INTRODUCTION

Hepatocellular carcinoma (HCC) remains the most common primary malignancy of the liver and a major contributor to cancer-related mortality worldwide, with over 900,000 new cases estimated annually.¹ Timely and accurate diagnosis is critical, as prognosis is strongly influenced by the stage at detection. In current clinical practice, noninvasive imaging plays a central role in the diagnosis of HCC, particularly in high-risk populations such as patients with cirrhosis or chronic hepatitis B infection.² For these individuals, dynamic contrast-enhanced imaging -typically using multiphasic computed tomography (CT) or magnetic resonance imaging (MRI)- can establish a diagnosis without the need for histologic confirmation when characteristic features are present. The radiological hallmarks of nonrim arterial phase hyperenhancement (APHE) followed by nonperipheral washout serve as the foundation of imaging-based diagnosis across major guidelines.²

Despite the strength of this imaging-based approach, false positive diagnoses remain a significant concern. A variety of benign and non-HCC malignant lesions may display overlapping enhancement patterns, leading to diagnostic uncertainty and potentially inappropriate treatment. This issue is further complicated when imaging criteria are applied in non-target populations where diagnostic specificity is lower.³ Although noninvasive confirmation of HCC is not recommended in these populations, misinterpretation of benign lesions as HCC can still lead to unnecessary interventions such as surgical resection. In such cases, accurate imaging-based differentiation becomes essential to avoid overtreatment and to guide appropriate clinical decision-making. Additionally, the diagnostic performance of imaging can vary depending on lesion size, underlying liver disease, and imaging modality, all of which contribute to interpretive complexity in real-world practice.

This review addresses these challenges by examining the principles and limitations of imaging-based diagnosis of HCC, highlighting a range of conditions that can mimic HCC on imaging, and outlining practical strategies for accurate interpretation of imaging findings and their integration into appropriate clinical management.

SPECIFICITY IN IMAGING DIAGNOSIS OF HCC: APPROACHES IN CURRENT GUIDELINES

Across major guidelines, including the Korean Liver Cancer Association-National Cancer Center (KLCA-NCC),⁴ Liver Imaging Reporting and Data System (LI-RADS),⁵ American Association for the Study of Liver Diseases (AASLD),⁶ European Association for the Study of the Liver (EASL),⁷ and Asian Pacific Association for the Study of the Liver (APASL),⁸ the combination of nonrim APHE followed by nonperipheral washout remains the core diagnostic criterion for identifying HCC in high-risk individuals. Although these guidelines differ in detail, they share the common goal of maximizing specificity while maintaining acceptable sensitivity, enabling noninvasive diagnosis without biopsy in lesions with a high probability of HCC.

LI-RADS, originally developed in North America, provides a structured lexicon and categorization system for imaging studies in high-risk populations. Notably, the AASLD⁶ and EASL guidelines⁷ have recently adopted the LI-RADS diagnostic algorithm. According to CT/MRI LI-RADS v2018, LR-5 represents ‘definite HCC’ and is assigned to lesions ≥10 mm with nonrim APHE and at least one additional major feature (nonperipheral washout, enhancing capsule, or threshold growth) except for 10-19 mm lesions, in which nonrim APHE combined with enhancing capsule alone is insufficient for LR-5 categorization.⁵ LR-5 is designed to maximize specificity, which has contributed to its high positive predictive value (>95%).⁹ To preserve this specificity, LI-RADS limits the assessment of washout to the portal venous phase (PVP) when hepatocyte-specific contrast agent is used, intentionally excluding hepatobiliary phase (HBP) findings.⁵

In contrast, Asian guidelines such as KLCA-NCC adopt a slightly different approach, aiming to improve sensitivity even at the cost of a small reduction in specificity. The 2022 KLCA-NCC criteria permit the use of hypointensity on the transitional phase (TP) or HBP as a surrogate for washout when gadoxetic acid is used.¹⁰ This strategy, however, introduces a risk of reduced specificity, as various non-HCC focal hepatic lesions can also demonstrate hypointensity during these phases due to altered hepatocyte function or contrast uptake mechanisms. For example, flash-filling hemangiomas may exhibit nonrim APHE followed by ‘pseudowashout’ on gadoxetic acid-enhanced MRI.¹¹ This apparent washout is not due to true lesion washout but rather results from the progressive enhancement of the surrounding hepatic parenchyma, potentially mimicking HCC enhancement patterns. To mitigate the risk of reduced specificity while still aiming for increased sensitivity, the KLCA-NCC strategy integrates ancillary imaging features. It specifically excludes lesions that exhibit a targetoid appearance or marked T2 hyperintensity from being classified as definitive HCC. This approach helps to differentiate HCC from potential mimickers, with validation studies reporting specificity values of approximately 90%.^12,13

Contrast-enhanced ultrasound (CEUS) is also accepted as a primary or complementary modality in HCC diagnosis. The CEUS LI-RADS v2017 algorithm defines LR-5 as a lesion ≥10 mm showing nonrim APHE followed by mild and late (>60 seconds) washout, using blood pool contrast agents.¹⁴ The KLCA-NCC 2022 guidelines adopt similar criteria but allow the use of either blood pool or Kupffer cell-specific contrast agents.¹⁰ The emphasis on ‘mild and late’ washout in both systems is designed to minimize false positives from intrahepatic cholangiocarcinoma (ICC) and other hypervascular malignancies.

Accurate application of imaging-based diagnostic criteria depends on appropriate patient selection. Noninvasive diagnosis is intended for individuals at sufficiently high risk for HCC, such as those with chronic hepatitis B or cirrhosis, although the specific definition of high-risk population may vary across guidelines (Table 1).² However, even among patients with cirrhosis, diagnostic performance can vary depending on the underlying etiology. For example, patients with cirrhosis due to vascular liver diseases (e.g., Budd-Chiari syndrome) are often excluded from the diagnostic target population due to their higher rates of false positive diagnoses.¹⁵ The applicability of noninvasive imaging-based diagnosis in non-cirrhotic patients with certain etiologies remains an area of ongoing investigation.^16,17 Metabolic dysfunction-associated steatotic liver disease is one such condition, where affected individuals are increasingly recognized as being at risk for HCC,¹⁸ but current evidence is insufficient to determine which subgroups may be appropriate candidates for diagnosis without histologic confirmation. Another example is chronic hepatitis C without cirrhosis, which is accepted as a target population in some Asian guidelines such as KLCA-NCC and APASL, but not in Western guidelines. Similarly, for chronic hepatitis B without cirrhosis, AASLD recognizes them as a target population for imaging diagnosis only when they are at higher risk based on their platelet, age, gender-hepatitis B (PAGE-B) score.⁶ Further research is needed to refine risk stratification and to more clearly define the boundaries of the diagnostic target population.

MALIGNANT MIMICKERS OF HCC

Intrahepatic cholangiocarcinoma

ICC is a well-recognized malignant mimicker of HCC on imaging, particularly in patients with cirrhosis. Although ICC typically exhibits a targetoid appearance across imaging phases, a subset of small duct type ICCs, especially those that are small in size, arise in cirrhotic livers, and are highly cellular, with prominent cholangiolocellular components, may deviate from this pattern.¹⁹ These lesions can demonstrate nonrim APHE with or without washout and may be categorized as definite or probable HCC on imaging (Fig. 1). This overlap reflects the shared risk factors between HCC and ICC -including cirrhosis and viral hepatitis- which complicate differential diagnosis in high-risk populations.

Avoiding false positive diagnosis of ICC is a key consideration in the design of imaging-based HCC diagnostic systems. The LI-RADS algorithm addresses this by classifying lesions with targetoid features as LR-M, which preserves specificity for HCC while retaining sensitivity for malignancy.⁵ CEUS LI-RADS also categorizes lesions with early or marked washout as LR-M, whereas LR-5 requires mild and late washout.¹⁴ Asian guidelines, such as those from KLCA-NCC and APASL, similarly emphasize specificity by excluding from noninvasive HCC diagnosis any lesion that demonstrates targetoid appearance on dynamic phases, the HBP, or diffusion-weighted imaging (DWI).^4,8 In addition, as mentioned earlier, the definition of washout on gadoxetic acid-enhanced MRI varies across guidelines. While emphasizing specificity can help minimize false positive diagnoses of ICC, it comes at the cost of reduced sensitivity for detecting HCC.

ICC cases that mimic HCC on imaging have been reported to have a relatively better prognosis compared to conventional ICC.^20,21 However, the clinical outcomes of patients who undergo treatment for presumed HCC, only to be subsequently diagnosed with ICC, remain insufficiently characterized. Further investigation is warranted to clarify the prognostic implications of imaging-based misclassification in such cases.

Combined hepatocellular-cholangiocarcinoma

Combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a rare primary liver malignancy characterized by histologic features of both hepatocellular and cholangiocellular differentiation within the same tumor. It accounts for approximately 1-5% of all primary liver cancers and occurs more frequently in cirrhotic livers.²²

Accurate imaging diagnosis of cHCC-CCA remains difficult, as it often lacks reliable imaging or biomarker signatures. On imaging, cHCC-CCA may present with a wide spectrum of features, ranging from HCC-like (nonrim APHE and washout) to ICC-like patterns (targetoid enhancement) or mixed appearances.^23-25 Lesions with predominant HCC differentiation are particularly prone to misclassification as definite or probable HCC, increasing the risk of false positive diagnosis (Fig. 2). The 2019 World Health Organization (WHO) classification refined the pathological criteria for cHCC-CCA by eliminating subtypes such as the stem cell variant and requiring unequivocal histologic evidence of both hepatocellular and cholangiocellular components.²² This redefinition has important implications for imaging-based diagnosis, and studies evaluating the diagnostic performance of imaging using older pathologic criteria should be interpreted with caution. Tumor marker profiles may offer additional clues. Although concurrent elevation of alpha-fetoprotein (AFP) and carbohydrate antigen 19-9 (CA19-9) can raise suspicion for cHCC-CCA, this pattern is observed in only a limited subset of patients.²⁶ Even biopsy may not provide a definitive diagnosis due to sampling error, particularly in tumors with spatially heterogeneous histologic components.

Recognizing cHCC-CCA as a mimicker of HCC is important, since misdiagnosis may result in treatment decisions, such as ablation or liver transplantation, that are based on HCC protocols but may be less appropriate or not well supported for cHCC-CCA.²⁷ When atypical imaging features or discordant tumor marker profiles are present, further diagnostic evaluation should be considered to ensure appropriate management and improve patient outcomes.

Primary hepatic lymphoma

Primary hepatic lymphoma (PHL) is a rare extranodal lymphoma confined to the liver at initial diagnosis. Although PHL typically presents as a large, solitary mass with rim-like or poor arterial enhancement, some lesions can occasionally mimic HCC by demonstrating nonrim APHE with or without washout appearance (Fig. 3).^28,29 However, several imaging characteristics may aid in differentiation. On DWI, lymphoma tends to show marked diffusion restriction due to high cellularity.³⁰ On CEUS, PHL usually shows relatively rapid washout,³¹ different from typical pattern of HCC. Additionally, most PHL demonstrates intense ¹⁸F-fluorodeoxyglucose (FDG) uptake on positron emission tomography (PET) imaging, helping differentiate it from well-differentiated HCC, which typically shows low or variable FDG avidity.³²

Clinical findings such as normal AFP levels, systemic symptoms (e.g., fever, weight loss, night sweats), or associated lymphadenopathy may further support the diagnosis. Recognition of these imaging and clinical features is essential, as PHL is typically treated with systemic chemotherapy rather than surgery or locoregional therapy.

Other primary malignancies mimicking HCC

Other primary hepatic malignancies can mimic HCC on imaging, particularly when they demonstrate APHE. Although these entities are rare, their recognition is important to avoid inappropriate management. Primary hepatic neuroendocrine tumor (NET) demonstrates variable imaging appearances without well-established characteristic features, and can occasionally present with APHE and washout appearance that mimics HCC. Although differentiation can be challenging, primary NETs often demonstrate internal necrosis, seen as non-enhancing areas on dynamic imaging, and relatively high signal intensity on T2-weighted sequences, features that can provide diagnostic clues.^33-35 Hepatic angiosarcomas represent another rare primary liver malignancy that can demonstrate hypervascular enhancement patterns mimicking HCC. Helpful differentiating features include high T1 signal intensity from blood products, progressive enhancement rather than washout, rapid growth over time, and T2 hyperintensity with hemangioma-like enhancement patterns,³⁶ though distinction from other hypervascular lesions such as epithelioid angiomyolipoma or atypical hemangioma can be challenging. Given the overlapping imaging features, tissue sampling is often required for definitive diagnosis of these rare primary hepatic malignancies.

Hypervascular metastases

Hypervascular metastases can mimic HCC in imaging studies, particularly in patients without known primary cancer or overt extrahepatic disease. NET and renal cell carcinoma are among the commonly reported sources, but other malignancies such as melanoma, breast cancer, and hepatoid adenocarcinoma can also give rise to hypervascular hepatic metastases that exhibit APHE.³⁷ Hepatoid adenocarcinoma is especially prone to misclassification, as it often presents with elevated AFP levels and HCC-like enhancement patterns, yet arises most frequently from a gastric primary (Fig. 4).^38,39

While multiple lesions favor a diagnosis of metastases, solitary hepatic metastases can be more difficult to distinguish from HCC. Clinical history is essential, but the diagnosis may remain uncertain when the primary malignancy is small, occult, or located outside the imaging field. The presence or absence of underlying liver disease provides valuable context, as HCC typically arises in cirrhotic livers, whereas hypervascular metastases more commonly occur in non-cirrhotic settings.

When a hypervascular liver lesion is suspected to represent a metastasis -either solitary or multiple- systematic efforts to identify the primary malignancy are essential. A thorough diagnostic workup may include cross-sectional imaging such as chest and abdominal CT, tumor marker evaluation, endoscopic studies, or PET/CT. In particular, when a NET is suspected, Gallium‑68 DOTA-(Tyr³)-octreotide (⁶⁸Ga-DOTATOC) PET/CT can be highly sensitive for detecting both the primary lesion and hepatic metastases (Fig. 5).⁴⁰ Biopsy of the liver lesion should be also considered to establish a definite diagnosis and guide management.

BENIGN MIMICKERS OF HCC

Focal nodular hyperplasia spectrum

Focal nodular hyperplasia (FNH) and FNH-like nodules represent a spectrum of benign hepatocellular lesions characterized by hyperplastic nodular transformation in response to abnormal vascular flow. Classic FNH occurs in otherwise healthy livers and is composed of hyperplastic hepatocytes arranged around a central stellate scar containing malformed arteries. In contrast, FNH-like nodules arise in the setting of altered hepatic perfusion, including vascular disorders such as Budd-Chiari syndrome, congenital or acquired portosystemic shunts, porto-sinusoidal vascular disease, and cirrhotic livers. These benign lesions can be particularly challenging HCC mimickers in patients with vascular liver diseases, which is why such patients are often excluded from noninvasive HCC diagnostic target populations, as discussed earlier. Although underlying pathophysiology and clinical context of these lesions differ, they show similar imaging appearances.

On dynamic imaging, both FNH and FNH-like nodules typically demonstrate homogeneous APHE with isoattenuation or isointensity during PVP and delayed phases. Additionally, these lesions typically appear nearly isointense on T1- and T2-weighted images, in contrast to HCC. On HBP imaging with gadoxetic acid, these lesions usually appear iso- to hyperintense due to preserved or even increased expression of organic anion transporting polypeptides 1B3 (OATP1B3). However, some FNH or FNH-like nodules may show atypical features such as washout on the portal or delayed phase and hypointensity on the HBP (Fig. 6), particularly when the characteristic central scar is not evident.⁴¹ When the diagnosis remains uncertain, CEUS can assist in diagnosis by demonstrating the characteristic spoke-wheel or centrifugal filling pattern during the arterial phase, which is highly specific for FNH or FNH-like nodules. The absence of washout on CEUS further supports the benign nature of these lesions.⁴²

Differential diagnosis is particularly challenging when imaging features overlap with those of atypical HCC. Approximately 10-15% of HCCs, especially well-differentiated tumors with β-catenin activation, can demonstrate iso- or hyperintensity on HBP due to preserved OATP1B3 expression.^43,44 Similarly, some subtypes of hepatocellular adenoma, notably β-catenin-activated and inflammatory subtypes, may show HBP hyperintensity,⁴⁵ complicating the distinction from FNH. Accurate diagnosis requires integration of imaging features, clinical context, and patient risk factors. In indeterminate cases, longitudinal follow-up or histopathologic confirmation may be necessary to avoid misclassification and ensure appropriate management.

Hepatocellular adenoma

Hepatocellular adenoma is a benign hepatocellular neoplasm with diverse molecular subtypes, each associated with distinct clinical, pathological, and imaging features. According to the 2019 WHO classification, these subtypes include hepatocyte nuclear factor 1α (HNF1α)-inactivated, inflammatory, β-catenin-activated, β-catenin-activated inflammatory, sonic hedgehog, and unclassified types.⁴⁶ Among these, the inflammatory and β-catenin-activated types are most relevant when considering HCC mimickers, given their frequent APHE.⁴⁷

The inflammatory subtype, the most common subtype, typically demonstrates APHE and may maintain iso- or hyperintensity on the PVP or TP without true washout (Fig. 7).⁴⁷ Although some inflammatory adenomas may appear iso- or hyperintense on the HBP, this finding is more typical of β-catenin-activated subtypes.^48,49 Ancillary features include a T2 hyperintense rim (atoll sign) and background hepatic steatosis.⁴⁷ This subtype is frequently associated with obesity, metabolic syndrome, and carries an increased risk of hemorrhage, especially in large or subcapsular lesions.

The β-catenin-activated subtype, more frequently seen in men, is associated with the highest risk of malignant transformation, particularly with exon 3 mutations. These lesions often appear large and heterogeneous and demonstrate iso- or hyperintensity on HBP due to upregulated OATP1B3 expression.^48,49 This HBP feature may serve as a noninvasive biomarker for identifying high-risk adenomas.

The HNF1α-inactivated subtype, not typically an HCC mimicker, is characterized by diffuse intracellular fat, which results in a signal drop on opposed-phase imaging. These lesions are usually hypointense on the hepatobiliary phase due to low OATP1B3 expression, aiding in differentiation from subtypes with higher malignant potential.⁵⁰

Key imaging features that help differentiate hepatocellular adenoma from HCC include persistent enhancement on delayed phases, absence of washout, lack of a capsule, and the presence of clinical or metabolic risk factors. In cases where imaging findings are indeterminate, biopsy with immunohistochemical staining may help identify high-risk subtypes and guide management decisions.

Angiomyolipoma

Hepatic angiomyolipoma (AML) is a rare benign mesenchymal tumor that belongs to the perivascular epithelioid cell tumor family.⁵¹ Although histologically benign in most cases, AML can present with imaging features that closely resemble HCC, particularly in non-cirrhotic livers. This resemblance may vary depending on the subtype, and accurate diagnosis is essential to avoid unnecessary surgical resection. Classic AML consists of variable proportions of blood vessels, smooth muscle, and macroscopic fat.⁵² The fat component is usually homogeneous and can be readily detected on unenhanced CT or chemical-shift MRI. However, fat-poor AMLs and epithelioid variants pose a greater diagnostic challenge. These lesions lack visible fat and may present as solid, hypervascular masses on imaging. Epithelioid AML, composed predominantly of epithelioid cells, may exhibit more aggressive histologic features such as nuclear atypia and increased mitotic activity.⁵¹

On CT or MRI, a distinctive ancillary feature of AML is the presence of early draining veins -small venous channels emerging from the lesion during the arterial phase and draining directly into hepatic or systemic veins (Fig. 8).^53,54 Although not exclusive to AML, this finding is uncommon in HCC and can serve as a helpful diagnostic clue when present.⁵³ On HBP imaging using gadoxetic acid, AMLs typically appear homogeneously hypointense due to the absence of functioning hepatocytes.⁵⁵ On CEUS, classic AMLs usually show rapid and homogeneous arterial enhancement, followed by no definite washout or only very late washout -findings that differ from the typical CEUS washout pattern of HCC.^56,57

Miscellaneous benign mimickers

Several additional benign entities can mimic HCC on imaging, including eosinophilic abscess, splenosis, and adrenal adenomas arising from adrenohepatic fusion. Recognition of these uncommon mimickers through their characteristic imaging features, relevant clinical context, and sometimes specialized imaging techniques can prevent misdiagnosis and unnecessary interventions.

Eosinophilic abscess

Eosinophilic abscess, also known as focal eosinophilic infiltration, typically occurs in patients with peripheral eosinophilia related to parasitic infections (particularly Clonorchis sinensis or Fasciola hepatica from raw freshwater fish), allergic reactions, or certain medications and health supplements. For suspected cases, clinicians should inquire about dietary history, supplement use, check peripheral eosinophilia, and consider parasitic serological testing.

On imaging, eosinophilic abscess may demonstrate APHE followed by washout appearance, potentially fulfilling imaging criteria for HCC.⁵⁸ One of characteristic imaging features suggesting eosinophilic abscess is a relatively smaller lesion size on unenhanced T1-weighted imaging compared to the HBP imaging (Fig. 9).⁵⁹ This size discrepancy reflects central necrosis surrounded by eosinophilic infiltration. In addition, the lesions often show a fuzzy margin and irregular shape, which can further support the diagnosis. Follow-up imaging typically reveals spontaneous regression or disappearance of the lesions after appropriate treatment of the underlying cause.⁶⁰

Splenosis

Splenosis represents auto-transplantation and subsequent growth of splenic tissue following traumatic splenic injury or splenectomy. While splenosis typically presents as multiple peritoneal implants, lesions adjacent to the liver capsule can mimic primary liver tumors, including HCC.⁶¹ These lesions may demonstrate APHE with variable washout on later phases and hypointensity on HBP images.

A history of splenic trauma or splenectomy should raise suspicion for this entity, particularly in non-cirrhotic patients with hypervascular subcapsular nodules. Definitive diagnosis can be achieved non-invasively through 99mTc-labeled heat-damaged red blood cell (RBC) scintigraphy with single photon emission computed tomography/computed tomography (SPECT/CT), which confirms the splenic nature of the tissue (Fig. 10).⁶² Recognition of splenosis is crucial as it represents a benign condition that generally requires no treatment, thereby avoiding unnecessary surgical intervention.

Adrenal cortical adenoma in adrenohepatic fusion

Adrenohepatic fusion, the anatomical continuity between liver and right adrenal gland without intervening connective tissue, found in 9.9% of adult autopsy specimens.⁶³ When adrenal cortical adenomas develop within these areas of fusion, they may present as apparent liver lesions with imaging features that can mimic HCC, including well-defined APHE and washout on PVP or delayed phases.⁶⁴

These lesions should be suspected in non-cirrhotic patients presenting with a solitary hypervascular nodule in the typical location for adrenohepatic fusion (posterior segments of the right hepatic lobe, particularly segment VII adjacent to the right adrenal gland) (Fig. 11). Chemical shift MRI can aid diagnosis by demonstrating signal dropout on opposed-phase images compared to in-phase images, confirming the presence of intracellular lipid, a characteristic feature of many adrenal adenomas.⁶⁵

PRACTICAL TIPS TO AVOID FALSE POSITIVE DIAGNOSIS

When a hepatic lesion suspicious for HCC is identified, the initial and crucial step involves a comprehensive assessment of clinical factors that significantly influence the pretest probability of HCC. This includes evaluating the presence or absence of underlying liver disease, reviewing relevant medical history (such as medications, prior malignancies, trauma, or surgery), and analyzing laboratory data, including tumor markers and eosinophil counts. This thorough clinical assessment is fundamental. It guides subsequent imaging interpretation and helps prevent misdiagnosis.

The fundamental principle of noninvasive HCC diagnosis lies in the strict application of validated imaging criteria, which is essential to ensure high specificity and avoid false positive diagnoses. Radiologic hallmarks such as unequivocal nonrim APHE and nonperipheral washout must be clearly and confidently identified. If they are equivocal, they should not be interpreted as positive. Specificity is preserved by adhering to major feature definitions, restricting washout assessment to validated phases, and applying tie-breaking rules when category assignment is uncertain. In addition, it is equally important to apply the concept of the high-risk population precisely. In non-target populations, noninvasive imaging-based diagnosis is not supported, even when lesions exhibit typical imaging features. In these patients, the goal is not to confirm HCC but to avoid misclassification of benign lesions or non-HCC malignancies, which could lead to unnecessary or inappropriate treatment.

In the differential diagnosis of HCC from its mimickers, imaging interpretation should be comprehensive and context-sensitive (Table 2). While major imaging features are central to diagnosis, ancillary findings that suggest alternative pathologies must also be actively evaluated. Imaging features should be interpreted in conjunction with clinical information, including underlying liver disease, serum tumor markers, and prior treatments. Furthermore, when a single imaging modality yields inconclusive results, a multimodality approach can enhance diagnostic confidence. CEUS may provide dynamic vascular information, including enhancement pattern and washout timing. Gadoxetic acid-enhanced MRI can assist in differentiation based on HBP signal characteristics. Nuclear medicine techniques, such as FDG PET/CT, DOTATOC PET/CT, and 99mTc-labeled RBC scintigraphy, are valuable adjuncts for distinguishing mimickers such as lymphoma, NET, and splenosis.

When diagnostic uncertainty remains despite comprehensive imaging, biopsy should be considered, particularly in non–target populations or when lesions do not fully meet the criteria for noninvasive diagnosis. Histologic confirmation helps clarify the nature of indeterminate lesions, distinguish between primary and metastatic tumors, and guide appropriate clinical management, especially when the primary malignancy is unknown or unexpected.

CONCLUSION

Noninvasive imaging has transformed the diagnosis of HCC, but its effectiveness depends on disciplined application to avoid false positive diagnoses. In high-risk populations, lesions with radiological hallmarks may proceed directly to HCC management, whereas those that do not fully satisfy the imaging criteria should be evaluated with short-term follow-up, complementary imaging, or biopsy, based on the clinical context. In non-target populations, biopsy is strongly recommended for any suspicious lesion when an alternative diagnosis cannot be confidently established. Taken together, these risk-stratified approaches are essential for reducing the risk of false positives. A risk-adapted, context-sensitive, and multidisciplinary team-based diagnostic strategy is essential to ensure accurate diagnosis while avoiding unnecessary or inappropriate treatment. This requires a thorough understanding of the imaging features of both HCC and its mimickers, thoughtful integration of clinical and laboratory data, and a patient-centered approach. Future refinement of imaging criteria and diagnostic strategies should continue to support tailored application across diverse clinical scenarios, thereby enhancing diagnostic accuracy and improving clinical decision-making.

Article information

Data Availability

Not applicable.

Authors Contributions

Conceptualization: IJ

Methodology: IJ

Writing - original draft: IJ

Figure 1.

Intrahepatic cholangiocarcinoma of small duct type in a 57-year-old man with chronic hepatitis B, confirmed by surgical resection. Gadoxetic acid-enhanced MRI shows a 1.5 cm nodule (arrow) in segment V of the liver. The lesion appears moderately hyperintense on T2- weighted imaging (A) and hypointense on unenhanced T1-weighted imaging (B). It demonstrates arterial phase hyperenhancement (C), washout appearance on portal venous phase (D), and hypointensity on hepatobiliary phase (E). Diffusion-weighted imaging with a b-value of 800 s/mm² shows diffusion restriction (F). The lesion fulfilled major imaging criteria for HCC, mimicking HCC in the setting of chronic liver disease. MRI, magnetic resonance imaging; HCC, hepatocellular carcinoma.

Figure 2.

Combined hepatocellular cholangiocarcinoma in a 57-year-old man with cirrhosis, confirmed by surgical resection. Liver CT shows a 1.8 cm exophytic nodule (arrow) in segment VIII with hypoattenuation on unenhanced imaging (A), nonrim arterial phase hyperenhancement (B), and washout on portal venous (C) and delayed phases (D). The lesion met LI-RADS category 5 criteria (definitely HCC). Surgical pathology revealed combined hepatocellular cholangiocarcinoma with 95% hepatocellular component. CT, computed tomography; LI-RADS, Liver imaging reporting and data system; HCC, hepatocellular carcinoma.

Figure 3.

Primary hepatic lymphoma in a 65-year-old woman without risk factors for HCC. Gadoxetic acid-enhanced MRI shows a 1.4 cm nodule (arrow) in segment V with hypointensity on unenhanced T1-weighted imaging (A), nonrim arterial phase hyperenhancement (B), and washout on portal venous phase (C). The lesion shows mild hyperintensity on T2-weighted imaging (D) and marked diffusion restriction on diffusion-weighted imaging with a b-value of 1,000 s/mm² (E). On ¹⁸F-FDG PET/CT, the nodule demonstrates intense hypermetabolism (F). Biopsy confirmed extranodal marginal zone B-cell lymphoma. MRI, magnetic resonance imaging; FDG, fluorodeoxyglucose; PET/CT, positron emission tomography/computed tomography.

Figure 4.

Hepatoid adenocarcinoma of the stomach with hepatic metastases in a 32-year-old man with markedly elevated serum alphafetoprotein level (to 30,000 ng/mL). Contrast-enhanced CT shows a 12 cm well-defined hepatic mass (arrows) in the right lobe with heterogeneous arterial enhancement (A) and washout on portal venous phase (B). Enhancing wall thickening and a polypoid mass are noted in the gastric cardia (asterisk). Portal venous phase images at different axial levels (C, D) show another 7 cm hepatic mass (arrow) and an enlarged perigastric lymph node (arrowhead of C), as well as portal vein tumor thrombus (arrowhead of D). Biopsy confirmed hepatoid adenocarcinoma in both the gastric and hepatic lesions. CT, computed tomography.

Figure 5.

Hypervascular liver metastases from rectal neuroendocrine tumor in a 50-year-old man. Liver CT shows multiple hypervascular nodules in both lobes on arterial phase imaging (A), with washout appearance on portal venous phase (B). An irregular enhancing soft tissue mass with perirectal extension is seen in the rectum (arrows) (C). ⁶⁸Ga-DOTATOC PET/CT demonstrates intense uptake in the hepatic lesions (D) and rectal mass (E), suggestive of neuroendocrine tumor, which was confirmed by biopsy. CT, computed tomography; PET/CT, positron emission tomography/computed tomography.

Figure 6.

Focal nodular hyperplasia in a 53-year-old woman with a history of rectal cancer surgery and adjuvant chemotherapy including oxaliplatin 3 years prior. Gadoxetic acid-enhanced MRI shows a 1.5 cm nodular lesion (arrow) in segment II of the liver with mild hyperintensity on T2-weighted imaging (A) and arterial phase hyperenhancement (B). The lesion demonstrates persistent enhancement on portal venous phase (C). On hepatobiliary phase imaging (D), the peripheral portion is slightly hyperintense, while the central portion remains hypointense. Surgical resection confirmed the diagnosis of focal nodular hyperplasia. MRI, magnetic resonance imaging.

Figure 7.

Hepatocellular adenoma of inflammatory subtype, confirmed by surgical resection, in a 53-year-old man. Gadoxetic acidenhanced MRI shows a 1.6 cm well-defined mass (arrow) in segment III of the liver with arterial phase hyperenhancement (A) and no washout on portal venous phase imaging (B). The lesion appears nearly isointense on transitional (C) and hepatobiliary phase images (D), shows mild hyperintensity on T2-weighted imaging (E), and demonstrates restricted diffusion on diffusion-weighted imaging with a b-value of 800 s/mm² (F). MRI, magnetic resonance imaging.

Figure 8.

Hepatic epithelioid angiomyolipoma, confirmed by surgical resection, in a 74-year-old woman. Liver CT shows a 4 cm mass (arrow) in the left lateral section of the liver with hypoattenuation on unenhanced imaging (A), nonrim arterial phase hyperenhancement (B), and washout on portal venous (C) and delayed phase imaging (D). An early draining vein sign is noted on arterial phase imaging, with early opacification of the left hepatic vein (arrowhead of B). CT, computed tomography.

Figure 9.

Eosinophilic abscess confirmed by surgical resection in a 52-year-old man with liver cirrhosis. CT shows a 1 cm ill-defined lesion (arrow) with arterial phase hyperenhancement in segment VI of the liver (A) and washout on portal venous phase imaging (B), fulfilling LIRADS category 5 criteria (definitely HCC). On MRI, the lesion shows moderate hyperintensity on T2-weighted imaging (C) and restricted diffusion on diffusion-weighted imaging with a b-value of 800 s/mm² (D). A size discrepancy is noted between unenhanced T1-weighted imaging (E) and hepatobiliary phase imaging (F), with the lesion appearing larger on the hepatobiliary phase, a finding that may suggest the possibility of eosinophilic abscess. CT, computed tomography; LI-RADS, Liver imaging reporting and data system; HCC, hepatocellular carcinoma; MRI, magnetic resonance imaging.

Figure 10.

Splenosis in a 55-year-old man with a history of splenectomy due to trauma. Gadoxetic acid-enhanced MRI shows a 2 cm welldefined subcapsular lesion (arrow) in segment III of the liver. The lesion appears hypointense on unenhanced T1-weighted imaging (A), demonstrates arterial phase hyperenhancement (B), and shows washout on portal venous phase (C). It also shows mild hyperintensity on T2-weighted imaging (D) and restricted diffusion on diffusion-weighted imaging with a b-value of 1,000 s/mm² (E). 99mTc-labeled heatdamaged red blood cell scintigraphy with SPECT/CT (F) shows intense uptake in the lesion, confirming the diagnosis of splenosis. MRI, magnetic resonance imaging; SPECT/CT, single photon emission computed tomography/computed tomography.

Figure 11.

Adrenal cortical adenoma arising from adrenohepatic fusion in a 39-year-old man. Gadoxetic acid-enhanced MRI shows a 1.5 cm well-defined nodular lesion (arrow) in the subcapsular area of segment VII of the liver, with mild hyperintensity on T2-weighted imaging (A). The lesion demonstrates arterial phase hyperenhancement (B), washout on portal venous phase (C), and restricted diffusion on diffusionweighted imaging with a b-value of 800 s/mm² (D). Opposed-phase imaging (E) shows diffuse signal drop compared with in-phase imaging (F), suggesting the presence of microscopic fat. Percutaneous biopsy confirmed the diagnosis of adrenal cortical adenoma. MRI, magnetic resonance imaging.

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