Introduction

Atopic dermatitis (AD), synonym atopic eczema, is an inflammatory, non-infectious, chronic, and recurrent skin disease, the symptoms of which are severely itchy and dry skin lesions, taking the form of erythema and papules [1–6]. The causes are believed to be environmental factors, dysregulation of the immune system, and genetic susceptibility, and treatment is aimed at relieving symptoms and improving the quality of life of patients because there is no method of complete cure [1–6]. Immunological disorders involved in the pathogenesis of AD concern T helper (Th) lymphocytes, especially Th1, Th17, and Th22, and the cytokines secreted by them, as well as hyperreactivity of Th2 lymphocytes, which leads to increased secretion of interleukins (ILs), mainly IL-4, IL-5, and IL-13, and also to an increase in the number of eosinophils and the synthesis of IgE antibodies [1–6]. Obesity is a chronic disease defined by a body mass index (BMI) above 30 kg/m², and its occurrence is associated with an impaired immune system (production of proinflammatory cytokines by adipocytes, such as TNF-α and IL-6); therefore, the risk of co-occurrence of many diseases (such as diseases stimulated by chronic inflammation, insulin resistance, or diabetes) as well as impaired response to the treatment of these diseases and their more frequent exacerbations should be taken into account [1, 2, 7–15]. Diabetes mellitus (DM) is a group of metabolic diseases in which hyperglycaemia occurs, which is a consequence of improper production or action of insulin, and among its types the most well-known are type 1 diabetes (T1D) – of autoimmune origin, in which the role is attributed, among others, to Th1 and Th17 lymphocytes, and type 2 diabetes (T2D) – which is mainly caused by environmental factors and excessive body weight, and for which insulin resistance is characteristic [3, 4, 8, 13–19]. Immunological, genetic defects and the influence of lifestyle, which underlie the disease, may constitute a predisposition to the co-occurrence of other diseases that have similar causes. Autoimmune thyroid diseases include Hashimoto’s disease (HT) and Graves-Basedow disease (GD) [9, 18, 20–25]. HT is characterised by the occurrence of antibodies against thyroid peroxidase (anti-TPO) and against thyroglobulin (anti-TG), and in its course it may develop hypothyroidism [9, 18, 20–25]. In GD, the presence of antibodies against TSH receptors (anti-TSHR, TRAb) is observed, and its effect is symptoms of hyperthyroidism [9, 20, 22–25]. These diseases have unclear causes, among which environmental factors (including stress, infections, eating habits), dysregulation of the immune system (disorders of the immune response dependent on Th1 lymphocytes), and genetic predisposition (related to human leukocyte antigens [HLA]) are indicated, and therefore the co-occurrence of other autoimmune diseases is observed. The commonness of the occurrence of the diseases described above, and their multifactorial causes, encourage the estimation of the risk of their co-occurrence, and in this paper the co-occurrence of AD and autoimmune thyroid diseases, DM, and obesity is analysed.

Methods

The aim of this study is to investigate the comorbidity of AD with obesity, diabetes, and autoimmune thyroid diseases. To achieve this, the authors conducted a review of relevant and current articles from the PubMed database. Clinical guidelines for AD were also reviewed: the European Dermatology Forum (EDF, 2025), the Japanese Guidelines for Atopic Dermatitis (ADGL, 2024), the American Academy of Allergy, Asthma, and Immunology/American College of Allergy, Asthma, and Immunology Joint Task Force (AAAAI/ACAAI JTF, 2023), and the Polish Dermatological Society, Polish Society of Allergology, Polish Paediatric Society, and Polish Society of Family Medicine (PDS, PSA, PPS, PSFM, 2020). Additionally, the authors referred to several of their earlier publications on related topics, co-authored with other researchers and not indexed in the PubMed database. In total, 32 sources were included in the review, with 31 published no later than 2020.

Atopic dermatitis and its diagnosis

Atopic dermatitis can affect both children and adults [26]. It is estimated that 13% of children and 7% of adults suffer from the condition [27]. Moreover, AD is the most common chronic inflammatory dermatologic condition [27]. AD often presents within the first few months of life, and most patients develop symptoms before the age of 5 years [28]. Approximately 60% of patients with AD eventually experience spontaneous remission [28].

Several diagnostic criteria sets have been proposed for AD, including the Japanese criteria from 2024, the United Kingdom Working Party (UKWP) criteria from 1994, and the Hanifin and Rajka criteria (HRC) from the 1980s [27, 29, 30]. There are also various clinical guidelines for AD, such as those of the EDF (2025), the ADGL (2024), the AAAAI/ACAAI JTF (2023), and the PDS, PSA PPS, PSFM (2020) [27, 28, 30–32].

Neither the EDF nor the PDS, PSA PPS, PSFM guidelines specify which criteria should be used to diagnose AD [28, 31, 32]. The AAAAI/ACAAI JTF did not introduce new diagnostic criteria but stated that the HRC and UKWP criteria are the most widely validated and adopted, and these were listed in the guidelines [27]. Notably, as early as 2020, it was observed that the HRC and UKWP criteria were the most commonly used in the literature [29].

Table 1 presents the HRC and UKWP criteria. The HRC are fulfilled when at least three major and three minor criteria are met. The UKWP criteria are met when the main criterion and at least three additional minor criteria are fulfilled [29]. Table 2 presents the Japanese criteria for AD; these are fulfilled when all three required conditions are met [30].

Obesity

The implications of obesity include the microbiome (both intestinal and elsewhere, especially skin), which results in changes in the production of immunomodulatory molecules and the epithelial barrier [1]. In their work, Shang and Zhao addressed the issue of the influence of compounds secreted by adipose tissue, such as adipokines, adiponectin, and leptin, and their impact on the immune system through their effects on Toll-like receptor (TLR) signalling pathways and changes in the levels of cytokines, such as IL-4, IL-6, IL-13, and TNF-α [1]. The role of intestinal microbiota disturbed by obesity was also emphasised – primarily the increase in the number of Escherichia coli, Clostridium difficile, and Staphylococcus aureus and the decrease in beneficial bacteria, such as Lactobacillus and Bifidobacterium, which leads, among others, to increased intestinal permeability and increased expression of inflammatory markers, especially TNF-a contributing to the exacerbation of AD symptoms [1]. It was indicated that a rational diet, based mainly on plant foods, contributed to improving the proportion of microbiota bacteria, and also, through a direct effect on normalising body weight, reduced the inflammation underlying AD [1]. Diet, and therefore also BMI, may have an impact on the skin microbiota, which was discussed, among others, in the work of McAleer [2]. AD is characterised by reduced lipid content in the skin, increased pH, and increased water loss, as well as dysbiosis consisting of a decrease in Streptococcus, Cutibacterium, and Malassezia and an increase in Staphylococcus aureus, which is why it is assumed that probiotic therapy and a proper diet could reduce skin inflammation [2]. The article also draws attention to the potential benefits of PPAR-γ stimulation, which, among others, due to Th17 suppression, could support AD therapy; however, further observations and a thorough assessment of the action of PPAR-γ modulators are needed, including the effect on adipose tissue [2]. The role of adipokines was emphasised in the work of Guo et al., who analysed the relationship between their concentration and the risk of developing AD [7]. It has been shown that obesity leads to adipocyte hypertrophy, increased expression of pro-inflammatory adipokines (mainly leptin), and decreased anti-inflammatory adipokines (mainly adiponectin) [7]. It is believed that obesity may be one of the factors underlying the development of AD and disease exacerbations, so in addition to pharmacological treatment, normalisation of body weight is recommended.

Diabetes

It is thought that the development of DM (both type 1 and type 2) and AD is due to environmental and genetic factors, as discussed in Sendrea and Salavastru’s work [3]. Genetic predispositions may be the cause of both T1D and AD, so patients suffering from one of these diseases should be monitored for the risk of co-occurrence of another [3]. Obesity promotes the occurrence of insulin resistance, T2D, as well as AD, so normalisation of body weight may bring multidimensional benefits in the context of preventing these diseases or reducing the severity of existing ones [3]. The publication also draws attention to the tendency towards reduced physical activity observed in AD patients, which may result, among other things, from sleep disorders, which in turn increases the risk of obesity, T2D, and increased inflammation, which may then result in exacerbation of AD and reduced quality of life [3]. The work of Zhou et al. draws attention to the immunological pathways that cause autoimmune diseases, which include T1D [4]. In the course of AD, the function of regulatory T lymphocytes (Treg) may be impaired, resulting in the activation of autoreactive T lymphocytes and destruction of β-cells of the islets of Langerhans of the pancreas, which leads to T1D [4]. In addition, AD is characterised by increased production of proinflammatory cytokines by Th17, which additionally promotes the development of T1D [4]. The potential relationship between AD and T2D resulting from similarities in molecular mechanisms was pointed out by Zhang et al. [8]. In the described studies, the LTF, LTB4R, and CCR1 genes were identified, the expression of which on specific cells may be important in the pathogenesis of diseases [8]. It was suggested that due to the strong affinity to the CCR1 binding site by dioscin, camptothecin, and albamycin, they could be potential therapeutic methods, which requires further research and observation [8]. In addition, common signalling pathways including Toll-type receptors and NF-κB, important in the inflammatory response, were indicated [8]. Further studies on the molecular similarities of AD and T2D could help to determine biomarkers and therapeutic targets [8].

Autoimmune thyroid diseases

Both thyroid autoimmune diseases and AD result from immune system disorders, so the study described in Mendiratta et al. addressed the issue of the coexistence of these diseases [5]. The study included children with AD, and the assessment included the clinical severity of AD, antinuclear antibody (ANA), anti-TPO, absolute eosinophil count, serum IgE, and vitamin D level [5]. Thyroid autoimmunity was diagnosed in 18.9% of children, which may be related to AD, because Th17 and Treg lymphocytes, whose disorders occur in AD and may lead to autoimmunity, are involved in the pathogenesis [5]. The study also emphasised the role of vitamin D supplementation because it may have a beneficial effect on the immune system and reduce inflammation that exacerbates AD symptoms and creates the risk of coexisting other diseases [5]. Further studies are needed to clarify the frequency of co-occurrence of AD and autoimmune thyroid diseases [5]. Similarities in the development of autoimmune thyroid diseases and AD were discussed in the work of Carlucci et al. [6]. The thyroid and skin show combined embryological development, which may indicate genetic predisposition to the coexistence of diseases of these organs [6]. An important role is attributed to the expression of major histocompatibility complex (MHC) molecules, necessary for the recognition of one’s own and potentially harmful tissues [6]. In addition, CTLA-4 mutations and IL-23 gene variants may be important in the pathogenesis of AD and autoimmune thyroid diseases, which additionally emphasises the importance of a genetic factor in the development of these diseases [6]. Based on these observations, there is a need for further studies focused on immunological treatment, as well as preventive thyroid tests (including ultrasonography, testing of anti-TPO and anti-TG antibody levels, and hormonal tests) in patients affected by AD [6]. In the course of autoimmune thyroid diseases, an increase in the levels of anti-TPO and anti-TG autoantibodies is observed, and their potential impact on atopic and allergic diseases is described in the work of Zhang et al. [10]. Based on the analysis of the results of studies of patients with allergic diseases, it was shown that the presence of these autoantibodies, mainly anti-TG, was associated with an increased risk of allergic disorders [10]. This indicates the need to monitor patients with increased levels of thyroid autoantibodies for AD, as well as control the thyroid status in patients already diagnosed with AD [10].

Conclusions

Based on the above considerations, it can be concluded that there is a relationship between the occurrence of AD and obesity, DM, and autoimmune thyroid diseases, which may be the result of common risk factors, including genetic and environmental, as well as the implication of inflammation in the course of these diseases (Table 3). Improved lifestyle, normalisation of body weight, and prevention and interdisciplinary control of co-occurring diseases are undoubtedly necessary. Further detailed studies focused on common risk factors for the development of these diseases may facilitate individual treatment selection, supplementation, and lifestyle modification, and ultimately improve the quality of life of patients affected by AD.