Endocrine-disrupting chemicals (EDCs) are a diverse, comprehensive group of mostly synthetic chemicals that disrupt many physiological functions in humans and animals. EDCs are particularly disruptive to the female reproductive system. Reproductive function in women is a dynamic process regulated by the hypothalamic–pituitary–ovarian axis. EDCs show their effects on the reproductive system through estrogenic, antiestrogenic, androgenic, and antiandrogenic effects or by directly affecting gonadotropin-releasing hormone secretion. Disruption in the menstrual cycle, decrease in fertility, infertility, increased risk of miscarriage, polycystic ovary syndrome, endometriosis, early or delayed puberty, and hormone-sensitive cancers can be listed as the main negative effects of endocrine disruptors on the female reproductive system. In this review, findings on the effects of the most studied EDCs, bisphenol A, phthalates, methoxychlor ethane, tetrachlorodibenzo-p-dioxin, atrazine, per- and polyfluoroalkyl substances, and micro- and nanoplastics on the female reproductive system are summarized.

Background/Objectives: Dry eye disease (DED) is now widely considered to be the most prevalent ocular surface-related disease and has attracted increasing clinical attention in recent years. DED is well-studied in thyroid orbitopathy, but scarce data are available in patients with papillary thyroid carcinoma (PTC). Methods: We analyzed 29 PTC cases with radioactive iodine (RAI) treatment (Group 1), 22 PTC cases without RAI (Group 2), and 26 normal control individuals (Group 3). All participants were evaluated with the Ocular Surface Disease Index (OSDI), meibomian gland secretion quality, and lid margin grading. Non-contact meibography and non-invasive tear breakup time measurements were completed using the Sirius Scheimpflug camera. Thyrotropin (TSH), free thyroxine, and free triiodothyronine were measured. Results: TSH values were significantly lower in both patient groups than in controls (p < 0.001). The proportion of participants with a lower meibomian gland secretion quality score ≥ 1 was 34.5% in Group 1, 22.7% in Group 2, and 7.1% in Group 3 (p = 0.002). There was a higher proportion of a meibomian gland atrophy score ≥ 1 in Groups 1 and 2 than in controls (p = 0.007). No differences were found between groups in lower lid margin score, Oxford values, upper meibomian gland expressibility or upper meibography scores (p = 0.485, p = 0.064, p = 0.256, p = 0.069). OSDI scores were higher in both PTC groups than in controls (6.25 and 8.12 vs. 2.52), with borderline overall significance (p = 0.050) and higher pairwise scores versus controls (both p = 0.034). Conclusions: Meibomian gland dysfunction was observed in PTC patients regardless of RAI treatment, suggesting that TSH suppression itself may contribute to the development of ocular surface changes.

Background: Insulin-like growth factor-1 (IGF-1) plays a role in metabolism and immune regulation. Although obesity is associated with chronic inflammation, the relationship between IGF-1 levels and systemic inflammatory markers remains unclear. This study aimed to examine the association between IGF-1 levels, systemic inflammation, and metabolic comorbidities in individuals with obesity. Methods: This retrospective cross-sectional study included 214 adults with a BMI ≥35 kg/m ² evaluated between June 2019 and March 2025. Participants were classified as low IGF-1 (standard deviation score [SDS] ≤ −2.0) or standard IGF-1 (−2.0 < SDS < 2.0). Clinical and laboratory data were analyzed, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio, systemic immune-inflammation index (SII), systemic inflammation response index, and systemic inflammation aggregate index. Results: Low IGF-1 was identified in 8.88% of patients. No differences were found between groups regarding diabetes, dyslipidemia, or hypertension. NLR (2.21 vs. 1.79; p = 0.005) and SII (614.6 vs. 521.8; p = 0.041) were significantly higher in the standard IGF-1 group. SII was positively correlated with systolic blood pressure, alanine aminotransferase, and insulin. IGF-1 SDS was not correlated with inflammatory markers. Conclusions: Lower IGF-1 levels were not associated with higher systemic inflammation. These findings highlight the heterogeneity of inflammatory responses in obesity and suggest the need for further research.

Background/Objectives: Atypia of undetermined significance (AUS; Bethesda category III) remains a challenging thyroid cytological diagnosis because of its heterogeneous malignancy risk and limited preoperative certainty. Molecular testing can improve risk stratification but is not universally available. This study evaluated the diagnostic and incremental predictive value of preoperative complete blood count-derived systemic inflammatory indices in surgically treated Bethesda III thyroid nodules. Methods: This retrospective cohort included 352 patients who underwent thyroidectomy for Bethesda III thyroid nodules. Preoperative neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI) were evaluated. Postoperative histopathology served as the reference standard. Receiver operating characteristic analysis and multivariable logistic regression were performed, followed by incremental model assessment, bootstrap internal validation, Hashimoto thyroiditis interaction analysis, and exploratory molecular subgroup analysis. Results: Among 352 patients, 197 (56.0%) had malignant histopathology. Malignant nodules showed higher NLR, PLR, SII, SIRI, and AISI and lower LMR. All six indices remained independently associated with malignancy after multivariable adjustment, with the strongest positive associations observed for SII (adjusted OR, 2.09; 95% CI, 1.60–2.72) and NLR (adjusted OR, 1.96; 95% CI, 1.51–2.54). SII demonstrated the numerically highest individual discrimination (AUC 0.687; 95% CI, 0.631–0.740), followed by NLR (AUC 0.661) and AISI (AUC 0.659); SII and NLR did not differ significantly (DeLong p = 0.182). Addition of SII increased the AUC of the clinico-ultrasonographic model from 0.695 to 0.761, with an optimism-corrected AUC of 0.721. Hashimoto thyroiditis did not significantly modify these associations. In the molecular subgroup, mutation status increased model discrimination from 0.765 to 0.824, whereas no statistically significant additional improvement with SII was detected in the exploratory molecular subgroup. Conclusions: Preoperative systemic inflammatory indices, particularly SII, provide modest but incremental predictive information beyond conventional clinical and ultrasonographic variables in surgically treated Bethesda III thyroid nodules. Their role appears complementary rather than diagnostic when used in isolation, particularly when comprehensive molecular testing is unavailable. Prospective external validation is required before clinical implementation.

Hypertension remains one of the leading causes of global morbidity and mortality and is the leading modifiable risk factor for cardiovascular disease worldwide. The inability of conventional risk factors alone to fully explain the global prevalence of hypertension, together with accumulating evidence implicating endocrine-disrupting chemicals (EDCs) in the pathogenesis of hypertension, has led to growing scientific interest in this field over recent years. EDCs are exogenous environmental chemicals capable of disrupting hormone synthesis, transport, metabolism, and signaling pathways, thereby adversely affecting vascular and metabolic homeostasis. In particular, per- and polyfluoroalkyl substances (PFASs), bisphenol A, phthalates, PCBs, heavy metals, and pesticides have been associated with hypertension and may influence blood pressure regulation through multiple interconnected mechanisms, including oxidative stress, endothelial dysfunction, inflammation, epigenetic modifications, and activation of the renin–angiotensin–aldosterone system. Moreover, prenatal exposure to EDCs has been associated with hypertensive disorders of pregnancy, including gestational hypertension and preeclampsia, with potential implications for long-term maternal cardiovascular health. This review provides a comprehensive overview of the experimental and epidemiological evidence linking endocrine-disrupting chemicals to hypertension, with particular emphasis on the underlying molecular mechanisms, emerging clinical evidence, and future research directions.

Background/Objectives: This study aimed to evaluate pancreatic steatosis and its association with the triglyceride index in patients with pheochromocytoma and paraganglioma (PPGL). Methods: In this retrospective single-center study conducted between 2 January 2019 and 30 April 2024, thirty-three patients with confirmed PPGL and thirty-three age-, sex-, and body mass index (BMI)-matched healthy controls were evaluated. The mean age of the study population was 49.7 ± 12.3 years, and 32 participants (48.5%) were female. Pancreatic fat infiltration was assessed via computed tomography (CT). Body composition parameters, including visceral fat area (VFA), subcutaneous fat area (SFA), skeletal muscle area (SMA), and skeletal muscle area index (SMAI), were also measured. Laboratory data, including lipid profiles, glucose, hemoglobin A1c (HbA1c), and triglyceride index (TyG), were analyzed. Results: Pancreatic steatosis, as indicated by significantly lower pancreatic attenuation values, was markedly higher in the PPGL group compared to controls (p < 0.001). No significant differences were observed between the groups in terms of VFA (p = 0.218), SFA (p = 0.413), SMA (p = 0.669), or SMAI (p = 0.562). Pancreatic fat was positively correlated with triglyceride levels, VLDL, TyG index, BMI, and VFA. No correlation was found between catecholamine levels and pancreatic steatosis. Conclusions: Our findings indicate an increase in pancreatic steatosis in patients with PPGL, suggesting a potential association between catecholamine excess and the development of ectopic fat deposition. These results support considering pancreatic fat as a marker of metabolic dysfunction in PPGL.