INTRODUCTION:Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction,and metabolic disturbances. Chronic low-grade inflammation and insulin resistance are key components of its pathophysiology.Helicobacter pylori (H. pylori) infection has been associated with systemic inflammation and metabolic alterations and may potentially affectendocrine function. The aim of this study was to assess whether H. pylori infection is associated with changes in hormonal parameters,including increased severity of hyperandrogenism, in women with PCOS. MATERIAL AND METHODS:A total of 150 patients aged 18-40 years were included and classified according to PCOS diagnosis and H. pyloriinfection status into four groups. PCOS was diagnosed based on the Rotterdam criteria. Active H. pylori infection was assessed usinga stool antigen test. Anthropometric measurements were obtained, and fasting blood samples were analyzed for hormonal (including totaland free testosterone, androstenedione, DHEAS, SHBG, LH, FSH, AMH, prolactin, cortisol) and metabolic parameters (glucose, insulin,HOMA-IR). Statistical analysis included non-parametric tests for between-group comparisons and categorical analyses, with correctionfor multiple comparisons where appropriate. RESULTS:No significant differences in age, BMI, or WHR were observed between H. pylori-positive and H. pylori-negative groups. Amongpatients with PCOS, H. pylori infection was not associated with significant differences in androgen concentrations (total and free testosterone,androstenedione, DHEAS, 9FAI) or other hormonal parameters. No significant differences were observed in gonadotropins, AMH,prolactin, cortisol, or metabolic parameters, including glucose, insulin, and HOMA-IR. In patients without PCOS, minor differences inhormonal parameters were observed; however, these were not statistically significant after correction for multiple comparisons. The frequencyof abnormal laboratory results did not differ between groups. CONCLUSIONS:In this cohort of young women, H. pylori infection, detected using a stool antigen test, was not associated with clinicallymeaningful alterations in androgen levels or ovarian reserve in women with PCOS. These findings suggest that the endocrine profile inPCOS is primarily determined by intrinsic pathophysiological mechanisms of the syndrome, which may mask the potential impact ofchronic H. pylori infection.
Introduction: Cushing’s disease (CD) results in chronic hypercortisolism with multisystem complications. Although glucocorticoids affecthematopoiesis, sex-specific hematological alterations and their reversibility following treatment remain incompletely characterized.Most previous studies have compared patients with CD with healthy controls, limiting the ability to isolate cortisol-specific effects fromtumor- or surgery-related confounders. We investigated hematological parameters in patients with CD at diagnosis and after remission,using patients with non-functioning pituitary adenoma (NFA) as controls to specifically identify hypercortisolism-driven changes. Material and methods: This retrospective study included 117 patients: 59 with CD and 58 with NFA who underwent transsphenoidal surgery. Complete blood count and hormonal parameters were evaluated at diagnosis and 3 months postoperatively. Changes in hematologicalparameters were compared between groups using repeated-measures analysis of variance, with subgroup analyses examiningremission status and sex-specific differences. Results: At baseline, patients with CD showed significantly elevated white blood cell (WBC) counts (9.50 ± 2.67 vs. 7.32 ± 1.71 × 10³/μL, p < 0.001), neutrophil counts (6.41 ± 2.35 vs. 4.30 ± 1.44 × 10³/μL, p < 0.001), neutrophil-to-lymphocyte ratio (NLR) (3.27 ± 2.03 vs.2.04 ± 0.91, p < 0.001), and red blood cell (RBC) counts (4.70 ± 0.50 vs. 4.51 ± 0.46 × 10⁶/μL, p = 0.03), with significantly lower eosinophilcounts (0.111 ± 0.093 vs. 0.166 ± 0.140 × 10³/μL, p = 0.01) compared with NFA patients. No sex-specific differences were observed inbaseline hematological parameters within the CD group. At 3 months postoperatively, significant decreases in hemoglobin (p = 0.02),WBC (p < 0.001), neutrophil counts (p < 0.001), and NLR (p = 0.006) were observed in patients with CD compared with NFA controls. Importantly, the magnitude of postoperative reductions in WBC (p = 0.01) and neutrophil counts (p = 0.009), as well as increases in eosinophil counts (p = 0.03), was significantly associated with achieving biochemical remission. Neutrophil recovery was greater in women (p = 0.03). No correlations were found between baseline cortisol levels and hematological parameters. Conclusions: Cushing’s disease demonstrates specific hematological alterations — elevated WBC, neutrophils, NLR, and RBC, with decreasedeosinophils — that are attributable to hypercortisolism rather than the presence of a pituitary tumor. These parameters normalizerapidly following surgical remission, with changes correlating with biochemical cure. Routine complete blood counts may serve as accessiblebiomarkers for monitoring disease activity and treatment response in CD.
INTRODUCTION:Ectopic fat deposition in the liver and pancreas is common in people with overweight or obesity and shares metabolic riskfactors. The relationship between intrapancreatic fat deposition (IPFD) and hepatic fat deposition, and the mediating role of visceral fat,remain unclear. This study investigated their association and the influence of visceral adipose tissue in young and middle-aged adultswith overweight or obesity. MATERIAL AND METHODS:This cross-sectional study included 197 adults (aged 18-50 years) with overweight or obesity. Hepatic and pancreatic fat contents were quantified using non-contrast computed tomography, while visceral and subcutaneous adipose tissue areas weremeasured via dual bioelectrical impedance analysis. Pearson correlation and multivariable linear regression analyses were performed,with adjustment for age, sex, and body mass index (BMI). RESULTS:Among participants, 131 (66.5%) had abdominal obesity. The association between pancreatic and hepatic fat was significantly modified by abdominal obesity (p = 0.041). Subgroup analysis showed a positive correlation only in those without abdominal obesity. CONCLUSIONS:Abdominal obesity significantly modified the association between IPFD and hepatic fat (p for interaction = 0.041). A positive correlation was observed only in participants without abdominal obesity, while no significant association was found in those withabdominal obesity. Abdominal obesity, reflecting visceral fat accumulation, weakened the pancreas-liver fat association. This suggestsa potential modulatory role of visceral fat in ectopic fat interrelationships, although causality cannot be inferred due to the cross-sectionaldesign.
INTRODUCTION:The C-reactive protein-triglyceride-glucose index (CTI) is an emerging composite biomarker reflecting insulin resistanceand systemic inflammation. Research regarding the relationship between CTI and risks of all-cause and cardiovascular mortality remainslimited and inconsistent. MATERIAL AND METHODS:Data from 9,264 USA adults aged ≥ 20 years were obtained from the National Health and Nutrition Examination Survey (1999-2010). Mortality status was determined through linkage to the National Death Index through 31 December 2019. Hazardratios (HRs) for all-cause and cardiovascular mortality were estimated using weighted Kaplan-Meier methods, restricted cubic spline(RCS) models, and multivariable Cox proportional hazards regression models. Prespecified subgroup analyses and sensitivity analyseswere conducted to assess the robustness of the findings. RESULTS:Over a median follow-up of 12.8 years, 2,644 deaths occurred, including 2,009 attributable to all causes and 635 to cardiovascular causes. After adjustment for potential confounders, each one-unit increment in CTI was associated with a 26% higher risk of all-causemortality [HR, 1.26; 95% confidence interval (CI), 1.15-1.38; p < 0.001) and a 25% higher risk of cardiovascular mortality (HR, 1.25; 95% CI,1.03-1.51; p = 0.021). Participants in the highest CTI quartile demonstrated a 33% higher risk of all-cause mortality compared with thosein the lowest quartile (HR, 1.33; 95% CI, 1.07-1.64; p = 0.010). RCS analyses indicated a nonlinear association between CTI and all-causemortality (p for nonlinearity = 0.018), with an inflection point at a CTI value of 9.25, whereas a linear association was observed for cardiovascular mortality (p for nonlinearity = 0.072). No statistically significant interactions were identified across prespecified subgroups. The results remained consistent after exclusion of early deaths (≤ 2 years) and after exclusion of participants with neoplasms. CONCLUSIONS:Higher CTI levels were independently associated with increased risks of all-cause and cardiovascular mortality among USA adults. These findings suggest that CTI may serve as a clinically relevant biomarker for early identification of individuals at elevated mortality risk, with potential implications for risk stratification, targeted prevention strategies, and healthcare resource allocation.
Introduction: Cognitive dysfunction is a common complication of the central nervous system in diabetic patients. To explore the molecularmechanism of diabetic cognitive dysfunction (DCD). Material and methods: The db/db mice and high-glucose (HG)-treated human brain astrocytes (SVG p12) and mouse hippocampalneuron cells (mHNCs) were used for mechanistic exploration. Learning and memory abilities in mice were tested using the Morris watermaze assay. The expression of lncRNA NEAT1 and miR-30e-5p and the mRNA levels of FLT1, NGF, and GPX4 were detected by RT-qPCR.Western blotting was used to analyze FLT1 and p-tau protein levels. Cell viability and apoptosis were evaluated using the CCK-8 methodand flow cytometry. Ferroptosis was assessed by measuring Fe2+ and 4-HNE levels and GPX4 expression. Target sites among NEAT1,miR-30e-5p, and FLT1 were detected using a dual-luciferase reporter assay, and their predictive value for DCD was assessed using ROCcurves and binary logistic regression analysis. Results: The db/db mice showed significant cognitive deficits. NEAT1 and FLT1 were highly expressed in the hippocampus of db/db mice and HG-treated nerve cells, whereas miR-30e-5p was expressed at low levels. Silencing NEAT1 rescued HG-induced nerve cell viabilityimpairment and ferroptosis. NEAT1 directly targeted miR-30e-5p and negatively regulated it, and miR-30e-5p directly targeted FLT1.The miR-30e-5p inhibitor partially reversed the effects of NEAT1 silencing, whereas silencing FLT1 rescued the effects of the miR-30e-5pinhibitor. NEAT1, miR-30e-5p, and FLT1 were classifiers for differentiating patients with diabetes mellitus from those with DCD, withareas under the curves (AUCs) of 0.718, 0.816, and 0.716, respectively. Their combination showed more reliable diagnostic performance(AUC = 0.896). Conclusions: The NEAT1/miR-30e-5p/FLT1 axis may mediate DCD pathogenesis by regulating ferroptosis in brain nerve cells under HG conditions. These molecules may serve as new biomarkers of DCD occurrence.
Introduction: One of the core pathological features of type 2 diabetes mellitus (T2DM) is pancreatic β-cell dysfunction. MicroRNAs, askey regulatory molecules, have emerged as pivotal post-transcriptional regulators of β-cell homeostasis, but their specific regulatorymechanisms require further clarification. This study aimed to investigate the expression characteristics and diagnostic value of miR-506-5pin T2DM and its regulatory mechanism in pancreatic β-cell function. Material and methods: A total of 45 healthy controls and 48 patients with T2DM were enrolled. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to quantify peripheral blood miR-506-5p and p21-activated kinase 1 (PAK1) levels, and theircorrelations with clinical indicators and diagnostic efficacy were analyzed. Using INS-1 cells as the model, overexpression or knockdown ofmiR-506-5p was achieved by transfecting miR-506-5p mimic/inhibitor. Combined with a dual-luciferase reporter gene assay and functionalrescue experiment, the target molecule and regulatory role of miR-506-5p were clarified. Results: miR-506-5p expression was significantly elevated in patients with T2DM, whereas PAK1 expression was significantly decreased. The area under the curve (AUC) of miR-506-5p for diagnosing T2DM was 0.904, and it was positively correlated with fasting plasmaglucose (FPG) and glycated hemoglobin (HbA1c). Cell experiment results showed that high glucose could upregulate miR-506-5p expression. Overexpression of miR-506-5p suppressed pancreatic β-cell viability, promoted apoptosis, and reduced insulin secretion, whereas knockdown reversed these effects. miR-506-5p could directly target PAK1 and negatively regulate its expression, and knockdown of PAK1 could reverse the protective effect of miR-506-5p inhibitor. Conclusions: miR-506-5p is highly expressed in T2DM, regulates pancreatic β-cell function by targeting and inhibiting PAK1, and participatesin the pathogenesis of T2DM.
Introduction: Renal cell carcinoma (RCC) is a common neoplasm with well-characterized risk factors, including obesity. The relationshipbetween adipocytokines and neoplasms remains an area of ongoing research. This study aimed to evaluate the activity of the adipocytokinenetwork in patients with RCC. Material and methods: The study group comprised 28 patients with newly diagnosed RCC and 20 controls. Serum levels of adipocytokines (adiponectin, irisin, omentin, visfatin, chemerin, resistin, apelin, vaspin, and nesfatin-1) were measured using enzyme-linkedimmunosorbent assay (ELISA). All subjects had a BMI < 30 kg/m² and normal renal function and did not have any of the diseases listedin the exclusion criteria. Results: Patients in the RCC group had lower serum levels of irisin (3.78 vs. 5.34 μg/mL, p < 0.001), adiponectin (4.92 vs. 6.89 μg/mL, p = 0.013), and nesfatin-1 (1291.0 vs. 1884.3 pg/mL, p = 0.019) than those in the control group. Resistin levels were higher in the RCC group (7.64 vs. 6.38 ng/mL, p = 0.044). We found no significant differences in the concentrations of chemerin, visfatin, apelin, vaspin, and omentin.We observed differences in correlations among adipocytokines across the study groups. In patients with RCC, positive correlations wereobserved between resistin and chemerin, resistin and vaspin, resistin and omentin, and vaspin and omentin; negative correlationswere observed between chemerin and adiponectin, resistin and irisin, and vaspin and irisin. In controls, positive correlations were observedbetween visfatin and resistin, visfatin and vaspin, chemerin and nesfatin-1, resistin and vaspin, and nesfatin-1 and apelin. Conclusions: The adipocytokine profile in patients with RCC differs from that of controls. This suggests their potential role as prognostic, diagnostic, and monitoring tools in RCC. It also suggests that patients with RCC have distinct metabolic profiles.
INTRODUCTION:Rapid on-site evaluation (ROSE) is thought to increase the adequacy of thyroid fine-needle aspiration (FNA) biopsiesand reduce overall cost. MATERIAL AND METHODS:We conducted a retrospective review of thyroid FNA cases from patients who presented to the endocrinology outpatient clinic of a tertiary center between May 2018 and March 2023. A cytopathologist performing ROSE in an FNA room in the endocrinologyclinic was available during the period June 2019-March 2023. Between May 2018 and June 2019, ROSE was not available. RESULTS:Of 1614 FNAs, 1212 were performed with ROSE by a cytopathologist and 402 without ROSE. The number of nondiagnostic FNA cases was 297 (24.6%) with ROSE and 140 (34.8%) without ROSE. In Group A (with ROSE), a total of 94 of 1212 nodules underwent repeatbiopsy, corresponding to a rate of 7.75%. In Group B (without ROSE), 59 of 402 nodules required repeat biopsy, yielding a rate of 14.7%. CONCLUSIONS:Although cytopathologist assistance during thyroid FNA increases costs, it lowers insufficiency rates by reducing the need for repeat procedures and expedites the time to definitive diagnosis.
Introduction: This prospective cohort study systematically compared neuropsychological impairments in Cushing’s disease (CD),non-functioning pituitary adenomas (NFPA), and healthy controls (HCs), and investigated the roles of HPA axis hormones (ACTH, cortisol)and inflammatory markers in cognitive dysfunction. Material and methods: A total of 107 CD patients, 110 NFPA patients, and 84 HCs were enrolled from the Chinese PLA General Hospital.Participants underwent preoperative comprehensive neuropsychological assessments, including the Mini-Mental State Examination(MMSE) and Montreal Cognitive Assessment (MoCA), Self-Rating Anxiety Scale (SAS), Self-Rating Depression Scale (SDS), PittsburghSleep Quality Index (PSQI), and Quality of Life (QOL) Scale. Clinical data were also collected. Longitudinal neuropsychological changeswere evaluated in 90 CD patients post-surgery. Statistical analyses included FDR-corrected group comparisons, correlation analyses,and multivariable regression. Results: Cushing’s disease patients exhibited significantly greater deficits in global cognition (MMSE/MoCA, q < 0.001), depression/anxiety (SDS/SAS, q < 0.006), and quality of life compared with NFPA and HCs. Critically, morning ACTH levels (8 A.M.) predicted cognitive decline, whereas cortisol showed no significant correlation. Paradoxically, inflammatory markers (WBC, neutrophils, lymphocytes) positively correlated with MMSE scores (q < 0.024), suggesting compensatory neuroprotection, which needs further investigation. Postoperatively, significant improvements occurred in affective symptoms and cognition, with maximal recovery in memory and attention. Conclusions: The CD-specific neuropsychological impairments exceed tumor mass effects in NFPA, driven by HPA hyperactivation. ElevatedACTH is an associated predictor of cognitive decline, advocating for its prioritization in clinical monitoring. Surgical remission partiallyreverses deficits, while neuroendocrine-immune crosstalk bidirectionally modulates cognition. Adrenocorticotropic hormone-centricmanagement and targeted rehabilitation may optimize long-term outcomes.
Chronic stress and sustained activation of the hypothalamic-pituitary-adrenal (HPA) axis result in elevated cortisol secretion, which caninterfere with regulation of the hypothalamic-pituitary-thyroid (HPT) axis and affect thyroid hormone metabolism and immune-mediatedmechanisms. The aim of this review is to present current evidence on the influence of stress and cortisol on thyroid function, including their effects onthe HPT axis, peripheral thyroid hormone metabolism, and autoimmunity, and to discuss potential clinical implications. A comprehensive literature search was conducted covering the last decade's clinical, population-based, and experimental studies addressingthe associations between psychological stress, cortisol levels, thyroid axis dysregulation, deiodinase activity, and autoimmune thyroiddisease. Mechanistic pathways and therapeutic perspectives are summarized. Evidence indicates that cortisol suppresses TRH and TSH secretion and disrupts the circadian rhythm of TSH secretion, while also influencingthyroid hormone transport proteins and deiodinase activity (↓ D1/↓ D2, ↑ D3), leading to reduced T3 and increased rT3. Thesemechanisms contribute to subclinical hypothyroidism and the non-thyroidal illness syndrome (NTIS) phenotype. Chronic stress alsodisturbs immune homeostasis (Treg/Th17 imbalance, elevated IL-6, TNF-α), increasing susceptibility to autoimmune thyroid diseases suchas Hashimoto's thyroiditis and Graves' disease. Emerging data suggest that stress-reduction interventions, optimization of micronutrientstatus (selenium, vitamin D, zinc), and modulation of the HPA axis may complement standard thyroid therapy. Stress and cortisol are significant but often underrecognized moderators of thyroid regulation through endocrine, metabolic, and immunologicalpathways. Incorporating assessment of chronic stress and HPA-axis activity into the diagnostic workup of thyroid disordersmay enhance clinical evaluation, and stress-targeted adjunctive interventions may improve management, particularly in patients withautoimmune thyroid disease.
Introduction: This study used optical coherence tomography angiography (OCTA) to investigate the early diagnostic value of OCTA parameters for diabetic kidney disease (DKD) in patients with non-proliferative diabetic retinopathy (NPDR). Material and methods: This prospective study enrolled patients with type 2 diabetes mellitus (T2DM) into three groups: those with T2DM without retinopathy (group A), those with non-proliferative diabetic retinopathy (NPDR) without DKD (group B), and those with NPDR and DKD (group C). All participants underwent OCTA imaging to measure vessel density (VD) in the superficial capillary plexus (SCP) and deep capillary plexus (DCP), as well as the foveal avascular zone (FAZ) area, perimeter (PERIM), and acircularity index (AI). Pearson or Spearman correlation analysis was used to explore the relationships between OCTA parameters and renal function indicators, including 24-hour urinary microalbumin, urinary albumin-to-creatinine ratio (UACR), and blood urea nitrogen (BUN). Multivariate logistic regression was performed to identify independent factors associated with NPDR with DKD. Receiver operating characteristic (ROC) curves were generated to assess the diagnostic performance of individual and combined OCTA parameters. Results: Significant differences in OCTA parameters and renal function indicators were observed among the three groups. Correlation analysis revealed that SCP-VD and DCP-VD were negatively correlated with 24-hour urinary microalbumin, UACR, and BUN, whereas FAZ area, PERIM, and AI were positively correlated with these renal markers. Multivariate logistic regression identified SCP-VD [odds ratio (OR) = 0.67], DCP-VD (OR = 0.68), PERIM (OR = 1.30), and AI (OR = 1.04) as independent factors associated with NPDR and DKD. Analysis of diagnostic performance showed that among the single parameters, SCP-VD had the best diagnostic value [area under the curve (AUC) = 0.80]. Among the different combination models, the combination of all four parameters demonstrated the highest diagnostic performance (AUC = 0.94). Conclusions: OCTA parameters (SCP-VD, DCP-VD, PERIM, AI) are closely associated with NPDR and DKD. A combined multiparameter model demonstrated excellent diagnostic efficacy for early detection. Retinal OCTA parameters may reflect early microvascular alterations associated with diabetic kidney disease.
INTRODUCTION:Papillary thyroid carcinoma (PTC) has a high incidence, and identifying key molecules is crucial for improving its treatment.This study aimed to clarify the expression, prognostic value, biological function, and regulatory mechanism of CSDE1 in PTC. MATERIAL AND METHODS:Bioinformatics analysis of TCGA data, RT-qPCR, and western blot assays were used to detect CSDE1/METTL3expression in PTC tissues and cells. CCK-8, colony formation, wound-healing, and Transwell assays were used to evaluate cell phenotypes.MeRIP-qPCR was used to detect m⁶A modification. A dual-luciferase reporter assay was used to confirm regulatory relationships. Pearsoncorrelation analysis was used to evaluate clinical correlations. RESULTS:CSDE1 was highly expressed in PTC and correlated with advanced clinical features and poor prognosis. CSDE1 knockdownsuppressed the proliferation, migration, invasion, and EMT of PTC cells. CSDE1 activated the Wnt/β-catenin pathway. Moreover, METTL3negatively regulated CSDE1 expression via m⁶A modification. CONCLUSIONS:CSDE1 promotes PTC progression through the Wnt/β-catenin pathway under the regulation of METTL3-mediated m⁶A modification, serving as a promising prognostic biomarker and therapeutic target.
INTRODUCTION:Posterior pituitary tumors (PPTs) are rare pathologies universally identified by positive immunoreactivity for thyroidtranscription factor-1 (TTF-1). They include four subtypes: pituicytoma (PC), granular cell tumor (GCT), spindle cell oncocytoma (SCO),and sellar ependymoma (SE). Because these tumors are rare, data regarding the optimal treatment strategy and prognosis are lacking. The aim of our study was to describe a large single-center cohort of patients with PPTs. MATERIAL AND METHODS:We retrospectively analyzed data from 15 patients diagnosed with PPTs among 2108 patients who underwent pituitary surgery at our institution between 2009 and 2024, examining their clinical presentations, imaging studies, surgical techniques, and recovery trajectories. The mean age was 50.5 years (range, 18-74 years). The mean follow-up time was 6.4 years (range, 0-15 years). RESULTS:We describe eight cases of PC, four of SCO, and three of GCT. The most common symptoms were visual impairment (46.7%) and headache (40.0%). Thirteen patients (86.7%) underwent endoscopic transsphenoidal surgery, ten of whom achieved gross total resection (GTR). CONCLUSIONS:The endoscopic transsphenoidal approach has proven to be a safe and highly effective method for achieving GTR in patients with PPTs. Spindle cell oncocytoma, with a higher level of vascularization than PC and GCT, poses a greater risk of surgical complicationsand may result in non-GTR.
