Hepatic sinusoidal obstruction syndrome (SOS) is characterized by hepatic sinusoidal endothelial cell injury and detachment, hepatic sinusoidal congestion, and hepatic cell necrosis. Currently, limited data exist concerning changes during the recovery period, especially histopathological changes. The purpose of this study was to investigate the evolution of pathology in patients with pyrrolizidine alkaloid (PA)-induced SOS and in a monocrotaline-induced SOS rat model.

Patients diagnosed with PA-induced SOS who underwent liver biopsy after achieving clinical remission were consecutively enrolled in this retrospective study. To compare the clinical and pathological differences between patients with acute and convalescent SOS, a 2:1 matched analysis was performed based on age, sex, treatment regimen, and baseline Drum Tower Severity Scoring (DTSS) during the acute phase. Additionally, an animal model of PA-induced SOS was established through the administration of monocrotaline.

Fourteen consecutive patients with SOS who had adequate liver biopsy specimens obtained during recovery were identified. During convalescence, most laboratory and imaging findings, such as the map-like enhancement observed on computed tomography, also disappeared. However, histopathological analysis revealed a distinct shift from hepatic sinusoidal endothelial cell injury in the acute phase to portal tract abnormalities, primarily characterized by portal vein stricture, in the recovery phase. These pathological changes were corroborated in our animal model.

Our study suggests that both patients with PA-induced SOS and rats in the convalescent stage may exhibit porto-sinusoidal vascular disease-like changes. Regular follow-up and dynamic pathological assessment are therefore recommended to facilitate the early detection of potential signs of portal hypertension.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly prevalent worldwide and is frequently encountered in patients undergoing liver transplantation and hepatic surgery. Although hepatic steatosis was once considered a relatively benign condition, accumulating evidence indicates that MASLD is associated with reduced tolerance to ischemic stress and increased susceptibility to ischemia–reperfusion injury, which may contribute to graft dysfunction and postoperative liver injury. In this mini review, we used the concept of hepatic resilience, referring to the ability of the liver to maintain homeostasis during stress and recover after injury. We discussed how MASLD may reduce hepatic resilience through mechanisms involving lipotoxicity, mitochondrial dysfunction, oxidative stress, inflammatory activation, regulated cell death, and impaired regeneration. MASLD represents a heterogeneous disease spectrum, and susceptibility to ischemia–reperfusion injury may differ according to disease stage and phenotype, particularly in the presence of progressive inflammation and fibrosis. We further summarized strategies aimed at improving hepatic resilience, including metabolic optimization, mitochondrial protection, modulation of reperfusion-associated inflammation, and enhancement of tissue repair. However, current evidence remains limited by the paucity of human studies and validated approaches for assessing hepatic resilience. Further investigation of these mechanisms may help develop individualized strategies to protect the liver in patients with MASLD during hepatic surgery and transplantation.

Since their first inception, neuroendocrine neoplasms of the breast have undergone many iterations of classification and definition. Taken together with their extremely low incidence, the ever-evolving landscape has made diagnosis, treatment, and research exceedingly challenging.

Our patient is a 45-year-old female who had a breast mass with clinical workup favoring a breast primary. A diagnosis of small cell carcinoma was established after an extensive clinical and pathologic workup. The mass did not respond to traditional neoadjuvant platinum-based chemotherapy, and she underwent a total mastectomy. Shortly thereafter, imaging revealed widely metastatic disease involving the brain, chest, abdomen, and pelvis. She received whole-brain radiation and, given the previous lack of response to chemotherapy, was recommended to try off-label tarlatamab. To date, with a short-term follow-up of 5 months, after whole-brain radiotherapy administered concurrently with the first cycle of tarlatamab, subsequent imaging showed near-complete radiographic resolution of extracranial metastatic disease, while the brain lesions also showed radiographic resolution on follow-up MRI.

We report the novel and preliminary use of tarlatamab in a patient with small cell neuroendocrine carcinoma of the breast, with short-term follow-up. We also discuss the most critical challenges associated with this rare pathologic diagnosis and the important elements to consider to ensure that metastatic disease is excluded.

EWSR1 fusions are recurrent genetic alterations in a wide spectrum of mesenchymal tumors and are often associated with specific clinicopathologic entities. However, the presence of an EWSR1 rearrangement does not always indicate a functional or disease-defining fusion.

We report a case of undifferentiated pleomorphic sarcoma with high-grade morphologic features harboring an EWSR1 rearrangement detected by fluorescence in situ hybridization. It was subsequently characterized by RNA sequencing as a likely nonfunctional fusion of EWSR1 exon 1 and NF2 intron 1. Histologically, the tumor was composed of pleomorphic spindle cells with brisk mitotic activity and lacked a specific line of differentiation. Immunohistochemically, the tumor showed diffuse cytoplasmic S100 positivity, with nuclear staining in a subset of tumor cells, while the overall immunophenotype did not support a specific line of differentiation. The EWSR1::NF2 fusion was inferred to have a tail-to-tail configuration, and additional KRAS and TP53 alterations were detected.

This case highlights that an EWSR1 rearrangement detected by fluorescence in situ hybridization should be interpreted cautiously and does not necessarily represent a functional or disease-defining fusion. Comprehensive molecular evaluation is important for the accurate interpretation and classification of sarcomas with atypical EWSR1 rearrangements.

Hepatitis B virus (HBV) reactivation is a well-recognized complication in patients with lymphoma receiving immunosuppressive therapy, particularly rituximab-containing regimens. We describe a 58-year-old man with diffuse large B-cell lymphoma and an atypical baseline HBV serological profile: hepatitis B surface antibody (anti-HBs) positivity (102.00 U/L), antibody to hepatitis B core antigen negativity, a low-level hepatitis B surface antigen (HBsAg) result (0.35 COI, reported as negative by the local laboratory), and undetectable HBV DNA. Thirteen days after initiation of the fourth cycle of modified R-CHOP (rituximab, cyclophosphamide, pirarubicin, vinorelbine and dexamethasone) chemoimmunotherapy, the anti-HBs titer had decreased to 1.31 S/CO, the HBsAg level to 0.02 S/CO, and HBV DNA was not reassessed until reactivation. Approximately 16 weeks after treatment completion, the patient developed fatigue, anorexia, and jaundice. HBsAg increased from 28.66 S/CO to 8048.30 IU/mL, hepatitis B e antigen became positive, and HBV DNA increased to 1.94 × 109 IU/mL. Despite treatment with tenofovir alafenamide fumarate and plasma exchange, the patient died of refractory liver failure and hepatic encephalopathy. These findings suggest that atypical serological profiles may not reliably indicate a low risk of severe HBV reactivation during intensive immunosuppressive therapy. Comprehensive pretreatment risk assessment and long-term monitoring of anti-HBs titers, HBsAg, and HBV DNA during and after therapy may facilitate earlier detection and intervention.

Watertight-intent dural reconstruction may reduce incisional cerebrospinal fluid (CSF) leakage after decompressive craniectomy but may prolong surgery. We aimed to evaluate whether watertight-intent reconstruction, compared with non-watertight management, was associated with direct postoperative incisional CSF leakage and operative time.

Five databases were searched through August 1, 2026. Comparative studies with explicit watertight or sealing-intent reconstruction and non-watertight comparators were included. The primary outcome was direct incisional CSF leakage; secondary outcomes included operative time, wound or surgical-site infection, hydrocephalus, mortality, and functional outcomes. Binary outcomes were expressed as risk ratios (RRs), and continuous outcomes as mean differences. Random-effects meta-analysis used restricted maximum likelihood estimation with Wald 95% confidence intervals (CIs); randomized and observational studies were examined as subgroups, with Hartung–Knapp sensitivity analyses. Certainty of evidence was assessed using the Grading of Recommendations Assessment, Development and Evaluation framework.

Twelve studies were included; nine (1,314 participants) reported direct incisional CSF leakage. Watertight-intent reconstruction was associated with fewer reported leaks (RR, 0.54; Wald 95% CI, 0.34–0.86; I² = 23.3%), although the prediction interval included the null value (0.24–1.20). The randomized subgroup was imprecise (RR, 0.75; 95% CI, 0.32–1.73), whereas the observational subgroup favored reconstruction (RR, 0.43; 95% CI, 0.20–0.90); its Hartung–Knapp interval (0.14–1.32) crossed 1. Infection and hydrocephalus estimates were imprecise; mortality and function were not pooled. Reconstruction was associated with longer operative time (mean difference, 39.85 minutes; 95% CI, 25.14–54.56; I² = 97.4%). Certainty was very low for all key outcomes.

Watertight-intent reconstruction is associated with fewer reported incisional CSF leaks and longer operations, although certainty is very low. Limited study and event numbers, imprecise design subgroups, and multicomponent techniques preclude causal or universal treatment conclusions. Effects on infection, hydrocephalus, mortality, and function remain uncertain.