In this editorial, we comment on the article published by Qiu et al. Pyogenic liver abscess is a serious clinical condition requiring timely and effective intervention. Ultrasound (US)-guided techniques - whether needle aspiration (NA) or catheter drainage - are key minimally invasive treatments, especially in patients with multiple or deep-seated abscesses where conventional surgery is often impractical. The timing and choice of evacuation method significantly influence clinical outcomes. Although catheter drainage may be necessary for larger or refractory collections, NA represents a less invasive alternative that is often sufficient for smaller abscesses - particularly multiloculated ones - and can avoid multiple catheter placements. This consideration is especially important in the early phase of the disease, when the abscess collection is poorly demarcated from surrounding tissue and more prone to bleeding during or after intervention. Traditional practice delays intervention until liquefaction occurs; however, emerging evidence supports early US-guided evacuation - even in partially liquefied or non-liquefied abscesses - as both safe and effective. Early intervention, particularly via NA when feasible, is associated with faster symptom resolution, shorter hospitalization, and fewer complications. This editorial explores the role of US-guided interventions in pyogenic liver abscess manaement, emphasizing the importance of individualized, timely approaches that optimize disease outcomes while minimizing procedural risk.

The liver is a central metabolic organ that regulates numerous physiological processes, including glucose and lipid metabolism, detoxification, and the synthesis of essential proteins and bile. Bile acids (BAs), synthesized from cholesterol in hepatocytes, not only facilitate the emulsification and absorption of dietary fats but also act as potent signaling molecules through receptors such as the farnesoid X receptor (FXR) and Takeda G-protein-coupled receptor 5. Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease globally, closely linked with obesity, insulin resistance, and other components of metabolic syndrome. In MASLD, the metabolism of BAs is markedly disrupted, resulting in alterations in their synthesis, composition, and signaling activity. These changes contribute to hepatic steatosis, inflammation, and fibrosis, thereby exacerbating metabolic dysfunction and liver damage. The altered profiles and signaling activity of BAs in MASLD patients suggest that BAs act not only as biomarkers of disease severity, but also as active mediators of its pathogenesis. Modulators of BA signaling pathways, especially FXR agonists, are the focus of intense research for their potential to beneficially influence liver steatosis and inflammation in MASLD. Recent research has yielded promising results, indicating potential therapeutic application and the introduction of novel agents aimed at modulating BA homeostasis and function. This minireview outlines the physiological roles of BAs, seeks to advance the elucidation of the mechanisms by which their dysregulation contributes to MASLD progression, and highlights current and emerging therapeutic approaches. A deeper understanding of these complex interactions is essential for improving the diagnosis, prognosis and treatment of MASLD.

The liver is a central metabolic organ that regulates numerous physiological processes, including glucose and lipid metabolism, detoxification, and the synthesis of essential proteins and bile. Bile acids (BAs), synthesized from cholesterol in hepatocytes, not only facilitate the emulsification and absorption of dietary fats but also act as potent signaling molecules through receptors such as the farnesoid X receptor (FXR) and Takeda G-protein-coupled receptor 5. Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease globally, closely linked with obesity, insulin resistance, and other components of metabolic syndrome. In MASLD, the metabolism of BAs is markedly disrupted, resulting in alterations in their synthesis, composition, and signaling activity. These changes contribute to hepatic steatosis, inflammation, and fibrosis, thereby exacerbating metabolic dysfunction and liver damage. The altered profiles and signaling activity of BAs in MASLD patients suggest that BAs act not only as biomarkers of disease severity, but also as active mediators of its pathogenesis. Modulators of BA signaling pathways, especially FXR agonists, are the focus of intense research for their potential to beneficially influence liver steatosis and inflammation in MASLD. Recent research has yielded promising results, indicating potential therapeutic application and the introduction of novel agents aimed at modulating BA homeostasis and function. This minireview outlines the physiological roles of BAs, seeks to advance the elucidation of the mechanisms by which their dysregulation contributes to MASLD progression, and highlights current and emerging therapeutic approaches. A deeper understanding of these complex interactions is essential for improving the diagnosis, prognosis and treatment of MASLD.

liver

Insertion/deletion polymorphism of the angiotensin converting enzyme (ACE) gene is a key component of the Renin-Angiotensin-Aldosterone System (RAAS). It has been proposed as an independent factor for hypertension and other cardiovascular diseases. Consequently, it has been extensively studied in various populations. The aim of this study is to investigate I/D polymorphism of ACE gene and its connection to hypertension in population of Tuzla Canton (Bosnia & Herzegovina). The study included 60 hypertensive subjects and 60 healthy control subjects with no risk factors for hypertension. I/D polymorphism was genotyped by polymerase chain reaction followed by gel electrophoresis and data obtained were statistically analysed using Chi square test. Odd’s ratios were calculated with a 95% confidence interval. P-value < 0.05 was considered significant. Odd’s ratios were calculated with a 95% confidence interval. P-value <0.05 was considered significant. Higher frequency of genotype D/D and allele D was determined in subjects with hypertension compared to control subjects but there is no statistical significance (p>0.05). However, statistically significant association was found in compared groups of subjects with genotypes DD + ID, in regards to genotype I/I (p<0.05). The results indicate the conclusion that ACE I/D polymorphism cannot be considered the main risk factor for development of hypertension, but its influence should be investigated together with other genetic and acquired risk factors that are associated with hypertension. This research contributes to the on-going exploration of molecular-genetic associations with hypertension.

Portal vein aneurysm (PVA) is a rare vascular abnormality, representing 3% of all venous aneurysms in the human body, and is not well understood. It can be congenital or acquired, located mainly at the level of confluence, main trunk, branches and bifurcation. A PVA as an abnormality of the portal venous system was first reported in 1956 by Barzilai and Kleckner. A review from 2015 entitled “Portal vein aneurysm: What to know” considered fewer than 200 cases. In the last seven years, there has been an increase in the number of PVAs diagnosed thanks to routine abdominal imaging. The aim of this review is to provide a comprehensive update of PVA, including aetiology, epidemiology, and clinical assessment, along with an evaluation of advanced multimodal imaging features of aneurysm and management approaches.