, it has been suggested that disruption of superficial capillaries during the wet-cupping process activates the innate immune response and induces the production of heme oxygenase-1 (HO-1) (18). Activation of the HO-1 enzyme system has been shown to have many downstream actions, including antioxidant, anti-inflammatory, and immunomodulatory effects (17). In a pilot study, thirteen women received 3 months of adjunctive wet cupping therapy, with one wet-cupping session, alongside conventional thyroid hormone treatment (18). Patients in this study demonstrated improvement across several aspects of HT, including hormonal, structural, and clinical parameters. Wet cupping was associated with a statistically significant reduction in anti-thyroid autoantibody levels and a decrease in TSH despite stable thyroid hormone dosing (18). In addition, a statistically significant reduction in erythrocyte sedimentation rate, an inflammatory marker, was observed. Thyroid ultrasound findings further demonstrated structural improvement, including normalization of gland size, echogenicity, and vascularity (18). Patients additionally reported symptomatic improvements in mood, energy, and bowel function. Although limited by a small sample size and short study duration, these findings suggest that wet cupping may serve as a useful adjunctive therapy for HT.

Acupuncture

Several studies have investigated the effects of acupuncture in patients with HT (19,20). Acupuncture, a traditional therapeutic technique widely practiced in Eastern Asian countries that involves inserting fine needles at specific body points, has been proposed to modulate immune activity. Preclinical animal studies suggest that acupuncture may reduce thyroid follicular cell apoptosis by regulating intestinal microbiota-palmitoleic acid metabolism, though this mechanism has not yet been demonstrated in human studies (21). According to a meta-analysis of 14 randomized control trials, when used as an adjunct to hormone replacement therapy, acupuncture was associated with a statistically significant reduction in thyroid autoantibody titers (TPOAb and TgAb) and modest improvements in quality of life (QOL) measures compared with hormone replacement therapy alone (19). However, many of the included studies are limited by inadequate control groups and short-term follow-up, underscoring the need for more rigorous clinical studies. The largest study to date (n=284), which included an adequate control group with a one-year follow-up, demonstrated significant reductions in TPOAb and TgAb titers (20). The protocol outlined in this study consisted of 36 sessions given over consecutive 12 weeks, with thyroid function and thyroid antibody tests measured at 0, 4, 8, and 12 weeks (20). Given the relatively low cost and consistent benefits reported across studies, acupuncture may be a reasonable adjunct therapy for HT patients who remain symptomatic despite optimal medical management.

Diet

Numerous studies have demonstrated alterations in the gut microbiome in patients with HT and other autoimmune conditions. In 2021, Cayres et al. reported statistically significant differences in gut microbiota composition and increased intestinal permeability in patients with HT compared with healthy controls, despite appropriate treatment with thyroid hormone replacement therapy (22). These findings suggested that standard hormone replacement does not fully address underlying gut-related immune dysregulation. The authors further noted that dietary patterns differed significantly between groups, including intake of vegetables, fruits, proteins, dairy products, saturated fats, and carbohydrates, suggesting a potential dietary influence on microbiome composition. Supporting this association, other studies have shown that HT patients with more pro-inflammatory dietary patterns, characterized by higher consumption of animal meat and processed foods, exhibited higher TSH and total thyroxine levels (23,24). One theory proposes that gut barrier dysfunction allows microbial products to cross and activate both the innate and adaptive immune response, contributing to systemic autoimmunity (25). Collectively, these observations support the hypothesis that alterations in gut barrier function may contribute to persistent HT symptoms by permitting translocation of immunogenic compounds into the systemic circulation (25). A multifaceted approach has been proposed to address this gut barrier dysfunction linked to autoimmunity, including restoration of the intestinal barrier integrity, probiotics, and dietary modification (25). Given the consistent differences in microbiome composition, intestinal permeability, and dietary habits between HT patients and controls, dietary modification may represent a meaningful adjunct in the management of HT.

HT and celiac disease (CD) share common genetic susceptibility factors, HLA-DQ2 and HLA-DQ8, supporting the hypothesis that a gluten-free diet (GFD) may be beneficial in patients with HT (26,27). However, the evidence remains inconsistent, and the clinical utility of GFD in HT is widely debated. More recent meta-analyses have not shown a significant benefit of GFD in HT alone (28). Given the high rate of co-occurrence of HT and CD, with an estimated odds ratio of approximately 3, it remains challenging to determine whether reported benefits of GFD reflect effects on HT itself or improvement of unrecognized CD (29).

The Mediterranean diet (MedD) emphasizes minimally processed, plant-based foods, such as fruits, vegetables, and whole grains, with olive oil as the primary fat source and fish and seafood as the main protein sources, while limiting red meat and alcohol consumption. A pilot study examined the effects of the MedD and GFD in HT patients, comparing oxidative stress parameters at baseline and after 12 weeks (30). Patients adhering to the MedD demonstrated a significant improvement in systemic redox balance compared with both the GFD group and those who made no dietary changes. Similarly, a more recent study comparing the MedD diet and GFD reported a significant increase in free triiodothyronine (fT3) levels in both groups, with the greatest increase observed in the MedD group (31). Consistent with these findings, a recent meta-analysis concluded that the MedD is a promising complementary adjunct in the management of HT, with potential benefits including reduced disease activity, improvement in autoimmunity-related outcomes, and promotion of weight loss (32). Overall, the available evidence supports the benefit of a low-inflammatory dietary pattern, such as MedD, for patients with HT.

Physical activity

Physical activity provides substantial benefits for patients with HT and hypothyroidism, particularly in managing fatigue, mood disorders, and associated metabolic dysfunction (33). Exercise interventions, including aerobic fitness or resistance training, have demonstrated improvements in both physical and mental health, such as reduced fatigue and enhanced psychological well-being (33-37). While the direct effects of physical activity on thyroid hormone levels are modest and inconsistent, the overall impact on QOL and related outcomes, including increased energy, is clinically significant (33,38).

Recent studies suggest that, in addition to the well-established benefits, moderate-intensity physical activity may also help to improve persistent HT symptoms. Several studies have reported a reduction in TPOAb titers, along with some improvements in TSH and fT4 levels, particularly in women (33,36). There is moderate certainty of evidence for TSH and very low certainty for fT4. Importantly, exercise exerts well-established anti-inflammatory and immunomodulatory effects, which may be relevant for autoimmune thyroiditis; however, direct clinical implications are still being investigated (39,40).

For individuals with chronic conditions such as hypothyroidism, the United States Department of Health and Human Services in the Physical Activity Guidelines for Americans recommends including 150 min per week of moderate-intensity aerobic activity, along with muscle-strengthening exercises on two or more days per week (41). In patients with HT, where fatigue is often more persistent and exercise tolerance is lower, psychological barriers to physical activity should also be considered. Individualized exercise programs that progress gradually, monitor symptoms, and incorporate supportive strategies may help improve both safety and adherence (41,42).

Micronutrient supplementation: selenium, vitamin D, iron/ferritin, iodine

Micronutrient status is a modifiable factor in the management of HT, particularly with respect to immune modulation, thyroid hormone metabolism, and symptom intensity. The micronutrients with the most clinical evidence include selenium, vitamin D, iron, and iodine.

Selenium

Selenium is a trace element that is incorporated into selenoproteins such as glutathione peroxidases and iodothyronine deiodinases, which protect thyroid tissue from oxidative damage and facilitate the conversion of T4 to T3. Selenium exerts immunomodulatory effects by inhibiting pro-inflammatory cytokines and enhancing regulatory T cells (Treg) activity, reducing autoimmune activity in HT (43-45). Clinical studies have shown that selenium supplementation shows a small but statistically significant decrease in TPOAb titers and TSH levels, especially in patients not receiving levothyroxine treatment (43-47). The most consistently observed improvements in thyroid hormone indices occur after approximately 3–6 months of supplementation at doses of 100–200 µg/day, with a low likelihood of serious adverse events at these doses (43-48). The effects of selenium on clinical symptoms, including energy and mood changes, as well as on long-term thyroid function remain uncertain. In most studies, selenium supplementation was not significantly associated with fT4, fT3, or TgAb concentrations, and the available evidence is limited (43,45,49-52).

Meta-analyses and systematic reviews have suggested that the antibody-lowering effect of selenium is most pronounced in patients with selenium deficiency or high baseline TPOAb levels, whereas improvements in thyroid hormone indices and patient-reported outcomes are less consistent (43,45-52). Although high-dose or prolonged supplementation is generally well tolerated, potential toxicity should be considered. The signs and symptoms of selenium toxicity include gastrointestinal tract symptoms, garlic-like odor of the breath, alopecia, breaking or discoloration of the nails, mental depression and other neuropsychiatric changes (47,49). Baseline selenium levels should be assessed in regions or populations with variable selenium status such as parts of China and Europe, where there is variability in soil content and dietary intake (43,44). Patients should then be monitored for TPOAb and thyroid function to evaluate response (43,44,48). In selenium-replete regions such as the United States, routine measurement may be less critical, though it may be considered in individuals with restrictive diets or malabsorption syndromes. Current consensus supports the role of selenium as an adjunctive therapy in HT, particularly in patients with high antibody titers or low selenium intake. However, selenium supplementation should not replace established thyroid hormone replacement when indicated, and its long-term benefits and effects on disease progression remain uncertain (43,44,47,52).

Vitamin D

Vitamin D is an essential micronutrient with immunomodulatory effects relevant to autoimmune thyroid disease. Mechanistically, vitamin D enhances Treg function, suppresses pro-inflammatory T helper 17 (Th17) cells responses, and modulates the cytokine profiles, collectively contributing to reductions in thyroid autoantibodies and stabilization of thyroid function (53,54). Clinically, vitamin D supplementation in HT patients with vitamin D deficiency is associated with a 15–30% reduction in TPOAb and TgAb titers (53-56). Most studies investigating supplementation in HT have been conducted in patients with underlying vitamin D deficiency [serum 25-hydroxyvitamin D (25-OH vitamin D) <30 ng/mL], reflecting the high prevalence of deficiency and its association with elevated thyroid autoantibody titers and increased risk of progression to hypothyroidism (53-57).

Reductions in thyroid autoantibody levels are most consistently observed with daily supplementation administered for at least 8–12 weeks, with greater reductions seen with longer treatment durations (55-59). Cholecalciferol (vitamin D3) at doses of 2,000–4,000 IU daily, or equivalent weekly or monthly dosing regimens, has been most commonly studied. Daily supplementation may be preferable to intermittent dosing for reducing thyroid autoantibody levels (60). A meta-analysis found that continuous daily rather than weekly vitamin D supplementation for at least 3 months significantly reduced serum TPOAb levels in patients with autoimmune thyroid disorder with initial vitamin D deficiency (58). The most pronounced reductions have been observed in patients with baseline 25-OH vitamin D levels of <20 ng/mL (55,58,59). Supplementation durations exceeding 3–6 months appear to confer more sustained effects; however, the impact on thyroid hormone levels and progression to overt hypothyroidism remains uncertain (56,58,60-62).

Improvements in systemic symptoms such as fatigue, depressive symptoms, musculoskeletal pain, and sexual dysfunction have been reported in vitamin D deficient patients with HT following supplementation (53,54,57,59). In contrast, effects on standardized QOL and short-term outcome instruments such as the SF-36 and ThyPRO have generally been modest and inconsistent (54,59). No serious adverse events have been reported with these regimens, although monitoring for hypercalcemia is advised, with a target 25-OH vitamin D level of 30–50 ng/mL (55,57,61). Regular reassessment of thyroid function and autoantibody titers during therapy has also been recommended (55,56,62).

Accordingly, vitamin D supplementation should be considered an adjunct to standard thyroid hormone replacement therapy in patients with HT who have confirmed vitamin D deficiency. Supplementation is consistently associated with reductions in thyroid autoantibody titers and modest improvement in fatigue, mood, and musculoskeletal symptoms. However, the long-term effects on overall QOL and disease progression remain uncertain, underscoring the need for larger, well-designed randomized controlled trials with longer follow-up durations (44,53,54,57).

Iron and ferritin

Iron is an essential cofactor for thyroid peroxidase (TPO), a heme-dependent enzyme required for thyroid hormone synthesis. Iron deficiency impairs TPO activity, leading to reduced thyroid hormone production and potentially contributing to persistent hypothyroid symptoms in some patients, even when biochemical euthyroidism is achieved or levothyroxine therapy is in place, as is often observed in HT (63-66). Identification and correction of iron deficiency is particularly important in patients with coexisting autoimmune conditions, such as autoimmune gastritis, CD, as well as other malabsorption syndromes, and in individuals with excessive menstrual blood loss, all of which increase the risk of iron deficiency and low ferritin levels (63,64,67,68).

Clinically, achieving ferritin levels above 100 µg/L appears to be relevant, as observational studies suggest that restoring ferritin to this threshold may alleviate persistent hypothyroid symptoms and optimize thyroid hormone metabolism, particularly in reproductive-aged women (63,64,66,68). Iron deficiency has also been associated with alterations in fT4 and fT3 levels, increased thyroid autoantibody positivity, and a higher risk of overt or subclinical hypothyroidism in both reproductive-aged and pregnant women (66,68). Indications for iron supplementation depend on the underlying etiology of deficiency, and long-term therapy requires regular monitoring of ferritin, hemoglobin, and transferrin saturation to ensure efficacy and safety (64,68).

Iodine

Iodine is essential for the synthesis of T4 and T3; however, both iodine deficiency and excess can impair normal thyroid function and influence the development and progression of autoimmune thyroid disease, making iodine status particularly relevant in HT (69-72). Excess iodine has been shown to increase the immunogenicity of thyroglobulin, promote oxidative stress, and activate pro-inflammatory pathways, thereby exacerbating lymphocytic thyroiditis (66,68,71-73). Populations with high iodine intake (>300 µg/day) have been reported to exhibit higher thyroid autoantibody levels and increased rates of subclinical hypothyroidism, particularly among individuals with prior iodine deficiency or genetic susceptibility to autoimmune thyroid disease (66,71-73). Observational studies further suggest that reducing excessive dietary iodine intake may help restore euthyroidism in some patients with hypothyroid HT (72,73).

In contrast, iodine deficiency reduces the synthesis of iodine-dependent hormones and may lead to thyrocyte hyperplasia and clinical hypothyroidism in severe cases. Mild iodine deficiency has been associated with nodular thyroid disease and may result in paradoxical hyperthyroidism following iodine repletion (74-76). Although iodine deficiency is uncommon in developed countries, when deficiency is confirmed, supplementation should be limited to the recommended daily allowance (approximately 150 µg/day for adults) (69-71).

Current clinical guidelines recommend against routine iodine or kelp supplementation in non-pregnant adults with HT residing in iodine-sufficient regions, as excess iodine may exacerbate thyroid autoimmunity (69). During pregnancy and lactation, however, women, including those with pre-existing HT, should ensure adequate iodine intake to achieve total daily intakes of approximately 250 ug during pregnancy and 250–290 µg during lactation, with close monitoring of thyroid function (66,70-73). Kelp or seaweed-based supplements are not recommended due to their highly variable iodine content (63). A summary of the findings outlined in this review can be found in Table 2.

Discussion

Optimal management of HT remains challenging, as many patients continue to experience hypothyroid symptoms despite achieving biochemical euthyroidism with hormone replacement therapy (77). These persistent symptoms can profoundly affect QOL and highlight the need for adjunctive strategies that address immune and inflammatory mechanisms not targeted by levothyroxine. Although thyroid autoantibody titers are frequently used as surrogate markers in clinical studies, current evidence does not support a direct correlation between antibody levels and symptom severity once significant thyroid tissue damage has occurred (78). Accordingly, therapeutic approaches aimed at immune modulation must be evaluated primarily for their clinical, rather than serologic, benefit.

Adjunctive interventions explored in this review include wet cupping, acupuncture, dietary modification, physical activity, and micronutrient supplementation. Wet cupping and acupuncture have demonstrated reductions in thyroid autoantibody titers and subjective symptom improvement in small studies; however, the absence of rigorous, well-controlled trials precludes their routine clinical use. Similarly, low-inflammatory dietary patterns, such as the MedD, may reduce oxidative stress and modestly influence thyroid hormone parameters. Many studies have examined the benefits of MedD on numerous diseases, including breast cancer, osteoarthritis, and type 2 diabetes mellitus, among others (79-81). These studies attribute the benefits of the MedD diet to its antioxidant and anti-inflammatory effects, which support the theory that it would be beneficial in improving the inflammatory aspect of HT that is not addressed by hormone replacement therapy. The MedD diet also consists of minimal consumption of processed foods, which have been shown to be linked to obesity, hypertension, and dyslipidemia (82). It is reasonable to theorize that the MedD diet could have health benefits in HT patients, such as symptomatic improvement, given its antioxidative and anti-inflammatory effects and reduction in pro-inflammatory processed foods. Nonetheless, existing dietary studies are limited by small sample sizes, and further research is needed to distinguish the immunomodulatory effects from symptomatic improvements attributable to weight loss.

Regular physical activity has been associated with improvements in fatigue and mental health. Additional investigation is also warranted to clarify the mechanisms and clinical applications of structured physical activity in immune modulation, metabolism, and neuropsychiatric symptoms associated with HT (37,83). Interestingly, mouse models subjected to forced moderate-intensity exercise (8–12 m/min for 40 min, 5 days per week for 6 weeks) exhibited exacerbated colitis symptoms and increased inflammatory gene expression compared with sedentary mice and those allowed voluntary wheel running (84). These findings suggest the existence of an optimal threshold of physical activity for promoting anti-inflammatory effects, warranting further investigation.

Micronutrient supplementation, particularly selenium, vitamin D, and iron, has demonstrated modest benefits in reducing thyroid autoantibody levels and supporting thyroid hormone metabolism. Future research should prioritize large, controlled trials to assess the clinical relevance of these interventions in biochemically euthyroid patients with persistent symptoms such as fatigue, mood disturbances, and cognitive dysfunction. Additional evidence is needed to define optimal dosing, treatment duration, and patient selection for selenium and vitamin D supplementation, as well as to clarify their effects on long-term symptom control and thyroid function (37,54,71). The role of iron repletion warrants particular consideration, especially in women with low ferritin levels who continue to experience residual symptoms. Given the high prevalence of iron deficiency in this population, correction may improve QOL and cognitive function even when thyroid hormone levels have normalized (70,71).

Lifestyle and micronutrient-based interventions are generally safe, low-cost, and accessible, making them reasonable adjunctive options for patients who remain symptomatic despite optimized hormone therapy. While they should not replace standard treatment, incorporating dietary, physical activity, and targeted supplementation strategies into an individualized care plan may help alleviate persistent symptoms and improve QOL.

Conclusions

HT is a common autoimmune disease in which many patients continue to experience symptoms despite adequate thyroid hormone replacement therapy. This review evaluated adjunctive strategies aimed at optimizing patient outcomes beyond biochemical normalization of thyroid hormone levels. Wet cupping and acupuncture are generally low-risk interventions with potential immunomodulatory benefits, with preliminary studies reporting improvements in thyroid-related biomarkers, QOL, and thyroid histopathology. Anti-inflammatory dietary patterns, such as MedD, and regular physical activity have been associated with improvements in metabolic health and QOL, while offering potential immunomodulatory benefits. Regular physical activity and MedD have well-documented health benefits for a large variety of pathologies and can be protective against common diseases. These lifestyle changes are therefore reasonable recommendations for many patients, although individual patient needs should always be considered. Among micronutrients, selenium and vitamin D appear most effective in reducing thyroid autoantibodies, whereas iron repletion supports thyroid hormone synthesis and may alleviate persistent symptoms. Vitamin D supplementation can be particularly beneficial in HT patients who are vitamin D deficient, and checking vitamin D levels in patients with persistent HT symptoms despite achieving euthyroidism could be beneficial. Many of these adjunct approaches are low-risk and may be combined to develop individualized treatment strategies. However, the current evidence in the literature is limited by small sample sizes, methodological heterogeneity, and a lack of standardized outcome measures. Despite these limitations, integrating selected adjunctive interventions may provide symptomatic improvement for patients who remain refractory to optimized hormone therapy.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-554/rc

Peer Review File: Available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-554/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-554/coif). E.K. serves as an Editor-in-Chief of Gland Surgery from May 2024 to April 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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