Metabolic dysfunction-associated fatty liver disease (MAFLD) poses a significant challenge in modern medicine due to its high prevalence. The pathogenesis of MAFLD involves a complex dysmetabolic process consistent with the “multiple-hit” hypothesis. This process includes excessive triglyceride (TC) accumulation within hepatocytes, lipotoxicity, insulin resistance (IR), chronic low-grade inflammation, and increased oxidative stress. The role of leptin in the liver has been extensively studied, demonstrating both direct effects on hepatic cells and indirect actions mediated through the central nervous system (CNS). In MAFLD, leptin modulates several physiological processes: it improves glucose metabolism by enhancing insulin sensitivity and lowering glucose levels; regulates lipid metabolism by promoting β-oxidation and TC export while inhibiting lipogenesis; and contributes to fibrogenesis by upregulating transforming growth factor-β (TGF-β) expression and activating hepatic stellate cells (HSCs) and the immune response. This review explores the structure of leptin, its primary physiological functions, its potential role in MAFLD pathogenesis, and its promise as a novel therapeutic target.

Chronic subdural hematoma (CSDH) is a common disease in neurosurgery, with epidemiological characteristics showing an overall annual incidence of 1.7–20.6 per 100,000 people and a higher prevalence in the elderly. However, despite the increased disease burden, there have been limited breakthroughs in treatment options over the past 20 years. A significant gap exists in our understanding of the exact pathophysiological mechanism of CSDH, leading to a lack of specific clinical treatment options based on a clear pathological mechanism. Current research suggests that the development of CSDH involves dual mechanisms of trauma and inflammation, and that these pathologic processes together promote pathological changes such as angiogenesis, inflammatory response, and neovascularization. Therapies for CSDH encompass both surgical (e.g., twist-drill drainage, burr-hole drainage, craniotomy) and non-surgical approaches (e.g., clinical observation, medication, intracranial pressure monitoring, anticoagulation). Meanwhile, middle meningeal artery embolization, as an emerging minimally invasive interventional technique, has shown good prospects for clinical application. This review aims to bridge the gap between current treatment options and the need for effective strategies by providing a comprehensive summary of the epidemiological trends, pathophysiological advances, and optimization of therapeutic strategies for CSDH.

Various devices are used to study the unique electrical properties of acupuncture points (APs), with Voll’s electropuncture diagnostics (EAV) occupying a prominent role. The technical design of EAV allows for the testing of drugs to determine their individual selection and dosages. However, the physiological basis of this phenomenon remains unclear. This study investigated the feasibility of evaluating the electrodermal activity of APs to determine the daily dose of ribavirin using electroacupuncture according to the Voll diagnostic system in patients with long COVID.

This blind, randomized, placebo-controlled trial included 101 patients (aged 16 to 50) who met the definition of long COVID and were examined using an EAV testing system that measures the electrodermal activity of APs. Ribavirin was tested at the APs with established decreased electrical impedance readings to determine the daily doses. Fifty-two participants were randomized to the experimental group, and forty-nine to the placebo group. These patients were considered for data analysis.

The results of this study demonstrated the feasibility of using EAV to identify APs with decreased levels of electrodermal activity, followed by medicament testing (MT) of different ribavirin doses to restore the electrodermal activity at these points.

The results indicated that the tested doses of ribavirin in patients with long COVID correlate with electrodermal activity at certain APs along specific meridians. Higher doses of the drug were associated with lower electrodermal activity readings during MT using the EAV diagnostic system. However, further clinical and instrumental studies are needed to evaluate the clinical application of MT in the assessment of long COVID.

Further decompensation in cirrhosis is associated with increased mortality. However, reliable tools to predict further decompensation after transjugular intrahepatic portosystemic shunt (TIPS) are currently limited. This study aimed to investigate the incidence and risk factors of further decompensation within one year post-TIPS in patients with cirrhosis and to develop a predictive model for identifying high-risk individuals.

This retrospective cohort study enrolled 152 patients with cirrhosis undergoing TIPS for variceal bleeding and/or refractory ascites (January 2018–January 2024). Patients were stratified according to one-year decompensation outcomes. LASSO regression and multivariable logistic analysis were used to identify predictors, and a nomogram was constructed and internally validated using bootstrapping (1,000 replicates).

Among the 152 patients (median age 57.5 years [IQR 50.0–66.0]; 58.6% male; 58.6% viral/alcohol-associated etiology), 65.8% (100/152) achieved clinical stability at one year post-TIPS, while 34.2% (52/152) developed further decompensation. LASSO regression identified right hepatic lobe volume, spleen volume, and portal pressure gradient (PPG) reduction as key predictors, all independently associated with further decompensation risk in multivariable analysis (OR [95% CI]: 0.683 [0.535–0.873], 1.435 [1.240–1.661], and 0.961 [0.927–0.996], respectively). The nomogram demonstrated superior discrimination compared with PPG reduction alone and benchmark prognostic scores (AUC 0.854 [0.792–0.915] vs. 0.619–0.652; ΔAUC +0.201–+0.235, p < 0.001) with 92.3% sensitivity. High-risk patients (score > 86) had a 10.7-fold higher risk of further decompensation than low-risk patients (60.0% vs. 5.6%; p < 0.0001).

This validated model, combining hepatosplenic volumetry and PPG reduction, accurately stratifies further decompensation risk post-TIPS and may guide targeted surveillance and preventive interventions.

Portal vein thrombosis (PVT) frequently occurs in patients with porto-sinusoidal vascular disease (PSVD), but its clinical characteristics and outcomes remain poorly understood. This study aimed to investigate the clinical features and outcomes of PVT in PSVD.

A total of 169 patients with PSVD confirmed by hepatic histology were included. PVT was diagnosed using contrast-enhanced magnetic resonance imaging or computed tomography. Demographic, clinical, and laboratory data, portal hypertension-related complications, comorbidities, and mortality were collected and compared between patients with and without PVT. The primary outcomes were baseline clinical characteristics and liver-transplantation-free mortality; the secondary outcome was the dynamic changes of PVT during follow-up.

At baseline, 45 (26.6%) PSVD patients had PVT. Compared to those without PVT, patients with PVT had significantly higher rates of esophageal variceal bleeding (62.2% vs. 29.0%), ascites (73.3% vs. 35.5%), antithrombin III deficiency (78.1% vs. 38.4%) (all p < 0.001), and a history of hematological disorders (11.1% vs. 0.8%, p = 0.005). After a median follow-up of 40.1 (23.4–62.3) months, liver-transplantation-free mortality rates were 7.9% (3/38) and 1.8% (2/112) in patients with and without PVT, respectively (log-rank p = 0.110). Among 41 patients followed for a median of 17.1 (7.4–39.3) months, PVT resolved in 9.1% (1/11) of those with baseline PVT and developed in 13.3% (4/30) of those without PVT at baseline. The one- and two-year cumulative incidence rates of PVT were 3.3% and 6.7%, respectively.

PSVD patients with PVT experience more portal hypertension-related complications, complex coagulation profiles, hematological disorders, and a higher risk of death compared to those without PVT.