Objective: We investigated the diagnostic value of first-trimester adipokines and placental markers in predicting macrosomia. Methods: Out of 328 women recruited during the prenatal diagnosis between 11th and 13th week of pregnancy and subjected to follow up until delivery, we selected 26 women who gave birth to macrosomic babies and 34 women who gave birth to normal weight neonates for the evaluation of first trimester serum levels of pregnancy associated plasma protein-A, free β-human chorionic gonadotropin, placental growth factor (PIGF), and selected adipokines. Results: The mothers of macrosomic infants had higher PIGF (p = .049) and irisin concentrations (p = .00003), and lower fetuin-A levels (p = .0002) than had the mothers of normal weight babies. Newborn’s weight correlated positively with maternal irisin (R = 0.454, p = .0003) and negatively with fetuin-A concentrations (R = −0.497, p = .00005). Multiple regression analysis showed that only serum irisin concentration was a significant predictor of birth weight (β = 0.329, p = .03), explaining 14% of its variability. The sensitivity and the specificity of irisin concentration in predicting macrosomia were 0.769 and 0.794, respectively (AUC = 0.818 [95%CI: 0.708–0.928], p = .00001) with a proposed cut-off value of 1725.4 ng/ml. Conclusions: Our results suggest that mother’s irisin may be an early biomarker of macrosomia.

Thyroid inflammation during pregnancy, particularly Hashimoto’s thyroiditis (HT) and postpartum thyroiditis (PPT), has a strong genetic and epigenetic basis. Susceptibility to these conditions is associated with specific HLA haplotypes (HLA-DR3, DR4, DR5) and immune-regulatory genes, including CTLA-4, PTPN22, FOXP3, as well as thyroid-specific genes such as TSHR, TG, and TPO. CTLA-4 polymorphism (CT60) is linked to increased thyroid autoantibody production, while PTPN22 R620W variant disrupts immune tolerance, exacerbating autoreactive lymphocyte activation. Epigenetic modifications play a crucial role in HT and PPT pathogenesis. Dysregulation of microRNAs (miRNAs), including miR-146a, miR-142, miR-301, and miR-155, affects immune pathways by modulating T-cell responses and inflammatory cytokine production. Aberrant DNA methylation in genes regulating immune function, such as FOXP3 and CTLA-4, contributes to altered immune tolerance and disease progression. Oxidative stress further modulates disease severity by inducing DNA damage and enhancing inflammatory responses, particularly in pregnancy. Reactive oxygen species (ROS) promote thyroid autoimmunity by affecting placental function and fetal neurodevelopment. Understanding the interplay between genetic susceptibility, epigenetic regulation, and oxidative stress is essential for developing personalized management strategies. This review highlights the molecular mechanisms underlying HT and PPT and the potential of epigenetic biomarkers for early diagnosis and targeted therapies.

It is hypothesized that growth hormone deficiency (GHD) is associated with increased oxidative stress (OS), contributing to elevated cardiovascular risk. This preliminary study evaluates changes in OS markers and cardiovascular biomarkers in 15 adult patients with severe GHD undergoing 12 months of recombinant human growth hormone (rhGH) therapy. IGF-1 concentrations increased significantly following 6 and 12 months of therapy (p = 0.0003 and p = 0.0001, respectively). These changes were accompanied by a significant decrease in endothelin-1 (ET-1) levels at 12 months (p = 0.007), as well as reductions in asymmetric dimethylarginine (ADMA) levels at both 6 and 12 months (p = 0.01 for each timepoint). Total oxidative capacity (TOC) decreased significantly after 6 months of therapy (p = 0.02), followed by a significant increase at 12 months (p = 0.04), whereas total antioxidant capacity (TAC) showed a significant increase at 12 months (p = 0.02). Tissue fat % showed significant reductions at 6 months (p = 0.006), suggesting early improvements in body composition. Correlation analyses indicated negative associations between IGF-1 and TOC (p < 0.006; R = −0.73), and positive associations with TAC (p < 0.001; R = 0.83). These findings suggest that rhGH therapy in adult patients with severe GHD reduces OS and cardiovascular risk through the modulation of biomarkers and improved body composition. This study explores the role of rhGH therapy in reducing cardiovascular risks in GHD, emphasizing the importance of individualized treatment approaches.

Graves' orbitopathy (GO) is an important problem in endocrinology. Currently used methods of assessing the degree of activity of the autoimmune process are not satisfactory. Therefore, there is a need to establish indicators of greater utility. The study included 35 patients: 15 with GO, 10 with Graves' disease (GD) without GO and 10 controls. Patients with GO received methylprednisolone (MP) for 12 weeks. Concentrations of thyrotropin receptor antibodies (TSHRab), interleukin 17 (IL-17) and 23 (IL-23) were obtained before administering the first dose of MP, after 6 and 12 weeks of therapy, and 3 months after treatment cessation. Patients were classified as responders (n ​= ​11) if a reduction of ≥2 points in the Clinical Activity Score (CAS) was observed. A significant decrease in exophthalmos, muscles' thickness and CAS value was demonstrated after MP treatment in responders group. Significantly higher concentrations were found in baseline IL-23 between the GD and GO groups compared to controls. No statistically significant differences in serum concentrations of IL-17 and IL-23 were observed during treatment with MP and 3 months after treatment cessation. A statistically significant reduction in TSHRab concentration was demonstrated 3 months after treatment cessation compared to baseline values in responders group. Low baseline IL-17 concentration, in addition to high TSHRab titre, serves as marker of disease activity. Although, we expect that low IL-23 concentration, in addition to high TSHRab titre, could be used as predictors of disease activity and a prognostic factor of response to immunosuppressive therapy in GO.

Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy associated with significant short- and long-term risks for both mother and offspring. Increasing evidence indicates that genetic susceptibility plays a central role in GDM pathogenesis, particularly through variants affecting insulin secretion and pancreatic β-cell function. This narrative review integrates molecular, clinical, and epidemiological perspectives, highlighting population-specific effects and gene–environment interactions. Improved understanding of the genetic risk architecture may support earlier risk stratification and enable the future development of personalized strategies for GDM prevention and management, with particular emphasis on genetic polymorphisms in SLC30A8, CDKAL1, and HHEX genes consistently implicated in glucose homeostasis and β-cell integrity. These genes contribute to distinct but complementary molecular pathways underlying GDM, including impaired insulin biosynthesis, defective zinc transport within insulin granules, and altered paracrine regulation within pancreatic islets. While associations between these variants and GDM have been repeatedly demonstrated, their clinical relevance and mechanistic impact remain incompletely understood. Available evidence suggests that CDKAL1 represents the strongest genetic determinant, followed by SLC30A8, while HHEX appears to play a modulatory role. This review summarizes current findings on the molecular functions and clinical significance of these polymorphisms, highlighting population-specific effects and gene–environment interactions. Improved understanding of genetic risk architecture may support earlier risk stratification and enable future development of personalized strategies for GDM prevention and management.