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Portal vein thrombosis (PVT) worsens the long-term prognosis of patients with cirrhosis; however, the optimal treatment remains to be determined. Reports on the efficacy of direct oral anticoagulants are increasing, and further evidence is needed. Therefore, we investigated the effectiveness of treatment with edoxaban in patients with PVT. We retrospectively reviewed the outcomes of edoxaban and warfarin as antithrombotic therapies for PVT. The median overall survival time was 4.2 years in patients with PVT, with a 1-year survival rate of 70.7% and a 5-year survival rate of 47.9%. The leading cause of death was hepatocellular carcinoma. The overall response rate for thrombolysis in the edoxaban group was 76.7% compared to 29.4% in the warfarin group, and edoxaban significantly improved PVT compared to warfarin. In addition, edoxaban provided long-term improvement of PVT. Warfarin, on the other hand, was temporarily effective but did not provide long-term benefits. The Child–Pugh and albumin-bilirubin scores did not change after edoxaban or warfarin use. No deaths occurred due to adverse events associated with edoxaban or warfarin. Edoxaban as a single agent can achieve long-term recanalization without compromising the hepatic reserves. Edoxaban is easy to initiate, even in an outpatient setting, and could become a major therapeutic agent for the treatment of PVT.

Although the addition of olanzapine to conventional antiemetic therapy has been reported to be useful for systemic chemotherapy with highly emetogenic agents such as cisplatin, no studies have evaluated its efficacy in transcatheter arterial chemoembolization (TACE) for patients with hepatocellular carcinoma (HCC). We evaluated the antiemetic efficacy of olanzapine in patients with HCC undergoing cisplatin-based TACE. This prospective study included 68 patients with HCC scheduled for cisplatin-based TACE between 2021 and 2022. Patients were divided into two groups: an olanzapine group receiving olanzapine 5 mg plus the conventional triple antiemetic combination and a control group receiving only the conventional triple combination therapy. The incidence of digestive symptoms and adverse events (AEs) in both groups were compared. For TACE-induced nausea and vomiting, the olanzapine group had similar antiemetic complete response (aCR) and complete control (CC) rates at 12 h post-TACE as the control group but significantly higher aCR and CC rates during the delayed-phase after 24 h and better patient satisfaction scores. No significant differences were noted in the occurrence of severe AEs in the two groups. The use of olanzapine, in addition to conventional antiemetics, may be a new standard for patients undergoing cisplatin-based TACE.

Patients with hepatocellular carcinoma (HCC) often sit at the crossroads of malignancy and chronic liver disease, where impaired hepatic reserve, systemic inflammation, and treatment-related stress accelerate loss of skeletal muscle mass and function. In this narrative review, we synthesize current evidence on the two-way relationship between sarcopenia and HCC management across curative and palliative settings. We outline key biological pathways—altered energy substrate use, amino acid imbalance, hyperammonemia-related signaling, and inflammatory and hormonal perturbations—that promote progressive muscle wasting, and we summarize how sarcopenia influences tolerance, complications, and outcomes of surgery, locoregional therapies, and systemic agents. We then translate the literature into practical supportive-care principles, including adequate energy and protein delivery, optimized meal distribution (including late-evening snacks), and selected supplementation alongside hepatic rehabilitation/exercise. Potential adjuncts discussed include branched-chain amino acids, L-carnitine, vitamin D, zinc, and other micronutrients. Because the available data are heterogeneous and largely derived from observational cohorts or extrapolated from cirrhosis populations, HCC-specific randomized trials and standardized intervention protocols remain limited. Therefore, nutritional and exercise recommendations should be individualized according to tumor stage, hepatic function, comorbidities, and treatment goals, and viewed as supportive guidance that requires confirmation in well-designed prospective studies.

Hepatitis B virus (HBV) infection is a major public health problem worldwide. The study aimed to evaluate the efficacy of pegylated interferon (Peg-IFN) alfa-2a treatment for seroclearance of HBs antigen (HBsAg) in HBe antigen (HBeAg)-negative chronic hepatitis B (CHB) patients. This retrospective study investigated 16 HBeAg-negative CHB patients who received Peg-IFN alfa-2a weekly for 48 weeks. Thereafter, the patients were followed-up for 48 weeks after the end of therapy. The following criteria were also used for inclusion: HBV-DNA < 5.0 log copies/mL and without nucleot(s)ide analogs. Four HBsAg-positive cases became HBsAg negative. The HBsAg levels of the 4 patients who achieved HBsAg seroclearance were lower significantly than that of the non-seroclearance group (p = 0.007). The mean HBsAg levels in these 4 cases were 68 IU/mL, while the mean HBsAg levels in the non-seroclearance group were 2,114 IU/mL. The mean HBV-DNA levels in the 4 HBsAg seroclearance cases were 2.8 log copies/mL as compared to 3.6 log copies/mL in HBsAg-non-seroclearance cases (p = 0.01). Cases that are HBeAg negative, with HBV-DNA levels < 5 log copies/mL, and HBsAg titers < 120 IU/mL cases may achieve HBsAg clearance with Peg-IFN therapy.

Background/Objectives: Constipation is a common gastrointestinal problem in older adults and is associated with reduced quality of life, functional decline, frailty, and an increased risk of delirium and cognitive impairment. Its pathogenesis is multifactorial, involving age-related changes in gastrointestinal motility, neural regulation, comorbidities, and polypharmacy. However, this condition has traditionally been regarded as a localized gastrointestinal disorder, which may not fully reflect its systemic clinical significance in older populations. While prior narrative reviews have described multifactorial contributors to constipation, none have formally applied a geriatric syndrome framework to integrate these dimensions. This review proposes a three-criterion operational definition—multifactorial pathogenesis, association with functional decline and frailty, and contribution to adverse systemic outcomes—to characterize constipation in older adults as a “systemic geriatric syndrome,” and evaluates available evidence against each criterion. Methods: A narrative literature search was conducted using PubMed to identify relevant studies published between 1 January 2023, and 31 December 2025. MeSH terms included “Constipation” [Major Topic] and “Aged” [MeSH Terms]. Eligible articles included English-language original studies, systematic reviews, and clinical or epidemiological studies involving individuals aged ≥65 years. Results: Diagnosis in older adults is often complicated by secondary causes, including medications and neurological disorders, as well as atypical symptom presentations in individuals with cognitive impairment. Key pathophysiological mechanisms include reductions in interstitial cells of Cajal, impaired smooth muscle contractility, dysfunction of the enteric and autonomic nervous systems, and gut microbiota dysbiosis, which may promote chronic low-grade inflammation. Major contributing factors include physical inactivity, sarcopenia, dehydration, inappropriate defecation posture, and polypharmacy, particularly opioids and anticholinergic agents. Importantly, these factors interact through the brain–gut–microbiota axis, contributing not only to gastrointestinal dysfunction but also to systemic outcomes such as frailty, cognitive decline, and increased healthcare burden, thereby supporting a multidimensional disease framework. Conclusions: The available evidence collectively supports the plausibility of framing constipation in older adults as a systemic geriatric syndrome, though formal validation of this classification requires further longitudinal and mechanistic research. Comprehensive and individualized management strategies, extending beyond simple laxative use, are essential to reduce complications and preserve functional health in aging populations. Further studies are required to validate this framework.

Hepatocellular carcinoma (HCC) is the most common primary liver cancer and a major cause of cancer mortality worldwide. Because HCC usually arises in cirrhotic livers, prognosis is shaped by the dual threats of tumor progression and hepatic decompensation, requiring treatment decisions that balance anticancer efficacy with preservation of liver function, portal hypertension control, and quality of life. In recent years, management has shifted from a predominantly locoregional approach to an integrated continuum that spans curative resection, ablation, and transplantation; refined transarterial and radiotherapy techniques; and modern systemic therapy dominated by immunotherapy-based combinations. These advances have improved response rates, enabled downstaging and conversion in selected patients, and expanded opportunities for sequential and multimodal treatment. However, challenges persist, including therapeutic decision-making in patients with Child–Pugh B liver function, lack of robust predictive biomarkers, and resistance after initial response. Emerging tools—liquid biopsy, radiomics, AI-assisted imaging, and microbiome modulation—may support future precision strategies and optimized treatment allocation. In this review, we summarize current evidence guiding staging and therapy selection, outline practical considerations across curative, locoregional, and systemic modalities, and discuss evolving biomarkers and next-generation immunotherapy as key steps toward more personalized, durable, and equitable global HCC care.

Drug resistance to molecular targeted agents, such as lenvatinib, is an important issue. The aim of this study was to explore the mechanism of lenvatinib resistance and to investigate potential drugs that may improve the treatment of lenvatinib-resistant (LR) hepatocellular carcinoma (HCC). LR cells were developed by long-term culture under lenvatinib exposure. We analyzed the biological characteristics of LR cells in vitro, and investigated the antitumor effects and endogenous mechanisms of cisplatin in LR cells. The proliferative potential of LR cells was enhanced by activation of ERK signaling and changes in several miRNAs. Cisplatin inhibited cell proliferation of LR cells and induced G2/M cell cycle arrest. Furthermore, cisplatin triggered the DNA damage response, via the ATM/ATR-Chk1/Chk2 signaling pathway. Proliferation of LR cells was induced upon ERK signaling activation. Cisplatin exerted antitumor effects in LR cells and was involved in the regulation of miRNAs associated with drug resistance.

Endoscopic ultrasound‐guided cyst drainage (EUS‐CD) was performed for walled‐off pancreatic necrosis. Computed tomography performed the next day showed that the tip of the external drainage tube was located in the transverse colon, confirming an accidental EUS‐CD‐associated complication of mis‐puncture. A colonoscopy was performed to confirm the puncture site, which was identified as a defect measuring 2 mm in diameter. The external drainage tube was removed immediately via a guidewire. We intentionally retained the guidewire as a landmark for the puncture site in the colon. The defect was approximated using an endoclip under full vision, with the guidewire covered with surrounding mucosa. After removing the guidewire smoothly, complete closure was achieved with additional endoclips. Four days later, EUS‐CD was successfully repeated, resulting in the resolution of the walled‐off pancreatic necrosis. This is the first known case in which an accidental puncture of the transverse colon occurred during EUS‐CD for walled‐off pancreatic necrosis, and guidewire‐guided clip closure of the colon contributed to troubleshooting.

Background/Objectives: We aim to determine if cytokeratin-18 fragment (CK-18F) could be used to diagnose metabolic dysfunction-associated steatohepatitis (MASH). Methods: A total of 289 patients with metabolic dysfunction-associated steatotic liver disease (MASLD) were enrolled in the analysis. To evaluate the association between CK-18F levels and the histological features of MASH, weighted receiver operating characteristic (ROC) curve analyses were performed. The diagnostic utility of CK-18F was compared with that of the Mac-2 binding protein glycan isomer (M2BPGi). Additionally, we assessed the predictive performance of combining CK-18F with either the FIB-4 index or the FIB-3 index for diagnosing MASH and investigated predictors of future progression to cirrhosis. Results: CK-18F was more useful for MASH diagnosis than M2BPGi and the FIB-4 index in the multivariate analysis, with a sensitivity of 47% and specificity of 80% at a CK-18F cutoff value of 750 U/L. Because CK-18F decreases with advanced liver fibrosis, the combination of the FIB-4 or FIB-3 index with CK-18F was examined to identify cases with cirrhosis. The combination of the CK-18F level and the FIB-3 index better predicted MASH than the combination of the CK-18F level and the FIB-4 index. The FIB-3 index was the most useful predictor of cirrhosis on imaging five years after diagnosis with F2 or less disease. Conclusions: CK-18F is useful for MASH diagnosis, and the diagnostic algorithm combining CK-18F with the FIB-3 index may be more useful than the previously reported MASH diagnostic algorithm that combined it with the FIB-4 index.

Background Hepatocellular carcinoma (HCC) in autoimmune hepatitis (AIH) was considered rare but is increasing with prolonged prognosis. Its impact on the overall prognosis of AIH is unknown, and treatment has not been established. Aim To investigate the risk factors and prognosis of HCC in patients with AIH and identify appropriate management strategies. Methods We studied patients with AIH including background liver disease, sex, age, complications, treatment, response to treatment, liver fibrosis, prognosis, and treatment. Results In 131 patients, deaths due to liver failure were more common early after the onset of AIH; however, deaths due to HCC increased gradually. HCC was observed in 12 patients (median age, 70 years; male/female, 4/8; cirrhosis at onset, 11; median time to carcinogenesis, 7 years). Cirrhosis at diagnosis was identified as a risk factor for carcinogenesis in the multivariate analysis (odds ratio, 41.36; p  < 0.0001) and cumulative cancer rates were high. Multidisciplinary therapy other than immune checkpoint inhibitors was administered as treatment for HCC. Two of the three patients who used molecular-targeted drugs discontinued the treatment because of adverse events. Conclusion HCC is an important cause of death in patients with AIH. Currently available drug therapies are limited and early detection is desirable. Trial registration This trial was retrospectively registered in the Ethics Committee of Kagawa University School of Medicine under the identifier 2019 − 238, registered on 4 Feb 2020.