Background/Objectives: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, primarily developing in the context of chronic liver disease. Traditional prevention has focused on liver-specific interventions like antiviral therapies and surveillance. However, extrahepatic factors also significantly contribute to HCC risk. This review explores comprehensive strategies for HCC prevention, including both hepatic and extrahepatic factors. Methods: An extensive literature search of peer-reviewed articles up to October 2024 was conducted, focusing on studies addressing HCC prevention strategies. Studies that focused on both hepatic and extrahepatic factors were included. Data were extracted and synthesized to provide an overview of current prevention strategies and their effectiveness in reducing HCC incidence. Results: Hepatitis B vaccination and antiviral treatments for hepatitis B and C significantly reduce HCC incidence. Lifestyle modifications—such as reducing alcohol consumption, maintaining a healthy weight through diet and exercise, and smoking cessation—are crucial in lowering HCC risk. Environmental measures to limit exposure to aflatoxins and other hazards also contribute to prevention. Regular surveillance of high-risk groups enables early detection and improves survival rates. Emerging strategies like immunotherapy and gene therapy show potential for further reducing HCC risk. Conclusions: A comprehensive approach combining medical interventions, lifestyle changes, and environmental controls is essential for effectively decreasing HCC incidence globally. Implementing these combined measures could significantly reduce the global burden of HCC.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, particularly among individuals with chronic liver diseases. Early detection through surveillance significantly improves survival rates and current guidelines recommend semiannual ultrasound, with or without alpha-fetoprotein (AFP) testing, for high-risk populations. However, limitations in ultrasound sensitivity, physician adherence, and patient compliance affect the effectiveness of these surveillance efforts. This review explores both current and emerging strategies for HCC surveillance. Individualized surveillance approaches, utilizing risk stratification tools such as the aMAP and PAGE-B scores, enable tailored monitoring based on individual risk profiles, potentially reducing unnecessary screening in low-risk groups. Advanced imaging techniques, including contrast-enhanced ultrasound and abbreviated magnetic resonance imaging, demonstrate improved sensitivity over traditional ultrasound, particularly for early-stage HCC detection. Additionally, combining clinical characteristics with novel HCC biomarkers—such as the Gender, Age, AFP-L3, AFP, and Des-gamma-carboxy prothrombin (GALAD) score; HCC early detection screening score version 2 (HES V2.0) score; Gender, Age, AFP, and Des-gamma-carboxy prothrombin (GAAD) score; and AFP, Sex, Age, and Protein induced by vitamin K absence-II (ASAP) score—has shown higher sensitivity for early detection, with GALAD and HES V2.0 performing particularly well in phase 3 biomarker studies. Emerging molecular diagnostics, including liquid biopsy and genetic markers, also show promise in refining future HCC surveillance protocols. Despite these advancements, a limited number of at-risk patients currently undergo surveillance. Therefore, solutions must focus on enhancing awareness, adherence, and accessibility to surveillance tools. This review discusses various strategies for optimizing HCC surveillance, emphasizing a multifaceted approach that integrates risk-assessment tools, advanced imaging, and novel biomarkers to improve early detection and reduce mortality.

Background and Aim: Hepatocellular carcinoma (HCC) surveillance in hepatitis B virus (HBV) patients is currently based on age/sex/cirrhosis, uses ultrasound abdomen every 6–12 months, and is a resource burden. HCC risk scores have been developed to classify HCC risk for surveillance. The number of HBV patients needing surveillance when HCC risk scores are used may be different from the current recommendation with implications on the resources needed for HCC surveillance.Methods: HBV patients from the liver clinic were included and classified as non‐cirrhotic/cirrhotic and untreated/treated for analysis. Each subgroup was analyzed using REACH‐B, CU‐HCC, LSM‐HCC, GAG‐HCC, and mPAGE‐B risk scores as appropriate. The change in the number of patients needing HCC surveillance using the above risk scores was calculated.Results: Seven‐hundred and thirteen HBV patients were included, of whom 361 (50.6%) were male with mean age 55.43 years, and 76 (10.7%) had cirrhosis. In the untreated, non‐cirrhotic subgroup, the percentage change of patients needing HCC surveillance was −69.5, −58.9, −58.8, and −54.1% when GAG‐HCC, LSM‐HCC, CU‐HCC, and REACH‐B were used compared to traditional criteria, respectively. In the treated, non‐cirrhotic subgroup, the percentage change of patients needing HCC surveillance decreased by −80, −75.2, −75.2, and −2.8% when GAG‐HCC, CU‐HCC, REACH‐B, and mPAGE‐B were used, respectively. For the cirrhotic group, HCC risk scores did not make much difference.Conclusion: The use of HCC risk scores in non‐cirrhotic HBV patients reduced the number of patients needing surveillance greatly. HBV cirrhotic patients should have HCC surveillance without the need for risk score calculation. Patients with a family history of HCC should undergo surveillance until proven unnecessary in prospective trials.

A 63-year-old woman presented with jaundice and epigastric pain for 2 weeks. Physical examination revealed marked jaundice, and palpable gallbladder with right upper quadrant tenderness. Liver function test was remarkable for hepatocellular injury pattern. Antinuclear antibody and anti-smooth muscle antibody were positive with high titre and serum IgG was elevated more than upper normal range. Ultrasound and CT scan demonstrated mildly diffuse periportal oedema of liver parenchyma and markedly diffuse gallbladder wall thickening up to 2 cm. Liver histology showed focal interface hepatitis with prominent plasma cell infiltration and cluster formation, moderate lobular spotty necrosis and emperipolesis consistent with autoimmune hepatitis. The patient was treated with steroid and azathioprine. She had complete resolution of symptoms and normal biochemical laboratory results. Diffuse gallbladder thickening was seen in acute hepatitis from definite autoimmune hepatitis.

A 29-year-old 11-week pregnant multigravida woman without previous medical history presentedwith sudden onset of hematemesis. This case illustrates the occurrence of a rare complication (rupture of pseudoaneurysm of right hepatic artery inside the biliary system), appearing as upper gastrointestinal bleeding in a pregnant woman. The cause of the rupture is presumably pregnancy-related. We would like to emphasize the presence of pseudoaneurysm of the hepatic artery as a rare cause of gastrointestinal bleeding in pregnancy. Figure 1 and 2 CTA showed a lobulated contour of saccular aneurysmal dilatation at proximal right hepatic artery, measured about 3.5x3.2x1.6 cm in size and 2.6 mm in neck width; pseudoaneurysm is likely. There is perianeurysmal heterogeneously hyperdense non-enhancing lesion which shows flip-flop phenomenon, measured about 5.5x6.1x5.5 cm in size; Partially thrombosed pseudoaneurysm at proximal right hepatic artery is likely. This lesion causes stretching of the common hepatic artery and portal vein. Hyperdenselesion with flip-flop phenomenon is also seen within dilated bilateral IHD, CHD, CBD and gallbladder; Contrast extravasation into CHD, CBD, 1st, 2nd, 3rd, 4th part of duodenum and jejunum is detected in portovenous phase. hemobilia is suggested.