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M GEORGES SKROUMBIS

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Auteur de référence en rhumatologie
25 articles scientifiques publiés — un praticien à la pointe de la recherche

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Top publications · les plus citées

Aspirin dosing after acute coronary syndrome with suspected aspirin resistance: the ANDAMAN trial

European heart journal · 2026

📚 2 citations🩺 Clinique

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Abstract Background and Aims Despite current antithrombotic treatments, the recurrence of ischaemic events remains high in patients with diabetes mellitus (DM) or aspirin resistance after acute coronary syndrome (ACS). Whether twice-daily aspirin dosing reduces major adverse cardiovascular events (MACE) in this population remains unknown. Methods In this prospective multicentre, randomized trial, patients with ACS and DM or high-risk of aspirin resistance (HRAR) defined as: (i) an index event occurring while on aspirin; (ii) body mass index ≥27 kg/m2; or (iii) increased waist circumference were assigned to receive enteric-coated aspirin once daily (100 mg/day) or twice daily (100 mg morning and evening). The primary outcome was MACE, a composite of any death, myocardial infarction, stroke, urgent coronary revascularization, stent thrombosis, or acute arterial thrombotic event assessed using a time-to-first-event analysis. The main secondary outcome was major bleeding (Bleeding Academic Research Consortium type 3–5). Results In total, 2484 participants were enrolled (77.2% with DM, 55.5% with ST-elevation segment myocardial infarction). The median follow-up duration was 18 (interquartile range: 17.6–18.3) months. The primary outcome occurred in 95 of 1228 participants (7.7%) in the twice-daily aspirin group, and 110 of 1256 (8.8%) in the once-daily group (hazard ratio [HR] 0.90; 95% confidence interval [CI] 0.69–1.19; P = .42). Major bleeding rates were similar between the groups (1.9% vs 2.1%; HR 0.88; 95% CI 0.50–1.55). Conclusions In patients with ACS and DM or HRAR, twice-daily aspirin did not significantly reduce the risk of MACE compared to once-daily dosing. No significant difference was observed in major bleeding between groups. Trial Registration NCT02520921/EUDRACT No: 2015-000947-18.

Corticotropin-Releasing Hormone (CRH) in Murine Narcolepsy: What Do Genetic and Immune Models Tell Us?

Journal of sleep research · 2026

📚 1 citations🔓 Open Access📄 PDF gratuit ↗

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ABSTRACT Narcolepsy type 1 is a chronic sleep disorder of putative autoimmune aetiology, primarily caused by the loss of orexin‐producing neurons in the hypothalamus. An additional 88% reduction in corticotropin‐releasing hormone‐immunoreactive neurons of the paraventricular nucleus has been recently observed in post‐mortem brains of individuals with narcolepsy type 1. It is, however, unknown whether this reduction is specific to the paraventricular nucleus or involves other brain regions expressing corticotropin‐releasing hormone, such as the amygdala, which plays a central role in mood regulation, stress response and cataplexy. This study examined whether orexin neuron loss and/or hypothalamic neuroinflammation would affect the expression of corticotropin‐releasing hormone and other neuropeptides, including melanin‐concentrating hormone and histidine decarboxylase as a proof of concept. We used quantitative polymerase chain reaction to measure messenger RNA levels in three mice models of narcolepsy type 1: mice lacking orexin due to genetic disruption, mice with toxin‐induced orexin neuron ablation and mice with autoimmune‐mediated orexin neuron loss accompanied by hypothalamic neuroinflammation. We found no change in corticotropin‐releasing hormone expression in both the hypothalamus and amygdala across all models, regardless of the timeline or mechanism of orexin loss. Similarly, the expression of melanin‐concentrating hormone and histidine decarboxylase was unaffected. These findings suggest that the absence of orexin signalling alone is not sufficient to alter corticotropin‐releasing hormone expression. Alternative mechanisms may account for the observation made in human narcolepsy type 1 post‐mortem samples. Future human studies are warranted to identify the underlying processes and determine whether similar changes occur in other brain regions.

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M GEORGES SKROUMBIS

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Top publications · les plus citées

Publications scientifiques (25) — classées par pathologie

Transversal9

Revue générale5

Revue / méta-analyse3

Santé mentale / fatigue3

Essai clinique2

Génétique2

Recommandations2

Activité physique / Rééducation1

Risque cardio-vasculaire1

Vraie vie / RWE1

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