Sickle cell disease (SCD) causes pulmonary parenchymal and vascular complications with a major impact on mortality. Quantitative computed tomography (CT) assessment of pulmonary vascular “pruning” (rarefaction of small-caliber pulmonary vessels) may provide a non-invasive tool to better understand these complications. To evaluate vascular pruning in SCD and its association with clinical, functional respiratory, and imaging parameters. Non-contrast chest CT scans from 73 adult patients with SCD followed at Avicenne Hospital (Paris, France) were analyzed. Pulmonary vascular volumes were quantified using the blood volume in vessels with a cross-sectional area < 5 mm² (BV5) and the ratio of BV5 to total pulmonary blood volume (TBV), measured globally and in peripheral lung regions. These biomarkers were compared with pulmonary function tests (PFTs), CT parenchymal abnormalities, and clinical history of vascular disease. In 73 patients (mean age 33 ± 14 years; 38 women), linear opacities (78
Dans le cadre d’un accord de partenariat entre l’ISPD et le RDPLF ( https://doi.org/10.25796/bdd.v4i3.63033 ), le RDPLF est le traducteur français officiel des recommandations de l’ISPD. Le RDPLF s’engage à traduire fidèlement le texte original sous la responsabilité de néphrologues connus pour leur expertise dans le domaine. La traduction est disponible sur le site de l’ISPD et dans le Bulletin de la Dialyse à Domicile. Cette traduction est, comme l’original, librement téléchargeable sous licence copyright CC By 4.0 https://creativecommons.org/licenses/by-nc/4.0/. Cette traduction est destinée à aider les professionnels de la communauté francophone à prendre connaissance des recommandations de l’ISPD dans leur langue maternelle. Toute référence dans un article doit se faire au texte original en accès libre : https://doi.org/10.1177/08968608261461639. Dans les articles rédigés pour des revues françaises, conserver la référence à la version originale anglaise ci-dessus, mais ajouter « traduction française : https://doi.org/10.25796/bdd.v9i3.87129
Background: Cancer-related cognitive impairment (CRCI) affects quality of life, daily functioning and return-to-work. However, CRCI remains under-addressed in cancer care. Since cognitive complaints often co-occur with fatigue and psychological distress, a multimodal approach is warranted. We developed Integrative Neuro-Cognitive Remediation Therapy (INCRT), a multidisciplinary survivorship program combining personalized cognitive function and strategy training with group-based psychoeducation, cognitive-behavioral therapy and Acceptance and Commitment Therapy, and onco-yoga. Methods: Cancer survivors suffering from CRCI were eligible. Assessments included neuropsychological testing, patient-reported outcomes, and daily functioning at baseline (T0), post-intervention (T1), and 6-month follow-up (T2). Primary outcomes were objective and subjective neurocognitive functioning (NCF); secondary outcomes were psychological distress, fatigue, metacognition, and daily functioning. Changes were analyzed using linear mixed models. Results: Between November 2022 and January 2025, 44 of 56 eligible survivors enrolled; 38 completed the program (71.1% female; median age 53.5). Objective and subjective NCF improved significantly at T1 and T2 (ps < 0.001). Psychological distress, fatigue, and unhelpful metacognitions decreased over time (ps < 0.05). Participants reported greater emotional and cognitive insight and improved daily functioning. Conclusions: INCRT improves cognitive functioning, reduces psychological distress and fatigue, and enhances daily functioning, with benefits maintained at follow-up. The integrative design supports sustained effects by promoting internalization and daily application of learned strategies.
BACKGROUND & AIMS:Severe alcohol-related hepatitis (AH) has high short-term mortality, and corticosteroid therapy is recommended in the absence of contraindications. However, its benefit in patients with early spontaneous bilirubin improvement remains unknown. We aim at determining whether corticosteroid therapy improves survival compared with placebo in this specific population. METHODS:In this multicenter, randomized, placebo-controlled trial conducted in 10 Belgian hospitals (from February 2018 to May 2024), patients aged ≥18 yr with biopsy-proven severe AH and spontaneous bilirubin decline >10% between admission and Day 5-10 were randomized 1:1 to methylprednisolone 32 mg daily or placebo for 28 days. The primary outcome was 90-day survival; other outcomes included 30-day survival and cumulative incidence of infection at 90 days. RESULTS:We analyzed 69 (49%) of the 140 planned patients (38 corticosteroid, 31 placebo). Baseline characteristics were well balanced. At 90 days, survival was 79% (95% CI 67-93%) vs. 83% (95% CI 70-98%) (hazard ratio 1.19, 95% CI 0.39-3.63, p = 0.76). Eight deaths occurred in the corticosteroid arm vs. five in the placebo arm. At 30 days, survival was 95% vs. 94% (p = 0.83). Cumulative incidence of infection at 90 days was 47% vs. 34% (subdistribution hazard ratio 1.55, 95% CI 0.72-3.34, p = 0.26). Lille score was an independent predictor of 90-day mortality. CONCLUSIONS:In patients with severe AH and early spontaneous bilirubin improvement, corticosteroid therapy was not associated with improved survival, but the underpowered trial cannot exclude a benefit. A short observation period after admission may help identify patients who can be managed without corticosteroids. IMPACT AND IMPLICATIONS:Corticosteroid therapy is recommended for patients with severe alcohol-related hepatitis (AH), but whether this benefit extends to those who show early spontaneous improvement in bilirubin after admission was previously unknown. In this multicenter, randomized, placebo-controlled trial, corticosteroid therapy was not associated with improved 90-day or 30-day survival in patients with severe, biopsy-proven AH and a spontaneous bilirubin decline of >10% within 5-10 days of admission. Corticosteroids were associated with a numerically higher, though not statistically significant, risk of infection. These findings are most relevant to hepatologists and other clinicians managing severe AH, and to researchers designing future AH trials, as they identify a subgroup in whom the benefit of corticosteroids is uncertain. They support a risk-stratified approach in which a brief observation period after admission-incorporating bilirubin trend, infection screening, and liver biopsy-may help identify patients with a relatively favorable prognosis who can be spared corticosteroid therapy and its associated risks. However, because the trial was stopped early after enrolling only 69 of the 140 planned patients, it was underpowered, and a modest survival benefit of corticosteroids cannot be excluded. Therefore, these results should not be interpreted as definitive evidence against corticosteroid use in this population. Larger, adequately powered studies are required to validate these findings before informing clinical guidelines or being generalized to broader patient populations. CLINICAL TRIAL REGISTRATION:ClinicalTrials.gov (NCT03160651), EudraCT number: 2016-005136-16.
Extremes of Body Mass Index (BMI) spectrum have been linked to impaired executive functions, including inhibitory control. While altered neural responses are documented in overweight and obese individuals, less is known about the full BMI spectrum, particularly in underweight adults. This study examined behavioral and neural correlates of reactive inhibition across four BMI groups (underweight, normal-weight, overweight, obese) in 87 young adults (Mage = 22.82, SD = 4.18). Participants performed a Go/NoGo task in neutral and food-related contexts while EEG was recorded. Analyses focused on N2d and P3d components. No behavioral differences emerged between groups. However, P3d amplitudes (but not N2d) showed significant BMI-related modulation (F(3,83) = 2.76, p = 0.047), driven by larger amplitudes in overweight participants compared to underweight and normal-weight individuals. Curve estimation analysis revealed a significant quadratic relationship between BMI and P3d amplitude (R2 = 0.073, p = 0.041), which provided a superior fit compared to the linear model (R2 = 0.061, p = 0.021). Elevated BMI is associated with increased neural recruitment during inhibition, suggesting a compensatory mechanism to maintain behavioral performance. The quadratic pattern suggests that this compensatory efficiency reaches a plateau or begins to stabilize beyond the overweight range. These findings highlight the importance of indexing neural inhibitory markers to identify cognitive vulnerabilities in weight regulation.
