Background: The anti-inflammatory effects of omega-3 fatty acids and their derivatives are of considerable interest as a potential therapeutic agent in many diseases characterized by inflammation. Methods: This study aimed to measure the concentration of mediators derived from eicosapentaenoic (EPA) and docosahexaenoic (DHA) fatty acids. We included 33 women suffering from Hashimoto’s disease, with an average age of 37.58 ± 8.41 kg, in the study. The levels of EPA and DHA acids were examined using gas chromatography, and their derivatives were studied with liquid chromatography (HPLC). Patients were assessed after being put on a healthy and balanced diet supplemented with omega-3 fatty acids. Results: The results showed statistically significant correlations between the C-reactive protein (CRP) level and derivatives: resolvins E1 and D1 (RvE1, RvD1), 10S17R DiHDHA (Protectin DX), and 18RS HEPE (18-hydro(peroxy)-eicosapentaenoic acid) following the diet. There was also a significant correlation observed between Maresin 1 and free thyroxine (fT4). Moreover, a dependency between the RvD1 level and some anthropometric parameters was observed. Conclusions: The findings suggest that the chronic inflammatory state occurring in the course of Hashimoto’s thyroiditis (HT) is associated with increased synthesis of anti-inflammatory mediators of omega-3 fatty acids, particularly DHA derivatives. Consequently, these may affect the level of thyroid hormone synthesis, which should be considered in future research on biological drugs in Hashimoto’s therapy.

The incidence of Hashimoto’s disease (HD) increases with age and in people who have other autoimmune diseases. It is characterized by lymphocytic infiltration, fibrosis, and atrophy of the thyroid parenchyma with the simultaneous presence of thyroid peroxidase antibodies (ATPO) and/or thyroglobulin antibodies (ATG). Eicosanoids are formed via the cyclooxygenase (COX), lipoxygenase (LOX), and monooxygenase (CYP450) pathways with arachidonic acid (ARA), resulting in the production of epoxyeicosatrienoic acids (EETs) or hydroxyeicosatetraenoic acids (HETEs). These eicosanoids can act in an autocrine or paracrine manner on target cells. This study aimed to examine whether a gluten-free diet (GFD) can modulate the enzymatic pathways of the pro-inflammatory ARA cascade. The study material consisted of serum samples from Caucasian female patients with HD aged 18–55 years. Participants were enrolled in the study based on the presence of an ultrasound characteristic of HD, and elevated serum levels of anti-thyroid peroxidase antibodies and anti-thyroglobulin antibodies. Patients with confirmed celiac disease did not participate in the study. A total of 78 samples were analyzed, with 39 collected after 3 months of following a GFD. Eicosanoids (thromboxane B2, prostaglandin E2, leukotriene B4, and 16R-hydroxy-5Z,8Z,11Z,14Z-eicosatetraenoic acid (16-RS HETE)) were extracted using high-performance liquid chromatography. The contribution of leukotriene (LTB) was analyzed in the LOX pathway, prostaglandins (PGE2) and thromboxane (TXB2) were selected for the involvement of the COX pathway, and 16RS HETE was used for the CYP450 pathway. All parameters were analyzed before and after a 3-month dietary intervention that included a gluten-free diet. In the obtained results, only one mediator, leukotriene B4, was significant (p < 0.05). The mean level on the initial visit was 0.202 ± 0.11 (SD), while it was 0.421 ± 0.27 (SD) on the subsequent visit, indicating a significant increase in its level after implementing a GFD. Although there was a trend in the CYP 450 pathway of decreased 16-RS HETE, the presented correlations show that thromboxane B4 and 16RS-HETE were positively correlated with the body mass and body fat mass of the examined patients. There was a trend in the CYP 450 pathway of decreased 16-RS HETE after GFD. Thromboxane B4 and 16RS-HETE levels before GFD were positively correlated with the body mass and body fat mass of the examined patients. A gluten-free diet in HD does not suppress the synthetic pathways of LOX, COX, or cytochrome P450 (CYP450). The level of adipose tissue has a greater impact on the inflammatory processes in HD than a gluten-free diet. This study does not confirm the suppressive effect of a gluten-free diet on the pro-inflammatory arachidonic acid cascade in any of the three analyzed mediator synthesis LOX, COX, CYP450 pathways.

Background: Hashimoto’s thyroiditis (HT) is the result of a complex interplay between genetic, environmental, and epigenetic factors. The role of cellular and humoral immunity in the pathogenesis of the disease is well-established. Inflammatory infiltration of T and B lymphocytes is a key feature identified on ultrasound examination. The lack of data on the effect of L-thyroxine (LT-4) doses on the level of anti-TPO and anti-TG antibodies in Hashimoto’s thyroiditis and the relationship with anthropometric measurements resulted in the desire to fill this niche. Methods: A total of 70 Caucasian patients diagnosed with Hashimoto’s thyroiditis within the past two years were examined. The participants were divided into three groups based on their L-thyroxine dosage (≤50, 50–100, >100 μg). Results: The results revealed no correlation between the dosage of L-thyroxine and anthropometric measurements (age, height, body weight, and body fat content). No correlation was identified between the levels of anti-TPO and anti-TG and the dose of L-thyroxine in patients with Hashimoto’s thyroiditis. Conclusions: The mechanism regulating the levels of anti-TPO and anti-TG appears to be associated with a more advanced thyroid inflammation and disease process. Long-term observation of patients would be advisable. We present evidence of no effect of hormone dose on antibody levels in Hashimoto’s thyroiditis. Regardless of disease severity, immune regulation remains outside the scope of hormonal regulation.

Hashimoto’s thyroiditis (HT) is one of the most common autoimmune disorders with a complex etiology and pathogenesis, representing a significant challenge for medicine. Current pharmacological management of HT focuses on the treatment of hypothyroidism rather than addressing the underlying cause. Available scientific evidence provides limited and inconsistent data regarding the association between levothyroxine (L–T4), its dosage, and the levels of antibodies against thyroid peroxidase (anti–TPO) and thyroglobulin (anti–TG) in women with HT. Therefore, the aim of the study was to summarize current findings in this field. This narrative review was conducted using elements of the PRISMA 2020 guidelines. Literature analysis was performed using EMBASE, SCOPUS, and PUBMED databases. Articles published within the last 20 years were included. The search terms included “Hashimoto’s thyroiditis”, “Hashimoto’s disease”, “levothyroxine”, “L–thyroxine”, “anti–TPO”, “anti–TG”, “anti–thyroid antibodies”. Furthermore, to obtain a comprehensive overview of the available knowledge, the search terms were combined with “inflammation,” “treatment,” and “pregnancy”. Treatment with levothyroxine may potentially lead to a decrease in the levels of thyroid antibodies, primarily anti–TPO, in hypothyroid women with HT. Nevertheless, the direct effect of L–T4 on anti–thyroid antibody levels remains inconclusive and varies among individuals. Treatment with L–T4 in hypothyroid women with HT was also associated with improved fertility and pregnancy outcomes. The findings summarized in this review may contribute to systematizing current knowledge regarding L–T4 therapy in women with HT and its potential benefits related to fertility. Further clinical studies are required, particularly those addressing the immunological mechanisms of levothyroxine action, which may improve therapeutic precision in HT.

Polyendocrine Metabolic Ovarian Syndrome (PMOS) is one of the most commonly diagnosed endocrine disorders among women of reproductive age. The proposed term more accurately reflects the pathophysiology of the condition, emphasizing its multisystem nature rather than restricting it to ovarian dysfunction. Polycystic ovary syndrome (PCOS) is estimated to affect approximately 6–20% of women of reproductive age. The condition is characterized by considerable clinical heterogeneity, including menstrual irregularities, hyperandrogenism, difficulties conceiving, and abdominal obesity. In addition to hormonal disturbances, an important and often underestimated aspect of PMOS is its association with insulin resistance and chronic low-grade inflammation. Current evidence indicates that insulin resistance represents an important component of the pathogenesis of PMOS. In this context, the identification of biomarkers reflecting metabolic and inflammatory disturbances in affected women is of particular interest. Pro-inflammatory lipid mediators, such as hydroxyeicosatetraenoic acids (HETEs) and hydroxyoctadecadienoic acids (HODEs), are products of fatty acid oxidation and act as active modulators of the inflammatory response. Increased concentrations of these metabolites have been reported in individuals with type 2 diabetes, excessive body weight, cardiovascular diseases, and in women with PMOS. The study included 45 women diagnosed with PMOS, who were divided into groups according to the presence of insulin resistance assessed using the HOMA-IR index. Venous blood plasma was used as the biological material, and the concentrations of selected HETE and HODE metabolites were determined using high-performance liquid chromatography (HPLC). The obtained data were subjected to statistical analysis to assess the associations between lipid mediator concentrations, parameters of carbohydrate metabolism, and selected metabolic indices. Statistical analysis revealed no significant differences in the concentrations of the analyzed oxylipins (HETE and HODE) between patient groups stratified according to HOMA-IR. No significant direct correlations were observed between most of the analyzed metabolites and body mass index (BMI) or fasting blood glucose levels. However, a nominally significant association was identified for 12S-HETE (p = 0.0258), which did not remain significant after Bonferroni correction (adjusted p = 0.1806). Its concentration was nearly twofold higher in patients with PMOS who exhibited postprandial hyperinsulinemia, assessed two hours after an oral glucose tolerance test (OGTT), compared with women who had a normal insulin response. Among the seven oxylipin metabolites analyzed, only 12S-HETE showed a nominal association with postprandial hyperinsulinemia. At the same time, the findings suggest that HOMA-IR and glycemic parameters may not fully reflect changes in the oxylipin profile in patients during the early stages of metabolic dysfunction. The concentrations of several analyzed oxylipins were strongly correlated, whereas 16RS-HETE showed only weak correlations with the other metabolites. Further studies are needed to clarify the relationship between oxylipin concentrations and metabolic dysfunction in women with PCOS/PMOS.