IntroductionEndometriosis is a chronic disease associated with substantial impairment in health-related quality of life (HRQoL) and considerable financial burden. This study aimed to examine how patient-reported financial toxicity and disease acceptance are associated with HRQoL in women with endometriosis and to assess the potential mediating role of disease acceptance in this relationship.MethodsThis cross-sectional study included 411 women with endometriosis recruited in Poland through online patient communities, social media channels, endometriosis-related networks, and a collaborating Women's Health Center. Patient-reported financial toxicity, disease acceptance, and HRQoL were assessed using the COST-FACIT, Acceptance of Illness Scale (AIS), and Endometriosis Health Profile-30 (EHP-30), respectively. The potential mediating role of disease acceptance in the association between financial toxicity and HRQoL was examined using regression-based mediation analysis with 5,000 bootstrap samples, adjusting for age, household income, previous surgical treatment, and infertility treatment.ResultsHigher COST-FACIT scores, indicating lower financial toxicity, were associated with greater disease acceptance [B = 0.618, 95% CI (0.552; 0.683), p < 0.001] and better HRQoL [B = −0.537, 95% CI (−0.711; −0.362), p < 0.001]. Greater disease acceptance was also associated with better HRQoL [B = −0.963, 95% CI (−1.144; −0.784), p < 0.001]. Mediation analysis showed a statistically significant indirect association between financial toxicity and HRQoL through disease acceptance [B = −0.595, 95% CI (−0.731; −0.472)], while the direct association remained statistically significant. Older age and previous infertility treatment were independently associated with better HRQoL (lower EHP-30 scores), whereas household income and previous surgical treatment were not.ConclusionPatient-reported financial toxicity was associated with both disease acceptance and HRQoL in women with endometriosis. The observed indirect association through disease acceptance is consistent with the possibility that psychological adaptation may represent one component of the relationship between financial toxicity and HRQoL. however, the cross-sectional design does not allow the temporal ordering or causality of these associations to be established. These findings support considering financial well-being alongside psychological factors when evaluating the broader impact of endometriosis on patients’ quality of life.
The growing number of older adults undergoing surgery has increased interest in anesthetic strategies that preserve physiological stability without worsening postoperative neurocognitive outcomes. Remimazolam is an ultra-short-acting benzodiazepine that produces hypnosis through positive allosteric modulation of the γ-aminobutyric acid type A (GABA-A) receptor and is rapidly hydrolyzed to the low-activity metabolite CNS7054. This focused narrative review examines remimazolam in older surgical patients, with particular emphasis on postoperative delirium (POD) and hemodynamic stability. Randomized trials and meta-analyses generally report fewer hypotensive events with remimazolam than with propofol, but neurocognitive findings are heterogeneous. Earlier trials in orthopedic, hip, gastrectomy, and abdominal surgery largely reported similar POD incidence, and one trial in frail patients undergoing hip surgery reported a lower POD incidence with remimazolam. In contrast, a 2026 randomized non-inferiority trial involving 455 patients aged ≥65 years undergoing lung resection found a higher overall incidence of delirium with remimazolam (48% vs. 31%), driven predominantly by emergence delirium in the post-anesthesia care unit (46% vs. 28%), whereas delirium after post-anesthesia care unit discharge through postoperative day 3 was similar (4% vs. 5%). This temporal distinction indicates that outcome definitions and assessment windows materially influence apparent treatment effects. PACU delirium is also associated with subsequent adverse outcomes in observational studies, underscoring the clinical importance of this early phenotype. The relatively consistent hemodynamic advantage of remimazolam should therefore be regarded separately from neurocognitive benefit; reduced hypotension has not yet been shown to translate into delirium prevention. Preclinical anti-inflammatory and organ-protective pathways are biologically plausible but remain unconfirmed at clinically relevant neurocognitive endpoints. Current evidence supports individualized use rather than routine selection of remimazolam for delirium prevention.
Although objective imaging markers for rehabilitation assessment are available, lumbar disc herniation (LDH) and lumbar spinal stenosis (LSS) remain two common causes of chronic low back pain (CLBP). Diffusion tensor imaging (DTI) is a non-invasive imaging modality that allows estimation of water-molecule anisotropy and assessment of the microstructure of nerve roots and paraspinal muscles. Postoperative monitoring, preoperative prognostic assessment, evaluation of conservative treatment, detection of paraspinal muscle degeneration, and prevention of injuries during military training are examples of DTI applications in the rehabilitation and prevention of lumbar degenerative disease (LDD). There are two aspects of “prevention”: primary prevention, which concerns early warning of training injuries; and secondary prevention, which concerns the quality of rehabilitation to avoid long-term disability. Initial results suggest that DTI has the potential to identify progressive recovery of fractional anisotropy (FA) following surgery, act as a preoperative outcome predictor, evaluate the efficacy of conservative treatment, and detect age- and disease-related changes in the paraspinal muscle. These results have particular implications for military personnel, where DTI could be used to monitor training load and help reduce non-combat casualties. However, most findings remain preliminary and need to be confirmed in military populations.
Kidney outcomes vary substantially among people with similar body mass index (BMI), and conventional measures of obesity do not specify the adipose compartments that lie closest to the kidney or the biological state of those tissues. Human imaging, physiological studies, and paired-tissue analyses now permit a more anatomically explicit account of kidney adiposity. Perirenal adipose tissue (PRAT), renal sinus adipose tissue (RSAT), and intrarenal lipid are distinct constructs and should not be collapsed into a single ‘fatty kidney’ construct. This critical narrative review examines kidney adiposity at the obesity–CKD interface using a claim-conditioned translational evidence continuum spanning association, partial independence from systemic adiposity, prospective association, human mechanistic support, treatment-associated depot remodeling, depot–renal response linkage, causal mediation, and treatment-effect modification. Selected kidney-associated fat measures are associated with albuminuria, filtration, intrarenal haemodynamics, and CKD status, and some signals persist after adjustment for BMI or visceral adipose tissue. In paired tissue from healthy kidney donors, PRAT and RSAT show distinct metabolic and immune profiles. However, much of the human evidence derives from cohorts enriched for type 2 diabetes, which limits extrapolation to non-diabetic obesity-associated CKD. Acquisition, segmentation, normalisation, external validation, and clinically useful thresholds also remain unsettled. Intervention studies show that selected kidney-associated fat measures can change with lifestyle or sodium-glucose cotransporter-2 inhibition, whereas major kidney-outcome trials often did not measure kidney-adiposity compartments. These parallel observations do not establish that depot remodeling mediates renal protection. Compartment-resolved assessment of kidney adiposity should therefore be regarded as a research strategy rather than a clinical classification. Its future value depends on incremental prognostic or decision information beyond eGFR, albuminuria, and validated CKD risk models, and on direct testing of whether depot modification contributes causally to kidney response.
