BACKGROUND: Hepatocellular adenoma is a rare benign liver tumor. Typically, hepatocellular adenomas are solitary and are found in young women who use estrogen-containing contraceptives. The occurrence of multiple hepatocellular adenoma has been linked to higher body mass index, and as the prevalence of overweight increases, multiple hepatocellular adenomas are seen more often. An hepatocellular adenoma does not always necessitate treatment, as they can regress under conservative strategies. In incidental cases, an adenoma presents owing to bleeding, which is mostly self-limiting. If it is not, embolization of hepatic involved vessels is indicated.
METHODS: In this case report, we discuss a 42-year old Caucasian woman with multiple hepatocellular bleeds, treated by multiple endovascular procedures. After the first embolization of an adenoma in the right liver lobe, a second bleed occurred in the left lobe, necessitating additional endovascular intervention. During admittance, treatment was complicated by pulmonary embolism and a pneumonia. During follow-up, our patient was diagnosed with antiphospholipid syndrome.
CONCLUSIONS: Hepatocellular adenoma is a rare diagnosis that requires centralized expertise. This particular case illustrates the complexity of treatment strategies for associated intra-abdominal bleeding and possible complications. Although liver adenoma is often an incidental finding, it can also result in significant morbidity. Centralization of treatment leads to expertise in managing complex treatment strategies.

Hepatocellular adenomas are rare and benign primary neoplasms of phenotypically mature hepatocytes. Our understanding of this pathology has greatly improved due to advances in molecular and anatomic knowledge. This article provides an in-depth review of hepatic adenomas (HCA) while presenting the case of a 20-year-old patient with a giant inflammatory hepatocellular adenoma with an atypical presentation, in whom surgical intervention was performed via right hepatectomy. In the post-surgical course, the patient had an in-hospital stay of three days with no complications. During outpatient monitoring via laboratory tests and imaging at eight months, the patient did not present any trace of recurrence.

No sensitive tumor marker for hepatocellular carcinoma (HCC) is available for patients with glycogen storage disease type Ia (GSDIa), in whom alpha-fetoprotein and carcino-embryonic antigen levels often remain normal. We describe increased levels of the HCC tumor marker des-gamma-carboxy prothrombin (DCP) in GSDIa patients with HCC. In one case DCP levels normalized after liver transplantation. We recommend including DCP as a screening HCC tumor marker in the surveillance of patients with GSDIa.

Abernethy syndrome is a rare congenital anomaly characterized by an intrahepatic or extrahepatic portosystemic shunt. Most patients are asymptomatic; however, due to the alteration in, or lack of, a portovenous flow, patients with Abernethy syndrome are at high risk of developing sequelae of liver failure. Once these complications develop, the only definitive treatment is transplantation. Patients with Abernethy syndrome are also at a higher risk of developing benign and malignant liver lesions, including hepatic adenomas. Here, we describe the first case of deceased donor liver transplantation as a treatment for a patient with type 1 Abernethy syndrome complicated by large, unresectable hepatic adenoma, found to have focal hepatocellular carcinoma on pathologic examination. Our male patient was found to have elevated liver enzymes at age 33, during a routine outpatient medical appointment. Despite being asymptomatic, his history of prior liver resection prompted CT imaging, which revealed two large liver lesions concerning for hepatic adenomas. When surveillance imaging showed a significant growth of the liver lesions, biopsy was pursued, which confirmed a diagnosis of hepatic adenomas. However, given the size of these lesions, resection was not a viable option for the patient. Instead, the patient underwent liver transplantation at age 41, which he tolerated well. Our case demonstrates the utility of deceased donor liver transplantation as a treatment for patients with Abernethy syndrome complicated by unresectable adenomas.

Abernethy malformation or congenital extrahepatic portosystemic shunt is an extremely rare condition whereby the portomesenteric blood drains into a systemic vein and bypasses the liver through a complete or partial shunt. Severe complications include hyperammonemia and encephalopathy, benign and malignant liver tumors, and hepatopulmonary syndrome. We describe a case where a female adult diagnosed with congenital extrahepatic portosystemic shunt subsequently developed focal nodular hyperplasia and then hepatocellular carcinoma.

BACKGROUND: Due to their overlapping radiological characteristics, hepatic lesions, such as hepatocellular carcinoma (HCC) and hepatocellular adenoma (HCA), present a substantial diagnostic challenge. Accurate differentiation between HCC and HCA is essential for the best clinical treatment and therapeutic decision-making. This study aims to assess the potential role of DCE-MRI and Apparent Diffusion Coefficient (ADC) quantitation in the diagnosis of hepatocellular carcinoma (HCC) from hepatocellular adenoma (HCA).
METHODS: 103 patients (56 HCC, 47 HCA) with histopathologically proven hepatocellular lesions were the subjects of a cross-sectional investigation. A standardized imaging technique was used for DCE-MRI on all patients. Diffusion-weighted imaging (DWI) provided the ADC values. The diagnostic efficacy of DCE-MRI and ADC in differentiation was evaluated using statistical analyses, such as t-tests and receiver operating characteristic (ROC) curve analysis. SPSS VER 16 was used for the analysis of the collected data.
RESULTS: A total of 103 patients (female: male= 52:51, 57.14±3.09 years) were included in the study. The study revealed significant differences in DCE-MRI parameters and ADC values between HCC and HCA lesions. ADC value was significantly lower in HCC than in HCA (p < 0.001). The area under the curve (AUC) was 0.78 (95% CI: 0.69-0.87) for ADC, 0.84 (95% CI: 0.76-0.91) for Ktrans, and 0.72 (95% CI: 0.62-0.82) for Ve. Sensitivity and specificity for ADC were 76.59% and 71.42%, respectively. Also, PPV and NPV of ADC were 69.23% and 78.43%, respectively. Sensitivity and specificity for Ktrans were 82.14% and 76.59%, respectively. Also, PPV and NPV of Ktrans were 80.7% and 78.26%, respectively.
CONCLUSIONS: In conclusion, DCE-MRI-derived parameters, along with ADC values, exhibit promise as non-invasive tools for differentiating HCC from HCA.

暂无摘要。

UNASSIGNED: Hepatocellular adenomas (HCAs) are rare, benign, liver tumours classified at the clinicopathological, genetic, and proteomic levels. The β-catenin-activated (b-HCA) subtypes harbour several mutation types in the β-catenin gene (CTNNB1) associated with different risks of malignant transformation or bleeding. Glutamine synthetase is a surrogate marker of β-catenin pathway activation associated with the risk of malignant transformation. Recently, we revealed an overexpression of glutamine synthetase in the rims of exon 3 S45-mutated b-HCA and exon 7/8-mutated b-HCA compared with the rest of the tumour. A difference in vascularisation was found in this rim shown by diffuse CD34 staining only at the tumour centre. Here, we aimed to characterise this tumour heterogeneity to better understand its physiopathological involvement.
UNASSIGNED: Using mass spectrometry imaging, genetic, and proteomic analyses combined with laser capture microdissection, we compared the tumour centre with the tumour rim and with adjacent non-tumoural tissue.
UNASSIGNED: The tumour rim harboured the same mutation as the tumour centre, meaning both parts belong to the same tumour. Mass spectrometry imaging showed different spectral profiles between the rim and the tumour centre. Proteomic profiling revealed the significant differential expression of 40 proteins at the rim compared with the tumour centre. The majority of these proteins were associated with metabolism, with an expression profile comparable with a normal perivenous hepatocyte expression profile.
UNASSIGNED: The difference in phenotype between the tumour centres and tumour rims of exon 3 S45-mutated b-HCA and exon 7/8-mutated b-HCA does not depend on CTNNB1 mutational status. In a context of sinusoidal arterial pathology, tumour heterogeneity at the rim harbours perivenous characteristics and could be caused by a functional peripheral venous drainage.
UNASSIGNED: Tumour heterogeneity was revealed in β-catenin-mutated hepatocellular adenomas (b-HCAs) via the differential expression of glutamine synthase at tumour rims. The combination of several spatial approaches (mass spectrometry imaging, genetic, and proteomic analyses) after laser capture microdissection allowed identification of a potential role for peripheral venous drainage underlying this difference. Through this study, we were able to illustrate that beyond a mutational context, many factors can downstream regulate gene expression and contribute to different clinicopathological phenotypes. We believe that the combinations of spatial analyses that we used could be inspiring for all researchers wanting to access heterogeneity information of liver tumours.

OBJECTIVE: This study aimed to assess the effectiveness of using MRI-apparent diffusion coefficient (ADC) map-driven radiomics to differentiate between hepatocellular adenoma (HCA) and hepatocellular carcinoma (HCC) features.
METHODS: The study involved 55 patients with liver tumors (20 with HCA and 35 with HCC), featuring 106 lesions equally distributed between hepatic carcinoma and hepatic adenoma who underwent texture analysis on ADC map MR images. The analysis identified several imaging features that significantly differed between the HCA and HCC groups. Four classification models were compared for distinguishing HCA from HCC including linear support vector machine (linear-SVM), radial basis function SVM (RBF-SVM), random forest (RF), and k-nearest neighbor (KNN).
RESULTS: The k-nearest neighbor (KNN) classifier displayed the top accuracy (0.89) and specificity (0.90). Linear-SVM and KNN classifiers showcased the leading sensitivity (0.88) for both, with the KNN classifier achieving the highest precision (0.9). In comparison, the conventional interpretation had lower sensitivity (70.1%) and specificity (77.9%).
CONCLUSIONS: The study found that utilizing ADC maps for texture analysis in MR images is a viable method to differentiate HCA from HCC, yielding promising results in identified texture features.

Although benign hepatocellular adenomas (HCA) are very rare, recent observations have shown their occurrence in patients with diabetes mellitus. Consequently, most of these cases are treated by resection due to concerns regarding their potential progression to hepatocarcinoma (HCC). This decision is largely driven by the limited number of studies on HCC subtyping and the lack of molecular and biological insights into the carcinogenic potential of benign tumors. This study aimed to comprehensively investigate the subtype classification of HCA and to compare and analyze gene expression profiling between HCA and HCC tissues. One fresh inflammatory HCA (I-HCA), three non-B non-C HCCs, two hepatitis B virus-HCCs, and one normal liver tissue sample were subjected to single-cell RNA sequencing (scRNA-seq). Comparative analysis of scRNA-seq among different tissues showed that phospholipase A2 group IIA (PLA2G2A) mRNA was specifically expressed in I-HCA, following RNA-seq analysis in formalin-fixed paraffin-embedded tissues from other HCAs. Immunohistochemistry using the PLA2G2A antibody in these tissues indicated that the positive reaction was mainly observed in hepatocytes of I-HCAs and stromal cells surrounding the tumor tissue in HCC were also stained. According to a clinical database, PLA2G2A expression in HCC does not correlate with poor prognosis. This finding may potentially help develop a new definition for I-HCA, resulting in a significant clinical contribution, but it requires validation with other fresh HCA samples.