The process of thyroid autoimmunization develops against the background of genetic predispositions associated with class II human leukocyte antigens (HLA-DR), as well as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and forkhead transcription box protein P3 (FOXP3). Environmental factors, such as vitamin D deficiency, Zn, Se, and Mg, as well as infections, chronic stress, pregnancy, smoking, alcohol, medications, intestinal dysbiosis, and malnutrition, also play an important role. The first stage of autoimmunization involves the accumulation of macrophages and dendritic cells, as well as plasma cells. In the second stage, the mutual interactions of individual cells in the immune system lead to a decrease in the level of CD8+ in favor of CD4+, which intensifies the synthesis of T lymphocyte derivatives, especially Th1, Th17, Tfh, and Tc, reducing the level of Treg. Consequently, the number of the anti-inflammatory cytokines IL10 and IL2 decreases, and the synthesis of the pro-inflammatory cytokines IL-2, Il-12, Il-17, IL-21, IL-22, IFN-γ, and TNF-α increases. The latter two especially trigger the pyroptosis process involving the inflammasome. Activation of the inflammasome by IL-β and IL-18 produced by macrophages is one of the mechanisms of pyroptosis in the course of Hashimoto’s thyroiditis, involving Gram-negative bacteria and NLRC4. In the next step, the apoptosis of thyroid cells is initiated by the intensification of perforin, granzyme, and proteoglycan synthesis by Tc and NK cells. The current findings raise many possibilities regarding interventions related to the inhibition of pro-inflammatory cytokines and the stimulation of anti-inflammatory cytokines produced by both T and B lymphocytes. Furthermore, since there is currently no effective method for treating thyroid autoimmunity, a summary of the review may provide answers regarding the treatment of not only Hashimoto’s thyroiditis, but also other autoimmune diseases associated with autoimmunity.

Background: Hashimoto’s Thyroiditis (HT) is one of the most common autoimmune diseases worldwide, yet little is known about the role of lipid mediators in its pathogenesis. This study investigated whether there is a link between complete blood count (CBC) and arachidonic acid (AA) derivatives resulting from the activation of lipoxygenases (LOX) in 39 female patients with HT. Material and Methods: Blood samples were used as the research material. Liquid chromatography was employed to analyze the lipid mediators. Results: Neutropenia, lymphopenia and basopenia were observed in the women studied. An increase in mean corpuscular volume (MCV) and low haematocrit (HCT) and hemoglobin (HGB) levels were also noted. The highest amounts of hydroxyeicosatetraenoic acids (5S-HETE, 12S-HETE and 15S-HETE) and 5-oxo-eicosatetraenoic acid (5-oxo-ETE) were observed in the study group. The strongest positive correlations were observed between the acids and C-reactive protein (CRP), neutrophils (NEUT), and eosinophils (EOS). Furthermore, significant correlations between eicosanoids and anthropometric parameters were also presented. Conclusions: Eicosanoids may play a crucial role in the pathogenesis of HT, affecting complete blood count. Further research in this area could lead to the development of new diagnostic markers and therapeutic strategies, including those aimed at the anticancer treatment of this gland.

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.

Background: Edible and medicinal mushrooms contain bioactive compounds potentially relevant to metabolic syndrome (MetS). Methods: This narrative review was based on searches of PubMed and Embase from database inception to 10 April 2026. In vitro, in silico, animal and human studies, and systematic reviews were considered. Evidence was mapped by species, preparation, evidence level and outcome, distinguishing MetS diagnostic components from related outcomes. Results: The evidence was predominantly preclinical and addressed glucose and lipid metabolism, adiposity, inflammation, oxidative stress and gut microbiota. Human evidence was dominated by Ganoderma lucidum. The only randomized trial in participants with diagnosed MetS that assessed its diagnostic components (n = 84) found no effect of G. lucidum, alone or combined with Cordyceps sinensis, on glycemia, blood pressure, lipids, waist circumference or MetS status. Systematic reviews reported no significant effects on fasting blood glucose, blood pressure or lipid profile and a small reduction in body mass index without a corresponding change in waist circumference, although the certainty of evidence was very low. Individual, unreplicated trials reported improvements in specific components. Conclusions: Mechanistic plausibility has not translated into demonstrated clinical efficacy. Insufficient chemical characterization and standardization of preparations preclude species-specific recommendations. Trials of standardized preparations in participants with diagnosed MetS are needed.

Introduction: There is limited data in the literature on the effect of prostaglandins (PG) and thromboxanes (TX) on the development and severity of Hashimoto’s Thyroiditis (HT). This article aimed to analyze the association between blood count and the cyclooxygenase (COX) pathway in 39 women with HT. Methods: Biochemical analysis of PGE2 and TXB2 was performed using liquid chromatography (HPLC). Results: Morphological abnormalities were found in the women studied, particularly with regard to white blood cell parameters. An increase in thyroid-stimulating hormone (TSH) was associated with significantly higher levels of monocytes (p = 0.041). Correlations were also noted between the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) with TXB2 and PGE2. Furthermore, a very strong correlation was demonstrated for the first time between antibodies against tissue transglutaminase (anti-tTG) and antibodies against thyroglobulin (ATG) (r = 0.781; p = 0.007). Correlations between blood count and eicosanoids were also demonstrated. Conclusions: The results suggest the involvement of COX products in the pathogenesis of HT and hematopoiesis; therefore, this study may contribute not only to advancing knowledge, but also to developing new guidelines for diagnosing and treating autoimmune diseases.

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.