Search Results (289)

Background/Objectives: Allogeneic hematopoietic stem cell transplantation is associated with increased cardiovascular risk driven by endothelial dysfunction, chronic inflammation, and treatment-related metabolic disturbances, including dyslipidemia. In the contemporary era of post-transplant cyclophosphamide-based prophylaxis, the prognostic significance of dyslipidemia—particularly as assessed by non-HDL cholesterol—remains unclear. In this study, we aimed to compare the engraftment days, graft-versus-host disease (GVHD) development, relapse, overall survival rates, and cardiovascular mortality in patients using myeloablative/reduced intensity conditioning regimens with post-transplant cyclophosphamide (PTCy) 50 mg/kg/day for 2 days in patients with acute leukemias. Methods: A total of 95 adult patients with acute leukemias were included in their first remission who underwent matched sibling donor transplantation with PTCy (50 mg/kg on days +3 and +4). Patients were stratified according to pre-transplant non-HDL-C levels (<160 mg/dL vs. ≥160 mg/dL). Matched related donors were selected for the patients. All patients received either myeloablative or reduced-intensity conditioning based on EBMT criteria, with fludarabine-based combinations including busulfan, treosulfan, or TBI, along with ATLG administered at a total dose of 15 mg/kg. Peripheral blood stem cells were used for all transplants, and GVHD prophylaxis consisted of cyclosporine. Results: Platelet (median 13 vs. 14 days) and neutrophil (median 14 vs. 15 days) engraftment times and veno-occlusive disease (VOD) rates were comparable across groups (all p > 0.05); cumulative incidences of grade II–IV aGVHD at +100 days, grade III–IV aGVHD at +100 days, and moderate-severe cGVHD at 1 year, relapse-free survival, and non-relapse mortality at 1 year were comparable in two cohorts (all p > 0.05). GVHD-free/relapse-free survival (GRFS) at 1 year was also comparable across groups (p = 0.15). Median GRFS was 150 (95% CI: 120–330) days and 270 (95% CI: 154-not reached) days, respectively [HR was 0.68 (0.40–1.15), p = 0.15; GRFS at 1 year was 66.6% vs. 52.0%, respectively]. The groups were also comparable in terms of overall survival (OS). Follow-up ranged from 0.5 to 108 months, and median follow-up was 60 months in two cohorts. Median OS was not reached in non-HDL-C < 160 (95% CI: 70 months–not reached) and 67 months in non-HDL-C ≥ 160 groups (95% CI: 13 months–not reached) (Log rank = 0.21). No cardiovascular death events occurred during the follow-up period. Conclusions: In this homogeneous matched sibling donor transplant cohort with extended follow-up and uniform administration of post-transplant cyclophosphamide, cyclosporine-based GVHD prophylaxis, and anti-thymocyte lymphoglobulin (ATLG), pre-existing dyslipidemia was not associated with an adverse impact on GRFS, NRM, PFS, CMV reactivation, OS or long-term cardiovascular mortality. Full article

Background: Type 2 diabetes mellitus (T2DM) is characterized by chronic low-grade inflammation that contributes to cardiometabolic complications. While diabetes duration reflects cumulative metabolic exposure, its relationship with systemic inflammatory burden remains insufficiently defined. We aimed to investigate inflammatory patterns across diabetes duration and to explore their metabolic and cardio–renal correlates. Methods: This real-world cross-sectional study included 250 adults with T2DM. Diabetes duration was analyzed both continuously and across four predefined strata (0–4, 5–9, 10–14, and ≥15 years). Inflammatory burden was assessed using C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Given the skewed distribution of CRP, log-transformed CRP was used in regression analyses. Nonlinear associations were evaluated using quadratic regression models. This approach was selected because preliminary descriptive analyses suggested a non-monotonic relationship between diabetes duration and CRP levels. Inclusion of a quadratic term allowed formal testing of a potential curvilinear association between diabetes duration and inflammatory burden. Spearman correlations were performed to assess associations with metabolic, renal, and cardiovascular variables. Results: CRP showed a nonlinear cross-sectional association across diabetes duration strata. Median CRP values were higher in early (0–4 years: 0.62 mg/L) and long-standing diabetes (≥15 years: 0.77 mg/L) compared with intermediate-duration groups (p = 0.063). Quadratic regression confirmed a U-shaped relationship (adjusted β_duration = −0.079, p < 0.001; β_duration² = 0.0027, p < 0.001; R² = 0.326). ESR differed significantly across duration strata (p = 0.002), with the highest levels observed in long-standing diabetes. CRP correlated positively with BMI (ρ = 0.151; p = 0.017) and triglyceride-to-HDL ratio (ρ = 0.215; p < 0.001), but not with HbA1c. Both CRP and ESR were more strongly associated with functional CKD (ρ = 0.350 and 0.429, respectively; p < 0.001) than with ASCVD. Conclusions: Inflammatory burden in T2DM shows a nonlinear cross-sectional pattern across diabetes duration, characterized by elevated levels in early and long-standing disease. Systemic inflammation appears more closely linked to renal dysfunction than to established cardiovascular disease. These findings support a cardio–renal–inflammatory axis in which prolonged diabetes exposure contributes to renal decline, which in turn amplifies systemic inflammatory activation. Full article

Olive pomace, a byproduct of olive oil production, is a rich source of bioactive phenolic compounds with potential health benefits. This study aimed to characterize the chemical composition and evaluate the metabolic effects of a subcritical water extract from California olive pomace (SWE COP) obtained from Arbequina olives. The extract was mainly composed of carbohydrates (72.81%) and contained 66.62 ± 1.22 mg gallic acid equivalents/g of phenolics, with 3,4-DHPEA-EDA, hydroxytyrosol, and verbascoside identified as the predominant compounds. Male C57BL/6N mice were fed a standard diet (SD; n = 7), a high-fat and high-sugar diet (HFSD; n = 7), which was used to induce features of diet-associated metabolic syndrome, or an HFSD supplemented with 3% (w/w) SWE COP (n = 7) for 16 weeks. Supplementation with SWE COP significantly reduced plasma triglycerides and increased HDL cholesterol levels compared with the HFSD group. Moreover, SWE COP improved glucose tolerance, enhanced insulin sensitivity, and reduced mesenteric and epididymal adiposity. Histological analysis showed that SWE COP alleviated hepatic steatosis and lowered the NAFLD activity score. These findings demonstrate that phenolic-rich SWE COP exerts beneficial effects on glucose and lipid metabolism and reduces liver fat accumulation in diet-induced obese mice. Overall, SWE COP represents a promising functional ingredient derived from olive industry byproducts for mitigating metabolic dysfunctions associated with obesity. Full article

Kidney transplantation (KTx) corrects many uremia-related metabolic disturbances; however, dyslipidemia remains common in kidney transplant recipients and contributes to persistent cardiovascular risk. Lipoprotein(a) [Lp(a)] is a largely genetically determined proatherogenic lipoprotein that increases in advanced chronic kidney disease (CKD) and may decrease after restoration of renal function. Autotaxin (ATX), an enzyme involved in proinflammatory lipid signaling through the ATX–lysophosphatidic acid axis, has also been implicated in cardiovascular pathology, but its early post-transplant dynamics remain poorly characterized. In addition to quantitative lipid abnormalities, CKD is associated with high-density lipoprotein (HDL) dysfunction and reduced paraoxonase-1 (PON-1) activity; however, data on early post-transplant changes in PON-1 activity are limited. In this prospective observational study, lipid profile parameters, Lp(a) concentration, ATX activity, and PON-1 activity were assessed in 55 Caucasian patients with CKD stage 5, most of whom were dialysis-dependent, before and 2–3 weeks after KTx. All recipients received tacrolimus-based maintenance immunosuppression with corticosteroids and mycophenolate mofetil. After KTx, Lp(a) levels decreased by a median of 21% and ATX activity by 28% (both p < 0.001). Lp(a) and ATX showed no cross-sectional or longitudinal association either before or after transplantation, and their percentage changes were not correlated. In contrast, conventional lipid fractions increased significantly, including total cholesterol (+22%), LDL cholesterol (+27%), HDL cholesterol (+24%), and triglycerides (+55%) (all p < 0.001). PON-1 activity increased by approximately 13% after KTx (p < 0.001), and its percentage change correlated positively with the increase in HDL cholesterol. In exploratory analyses, the magnitude of Lp(a) reduction was associated with early graft function: patients with eGFR <45 mL/min/1.73 m² exhibited a significantly smaller decline in Lp(a) than those with better graft function (−4.8% vs. −26.7%, p = 0.009). Multivariable analysis showed that demographic characteristics, body mass index, tacrolimus exposure, and post-transplant eGFR did not independently predict the magnitude of Lp(a) reduction. Tacrolimus trough concentrations and cumulative corticosteroid exposure were not associated with lipid parameters or their changes, except for a single subgroup difference in PON-1 activity of uncertain clinical significance. In summary, in the early period after KTx under tacrolimus-based immunosuppression, Lp(a) concentration and ATX activity decrease, whereas conventional lipid fractions increase and PON-1 activity improves. These changes were not associated with tacrolimus exposure or cumulative corticosteroid dose. The reduction in Lp(a) was associated with early graft function in exploratory analyses, suggesting that recovery of renal function may contribute to early post-transplant Lp(a) dynamics; however, no independent causal relationship was established, and the findings should be interpreted cautiously given the limited sample size and exploratory design. The clinical significance of these changes for long-term cardiovascular and graft outcomes requires further investigation. Full article

Background/Objectives: Peritoneal membrane failure remains a major limitation of peritoneal dialysis (PD). Systemic inflammation contributes to membrane dysfunction, yet simple predictive biomarkers are lacking. The uric acid-to-HDL cholesterol ratio (UHR) represents a novel integrative marker of metabolic-inflammatory burden, but its association with membrane failure has not been investigated. Methods: This retrospective cohort study included adult patients who initiated PD between 1997 and 2023. Baseline UHR was calculated from laboratory measurements obtained within the first three months after PD initiation. The primary outcome was peritoneal membrane failure, defined as permanent transfer to hemodialysis due to ultrafiltration failure, inadequate solute clearance, or progressive membrane dysfunction. Receiver operating characteristic, Kaplan–Meier, and Cox regression analyses were used to evaluate the association between UHR and membrane failure. Results: Among 214 patients, 62 (29%) developed membrane failure during follow-up. Baseline UHR was significantly higher in patients with membrane failure. A UHR cut-off value of 14 was identified for risk stratification. In multivariable Cox regression analysis, UHR >14 was independently associated with an increased risk of membrane failure (hazard ratio 1.836, 95% CI 1.040–3.241). A history of kidney transplantation prior to PD initiation also emerged as a strong independent predictor of membrane failure. Conclusions: Elevated baseline UHR is independently associated with peritoneal membrane failure in PD patients. As a simple and readily available biomarker, UHR may support early risk stratification and individualized management. Prospective multicenter studies are warranted to validate these findings. Full article

Background: Spirulina supplementation combined with structured exercise may improve obesity-related metabolic dysfunctions. This research examined whether this combination enhances body composition, glucose levels, lipid profile, and cardiorespiratory fitness in overweight and obese adults. Methods: Following PRISMA 2020 guidelines, a systematic search of Scopus, PubMed, and Web of Science identified randomized controlled trials (RCTs) evaluating spirulina (1–6 g/day) combined with structured exercise in individuals with overweight and obesity (BMI ≥ 25). The search retrieved 91 records, of which 10 studies met the inclusion criteria and were included in the systematic review. Nine studies provided sufficient post-intervention data and were included in the quantitative meta-analysis using a random-effects model, with heterogeneity assessed using τ², Q, and I² statistics. Publication bias was evaluated using rank correlation, regression-based tests, trim-and-fill, and fail-safe N analyses. Results: Combined spirulina supplementation and structured exercise (6–12 weeks) was associated with reductions in BMI (−1.34 kg/m²), body fat percentage (−3.03%), fasting glucose (−14.47 mg/dL), LDL-C (−12.68 mg/dL), and triglycerides (−9.81 mg/dL), along with increases in VO2max (3.25 mL/kg/min) and HDL-C (4.21 mg/dL). Effect estimates were generally larger in combined exercise–spirulina subgroups, particularly in HIITsupp and R-AEsupp conditions, whereas supplementation-only comparisons demonstrated smaller and less consistent changes. Inflammatory markers and adipokines (CRP, TNF-α, MCP-1, IL-6, IL-8) showed favorable directional changes in individual trials. Conclusions: Spirulina combined with structured exercise was associated with changes in anthropometric, glycemic, cardiorespiratory, and lipid parameters in individuals with overweight or obesity. Full article

Background/Objectives: Coronary collateral circulation (CCC) reduces ischemic damage in patients with chronic total occlusion (CTO), yet collateral development varies considerably among individuals. Endothelial stress and systemic inflammation are key biological processes involved in collateral vessel formation. The Endothelial Activation and Stress Index (EASIX), calculated from lactate dehydrogenase, creatinine, and platelet count, is a simple marker reflecting endothelial dysfunction and inflammatory status. However, evidence regarding its relationship with angiographic coronary collateral development in CTO remains limited. Therefore, this study aimed to evaluate the association between EASIX and CCC grades in patients with CTO. Methods: This retrospective study included 186 patients with CTO who underwent coronary angiography. CCC was evaluated using the Rentrop–Cohen classification and categorized as poorly developed (grades 0–1) or well-developed (grades 2–3). Clinical and laboratory data, including EASIX, were collected. Univariate and multivariate binary logistic regression analyses were performed to identify factors associated with poorly developed CCC. EASIX was standardized (z-score), and odds ratios were reported per 1-standard deviation increase. The predictive performance of EASIX was assessed using receiver operating characteristic (ROC) curve analysis. Results: Poorly developed CCC was observed in 70 patients (37.6%). Patients with well-developed CCC had significantly lower EASIX values (median 0.44 vs. 0.67, p < 0.001) and higher HDL cholesterol levels (p = 0.043). Neutrophil-to-lymphocyte ratio was also higher in the poorly developed CCC group (median 2.59 [2.19–3.59] vs. 2.41 [1.59–3.49], p = 0.028). In multivariate analysis, standardized EASIX remained independently associated with poorly developed CCC (OR 2.536 per 1-SD increase, 95% CI 1.734–3.710, p < 0.001). ROC analysis showed that EASIX provided moderate discrimination for poorly developed CCC (AUC 0.718), with 72.9% sensitivity and 62.1% specificity at a cutoff of >0.51. Conclusions: Higher EASIX values were independently associated with poorly developed CCC in patients with CTO. These findings support a link between systemic endothelial stress and impaired collateral vessel formation. EASIX may serve as a simple, practical, and low-cost biomarker to support risk stratification in CTO patients; however, prospective studies are needed to confirm these results and clarify clinical implications. Full article

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder associated with insulin resistance (IR), visceral adiposity, and increased cardiometabolic risk. The visceral adiposity index (VAI) is a validated surrogate marker of adipose tissue dysfunction, but its relationship with circulating neurotrophins and adipokine balance in PCOS remains incompletely understood. In this study, 100 women with PCOS were stratified into lower- (n = 50) and higher-risk (n = 50) groups according to VAI. Anthropometric measures, fasting glucose and insulin concentrations, lipid profile, and serum levels of brain-derived neurotrophic factor (BDNF), nerve growth factor-β (NGFβ), leptin, adiponectin, and resistin were assessed. HOMA-IR, adipokine ratios and atherogenic indices were calculated. Multivariate regression showed that BDNF was independently associated with VAI and non-HDL cholesterol, whereas NGFβ was independently linked to HDL cholesterol and estradiol, highlighting neurotrophin relationships with metabolic and endocrine parameters beyond general adiposity. Correlation heatmap and network analyses demonstrated interconnected clusters linking visceral adiposity, IR, dyslipidemia, adipokine imbalance, and neurotrophins, with the leptin/adiponectin ratio emerging as a central integrative marker. These findings suggest that within a PCOS population, VAI-defined cardiometabolic risk is associated with distinct neurotrophin–adipokine signatures, highlighting neurotrophin–adipokine networks underlying visceral adiposity-driven cardiometabolic and endocrine risk. Full article

Background/Objectives: This study aimed to evaluate the predictive value of the triglyceride-glucose index with body mass index (TyG-BMI) and the triglyceride-to-high-density lipoprotein-cholesterol (TG/HDL-C) ratio for predicting the occurrence of metabolic dysfunction-associated steatotic liver disease (MASLD) in obstructive sleep apnea (OSA). Methods: Data from patients diagnosed with OSA were analyzed in this retrospective cohort study. The participants were stratified into two groups: OSA alone and OSA with MASLD. The clinical characteristics and polysomnography data were collected. TyG-BMI and TG/HDL-C ratios were categorized into tertiles. Logistic regression and receiver operating characteristic (ROC) curve analyses were conducted to identify risk factors and assess their predictive performance for MASLD in OSA. Results: Among the 133 patients with OSA, 104 (78.2%) were diagnosed with MASLD. Multivariate analysis identified alanine aminotransferase (ALT), alkaline phosphatase, and TyG-BMI as independent risk factors for MASLD development in patients with OSA. Both TyG-BMI and TG/HDL-C ratio were significant predictors of MASLD in this patient population. The optimal cut-off values for TyG-BMI and TG/HDL-C ratio were 0.546 (sensitivity, 79.6%; specificity, 75.0%) and 0.539 (sensitivity, 93.2%; specificity, 60.7%), respectively. Combining TyG-BMI with ALT improved the predictive accuracy, yielding a cutoff of 0.696 (sensitivity, 76.7%; specificity, 92.9%). Similarly, the combination of TG/HDL-C ratio with ALT resulted in a cutoff value of 0.728 (sensitivity, 83.5%; specificity, 89.3%). Conclusions: TyG-BMI and the TG/HDL-C ratio are effective predictors of MASLD in patients with OSA. A combined model incorporating these indices with ALT levels demonstrated enhanced predictive accuracy for MASLD in this population. These indices are well-suited for risk stratification in resource-constrained settings facing a rising dual burden of OSA and MASLD. Full article

Background: Coronary slow flow (CSF) is a microvascular disorder characterized by delayed perfusion despite the absence of significant epicardial stenosis. Although its exact pathophysiology remains unclear, endothelial dysfunction, oxidative stress, and atherogenic dyslipidemia have been implicated. Traditional lipid parameters may not fully capture the atherogenic burden, whereas atherogenic indices such as the atherogenic index of plasma (AIP), atherogenic coefficient (AC), and Castelli risk indices (CRI-I and CRI-II) may provide better predictive value. This study aimed to investigate the association between atherogenic indices and CSF in a large real-world angiographic cohort. Methods: This retrospective study included 25,486 patients who underwent coronary angiography between September 2020 and June 2024. A total of 464 patients with CSF (diagnosed by TIMI frame count criteria) and 408 controls with normal coronary flow (NCF) were identified. Atherogenic indices, including AIP, AC, CRI-I, CRI-II, and non-HDL cholesterol (non-HDL-C), were calculated. Multivariate logistic regression analysis identified independent predictors of CSF, while receiver operating characteristic (ROC) curve analysis was used to assess the diagnostic performance of each lipid-related parameter. Results: Patients with CSF had significantly higher AIP, AC, non-HDL-C, and CRI indices and lower HDL-C levels compared to controls (all, p < 0.05). Multivariate analysis identified AIP (OR: 1.73, 95% CI: 1.18–2.44, p = 0.004), age (OR: 1.02, 95% CI: 1.01–1.06, p = 0.014) and smoking (OR: 2.22, 95% CI: 1.36–2.84, p = 0.003) as independent predictors of CSF. ROC analysis showed modest but statistically significant discriminatory capacity for AIP (cut-off: 0.50; AUC: 0.629; 95% CI: 0.591–0.667; p < 0.001). AIP also demonstrated a weak yet significant correlation with mean TIMI frame count (rho = 0.245, p < 0.001), suggesting a potential link to microvascular dysfunction. Conclusions: Among the evaluated atherogenic indices, only AIP demonstrated an independent association with CSF. Despite modest discriminative performance that does not support standalone clinical prediction, AIP may reflect an underlying metabolic phenotype associated with CSF and serve as a complementary marker alongside traditional risk assessment. These findings should be interpreted as hypothesis-generating and warrant prospective validation. Full article

Background: Acne in adult women is increasingly recognized as a condition with systemic endocrine–metabolic correlates. Evidence linking acne to thyroid-related abnormalities and cardiometabolic risk markers remains mixed, and integrated real-world evaluations combining thyroid biochemistry, ultrasound metrics, inflammatory indices, and lipid profile are limited. Methods: We performed a cross-sectional observational analysis of 80 women with acne who underwent routine laboratory testing and thyroid ultrasound assessment. Thyroid status was defined using TSH (reference 0.4–4.5 mIU/L) and free T4 (0.8–1.8 ng/dL), with an additional TSH-only sensitivity definition (high TSH >4.5 mIU/L). Low HDL-cholesterol (HDL-C) was defined as <50 mg/dL. Group comparisons used Mann–Whitney U tests with Hodges–Lehmann shifts; associations were summarized using odds ratios (ORs) with Fisher’s exact tests; correlations used Spearman’s ρ (TSH log-transformed for correlation analyses) with confidence intervals. Multiple testing was controlled within panels using Benjamini–Hochberg FDR. Analyses were complete-case per comparison. Results: Thyroid dysfunction and metabolic–inflammatory abnormalities were common in this cohort. Low HDL-C was more frequent in thyroid dysfunction, and in the TSH-only sensitivity analysis, high TSH (>4.5 mIU/L) was strongly associated with low HDL-C (OR 13.13, 95% CI 1.48–116.04; p = 0.020). In a minimal adjusted model including NLR, high TSH remained associated with low HDL-C (adjusted OR 12.93, 95% CI 1.44–115.70; p = 0.022). HDL-C showed an inverse association with NLR (ρ = −0.28; p = 0.023). Endocrine profiling suggested a positive association between ACTH and log(TSH) (ρ = 0.62; p = 0.004), although this did not remain significant after FDR correction. Thyroid ultrasound metrics showed limited correspondence with thyroid biochemistry. Conclusions: In women with acne, elevated TSH is associated with substantially higher odds of low HDL-C, independent of inflammatory burden as proxied by NLR, while thyroid ultrasound morphology contributes limited functional information. These findings support integrated thyroid–metabolic assessment in adult female acne and motivate prospective studies incorporating acne severity measures and standardized testing to clarify clinical implications. Full article

Background: Menopause is accompanied by hormonal alterations that are closely linked to changes in body composition, insulin sensitivity, and cardiovascular risk in women. Gremlin-1 has recently been identified as an adipokine involved in metabolic and reproductive aging; however, its associations with endocrine and lipid biomarkers across the menopausal transition remain incompletely defined. Objectives: To evaluate the relationships between plasma Gremlin-1 and IGF-1, HDL cholesterol, estradiol, and age in reproductive-aged and postmenopausal women. Methods: This cross-sectional study included 88 women aged 18–65 years, stratified by menopausal status (reproductive-aged vs. postmenopausal). Plasma concentrations of Gremlin-1, growth hormone, IGF-1, insulin, estradiol (E2), glucose, HbA1c, and a standard lipid profile were measured. Results: Plasma Gremlin-1 concentrations were significantly higher in postmenopausal women compared with reproductive-aged women (p < 0.001). Age (p = 0.013), but not menopause status (p = 0.874), was associated with Gremlin-1 levels. Gremlin-1 showed a strong inverse association with IGF-1 (p = 0.003) and a negative correlation with HDL cholesterol (p = 0.03) in non-obese women; however this association disappeared after adjustment for age. Conclusion: Circulating Gremlin-1 primarily reflects chronological aging and associated endocrine–metabolic changes rather than menopausal status or adiposity per se. While unadjusted associations with metabolic biomarkers are detectable, these relationships are largely attributable to aging. Gremlin-1 may therefore serve as a marker of systemic aging-related endocrine–metabolic remodeling rather than a specific indicator of ovarian aging or adipose tissue dysfunction. Full article

Atherosclerosis is a progressive cardiovascular disease characterized by lipid accumulation, oxidative stress, and inflammation within the arterial walls. Environmental pollutants, including particulate matter (PM), diesel exhaust particles (DEPs), and heavy metals, contribute directly to the initiation and progression of arterial plaques by promoting LDL oxidation, endothelial dysfunction, foam cell formation, and vascular inflammation, whilst high-density lipoprotein (HDL) provides protective effects. This review examines the mechanistic links between environmental exposures, lipid dysregulation, and plaque formation, highlighting how both gaseous and particulate pollutants and toxic and essential metals, as well as endocrine disrupting chemicals, influence atherosclerotic risk. Potential antioxidant and lifestyle interventions to mitigate these pollutant-driven effects are also discussed. Full article

Background/Objectives: Background: Dyslipidaemia and oxidative stress (OS) are frequent in peritoneal dialysis (PD). The Lipoprotein Combine Index (LCI) integrates lipid parameters, but its relationship with peritoneal transport and OS is unclear. Methods: This cross-sectional study included 100 clinically stable adults on continuous ambulatory PD with preserved ultrafiltration and adequate dialysis. LCI was calculated as (total cholesterol × triglycerides × LDL-C)/HDL-C and analyzed by tertiles. Lipid peroxidation and antioxidant markers were measured in serum, erythrocytes, urine, and spent dialysate. Multivariable regression models examined associations between LCI, peritoneal solute transport, and dialysate OS markers. Results: Higher LCI was independently associated with lower peritoneal solute transport. LCI correlated inversely with the 4 h dialysate-to-plasma creatinine ratio (ρ = −0.32, p = 0.001) and remained significant after adjustment (adjusted R² = 0.224, p < 0.001). Increasing LCI was associated with higher malondialdehyde levels in serum, urine, and dialysate (all p ≤ 0.008) and impaired antioxidant defenses, including lower total peroxidase activity in erythrocytes and dialysate (both p = 0.001), reduced serum sulfhydryl groups (p = 0.011), decreased oxidative resistance of erythrocytes, and increased peroxide-induced hemolysis (both p = 0.001). In adjusted models, logLCI was independently associated with higher dialysate malondialdehyde (p < 0.001) and lower dialysate peroxidase activity (p = 0.005). Conclusions: In clinically stable PD patients, higher lipid burden assessed by LCI is independently associated with lower peritoneal solute transport and a marked increase in systemic and local OS. Our findings suggest that dyslipidaemia may contribute to early metabolic and oxidative changes even before overt peritoneal membrane dysfunction develops. Full article

Cardiovascular diseases and metabolic dysfunction-associated steatotic liver disease (MASLD) are increasing sharply worldwide and share overlapping pathophysiological pathways, including oxidative stress, inflammation, hyperglycemia, obesity, dyslipidemia, and hypertension. Dark chocolate, rich in cocoa flavanols such as epicatechin and catechin, exhibits antioxidant and anti-inflammatory effects. Based on these properties, this narrative review uniquely integrates evidence on chocolate’s effects on both cardiovascular and hepatic health, exploring shared mechanisms and clinical implications. Evidence from clinical studies suggests that chocolate modulates nitric oxide bioavailability and NADPH oxidase activity. Clinical findings demonstrate improvements in flow-mediated dilation, decreased NT-proBNP, reduced intestinal permeability and endotoxemia, improved lipid profile (increased HDL-c and reduced total cholesterol, LDL-c, and triglycerides), increased plasma polyphenols, improved platelet function, and attenuated hepatocyte apoptosis. These findings suggest a potential role for cocoa flavanol-rich dark chocolate in cardiometabolic health; however, the evidence remains preliminary and is limited by heterogeneous study designs, small sample sizes, and short intervention durations. Despite these limitations, current evidence supports the inclusion of moderate dark chocolate consumption as a possible adjunct strategy to mitigate cardiometabolic and hepatic metabolic risks. Further large-scale, long-term trials are needed to confirm these beneficial effects and to standardize the dosage and formulation of cocoa flavanols. Full article