Focal Nodular Hyperplasia-like Nodules Research Articles

Dynamic contrast-enhanced ultrasound findings of focal nodular hyperplasia-like nodules in cirrhosis: a description of two cases and literature analysis.

Dynamic contrast-enhanced ultrasound findings of focal nodular hyperplasia-like nodules in cirrhosis: a description of two cases and literature analysis.

Nodular Liver in Portosinusoidal Vascular Disease: A Case of Mistaken Identity

Background Portosinusoidal vascular disease (PSVD) has been proposed as a unifying term for vascular abnormalities of the small portal veins and sinusoids that occur in the noncirrhotic liver. This term supersedes other designations including incomplete septal cirrhosis, nodular regenerative hyperplasia, hepatoportal sclerosis, and obliterative portal venopathy. Most patients have noncirrhotic portal hypertension, but the latter is not required to establish a diagnosis of PSVD. Diagnosis requires a liver biopsy of adequate size (≥20 mm long) in the presence of accompanying clinical signs of noncirrhotic portal hypertension and/or histological changes of PSVD. We report a case of severe PSVD that caused severe liver atrophy and required transplantation for intractable hepatic encephalopathy. The explanted liver showed numerous focal nodular hyperplasia-like nodules. Case Report A 57-year-old man with neurofibromatosis type 2 and diabetes mellitus type 2 controlled with insulin developed ascites and signs of portal hypertension. He was presumed to have cirrhosis due to nonalcoholic fatty liver disease and underwent liver transplantation for intractable portal hypertension and severe hepatic encephalopathy. The explanted liver had a nodular appearance; however, histological sections showed no bridging fibrosis. Thin, incomplete curvilinear fibrous septa were seen emanating from portal tracts in a patchy distribution. Our case illustrates that PSVD may cause severe hepatic atrophy and lead to architectural abnormalities that may radiologically mimic the parenchymal nodularity of cirrhosis.

Porto-Sinusoidal Vascular Disease and Focal Nodular Hyperplasia-like Nodules in a Patient with Neurofibromatosis and Non-Cirrhotic Portal Hypertension

Abstract Introduction/Objective Non-cirrhotic portal hypertension (NCPH) is uncommon. The underlying pathophysiology appears to lie at the level of intrahepatic portal veins and sinusoids, hence the term “porto-sinusoidal vascular disease” (PSVD). We report a rare case of PSVD with focal nodular hyperplasia (FNH)-like nodules in a patient with neurofibromatosis type 2 (NF2). Methods/Case Report A 57-year-old male with NF2 and type 2 diabetes, presented with a large variceal bleed requiring blood transfusion and subsequent transjugular intrahepatic portosystemic shunt (TIPS). Imaging showed a nodular liver, presumed to be cirrhosis due to non-alcoholic liver disease. Liver biopsy was not done. Thereafter, he had several episodes of hepatic encephalopathy and TIPS was downsized to prevent recurrences. The patient required liver transplantation for intractable portal hypertension and severe hepatic encephalopathy; his liver synthetic function was near normal and MELD was 11. Portal vein was patent. The explanted liver was micronodular, soft and weighed 946 grams. Unencapsulated nodules, a few mm to 1 cm in size, were present. Microscopically, there was diffuse nodularity in the absence of bridging fibrosis. Thin, incomplete curvilinear fibrous septa were present. There were aberrant veins, hypervascular portal tracts, herniated portal veins and rare occluded portal veins. Trichrome and reticulin stains confirmed architectural abnormalities including nodularity, lack of bridging fibrosis and approximation of portal tracts. Immunohistochemistry for glutamine synthetase accentuated architectural distortion and revealed nodules with FNH-like geographic areas of staining. Results (if a Case Study enter NA) NA Conclusion This is a rare case of NCPH due to PSVD in a patient with NF2. Microscopy suggested incomplete septal cirrhosis (ISC), a pattern associated with both PSVD and regression of fibrosis in a cirrhotic liver. Isolated portal hypertension without loss of synthetic function favors primary PSVD over regression of fibrosis. FNH-like nodules are consistent with regenerative changes caused by localized abnormalities of blood flow.

Transjugular intrahepatic portosystemic shunt creation may be associated with hyperplastic hepatic nodular lesions in the long term: an analysis of 18 pediatric and young adult patients.

Retrospective studies have demonstrated the efficacy and safety of pediatric and adolescent transjugular intrahepatic portosystemic shunt (TIPS), but long-term outcomes warrant further investigation. To report on the development of hyperplastic hepatic nodular lesion development in children and young adults (<21 years) with TIPS patency >3years. Eighteen children and young adults, including 10 (55.6%) females and 8 (44.4%) males, underwent TIPS creation with >3years' patency and follow-up evaluation at a tertiary children's hospital. The mean age at the time of TIPS creation was 12.5±5.1 years (range: 1.5-20.0years). The mean model for end-stage liver disease (MELD) at the time of TIPS creation was 8.1±1.6 (range: 6-11). Indications for TIPS creation included acute variceal bleeding (8/18, 44.4%), primary (1/18, 5.6%) or secondary (7/18, 38.9%) prevention of varices, portal vein thrombosis (1/18, 5.6%), and splenic sequestration (1/18, 5.6%). Technical successes, intra-procedural parameters, hemodynamic and clinical successes, TIPS patencies, adverse events, imaging evaluations, and follow-ups were recorded. All (100%) TIPS placements were successful; however, a direct intrahepatic portosystemic shunt was created in one (5.6%) patient. Mean reduction of the portosystemic shunt gradient was 9.1±3.3mmHg (range: 4-16 mmHg). Seventeen (94.4%) patients demonstrated clinical success with resolution of their initial clinical indication for TIPS placement. The 3-year TIPS primary, primary-assisted, and secondary patencies were 83.3% (15/18), 94.4% (17/18), and 100% (18/18), respectively. Two (11.1%) patients developed mild, medically controlled hepatic encephalopathy. One (5.6%) patient developed hepatopulmonary syndrome. Nine (50%) patients developed single or multiple hepatic nodules at a mean imaging surveillance time after TIPS of 4.4±3.0years (range: 1.5-10.2years). Six (33.3%) patients developed nodules >1 cm with imaging features most consistent with focal nodular hyperplasia or focal nodular hyperplasia-like nodules. The mean follow-up duration was 5.7±2.9years (range: 3.0-13.1 years). Long-term (>3years) portosystemic shunting via TIPS is associated with the development of hepatic nodular lesions in children. Consequently, children with TIPS may need gray-scale assessment of hepatic parenchyma as part of routine ultrasound exams and extended imaging surveillance until more is understood regarding the natural history of induced nodularity.

Hepatocyte-specific contrast-enhanced MRI findings of focal nodular hyperplasia-like nodules in the liver following chemotherapy in pediatric cancer patients

We aimed to assess the MRI findings and follow-up of multiple focal nodular hyperplasia (FNH)- like lesions in pediatric cancer patients diagnosed by imaging findings. We retrospectively analyzed clinical data and MRI examinations of 16 pediatric patients, who had been scanned using gadoxetate disodium (n=13) and gadobenate dimeglumine (n=3). Hepatic nodules were reviewed according to their number, size, contour, T1- and T2-weighted signal intensities, arterial, portal, delayed and hepatobiliary phase enhancement patterns. Follow-up images were evaluated for nodule size, number, and appearance. All 16 patients received chemotherapy in due course. Time interval between the initial diagnosis of cancer and detection of the hepatic nodule was 2-14 years. Three patients had a single lesion, 13 patients had multiple nodules. The median size of the largest nodules was 19.5 mm (range, 8-41 mm). Among 16 patients that received hepatocyte-specific agents, FNH-like nodules appeared hyperintense in 11 and isointense in 5 on the hepatobiliary phase. During follow-up, increased number and size of the nodules were seen in 4 patients. The nodules showed growth between 6-15 mm. Liver MRI using hepatocyte-specific agents is a significant imaging method for the diagnosis of FNH-like lesions, which can occur in a variety of diseases. Lesions can increase in size and number in pediatric patients.

Benign Hepatic Nodules Mimicking Hepatocellular Carcinoma in the Setting of Fontan-associated Liver Disease: A Case Report

ABSTRACTFontan procedure, in which systemic circulation is redirected into pulmonary circulation by a baffle, is a palliative surgical strategy for patients born with single ventricle congenital heart disease. Hemodynamic changes secondary to Fontan procedure, also termed as Fontan physiology, result in end-organ damage, especially of the liver. Fontan-associated liver disease (FALD) represents a spectrum of pathologies ranging from mild liver fibrosis to advanced liver cirrhosis and hepatocellular carcinoma (HCC). Hepatic nodules, some of which have been documented as HCC in several case series and reports, are a recognized complicated feature of FALD. Herein, we report a case with benign hepatic nodules mimicking HCC by imaging characteristics, emphasizing the fact that arterially enhancing lesions with delayed washout appearance may reflect benign regenerative or focal nodular hyperplasia-like nodules in patients with Fontan physiology.How to cite this articleÇolaklar A, Lehnert SJ, Tirkes T. Benign Hepatic Nodules Mimicking Hepatocellular Carcinoma in the Setting of Fontan-associated Liver Disease: A Case Report. Euroasian J Hepato-Gastroenterol 2020;10(1):42–44.

Hepatic nodules with arterial phase hyperenhancement and washout on enhanced computed tomography/magnetic resonance imaging: how to avoid pitfalls

This essay aimed to illustrate the various hepatic nodules that may exhibit arterial phase hyperenhancement and washout on computed tomography/magnetic resonance imaging (CT/MRI). Hepatic nodules with arterial phase hyperenhancement and washout on CT/MRI include hepatocellular carcinoma, focal nodular hyperplasia-like nodules, serum amyloid A-positive hepatocellular neoplasms, intrahepatic cholangiocarcinoma, intrahepatic bile duct adenoma,hepatoblastoma, hepatocellular adenoma, hepatic epithelioid angiomyolipoma, and metastasis including neuroendocrine and gastrointestinal stromal tumors. Understanding the imaging findings is important to ensure correct diagnosis.

Uncommon imaging evolutions of focal liver lesions in cirrhosis.

The purpose of this article is to describe and illustrate uncommon imaging evolutions of benign (i.e., cyst, hemangioma, focal nodular hyperplasia-like nodules, and hepatic angiomyolipoma) and malignant (i.e., HCC and non HCC malignancies) lesions in a cirrhotic liver. The content highlights relevant pathogenesis and imaging clues for proper differential diagnosis. Revision of prior imaging and knowledge of these scenarios may help the abdominal radiologist to reach a noninvasive diagnosis and direct the patient to the most appropriate clinical management. Uncommon imaging evolutions of focal liver lesions in cirrhosis may represent a challenge for the abdominal radiologist, with atypical changes in size, and internal vascularization changes that may lead to misdiagnoses.

Personalized 3D-Printed Transparent Liver Model Using the Hepatobiliary Phase MRI: Usefulness in the Lesion-by-Lesion Imaging-Pathologic Matching of Focal Liver Lesions-Preliminary Results.

The aim of this study was to investigate the usefulness of a personalized, 3-dimensional (3D)-printed, transparent liver model with focal liver lesions (FLLs) for lesion-by-lesion imaging-pathologic matching. This preliminary, prospective study was approved by our institutional review board, and written informed consent was obtained. Twenty patients (male-to-female ratio, 13:7; mean age, 56 years) with multiple FLLs, including at least one presumed malignant, or an indeterminate lesion 10 mm or less on the preoperative gadoxetic acid-enhanced magnetic resonance imaging (MRI), were included. After digital segmentation of hepatobiliary phase MRI, a transparent, 3D-printed liver model with colored anatomical structures and FLLs was produced. During the gross examination of the liver specimen, the per-lesion detection rates were compared between those without (routine protocol) and those with the aid of the 3D-printed liver model. Among 98 MRI-detected FLLs (11.5 ± 12.5 mm), the per-lesion detection rate on gross examination using the 3D-printed liver model was 99.0% (97/98), which was significantly higher than that obtained on routine examination (82.7% [81/98]; P < 0.001). In the subgroup analysis, according to the tumor size, 23.9% (16/67) of FLLs 10 mm or less were additionally detected using the liver model, whereas none were additionally detected in greater than 10 mm. The additionally detected 16 FLLs in 12 patients included histologic diagnoses of viable metastases, pathologic complete response of metastases, hepatocellular carcinomas, focal nodular hyperplasia-like nodules, and hemangiomas. A personalized, 3D-printed liver model with FLLs may improve the lesion-by-lesion imaging-pathologic matching for small FLLs, thus leading to accurate pathologic tumor staging and obtaining a reliable reference for imaging-detected FLLs.

Problematic lesions in cirrhotic liver mimicking hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a unique malignancy that can be diagnosed and treated based on non-invasive imaging criteria without histological confirmation in cirrhotic patients, which opens the possibility, although rare, of false-positive diagnosis of the tumor. This brief review illustrates benign and non-HCC malignant lesions arising in cirrhotic liver that could have been erroneously diagnosed as HCC based on imaging criteria: focal nodular hyperplasia-like nodules, serum amyloid A-positive nodules, dysplastic nodules, spontaneously regressing lesions, combined hepatocellular-cholangiocarcinoma, cholangiocarcinoma, sarcomatoid carcinoma, lymphoepithelioma-like carcinoma, hepatoblastoma, and metastatic adenocarcinoma. To determine the potential differences in clinical courses and post-treatment outcome of HCC diagnosed by imaging alone and those histologically, we suggest the terms HCCi and HCCp to distinguish between lesions that are diagnosed as HCC based on imaging alone from those diagnosed based on pathological examination, respectively.Key Points • Benign lesions, such as focal nodular hyperplasia-like nodules, serum amyloid A-positive nodules, dysplastic nodules, and spontaneously regressing lesions, may show imaging findings that mislead to the diagnosis of HCC. • Non-hepatocellular malignant lesions, such as sarcomatoid carcinoma, lymphoepithelioma-like carcinoma, hepatoblastoma, and metastatic adenocarcinomas, can be erroneously diagnosed as HCC based on imaging findings alone, even in cirrhotic liver.

Magnetic Resonance Imaging of Liver Metastasis

Liver magnetic resonance imaging (MRI) is becoming the gold standard in liver metastasis detection and treatment response assessment. The most sensitive magnetic resonance sequences are diffusion-weighted images and hepatobiliary phase images after Gd-EOB-DTPA. Peripheral ring enhancement, diffusion restriction, and hypointensity on hepatobiliary phase images are hallmarks of liver metastases. In patients with normal ultrasonography, computed tomography (CT), and positron emission tomography (PET)-CT findings and high clinical suspicion of metastasis, MRI should be performed for diagnosis of unseen metastasis. In melanoma, colon cancer, and neuroendocrine tumor metastases, MRI allows confident diagnosis of treatment-related changes in liver and enables differential diagnosis from primary liver tumors. Focal nodular hyperplasia-like nodules in patients who received platinum-based chemotherapy, hypersteatosis, and focal fat can mimic metastasis. In cancer patients with fatty liver, MRI should be preferred to CT. Although the first-line imaging for metastases is CT, MRI can be used as a problem-solving method. MRI may be used as the first-line method in patients who would undergo curative surgery or metastatectomy. Current limitation of MRI is low sensitivity for metastasis smaller than 3mm. MRI fingerprinting, glucoCEST MRI, and PET-MRI may allow simpler and more sensitive diagnosis of liver metastasis.

Imaging findings of mimickers of hepatocellular carcinoma.

Radiological imaging plays a crucial role in the diagnosis of hepatocellular carcinoma (HCC) as the noninvasive diagnosis of HCC in high-risk patients by typical imaging findings alone is widely adopted in major practice guidelines for HCC. While imaging techniques have markedly improved in detecting small liver lesions, they often detect incidental benign liver lesions and non-hepatocellular malignancy that can be misdiagnosed as HCC. The most common mimicker of HCC in cirrhotic liver is nontumorous arterioportal shunts that are seen as focal hypervascular liver lesions on dynamic contrast-enhanced cross-sectional imaging. Rapidly enhancing hemangiomas can be easily misdiagnosed as HCC especially on MR imaging with liver-specific contrast agent. Focal inflammatory liver lesions mimic HCC by demonstrating arterial-phase hypervascularity and subsequent washout on dynamic contrast-enhanced imaging. It is important to recognize the suggestive imaging findings for intrahepatic cholangiocarcinoma (CC) as the management of CC is largely different from that of HCC. There are other benign mimickers of HCC such as angiomyolipomas and focal nodular hyperplasia-like nodules. Recognition of their typical imaging findings can reduce false-positive HCC diagnosis.

Focal lesions in cirrhotic liver: what else beyond hepatocellular carcinoma?

Detection and characterization of focal lesions in the cirrhotic liver may pose a diagnostic dilemma. Several benign and malignant lesions may be found in a cirrhotic liver along with hepatocellular carcinoma (HCC), and may exhibit typical or atypical imaging features. In this pictorial essay, we illustrate computed tomography and magnetic resonance imaging findings of lesions such as simple bile duct cysts, hemangioma, focal nodular hyperplasia-like nodules, peribiliary cysts, intrahepatic cholangiocarcinoma, lymphoma, and metastases, all of which occur in cirrhotic livers with varying prevalences. Pseudolesions, such as perfusion anomalies, focal confluent fibrosis, and segmental hyperplasia, will also be discussed. Imaging characterization of non-HCC lesions in cirrhosis is important in formulating an accurate diagnosis and triaging the patient towards the most appropriate management.

Serum amyloid A-positive hepatocellular neoplasms in the resected livers from 3 patients with alcoholic cirrhosis.

Twelve hepatocellular nodules were characterized in the resected livers from 3 patients (2 men and a woman) with alcoholic cirrhosis. Imaging techniques suggested that the nodules were hypervascular and may be hepatocellular carcinoma. Five nodules (4-31 mm in diameter) were serum amyloid A-positive hepatocellular neoplasm, which shares features with inflammatory hepatocellular adenoma. The remaining 7 nodules (5-8 mm) were focal nodular hyperplasia-like nodules showing focal or no immunostaining for serum amyloid A. The serum amyloid A-positive hepatocellular neoplasms showed increased cellular density, inflammatory infiltrate, sinusoidal dilatation, and ductular reaction to various degrees. These histologic features tended to be less extensive in focal nodular hyperplasia-like nodules. Three of 4 serum amyloid A-positive hepatocellular neoplasms showed slight hypointensity in the hepatobiliary phase on the magnetic resonance (MR) imaging with gadolinium ethoxybenzyl diethylenetriaminepentaacetic acid (Gd-EOB-DTPA) enhancement. In contrast, 3 focal nodular hyperplasia-like nodules showed iso-intensity in the hepatobiliary phase. This study further confirms characteristics of serum amyloid A-positive hepatocellular neoplasm arising in alcoholic cirrhosis that share features with inflammatory hepatocellular adenomas. Serum amyloid A-positive hepatocellular neoplasms sometimes co-exist with focal nodular hyperplasia-like nodules and may show different findings on Gd-EOB-enhanced MR imaging.

Case 183: Obliterative Portal Venopathy

Obliterative portal venopathy—which is characterized clinically by the presence of portal hypertension in the absence of liver insufficiency—has recently been described as a non–AIDS-defining hepatic disease in patients with the human immunodeficiency virus, and its imaging findings—other than the usual sings of portal hypertension—include liver morphologic changes, multifocal thrombosis of intrahepatic portal branches, parenchymal enhancement abnormalities, focal nodular hyperplasia-like nodules, and extrahepatic portal vein thrombosis.

Obliterative Portal Venopathy: Findings at CT Imaging

To retrospectively analyze the computed tomographic (CT) findings in a single-center series of adult patients with biopsy-proved obliterative portal venopathy (OPV) and to compare them with those observed in patients with cirrhosis. The requirement for informed consent was waived. This institutional review board-approved study included 42 consecutive patients with a histologically proved diagnosis of OPV who underwent CT at diagnosis. The clinical characteristics at diagnosis were recorded, and CT examination results were reviewed. Two radiologists evaluated portal vein patency and intrahepatic portal branches, the morphologic changes in the liver, the presence of hepatic nodules, and signs of portal hypertension in consensus. The control group consisted of 42 patients who had histologically proved cirrhosis. CT findings were compared between the OPV patient group and the cirrhotic group and also among the conditions associated with patients with OPV. The Fisher exact test was used. P values of .05 or less were considered to indicate significant differences. The following CT findings were observed significantly more frequently in OPV than in cirrhosis: extrahepatic portal vein thrombosis (18 [43%] of 42 vs five [12%] of 42); intrahepatic portal abnormalities (18 [58%] of 31 vs one [2%] of 42) such as reduced caliber, occlusive thrombosis, and lack of visibility; focal nodular hyperplasia-like nodules (six [14%] of 42 vs 0 [0%] of 42); and perfusion disorders (15 [36%] of 42 vs six [14%] of 42). Conversely, the combination of hypertrophy of the caudate lobe and atrophy of segment IV (27 [64%] of 42 vs 10 [24%] of 42) and nodular surface (37 [88%] of 42 vs seven [17%] of 42) were seen significantly more often in cirrhosis. Characteristic CT findings in patients with OPV that differ from those in patients with cirrhosis were shown, the most common being the presence of intra- or extrahepatic portal abnormalities.

Hepatic stellate cells are activated around central scars of focal nodular hyperplasia of the liver—a potential mechanism of central scar formation

Focal nodular hyperplasia of the liver is typically accompanied by a central scar, but cases that lack the central scar are occasionally encountered. This study was performed to clarify the mechanism of the central scar formation in focal nodular hyperplasia. Immunohistochemical analysis was performed for liver sections of focal nodular hyperplasia with and without a central scar. For comparison, liver specimens of focal nodular hyperplasia-like nodules and nodular regenerative hyperplasia were used. Immunostaining showed that activated hepatic stellate cells, as determined by alpha-smooth muscle actin expression, were invariably observed in all cases of focal nodular hyperplasia with a central scar, whereas focal nodular hyperplasia without a central scar and nodular regenerative hyperplasia lacked hepatic stellate cell activation. Hepatic stellate cell activation in focal nodular hyperplasia with a central scar was accompanied by the expression of 8-hydroxy-2'-deoxyguanosine and inducible nitric oxide synthase in the liver. Expression of 8-hydroxy-2'-deoxyguanosine and inducible nitric oxide synthase was rarely seen in focal nodular hyperplasia without a central scar, focal nodular hyperplasia-like nodules, or nodular regenerative hyperplasia. Overexpression of vascular endothelial growth factor was also observed in focal nodular hyperplasia with a central scar. These results suggest that the central part of focal nodular hyperplasia suffers from hyperoxic conditions due to arterial hyperperfusion; and the resultant oxidative stress may activate hepatic stellate cells, leading to central scar formation. In addition, vascular endothelial growth factor may contribute to the proliferation of abnormal vessels as an angiogenic inducer.

Glypican-3 Expression Distinguishes Small Hepatocellular Carcinomas From Cirrhosis, Dysplastic Nodules, and Focal Nodular Hyperplasia-like Nodules

Distinguishing small hepatocellular carcinoma (HCC) from other types of small focal lesions that occur in a cirrhotic liver can be difficult on the basis of morphologic features alone. We investigated whether the expression of glypican-3 (GPC3) could be an ancillary tool in the histopathologic diagnostic process. We performed immunohistochemistry for GPC3 on 16 low-grade dysplastic nodules, 33 high-grade dysplastic nodules, 13 focal nodular hyperplasia-like nodules, and 59 HCCs with a diameter less or equal to 3 cm present in the cirrhotic liver of 66 patients. Both resected lesions and lesions biopsied by needle were included and nonlesional cirrhotic parenchyma was also stained. In a subset of cases (23 samples of cirrhosis, 4 low-grade dysplastic nodules, 5 high-grade dysplastic nodules, 2 focal nodular hyperplasia-like nodules, and 18 HCCs), real time reverse transcriptase-polymerase chain reaction for GPC3 was performed. GPC3 expression was, both on immunohistochemistry and by real time reverse transcriptase-polymerase chain reaction, much higher in small HCCs than in cirrhosis and other types of small focal lesions, indicating that the transition from premalignant lesions to small HCC is associated with a sharp increase of GPC3 expression in a majority of cases. The sensitivity and specificity of a positive GPC3-staining for the diagnosis of HCC in small focal lesions was 0.77 and 0.96, respectively, in resected cases, and 0.83 and 1, respectively, for needle biopsies. Because the result of the staining was easily interpretable, immunohistochemistry for GPC3 is valuable ancillary tool in the histopathologic diagnosis of small focal lesions in cirrhosis.

Clinicopathological Features of Focal Nodular Hyperplasia-Like Nodules in 130 Cirrhotic Explant Livers

Focal nodular hyperplasia-like nodules (FNH-like nodules) are focal lesions occurring in liver cirrhosis and are morphologically very similar to classical FNH in an otherwise normal liver. They are sometimes misdiagnosed as hepatocellular carcinoma (HCC) on imaging because both types of lesions show arterial-phase enhancement. Although the morphological, immunohistochemical, and imaging features of FNH-like nodules are well-known, their pathogenesis and role in hepatocarcinogenesis have not been studied in detail. Therefore, we performed a detailed pathological evaluation of 130 cirrhotic explant livers and correlated these data with the clinical features of the patients. All cirrhotic explant livers were uniformly sliced at 5-mm intervals and all detected focal lesions were microscopically classified according to internationally accepted criteria. The obtained data regarding FNH-like nodules were then correlated with other pathological findings and with clinical data obtained during pretransplant evaluation and recorded in a database. FNH-like nodules were present in 15% of patients and their small size (75% of cases < 1 cm) appears to preclude detection by imaging in almost all cases. The presence of esophageal varices and pretransplant treatment with chemoembolization were independently and significantly associated with the presence of FNH-like nodules. There were no associations between FNH-like nodules on the one hand and low-grade dysplastic nodules, high-grade dysplastic nodules, and HCCs on the other hand. The clinicopathological features of FNH-like nodules support the hypothesis that vascular alterations in liver cirrhosis play an important role in their pathogenesis and that FNH-like nodules do not have an increased risk of malignant transformation.