Daily Endocrinology Research Analysis
Analyzed 28 papers and selected 3 impactful papers.
Summary
Longitudinal insulin resistance profiling in CKM stages 0–3 shows sustained IR burden predicts incident CVD, partly mediated by biological age acceleration. A PRISMA-compliant meta-analysis finds higher intracranial aneurysm prevalence among patients with pituitary adenoma, informing preoperative imaging strategies. A multimodality meta-analysis in MASLD demonstrates consistent associations with adverse imaging biomarkers (CAC, EAT, CAP, LSM), while emphasizing that incremental predictive value beyond clinical scores remains unproven.
Research Themes
- Longitudinal insulin resistance and biological aging in early CKM stages
- Endocrine–neurovascular interface: pituitary adenoma and intracranial aneurysms
- Imaging biomarkers for cardiometabolic risk stratification in MASLD
Selected Articles
1. Longitudinal associations of cumulative and repeated-measure patterns of insulin resistance surrogate indices with biological age acceleration and incident cardiovascular disease across cardiovascular-kidney-metabolic syndrome stages 0-3: evidence from CHARLS 2011-2020.
In 3948 adults with CKM stages 0–3, higher cumulative and unfavorable longitudinal patterns of TyG-based indices, METS-IR, CTI, and TG/HDL-C predicted incident CVD, whereas higher cumulative eGDR was protective and showed the best discrimination (AUC 0.613). Biological age acceleration (KDM and Light-BioAgeAccel) partially mediated IR–CVD links (up to 45.8% and 25.9%).
Impact: This study operationalizes longitudinal IR profiling and integrates biological aging metrics to explain CVD risk in preclinical CKM stages, offering a scalable framework for early prevention.
Clinical Implications: Incorporating cumulative eGDR and longitudinal IR patterns into risk assessments may help identify high-risk patients before overt CVD, informing timing and intensity of lifestyle or pharmacologic interventions.
Key Findings
- 19.1% developed incident CVD over 2011–2020; higher cumulative TyG-based indices, METS-IR, CTI, and TG/HDL-C were associated with increased CVD risk.
- Higher cumulative eGDR was protective and achieved the best discrimination (AUC 0.613; all DeLong P<0.05 vs other indices).
- K-means longitudinal pattern groups showed least favorable IR trajectories linked to higher CVD risk.
- Biological age acceleration partially mediated IR–CVD associations (up to 45.8% for KDM and 25.9% for Light-BioAgeAccel).
Methodological Strengths
- Prospective national cohort with repeated IR surrogate measurements and advanced competing-risk modeling.
- Comprehensive evaluation across 12 IR indices with pattern analysis and formal mediation by biological aging metrics.
Limitations
- Observational design limits causal inference; discrimination (AUC 0.613) is modest.
- Generalizability may be limited to middle-aged and older Chinese adults; IR surrogates are not clamp-based measures.
Future Directions: External validation in diverse populations, interventional trials guided by longitudinal IR profiles, and mechanistic studies targeting aging pathways to reduce CVD risk.
BACKGROUND: Cardiovascular-kidney-metabolic (CKM) syndrome stages 0-3 represent a critical window for preventing progression to overt cardiovascular disease (CVD). Insulin resistance (IR) is central to CKM pathophysiology, yet the comparative utility of longitudinal IR patterns (cumulative burden and longitudinal pattern groups) across multiple surrogates, and the mediating role of biological ageing, remain unexamined in this preclinical population. METHODS: We included 3948 participants with CKM stages 0-3 from the CHARLS 2011-2020. Twelve IR surrogates (TyG and derivatives, METS-IR, CTI, eGDR, TG/HDL-C) were assessed via cumulative exposure and K-means-derived pattern groups. Associations with incident CVD were evaluated using Fine-Gray competing risk models, spline regression, receiver operating characteristic analyses, and quantile-based models. Mediation analyses quantified the contribution of biological age acceleration. RESULTS: 756 (19.1%) of 3948 participants with CKM stages 0-3 developed incident CVD. Higher cumulative levels and the least favorable pattern groups of TyG-based indices, METS-IR, CTI, and TG/HDL-C were consistently associated with increased CVD risk, whereas elevated cumulative eGDR was protective. Cumulative eGDR demonstrated superior predictive performance for CVD risk (AUC: 0.613; all DeLong P < 0.05 vs. other indices) and was consistently identified as the top contributor by both WQS and Qgcomp analyses. Both KDM- and Light-BioAgeAccel partially mediated several IR-CVD associations (up to 45.8% and 25.9%, respectively). CONCLUSIONS: Sustained IR burden and unfavorable longitudinal IR patterns are linked to higher CVD risk in CKM stages 0-3, partly through accelerated biological aging. Integrating longitudinal IR profiling with aging metrics may sharpen early risk stratification and support scalable prevention targeting upstream metabolic drivers.
2. Pituitary adenoma and intracerebral aneurysms: case series, systematic review and meta-analysis.
Across 71 studies, the pooled prevalence of intracranial aneurysms among pituitary adenoma patients was 4% (95% CI 2–4%), with higher sex-specific prevalence than in the general population. Aneurysms were most often in the cavernous internal carotid segment, and macroadenomas predominated.
Impact: By quantifying aneurysm prevalence and anatomical patterns in pituitary adenoma, this meta-analysis directly informs preoperative vascular imaging and surgical risk mitigation.
Clinical Implications: Consider routine or selective CTA/MRA screening for intracranial aneurysms in pituitary adenoma—particularly macroadenomas and in women—during preoperative planning to prevent catastrophic intraoperative events.
Key Findings
- Pooled IA prevalence among PA patients: 4% (95% CI 2–4%; I²=92.1%).
- Sex-stratified prevalence higher than general population: females 8% (95% CI 6–9%), males 6% (95% CI 4–7%).
- IAs most commonly located in the cavernous internal carotid segment (33%); PAs predominantly macroadenomas (91.9%).
- IA diagnosis tended to occur later than PA diagnosis (p<0.01).
Methodological Strengths
- PRISMA 2020-compliant systematic review with separate analyses of individual-level and aggregate prevalence data.
- Risk-of-bias assessment using Joanna Briggs Institute tools and standardized meta-analytic methods (metaprop in R).
Limitations
- High heterogeneity (I²=92.1%) across prevalence studies limits precision and may reflect varying imaging strategies.
- Underlying data are observational; potential selection and publication biases cannot be excluded.
Future Directions: Prospective registries with standardized vascular imaging protocols in PA, and decision-analytic studies to optimize cost-effective IA screening strategies.
PURPOSE: Intracranial aneurysms (IAs) and Pituitary Adenoma (PA) coexistence has been reported for decades, yet available evidence remains fragmented. We performed a systematic review and meta-analysis following PRISMA 2020 guidelines to assess clinical features of patients with both conditions and quantify the prevalence of IAs in PA patients. METHODS: PubMed and Embase were searched up to December 15, 2025. Studies reporting coexistence of IAs and PAs were included. Individual patient-level data (Group 1) and aggregate prevalence data (Group 2) were analyzed separately. Risk of bias (RoB) was assessed using Joanna Briggs Institute tools. All analyses were performed using metaprop function from the meta package in R software. RESULTS: Seventy-one studies met inclusion criteria. Most studies have a low RoB. In Group 1 (74 patients), PAs were predominantly macroadenomas (91.9%), most frequently non-functioning (40.5%). IAs were mainly in the cavernous segment of the internal carotid artery (33%). IA diagnosis occurred significantly later than PA diagnosis (p < 0.01). In Group 2 (5264 patients), the pooled prevalence of IAs among PAs was 4% (95% CI 2-4%; I² = 92.1%, τ² = 1.1050, p < 0.0001). Sex-stratified prevalence was 8% (95% CI: 6%-9%) in females and 6% (95% CI: 4%-7%) in males. IAs sex-specific prevalence was significantly higher in both male and female PA patients as compared to the general population (p < 0.01). CONCLUSION: Patients with PAs show a higher IAs prevalence compared with the general population, likely reflecting combined hemodynamic, anatomical, and endocrine influences.
3. Imaging Biomarkers for Cardiometabolic Risk Stratification in MASLD: Incremental Value of CAC, EAT, CAP, and LSM Beyond Clinical Scores.
Across 16 observational studies (n=34,713), MASLD was consistently associated with higher odds and levels of CAC, EAT, CAP, and LSM, indicating concurrent adverse subclinical atherosclerotic and hepatic imaging burden. The study cautions that incremental predictive value beyond established clinical scores has not been established and requires prospective testing.
Impact: This multimodality synthesis consolidates quantitative evidence that MASLD coexists with adverse cardiometabolic imaging phenotypes, setting a rigorous benchmark and analytic framework for future incremental prediction studies.
Clinical Implications: Clinicians should recognize the higher burden of subclinical atherosclerosis and hepatic stiffness in MASLD, while avoiding overinterpretation of imaging as independently predictive beyond validated risk engines until prospective incremental analyses are available.
Key Findings
- MASLD associated with higher odds of modality-specific thresholds: CAC (OR 1.41), high EAT (OR 1.44), high CAP (OR 1.47), high LSM (OR 1.49).
- Continuous measures showed higher CAC by 49.2 Agatston units and higher LSM by 0.57 kPa in MASLD versus comparators.
- EAT and CAP continuous analyses (k=2 each) showed high heterogeneity and were exploratory, not suitable for precise point estimates.
- Authors emphasize these are concurrent imaging differences, not proof of incremental predictive value beyond established clinical scores.
Methodological Strengths
- Comprehensive search across four databases with REML random-effects and Hartung–Knapp adjustment.
- Modality-specific threshold and continuous analyses with explicit heterogeneity quantification (I², τ²).
Limitations
- Predominantly observational data with residual confounding; substantial heterogeneity for CAC and EAT/CAP continuous analyses.
- Incremental prediction beyond clinical risk scores was not assessed prospectively.
Future Directions: Prospective cohorts and trials with pre-specified incremental prediction metrics (discrimination, reclassification, net benefit) integrating CAC, EAT, CAP, and LSM into MASLD risk engines.
OBJECTIVES: To systematically synthesize evidence on the association between metabolic dysfunction-associated steatotic liver disease (MASLD) and imaging biomarkers of subclinical atherosclerosis and hepatic steatosis/fibrosis, and to quantify the magnitude of these associations across study populations. METHODS: We systematically searched PubMed, Embase, Web of Science Core Collection, and Cochrane Library (January 2000-February 28, 2026) for observational studies enrolling adults with MASLD (or historical NAFLD/MAFLD) that reported atherosclerotic cardiovascular disease (ASCVD)-related imaging outcomes. Primary outcomes were continuous coronary artery calcium (CAC; Agatston units), epicardial adipose tissue (EAT; cm3), controlled attenuation parameter (CAP; dB/m), and liver stiffness measurement (LSM; kPa). Weighted mean differences (WMDs) for continuous outcomes and odds ratios (ORs) for dichotomized thresholds were pooled using random-effects models with restricted maximum likelihood (REML) estimation and Hartung-Knapp adjustment where applicable; heterogeneity was quantified with I2 and τ2. RESULTS: Sixteen observational studies (n = 34,713; 6 cohort, 10 cross-sectional) from North America, Asia, and Europe were included. In modality-specific threshold analyses, MASLD was associated with higher odds of subclinical disease: CAC (OR 1.41, 95% CI 1.32-1.51; I2=75.0%), high EAT (OR 1.44, 95% CI 1.21-1.68; I2=0%), high CAP (OR 1.47, 95% CI 1.35-1.58; I2=0%), and high LSM (OR 1.49, 95% CI 1.31-1.66; I2=0%). For continuous outcomes, CAC was higher by 49.2 Agatston units (95% CI 46.8-51.7; I2=75.4%) and LSM was higher by 0.57 kPa (95% CI 0.46-0.68; I2=0%) in MASLD versus comparators. EAT (k = 2; n = 4,306): WMD 76.18 cm³ (95% CI 5.04-147.32; I2=98.3%) (exploratory only; not suitable for point estimation). CAP (k = 2; n = 6,652): WMD 45.12 dB/m (95% CI 0.96-89.27; I2=98.1%) (exploratory only; not suitable for point estimation). CONCLUSIONS: MASLD is consistently associated with greater calcific coronary burden, pericoronary adiposity, hepatic steatosis, and hepatic stiffness relative to non-MASLD comparators. These findings represent between-group imaging differences and should be interpreted as evidence of concurrent adverse imaging burden rather than formal demonstration of incremental predictive value beyond validated clinical risk engines. Whether these biomarkers improve discrimination, reclassification, or net clinical benefit beyond established scores (Pooled Cohort Equations [PCE], SCORE2, Framingham Risk Score [FRS]) requires prospective validation with pre-specified incremental prediction analyses. ADVANCES IN KNOWLEDGE: This study provides a comprehensive quantitative, multimodality synthesis demonstrating that MASLD is consistently associated with concurrent adverse changes across four key imaging biomarkers spanning subclinical atherosclerosis (CAC, EAT) and hepatic disease burden (CAP, LSM), establishing a critical evidence base to motivate prospective studies on integrating standardized imaging protocols to refine ASCVD risk characterization in MASLD populations.