Background Androgenetic alopecia (AGA) is the most common form of hair loss worldwide and has been linked to adverse psychological outcomes. This study aimed to investigate the status of AGA and depression in the Prospective Epidemiological Research Studies of the Iranian Adults (PERSIAN) Guilan Cohort Study (PGCS) population. Methods This cross-sectional study was conducted using data from 10,520 participants aged 35–70 years enrolled. AGA was diagnosed through dermatologist examination and classified using the Hamilton–Norwood scale in men and the Sinclair scale in women. Depression was defined as a documented diagnosis by a psychiatrist or psychologist and/or current antidepressant treatment. Logistic regression analyses were performed to evaluate the association between AGA and depression. Adjusted models controlled for demographic characteristics, socioeconomic status, lifestyle factors, body mass index, physical activity, substance use, and comorbidities. Results The prevalence of AGA and depression was 52.7% and 5.2%, respectively. AGA was significantly more common in men than women (65.8% vs. 41.2%, P < 0.001) and increased with age (P for trend < 0.001). Depression was more prevalent among women than men (7.3% vs. 2.8%, P < 0.001). No significant difference in depression prevalence was observed between participants with and without AGA (4.9% vs. 5.6%, P = 0.112). In multivariable logistic regression analyses, AGA was not associated with depression in the overall population (adjusted OR = 0.98, 95% CI: 0.82–1.18, P = 0.841). Similar null associations were observed in sex-stratified analyses among men and women. Conclusions Our findings illustrated that, although AGA was highly prevalent among adults and strongly associated with age and sex, it was not independently associated with depression in these population.
Background In recent years, evidence has shown that miRNAs play a crucial role in initiating and progressing many physiological-pathological processes, including diabetes and exercise. Although exercise and diabetes have been shown to affect miRNA expression, little is known about their potential roles and mechanisms. This study investigated the effects of continuous endurance training (CET) and high-intensity interval training (HIIT) on plasma miR-98-5p and miR-135-5p expression in diabetic rats. Methods and results Current study investigated the effects of CET and HIIT on plasma miR-98-5p and miR-135-5p expression in diabetic rats. Diabetes was induced in the rats by a high-fat high-fructose diet (HFHFD). They were then divided into three categories: diabetics, CET, and HIIT groups. The expression of miR-98 and miR-135 were examined after eight weeks of exercise. Compared to CET, HIIT efficiently increased miR-98 and miR-135 expression in diabetic rats. In_silico investigation shows that both miRs influence biological pathways associated with diabetes, including the insulin signaling pathways. Conclusions Our results indicated that the miR-98-5p and miR-135-5p expression levels are deregulated in the diabetic rats. Furthermore, exercise, especially HIIT, is an effective strategy for increasing miR-98-5p and miR-135-5p and improving glycemic control, lipid profile, and insulin resistance.
Background Thyroid nodules (TNs) are a common clinical condition with a certain percentage of thyroid cancer. There are no studies in Vietnam surveying the prevalence of this disease in the community. This study is carried out to investigate the prevalence of thyroid nodules and some key associated factors in adults in Thanh Tri District, Hanoi. Methods A Descriptive Cross-Sectional Study was conducted to determine the prevalence of thyroid nodules in the community, clinical and paraclinical characteristics, and their correlation with several other factors. A total of 1473 randomly selected residents over 18 years of age in Thanh Tri District, Hanoi, were included in the study. After completing the consent form, the selected participants will undergo medical history taking, clinical examination, urine iodine sampling, and thyroid ultrasound. Result A total of 1141/1473 (77,5%) cases were found to have thyroid nodules; the prevalence of thyroid nodules significantly increases with age with the highest incidence in the 61–70 age group (89.4%); the female/male ratio was 5/1. In the group with thyroid nodules, the majority were multinodular (63.9%), affecting both lobes (58.3%), size <10 mm (70.4%), TIRADS 3 (43.2%). Factors such as age ≥ 55, female gender, history of hypertension, diabetes mellitus, and dyslipidemia had a statistically significant effect on the prevalence of thyroid nodules (P < 0.05). Multivariate Logistic Regression identified two independent prognostic factors with statistical significance (p < 0.05): gender (female) and age (≥ 55 years). Conclusion This study showed that screening for endocrine disorders is crucial for individuals aged 55 and over, female, and those with a history of diabetes, hypertension, or dyslipidemia.
Aims The study evaluated the efficacy and safety of once-daily oral semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1 RA), during the 2023 Ramadan fast. Methods This prospective, observational study is a sub-analysis of the O-SEMA–FAST study that includes 87 adults with type 2 diabetes in Kuwait. Endpoints were assessed pre-Ramadan and after 20 weeks. Adjusted means and changes in HbA1c (%) and body weight were estimated using a regression model controlling for covariates. Results Mean HbA1c (%) decreased from 6.7 (50 mmol/mol) ± 1.33 at baseline to 6.4 (46 mmol/mol) ± 1.20 at study end. After adjustment for age, sex, baseline weight and HbA1c, the mean difference was 0.32% (p = 0.021). Mean body weight decreased from 90.41 kg ± 18.86 to 88.44 ± 19.68 kg (p < 0.001), while adjusted weight declined from 88.64 kg to 88.16 kg [95% CI = 87.33–88.98], (p = 0.045). Mean BMI decreased from 32.65 ± 5.98 kg/m2 to 32.28 ± 6.0 kg/m2 at the end of the study (p < 0.001). Conclusion Oral semaglutide use during Ramadan fasting was associated with modest improvements in HbA1c, body weight, and BMI, with few reported adverse events.
Monosodium glutamate (MSG; food additive E621) is a widely used flavor enhancer in processed foods and cooking, imparting a characteristic savory umami taste. Despite its culinary utility, the toxicological profile of MSG remains a topic of scientific discussion. A significant body of research, predominantly from rodent models, indicates that MSG exposure can adversely affect the hypothalamic-pituitary-gonadal (HPG) axis. Neurotoxic effects within the hypothalamus, particularly in the arcuate nucleus (ARC) and suprachiasmatic nucleus (SCN), are linked to subsequent metabolic and circadian disruptions, including obesity. Furthermore, MSG exposure has been associated with structural alterations in the pituitary gland and gonads (testes and ovaries), concomitant with dysregulation of key reproductive hormones such as testosterone, progesterone, and estradiol. These central and peripheral changes collectively compromise reproductive morphology and function. This literature review provides a comprehensive synthesis of the structural and functional impairments induced by MSG exposure—administered via subcutaneous, intraperitoneal, or oral (gavage) routes—on the hypothalamus, pituitary gland, testes, and ovaries.
Background Androgenetic alopecia (AGA) is the most common type of hair loss worldwide and may be linked to systemic metabolic abnormalities such as dyslipidemia. This study evaluated the associations between androgenic alopecia and dyslipidemia among the Prospective Epidemiological Research Studies of the Iranian Adults (PERSIAN) Guilan Cohort Study (PGCS) population. Methods This cross-sectional study included 10,520 adults aged 30–70 years. Demographic, lifestyle, and clinical data were collected. Lipid profiles, including triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), and low-density lipoprotein cholesterol (LDL), were measured. AGA was diagnosed and classified by dermatologists using the Norwood–Hamilton scale in men and the Sinclair Scale in women. Data was analyzed using SPSS software version 16, and GraphPad Prism software version 8.0.1. A significant level was set at 0.05. Results Dyslipidemia prevalence was 75.8%, higher in females than in males (P < 0.001). AGA was observed in 52.7% of participants, more common in males than in females (65.8% vs. 41.2%, P < 0.001). Overall, AGA showed no significant association with dyslipidemia (P = 0.230). However, in females, dyslipidemia was associated with higher odds of AGA (aOR = 1.16; 95% CI: 1.01–1.34; P = 0.040). A dose-response trend was observed as the number of dyslipidemia components increased (P = 0.007). Low HDL was the strongest predictor in women (aOR = 1.24; 95% CI: 1.11–1.39; P < 0.001). In contrast, no significant associations were detected in males, while paradoxical inverse relationships were noted for hypercholesterolemia and elevated LDL. Conclusion This study revealed a sex-specific association between dyslipidemia and AGA, with low HDL and multiple lipid abnormalities increasing risk in females but not in males, underscoring the need to consider gender differences in clinical evaluation and management.
Introduction Growth hormone deficiency (GHD) is an important cause of short stature, but GH stimulation tests are costly, time-consuming, and imperfect. Insulin-like growth factor-1 (IGF-1) has been proposed as a potential screening or diagnostic tool, but its accuracy is uncertain. Methods We performed a retrospective review of 431 children referred for evaluation of growth disorders between 2010 and 2020. 357 patients were included in the analysis. IGF-1 standard deviation scores (SDS), normalised for age and sex, were compared with peak GH concentrations. GHD was defined using four GH cut-offs (<3, <5, <7, and <10 ng/mL). IGF-1 SDS was evaluated using quantile regression and 2 × 2 confusion matrices to derive sensitivity, specificity, accuracy, the no-information rate (NIR), and Cohen's kappa as a chance-corrected agreement statistic, as well as ROC curve analysis. Results Peak GH concentration showed a statistically significant but very weak association with IGF-1 SDS (0.04 SDS per 1 ng/mL GH; p = 0.002). Median IGF-1 SDS did not differ materially between GHD and non-GHD groups at any GH cut-off. Sensitivity was low across GH thresholds, ranging from 18.8% to 44.1%, whereas specificity remained relatively high, ranging from 86.7% to 88.1, and accuracy did not significantly exceed the NIR at any GH threshold. Agreement between IGF-1 and GH-defined GHD was low (Cohen's kappa 0.055–0.234). Conclusion IGF-1 had poor sensitivity and limited overall diagnostic accuracy for predicting GHD across all GH cut-offs, despite relatively high specificity. Our findings support the view that IGF-1 should be interpreted as an adjunct to clinical and auxological assessment and dynamic testing, rather than as a stand-alone screening test for paediatric GHD.
Introduction The number of patients living with diabetes in Lebanon is likely an underestimate. Obesity (OBS) can be one of the precursors for cardiometabolic diseases like prediabetes (PT2DM) and type 2 diabetes mellitus (T2DM) in the young population. Our aim was to describe OBS, overweight (OWT), PT2DM, and T2DM in 10–55 years old Lebanese outpatients. We also aimed to assess how many of these patients did not seek out glycemic and weight management plus the reasons behind that. In addition, we attempted to evaluate these aims with respect to religious sects. Methods This was an observational retrospective study based on outpatients' medical record forms who presented to Ain Wazein Medical Village (AWMV) and to our private outpatient clinic over a near course of 9 months. Results 56.9% of OWT and 52.1% of OBS CI were Druze. 75.0% of OBS CIII and 66.7% of OBS CII were non-Druze (p-value < 0.05). 57.4% of PT2DM cases were non-Druze while 58.8% of T2DM patients were Druze (p-value < 0.05). 39.6% did not have OWT/OBS as a primary complaint but clinically had it. 22.7% did not consider themselves having OWT/OBS while clinically they did. 13.0% of patients were not aware of their impaired glycemia, and 100% of them had PT2DM. 12.6% regarded their glycemic status as normal while all of them had PT2DM. Conclusion There is a Druze prominence of T2DM, hypertension, and dyslipidemia, along with the considerable percentages of OWT and OBS CI. Efficient medical education is key in developing awareness among patients.
Bone formation is governed by a complex regulatory network in which osteoblast differentiation and activity are tightly controlled by transcriptional, epigenetic, metabolic, and mechanical cues. Among these regulatory layers, microRNAs (miRNAs) have emerged as critical post-transcriptional modulators that fine-tune osteogenic signaling. Increasing evidence demonstrates that a distinct subset of miRNAs functions as potent endogenous inhibitors of bone formation by directly targeting essential osteogenic genes, including RUNX2, ATF4, SMADs, β-catenin, BMP receptors, and mitochondrial regulators, and by converging on pathways such as Wnt/β-catenin, BMP/Smad, TGF-β, mechanotransduction, and mitochondrial homeostasis. Furthermore, inhibitory miRNAs operate not only within osteoblast lineage cells but also through intercellular communication, particularly via osteoclast- and MSC-derived exosomes that transfer anti-osteogenic miRNAs to recipient cells, thereby coupling resorption to suppressed bone formation. This article curates miRNAs that act as bone-formation inhibitors, providing a reference of their targets, pathways, and outcomes, and highlights their potential translational utility as therapeutic agents in conditions where suppression of bone formation is desirable, such as heterotopic ossification, fibrodysplasia ossificans progressiva, and pathological bone overgrowth.
The proliferation of plastic pollution has driven the pervasive environmental contamination by microplastics (MPs, <5 mm) and nanoplastics (NPs, <1 μm), leading to chronic human exposure through ingestion, inhalation, and transplacental transfer. This review critically examines the current state of knowledge regarding internal MPs exposure and its profound impact on human health. We synthesize evidence demonstrating that MPs act not only as physical contaminants but also as potent vectors for chemical additives—such as phthalates, bisphenols, and organotins—which acts as endocrine-disrupting chemicals (EDCs) and environmental obesogens. Mechanistically, MPs and their leachates are shown to dysregulate molecular signaling activation, and drive systemic metabolic dysfunction. These include the induction of chronic, low-grade inflammation (linked to metabolic endotoxemia and insulin resistance), mitochondrial dysfunction and oxidative stress, and the alteration of the gut microbiome composition. Furthermore, we highlighted preclinical evidence linking MPs exposure to the pathogenesis of neurodegenerative conditions, including Alzheimer's disease (AD) and Parkinson's disease (PD), mediated by blood–brain barrier disruption, neuroinflammation, and the accelerated aggregation of pathological proteins. Despite clear mechanistic insights, the precise causal relationship in human populations is obscured by a lack of standardized analytical methods and comprehensive epidemiological data. We conclude by advocating for urgent, interdisciplinary strategies—integrating high-resolution biomonitoring, advanced in vitro models, regulatory policy, and public health initiatives—to mitigate exposure and safeguard metabolic and neurological health globally.
Background Elevated serum ferritin is associated with an increased risk of Type 2 Diabetes Mellitus (T2DM), but the precise dose-response relationship, particularly potential non-linear patterns and the modifying role of erythrocyte parameters, remains unclear. Methods This cross-sectional study enrolled 4148 participants, of whom 775 had T2DM (18.7%). We used multivariable logistic regression, with restricted cubic splines (RCS), to analyze the non-linear association between log10-transformed ferritin and T2DM risk, incorporating interaction terms for erythrocyte parameters. Robustness was confirmed using stratified analysis and propensity score weighting (PSW). Results Serum ferritin levels were significantly higher in the T2DM group (P < 0.001). RCS analysis revealed a J-shaped relationship between log10-transformed ferritin and T2DM risk (P for non-linearity < 0.001), with an inflection point at a ferritin level of approximately 316 μg/L, beyond which the risk increased sharply. An S-shaped non-linear association was also observed for MCV. In stratified analyses, log10-transformed ferritin was inversely associated with T2DM risk in non-anemic participants (OR = 0.149, 95% CI: 0.063–0.350, P < 0.001), while a positive trend was observed in the anemic group (OR = 2.999, 95% CI: 0.616–14.588, P = 0.174; P_interaction = 0.189). After PSW adjustment, high ferritin (Q4 vs. Q1) was confirmed as a robust independent risk factor (OR = 2.212, 95% CI: 1.655–2.956). Conclusion A non-linear, J-shaped relationship exists between ferritin and T2DM risk, suggesting a threshold effect. This association potentially varies by anemia status. These findings emphasize the necessity of considering both non-linear effects and erythrocyte parameters in T2DM risk assessment.
Background Beyond its classical reproductive and social functions, the neuropeptide oxytocin has been hypothesized to influence eating behavior and metabolic regulation. However, most human evidence remains observational, and the directionality of associations is uncertain. Objective To estimate associations between endogenous plasma oxytocin concentrations and key behavioral and metabolic outcomes using a Bayesian target-trial emulation framework designed to reduce measured confounding while explicitly acknowledging the cross-sectional nature of the data. Methods In a cohort of 99 adults examined at the Republican Specialized Scientific-Practical Medical Center of Endocrinology (Tashkent, Uzbekistan), we emulated a two-arm trial comparing high (≥ 37.6 pg/mL) versus low (< 37.6 pg/mL) plasma oxytocin concentrations. Bayesian augmented inverse-probability weighting with overlap weighting (adjusting for age, sex, and BMI) estimated posterior associations for disordered-eating severity (Eating Disorder Examination Questionnaire [EDE-Q] global score) and metabolic indices—the hepatic steatosis index (HSI) and visceral adiposity index (VAI). Restricted cubic-spline models examined continuous dose–response relationships. Results Higher oxytocin concentrations were strongly associated with lower EDE-Q scores (posterior mean ATE = −1.20; 94% HDI = −1.65 to −0.75; P(ATE <0) = 1.000). Associations with HSI and VAI were directionally favorable but imprecise, with wide uncertainty intervals. Spline analyses suggested a monotonic reduction in EDE-Q scores across an observed assay-specific concentration interval of approximately 80–120 pg/mL. Because oxytocin and outcomes were measured concurrently, reverse causality cannot be excluded. Conclusions Within a causal-emulation analytical framework, higher endogenous oxytocin concentrations were consistently aligned with healthier behavioral–metabolic profiles.Findings are hypothesis-generating and should not be interpreted as evidence of causality or as establishing a universal clinical threshold, particularly given assay-specific measurement considerations. Confirmation in longitudinal and interventional studies is required before clinical translation.
Aim To identify predictors of incident cardiovascular disease (CVD) in patients with type 2 diabetes mellitus (T2DM) over more than four years of follow-up. Methods A total of 190 patients with T2DM were followed for a mean duration of 4.76 years. Baseline demographic, anthropometric, laboratory, and CVD-related biomarker profiles were obtained at baseline and follow-up. At baseline, 105 patients (55.3%) had established CVD. The remaining 85 patients without CVD were classified as CVD progressors (developed CVD at follow-up, n = 31) or non-progressors (no CVD at follow-up, n = 54). Between-group comparisons, delta-change analysis, and multivariable logistic regression (adjusted for demographics, diabetes duration, medications, comorbidities, and smoking) were performed to determine independent predictors of CVD development. Results At baseline, the cohort had a mean age of 50.23 ± 7.3 years, 51.6% were males, and the mean diabetes duration was 12.02 ± 5.9 years. Over follow-up, significant increases were noted in systolic blood pressure, AST, total bilirubin, alkaline phosphatase, HDL, and multiple CVD biomarkers (A2M, fetuin, L-selectin, SAP, adipsin) (all p < 0.05), while BMI, waist/hip circumference, GGT, albumin, and HbA1c significantly decreased (p < 0.01). Among the 85 patients without baseline CVD, 31 (36.5%) developed CVD. Progressors had a greater decline in platelet count (−19.42 vs +8.92, p = 0.011) and a greater increase in PF4 (+0.80 vs +0.01, p = 0.009). Platelet decline correlated negatively with CVD risk (r = −0.296, p = 0.006), whereas PF4 elevation correlated positively (r = 0.284, p = 0.009). Multivariable regression consistently identified decreasing platelet count (OR 0.981–0.985, p ≤ 0.015) and increasing PF4 levels (OR 1.557–1.760, p ≤ 0.026) as independent predictors of incident CVD. SGLT2 inhibitor use was associated with a significantly lower risk of CVD (adjusted OR 0.311, 95% CI 0.119–0.817, p = 0.018), while GLP-1 receptor agonists and DPP-4 inhibitors use showed non-significant trends towards risk reduction. Conclusion In patients with T2DM, a decrease in platelet count and an increase in PF4 independently predict incident CVD, highlighting the contribution of platelet activation to cardiovascular risk. In addition, SGLT2 inhibitor therapy appears to confer a significant protective effect against CVD in this high-risk population.ClinicalTrials.gov IDNCT05697991
Bisphenol A (BPA), a widely prevalent environmental endocrine disruptor, has been implicated in the induction of testicular oxidative stress and subsequent impairment of male reproductive function. This study investigated the ameliorative effects of N-acetylcysteine (NAC), α-tocopherol, and A. esculentus on BPA-induced oxidative stress and testosterone alterations in male Wistar rats. Thirty-six adult male Wistar rats were randomly assigned into six groups (n = 6): control, BPA only, BPA + A. esculentus, BPA + N-acetylcysteine (NAC), BPA + A. esculentus + NAC, and BPA + A. esculentus + α-tocopherol. Following exposure and intervention, testicular oxidative stress biomarkers; including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and nitric oxide (NO) as well as serum testosterone levels were evaluated. BPA exposure resulted in significant oxidative perturbations, evidenced by elevated lipid peroxidation (MDA) and nitric oxide levels, accompanied by disruptions in endogenous antioxidant defenses (SOD, CAT, and GSH) and a marked reduction in serum testosterone. Co-administration of NAC, α-tocopherol, and A. esculentus elicited variable yet generally favorable responses, including attenuation of lipid peroxidation and partial restoration of antioxidant enzyme activity and testosterone levels. However, some oxidative stress markers remained significantly altered compared to controls, indicating incomplete recovery. In conclusion, BPA induces pronounced oxidative stress and hormonal disruption in male Wistar rats. Antioxidant interventions involving NAC, A. esculentus, and α-tocopherol-containing combinations demonstrated partial modulatory effects against BPA-induced oxidative stress and testosterone disruption. These findings highlight the potential of antioxidant-based interventions as supportive strategies against environmental toxicant-induced reproductive dysfunction.
Introduction: Atherogenic dyslipidaemia is a common feature of type 2 diabetes mellitus (T2DM) and contributes substantially to increased cardiovascular risk. Antidiabetic therapies may exert differential effects on lipid metabolism and atherogenic markers. Methods: This retrospective study included 80 patients with T2DM, equally divided into two groups (n = 40 each) according to treatment regimen: metformin or sulfonylurea. Clinical and biochemical parameters including fasting blood glucose (FBG), glycated hemoglobin (HbA1c), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), and non-high-density lipoprotein (non-HDL) cholesterol were assessed at baseline and after 3 months of therapy. Correlation and regression analyses were performed to evaluate associations between glycaemic parameters and lipid profile. Results: Metformin achieved significantly greater reductions in HbA1c, total cholesterol, and non-HDL cholesterol compared with sulfonylurea (p < 0.05), while differences in FBG, TG, and HDL were not statistically significant (p > 0.05). Regression analysis identified FBG and HbA1c as independent predictors of non-HDL cholesterol levels. Pearson correlation analysis demonstrated significant positive correlations between glycaemic parameters (FBG and HbA1c) and atherogenic lipids (TC, TG, and non-HDL), whereas HDL showed inverse correlations. A strong correlation between total cholesterol and non-HDL cholesterol was also observed. Clustering of cardiometabolic risk factors, including body mass index and blood pressure, was more pronounced in the sulfonylurea group. Conclusion: Metformin appears to be more effective than sulfonylurea in improving both glycaemic control and atherogenic lipid profile. These findings suggest that metformin may confer additional cardiovascular benefits in patients with T2DM by reducing atherogenic risk.
Purpose To investigate the relationship between proliferative diabetic retinopathy (PDR) and ocular hemodynamics by measuring ophthalmodynamometric pressure (ODP) during pars plana vitrectomy (PPV) and compare the results with non-diabetic, non-vascular vitreoretinal disorders. Methods This cross-sectional study included 53 patients who underwent PPV under general anesthesia by a single surgeon. One group included 18 individuals with PDR, while the other group included 35 non-diabetic patients with conditions such as rhegmatogenous retinal detachment, macular hole, or epiretinal membrane. We used a vented-gas forced-infusion (VGFI) system to measure ODP during the operation. Systemic diastolic blood pressure (DBP), systolic blood pressure (SBP), and mean arterial pressure (MAP) were measured simultaneously. Linear mixed-effect models (LMMs) were employed to compare adjusted ODP values. Results The median age of PDR cases and non-vascular vitreoretinal cases was 65.0 and 64.0 years, respectively, without a significant difference. The mean ODP in the PDR group was 47.8 mmHg (95%CI: 44.3–51.3), and the corresponding value in the non-diabetic cases was 46.9 mmHg (95%CI: 43.7–50.0), without any significant difference (p = 0.713). The adjusted ODP values for DBP, SBP, and MAP also showed no significant difference between the groups. The DBP and MAP were substantial predictors of ODP (βs: 0.676 and 0.278, respectively). Conclusion ODP values may not differ in PDR cases compared with other non-vascular indications of PPV. The DBP is the most crucial predictor of ODP, followed by MAP. The DBP should be more closely monitored during the intraoperative period to decrease the risk of retinal ischemic events during PPV due to excessively reduced ODP.
The C-reactive protein–triglyceride glucose index (CTI) has recently emerged as an integrative biomarker capturing both inflammation and insulin resistance (IR). A growing body of evidence suggests that CTI is potentially associated with an elevated risk of cardiovascular disease (CVD). Nevertheless, the application of CTI in the context of CVD has not been comprehensively reviewed, and its potential limitations remain underexplored. In the narrative mini-review, we summarized evidence showing that higher CTI was consistently associated with an increased risk of CVD, including stroke. For instance, for each 1-unit increase in CTI, the hazard ratios (HRs) or odds ratios (ORs) for CVD ranged from 1.06 to 2.85, with a pooled effect estimate (eOR) of 1.30 (95% CI: 1.13–1.50). Similarly, each 1-unit increase in CTI or cumulative CTI (cuCTI) was associated with a 10–33% increased risk of self-reported stroke, with a pooled eOR of 1.20 (95% CI: 1.13–1.29). However, several knowledge gaps remain: (1) population-specific CTI formulas require development and validation across different demographic and clinical groups; (2) the predictive performance of CTI should, wherever feasible, be compared with that of its individual components; and (3) consistency between formula application and descriptive results must be ensured to allow meaningful comparisons.
Introduction Anastomosing hemangioma is a rare benign vascular tumor. Since its initial description, only a few cases have been reported in the literature. The adrenal gland is among the rarest locations for this tumor. These benign lesions are most often seen in patients in their fifth or sixth decades of life.Anastomosing hemangiomas are usually asymptomatic, and their diagnosis is often incidental during imaging performed for other reasons. Hypertension due to compressive mass effect from both malignant and benign lesions of the adrenal glands or kidneys has been reported in case studies. However, anastomosing hemangioma as a cause of persistent hypertension in young individuals has not been previously described. To the best of our knowledge, this is the first reported case of an adrenal anastomosing hemangioma causing persistent hypertension. Case presentation A 29-year-old male presented with a complaint of epigastric swelling of 20 years' duration, which had worsened over the past four years and became particularly bothersome one week prior to presentation. He also had a history of hypertension for the past two years, managed with three antihypertensive medications and lifestyle modifications; however, his blood pressure remained uncontrolled.An abdominal ultrasound was performed to evaluate the epigastric swelling, revealing a right adrenal mass. A subsequent contrast-enhanced computed tomography (CT) scan was obtained for better characterization, which showed an avidly enhancing right adrenal mass with central necrosis. Differential diagnoses included lipid-poor adenoma and pheochromocytoma.Due to the unavailability of percutaneous biopsy, surgical excision was planned. A simple right adrenalectomy was performed, and the specimen was sent for histopathologic evaluation. The patient recovered from surgery without complications. Histopathology revealed an anastomosing hemangioma.During follow-up at the outpatient department, the patient's blood pressure normalized, and he was subsequently discharged. Conclusion Anastomosing hemangioma of the adrenal gland is one of the rarest locations for this benign vascular tumor. The diagnosis is often incidental. In young patients presenting with persistent hypertension, secondary causes should always be considered. Although benign masses causing hypertension due to a mass effect are rare, they have been reported in the literature. Surgical excision is recommended to correct the blood pressure before end-organ damage occurs.
Neuropsychological stress has been implicated in male reproductive dysfunction; however, the mechanistic pathways linking stress exposure to fertility impairment remain insufficiently defined. Activation of the hypothalamic–pituitary–adrenal (HPA) axis during stress elevates glucocorticoids, which may suppress androgen signalling and compromise spermatogenesis. This study investigated whether neuropsychological stress impairs male fertility through glucocorticoid-mediated endocrine disruption and testosterone-dependent spermatogenic failure in male rats. Sixty Wistar rats were randomized into control and stress-exposed groups subjected to swinging stress for 3, 7, 14, or 21 days. Stressed males were paired with non-stressed female rats to assess reproductive outcomes. Serum corticosterone and testosterone concentrations, semen quality indices (sperm count, motility, morphology), testicular weight and volume, litter characteristics, and testicular histology were evaluated. Neuropsychological stress produced a graded, duration-dependent increase in serum corticosterone accompanied by a significant reduction in testosterone levels. These endocrine alterations were associated with declines in sperm count, progressive motility, and normal morphology, together with reductions in testicular weight and volume. Reproductive success decreased progressively with increasing stress duration, and mating failure occurred following 21-day exposure, whereas pup weight and litter size were not significantly altered in matings that resulted in pregnancy. Qualitative H & E evaluation did not reveal overt structural disruption of seminiferous tubules or leydig cell distribution; however, quantitative morphometric analysis was not performed. These findings are consistent with glucocorticoid-associated suppression of androgen signalling and testosterone-dependent spermatogenic failure, rather than overt testicular structural damage. Although LH, FSH, and GnRH were not directly measured, the observed endocrine pattern suggests possible HPA–HPG axis interaction linking stress exposure to male infertility.
