As an alternative to perfluorooctanesulfonic acid (PFOS), sodium perfluorononenyl oxobenzene sulfonate (OBS) is widely used due to its cost-effectiveness. Multiple studies have shown that the liver is a classic target organ for OBS. However, there is currently no systematic review on the hepatotoxic effects of OBS. This review systematically summarizes the exposure characteristics of OBS in the environment and human populations, as well as its mechanisms of liver toxicity. In vivo studies consistently demonstrate that OBS induces hepatotoxic effects, such as hepatomegaly, vacuolization, elevated serum transaminases, and lipid dysregulation, though the manifestation of these phenotypes varies across species and exposure routes. In vitro evidence further shows that OBS reduces cell viability and survival, and triggers necrosis accompanied by inflammation. Mechanistically, oxidative stress, inflammatory signaling, and metabolism disorder are implicated. Critically, most existing work addresses subacute or subchronic exposure, leaving a gap in chronic risk assessment for long-term, low-dose OBS exposure. Moreover, mechanistic studies have focused predominantly on downstream transcriptional and signaling changes, with limited exploration of upstream epigenetic controls. Overall, this study aims to provide a comprehensive reference for future toxicological investigations and liver injury risk assessments related to OBS exposure.

Liver cirrhosis represents the irreversible end-stage of various chronic liver diseases, whereas hepatic fibrosis, characterized by hepatic stellate cell (HSC) activation, constitutes the critical pathological intermediate in this progression. In this study, we investigated the antifibrotic effects of loganin, a natural iridoid glycoside, and elucidated its underlying mechanisms in bile duct ligation (BDL)-induced cholestatic liver injury and hepatic fibrosis and in TGF-β1-stimulated HSCs. Sprague-Dawley rats subjected to BDL surgery received loganin for 14 days, resulting in marked amelioration of hepatomegaly, inflammatory infiltration, hepatocyte necrosis, and collagen deposition, alongside restoration of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (T-BIL) levels and suppression of fibrogenic gene expression (collagen type I alpha 1 chain [COL1α1], alpha-smooth muscle actin [α-SMA], and fibronectin). Moreover, loganin attenuated hepatic autophagy, as evidenced by reduced Beclin-1 expression and LC3B-II/I ratio, with decreased colocalization of α-SMA and LC3B. Bioinformatics analysis and molecular docking indicated that epidermal growth factor receptor (EGFR) may be the target protein through which loganin exerts its antifibrotic effect. Experimental validation demonstrated that loganin suppressed BDL-induced EGFR phosphorylation in vivo. In TGF-β1-activated HSC-T6 cells, loganin inhibited cell activation, downregulated fibrosis markers, impaired autophagic flux, and suppressed TGF-β1-induced upregulation of Beclin-1 and LC3B-II/I. Critically, cotreatment with the EGFR agonist EGF reversed the autophagy-inhibitory and antifibrotic effects of loganin, whereas the EGFR inhibitor AG-1478 mimicked loganin's actions, confirming EGFR signaling as the functional mediator. Overall, these results indicated that loganin could alleviate liver injury and hepatic fibrosis in BDL rats by inhibiting autophagy and activation of HSCs, and this protective effect is mediated by the EGFR pathway.

Brucellosis is a common zoonosis worldwide, yet large-scale pediatric data are scarce. This nationwide multicenter study from Türkiye, a highly endemic country, aimed to characterize pediatric brucellosis and identify independent risk factors for complications, relapse, and hospitalization. A retrospective cohort was conducted across 32 hospitals between January 2019 and June 2024. Children aged 0-18 years with confirmed brucellosis were included. Data were analyzed by multiple backward logistic regressions, with Firth penalization for the complication and relapse models. A total of 1052 children were included (median age 12 years; 69.9% male). Complications occurred in 87 patients (8.3%), most frequently osteoarticular (spondylitis, sacroiliitis, and osteomyelitis), whereas neurobrucellosis was rare (0.9%); relapse occurred in 34 patients (3.2%). Complications were independently associated with headache (adjusted OR 3.566, 95% CI 1.861-6.637), arthralgia/arthritis, culture positivity, night sweating, and myalgia. Relapse was independently associated with female sex (adjusted OR 3.675, 95% CI 1.617-8.568), whereas treatment compliance was protective (adjusted OR 0.254, 95% CI 0.092-0.857). Hospitalization (34.1%) was independently associated with headache, diarrhea, hepatomegaly, lymphadenopathy, fever, elevated CRP, and lower hemoglobin, whereas diagnosis through household contact screening was protective. Conclusion: Pediatric brucellosis in Türkiye generally follows a favorable course, with low complication and relapse rates. Readily identifiable musculoskeletal and constitutional symptoms at presentation may help predict complicated disease, while treatment adherence remains the key determinant of relapse. Early detection through household contact screening may reduce disease burden in endemic regions. What is Known: • Brucellosis is a common zoonosis with limited pediatric data worldwide. Early detection and treatment adherence are critical for favorable outcomes. • Complications and relapse are recognized but poorly defined in children What is New: • This is one of the largest nationwide pediatric brucellosis cohorts reported to date, including 1052 children. Household contact screening shown protective against hospitalization. • Treatment adherence, rather than disease severity or complications, was the key determinant of relapse in pediatric brucellosis.

Postpartum autoimmune hepatitis (AIH) is a rare but serious condition triggered by immune rebound after delivery. Diagnosis is typically supported by elevated immunoglobulins and positive autoimmune markers; however, seronegative presentations remain diagnostically challenging. We present the fourth reported worldwide case of seronegative postpartum AIH in a 36-year-old woman who developed jaundice, pruritus, pale stools, and dark urine 4 months after delivery. Laboratory evaluation revealed severe hepatocellular injury with aspartate aminotransferase 1373 U/L, alanine aminotransferase 2137 U/L, and marked hyperbilirubinemia. Viral, toxic, metabolic, and rheumatologic investigations were negative, while autoimmune serologies and immunoglobulin levels remained normal. Imaging demonstrated hepatomegaly without biliary obstruction or vascular abnormalities. Liver biopsy revealed acute-on-chronic autoimmune-mediated hepatitis with necrosis, confirming seronegative postpartum AIH. This case emphasizes seronegative AIH as a critical consideration in postpartum acute hepatitis, with liver biopsy essential for diagnosis and early treatment.

Veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome (SOS), is a life-threatening complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT) characterized by endothelial injury and post-sinusoidal portal hypertension. Classical diagnostic criteria rely on clinical signs such as ascites, weight gain, and painful hepatomegaly; however, these features may be altered in patients with modified portal hemodynamics. We report the case of a 46-year-old woman with primary myelofibrosis who underwent transplantation after placement of a transjugular intrahepatic portosystemic shunt to manage severe portal hypertension. To our knowledge, this is the first reported case of VOD occurring after transplantation in a patient with a pre-existing transjugular intrahepatic portosystemic shunt, representing a unique diagnostic challenge. Early after transplantation, the patient developed rapidly progressive hyperbilirubinemia without the typical manifestations of VOD, leading initially to an alternative diagnostic hypothesis and delayed initiation of defibrotide therapy. The presence of the shunt likely attenuated hallmark clinical signs by decompressing the portal venous system, thereby masking the syndrome until advanced liver failure occurred. Despite treatment, the patient experienced progressive hepatic dysfunction and died. This case highlights a previously underrecognized diagnostic pitfall: standard diagnostic criteria for VOD may be unreliable in patients with altered portal circulation. Clinicians should maintain a high index of suspicion in this setting and consider early treatment when biochemical abnormalities emerge, as prompt recognition remains critical for improving outcomes.

BACKGROUND Hydatid disease, caused by Echinococcus granulosus, is an endemic parasitic infection that predominantly affects the liver. Although slow-growing and asymptomatic, large hepatic cysts lead to catastrophic vascular complications, including inferior vena cava (IVC) thrombosis and pulmonary embolism (PE). Although rare, life-threatening events require prompt recognition and multidisciplinary management to optimize outcomes. CASE REPORT A 68-year-old woman with paroxysmal atrial fibrillation presented with right upper-quadrant pain, fever, and poor oral intake for several weeks. Examination revealed abdominal distension, hepatomegaly, and mottled, cold lower limbs. Laboratory findings showed severe metabolic acidosis and leukocytosis, indicating significant systemic involvement and possible sepsis. Computed tomography (CT) angiography demonstrated a pulmonary embolism, a giant (29×18 cm) right hepatic cyst exerting a mass effect, and extensive thrombosis extending from the infrarenal IVC to both external iliac veins. Echocardiography showed extrinsic cardiac compression without signs of tamponade but with functional compromise related to mass effect. Management included anticoagulation, albendazole, broad-spectrum antibiotics, vasopressors, and continuous renal replacement therapy. Ultrasound-guided percutaneous drainage of the cyst yielded 4 L of purulent fluid, with transient improvement in limb perfusion suggesting partial decompression of venous outflow obstruction. An IVC filter was inserted, but despite intensive therapy, the patient developed refractory shock and died due to progressive hemodynamic collapse and multiorgan failure. CONCLUSIONS Massive hepatic hydatid cysts can precipitate IVC thrombosis and PE through mechanical compression or infection-related inflammation. Early diagnosis, multidisciplinary coordination, and timely surgical or percutaneous decompression are vital to prevent death.

Hepatic sinusoidal obstruction syndrome (HSOS) is a hepatic vascular disease initiated by injury to hepatic sinusoidal endothelial cells. Its main clinical manifestations include hepatomegaly, elevated bilirubin, ascites and weight gain. The incidence of HSOS has been increasing year by year. Nevertheless, due to its non-specific clinical manifestations, limited effective diagnostic methods and imperfect relevant diagnostic criteria, it is highly likely to be misdiagnosed as other liver diseases. This study reports a case of HSOS induced by ingestion of Gynura segetum.