Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease, with a global prevalence estimated at approximately 25%. NAFLD is also the leading cause of liver cirrhosis, hepatocellular carcinoma, and death. Additionally, the risk of cardiovascular disease increases with greater NAFLD severity. The liver- and cardiovascular disease-related mortality incident rate ratios among the NAFLD population were 0.77 and 4.79 per 1,000 person-years, respectively. We intend to discuss the risk factors associated with NAFLD in terms of development and progression. Obesity or higher body mass index is closely associated with NAFLD in a dose-dependent manner, but growing evidence suggests that central obesity plays a more important role in the development of NAFLD. Saturated fat and fructose have been reported to be closely related to NAFLD. Fructose intake promotes lipogenesis and impairs mitochondria fat oxidation. The presence of type 2 diabetes is the most powerful predictive risk factor for hepatic fibrosis in patients with NAFLD. Single nucleotide polymorphism is not only associated with the prevalence of NAFLD but also associated with increased liver disease mortality. Obstructive sleep apnea, intestinal dysbiosis, and sarcopenia are associated with the development of NAFLD

Steatotic liver disease was suggested as an overarching term encompassing various etiologies of hepatic steatosis. Experts from multinational liver societies went through the Delphi process, including four rounds of surveys, and consented to adopt a new nomenclature and definition instead of the conventional nonalcoholic fatty liver disease (NAFLD). This was to improve the understanding of the patients and primary care physicians, with an explanation of the pathophysiology in the name of the disease. Also, it could minimize the stigmatization of patients by using the histological neutral term “steatosis” instead of “fatty”. Herein, we will discuss the changes and continuity between the two nomenclatures, metabolic dysfunction-associated steatotic liver disease (MASLD) and NAFLD, as well as the challenges to MASLD which need to be addressed in future.

Lipiodol based conventional transarterial chemoembolization (TACE) is a standard of care for unresectable, non-invasive, and multinodular Hepatocellular carcinoma (HCC)s. The procedure relies on the intra-arterial administration of lipiodol/cytotoxic agent emulsion followed by the infusion of embolic material. Lipiodol, with its oily nature and radiopacifying properties, is in the center of the TACE procedure. Unstability and unpredictable therapeutic effect of hydrophilic cytotoxic drugs emulsified in the lipiodol and technical problems lie beyond the control of clinicians. Thus, interest in the properties and respective roles for lipiodol in the management of HCC is essential for the clinicians.
Carcinoma, Hepatocellular* ; Ethiodized Oil* ; Standard of Care

Fever is a common complication of endoscopic variceal obturation (EVO) therapy for gastric variceal bleeding. However, fungemia related to EVO therapy has not yet been reported. Herein, we report two cases of post-EVO fungemia in cirrhotic patients who underwent therapeutic EVO for gastric variceal bleeding. Both patients developed sustained high fever after repeated EVO procedures while on prophylactic antibiotic use. In both patients, blood cultures revealed yeast, and they were finally diagnosed with Candida infection. Candida is a common member of the intestinal flora; however, it can cause invasive infection with consequent poor prognosis in cirrhotic patients. The route of Candida invasion is unclear; however, repeated EVO may predispose patients to Candida infection, particularly those who are in the end stage of liver disease and receiving prophylactic antibiotics. Our cases highlight that repeated invasive procedures can increase the risk of fungal infections, and fungemia should be considered in the differential diagnosis of post-EVO fever.