Kenichi Ikejima

Background: Spleen stiffness (SS) is a noninvasive marker of portal hypertension; however, the clinical significance of early changes in SS after endoscopic treatment for esophageal varices remains unclear. We evaluated whether SS and its early post-treatment changes are associated with variceal recurrence. Methods: This retrospective pilot study included 20 patients who underwent endoscopic treatment for esophageal varices. Liver stiffness (LS) and spleen stiffness (SS) were measured before treatment, approximately 1 week after the final treatment session (1W), and at 1 month and 1 year after treatment. The clinical outcome of interest was variceal recurrence within 1 year. Early changes in stiffness were calculated from 1W to 1M (Δ1M − 1W). Results: Eleven patients (55.0%) developed variceal recurrence. LS did not differ significantly between the non-recurrence and recurrence groups at any time point during follow-up. SS was comparable between the groups before treatment and at 1W but was significantly higher in the recurrence group at 1M (median [IQR], 2.75 [2.70–2.86] vs. 3.40 [3.06–3.81] m/s in the non-recurrence and recurrence groups, respectively; p = 0.003). ΔSS-VTQ (1M − 1W) was significantly greater in the recurrence group than in the non-recurrence group (−0.13 [−0.62–−0.04] vs. 0.25 [−0.05–0.40] m/s, respectively; p = 0.013), whereas no significant between-group differences were observed in changes in LS. Conclusions: SS at 1 month after endoscopic treatment and its early post-treatment change were associated with variceal recurrence. Serial assessment of SS may provide useful information for early post-treatment risk assessment, although validation in larger prospective studies is needed.

The hepatic sinusoid is increasingly recognized as a multicellular, spatially organized, and therapeutically actionable regulatory niche rather than merely a specialized microvascular bed. Liver sinusoidal endothelial cells, HSCs, KCs, recruited leukocytes, lymphocytes, cholangiocytes, hepatocytes, and extracellular matrix components form dynamic networks that coordinate vascular exchange, immune surveillance, metabolic zonation, tissue repair, and systemic communication. Recent advances in single-cell and spatial omics, quantitative imaging, mechanobiology, and human tissue models have revealed how endothelial dedifferentiation, macrophage and T-cell programming, stellate cell plasticity, extracellular matrix remodeling, and stromal control of cancer immunity interact across disease stages. These insights recast fibrosis, portal hypertension, metabolic dysfunction–associated steatotic liver disease, and liver cancer as disorders of sinusoidal communication and niche organization, while linking sinusoidal dysfunction to aging and extrahepatic axes. In this review, we trace the evolution of sinusoidal research from cellular specialization to integrated niche biology, focusing on the next unresolved layer: which cell-cell interactions are causal, how they change with disease stage, and how they can be measured or perturbed in human tissue. We define priorities for mapping disease-stage–specific human niches, restoring protective functions, developing composite biomarkers, and standardizing translational platforms. We propose that the hepatic sinusoid be considered as a tissue-level regulatory unit whose failure can be interrogated through coupled vascular, stromal, immune, metabolic, and mechanical readouts.

Introduction: Cell‐free and concentrated ascites reinfusion therapy (CART) alleviates the symptoms of malignant ascites but may trigger inflammation. We investigated why AHF‐MO filter (A‐A)–processed concentrates showed weaker bioactivity than EC20W filter (A‐E)–processed concentrates. Methods: Ascites from three patients with ovarian cancer were processed into untreated ascites (UA), A‐A, or A‐E. Whole ascites, extracellular vesicles (EVs), and EV‐depleted supernatants were injected intraperitoneally into mice. Serum cytokines were measured, and label‐free proteomics was used to identify inflammatory pathways. Results: A‐E induced the strongest proinflammatory and Th17/type I interferon responses compared to UA. A‐A produced intermediate activation. EV‐depleted A‐E supernatants remained highly bioactive. A‐E was enriched in proteins associated with cellular damage pathways and proinflammatory signaling. A‐A exhibited attenuated changes and preserved regulatory proteins. Conclusion: A‐A yields a more balanced inflammatory and proteomic profile than A‐E. Our findings provide a preliminary mechanistic rationale for its use in CART and offer targets for membrane optimization.

Metabolic dysfunction‐associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disease worldwide, with an increasing number of patients progressing to cirrhosis and hepatocellular carcinoma (HCC). Early identification of individuals at high risk for advanced fibrosis is essential for preventing liver‐related events and improving long‐term outcomes. This guideline summarizes current evidence and provides practical recommendations for the diagnosis, risk stratification, and management of MASLD in clinical practice. These recommendations were developed through systematic evaluation of the literature and expert consensus. Diagnostic approaches, including noninvasive fibrosis assessment tools, imaging, biochemical testing, and indications for referral to gastroenterology/hepatology specialists, were reviewed. Advanced fibrosis is the major determinant of liver‐related morbidity and mortality in MASLD. The Fibrosis‐4 (FIB‐4) index is a widely accessible and reliable first‐line noninvasive tool for fibrosis risk stratification. Patients with elevated FIB‐4 values or clinical features suggestive of progressive liver injury should undergo secondary assessment with elastography and be referred to a specialist when appropriate. Liver biopsy is not routinely required for the diagnosis of MASLD but remains essential for establishing a definitive diagnosis of at‐risk metabolic dysfunction–associated steatohepatitis (MASH), assessing inflammatory activity, resolving discrepancies between noninvasive tests, and differentiating MASLD from other chronic liver diseases. Lifestyle modification remains the foundation of management, with pharmacological therapy considered for patients with a high likelihood of at‐risk MASH. MASLD represents a heterogeneous disease spectrum in which advanced fibrosis is the key prognostic factor. These guideline recommendations aim to standardize clinical practice and support evidence‐based management of MASLD in Japan.

Background: In many inpatient settings, physician coverage is organized around single-attending responsibility, which can create challenges in supervision and workload distribution, particularly in procedurally intensive environments. To address these issues, our department introduced a junior–senior inpatient team model in which multiple physicians jointly share responsibility for hospitalized patients. This study examined physicians’ perceptions of how this restructuring influenced clinical workflow, supervision, and workload. Methods: We performed a mixed-methods cross-sectional survey two months after implementation. Twenty-two physicians (13 junior, 9 senior) completed five-point Likert-scale items and open-ended questions. Responses were analyzed using non-parametric group comparisons. Qualitative comments were examined thematically to identify recurring perspectives on supervision and workload. Results: Junior physicians reported more favorable perceptions across several domains. Significant differences between junior and senior physicians were observed for reassurance during off-site duties (p = 0.013) and perceived reduction in burden when managing critically ill patients (p = 0.002). Qualitative findings indicated that junior physicians experienced greater shared responsibility and easier access to consultation, whereas senior physicians described increased supervisory demands, responsibility extending beyond subspecialty areas, and heavier weekend or holiday duties. Both groups emphasized the importance of flexible patient redistribution during staffing variability. Conclusions: The junior–senior inpatient team model was associated with improved perceived accessibility of supervision and collective support for junior physicians while increasing supervisory demands on senior staff. These findings suggest the potential importance of workload-sensitive implementation strategies and explicit role definition when introducing physician team–based coverage in high-acuity inpatient settings.

This study investigated the impact of partial splenic embolization (PSE) on portal hypertensive gastropathy (PHG). We retrospectively analyzed endoscopic findings and the portal venous system of 31 cirrhotic patients with PHG. The improved group was defined as the amelioration of PHG findings using the McCormack classification. Child–Pugh scores of the improved group (18 of 31 patients) were significantly lower compared with those of the non-improved group (p = 0.018). The changes in the diameters of the portal trunk and those of the spleno-portal junction and spleen hilum in the splenic vein of the improved group were significantly larger than those of the non-improved group (p = 0.007, p = 0.025, and p = 0.003, respectively). The changes in the diameters of the portal vein and splenic hilum of the splenic vein showed significant correlations with Child–Pugh score (r = 0.386, p = 0.039; r = 0.510, p = 0.004). In a multivariate analysis of baseline factors related to the improved group, Child–Pugh grade A was significantly associated with the improvement of PHG (odds ratio 6.875, p = 0.033). PSE could be useful for PHG, especially in patients with Child–Pugh grade A, at least in the short term.