scholarly journals Overview of Hepatocellular Adenoma in Japan

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Motoko Sasaki ◽  
Yasuni Nakanuma
Keyword(s):  
Oral Contraceptives ◽  
Hepatocellular Adenoma ◽  
Alcoholic Cirrhosis ◽  
Hepatocyte Nuclear Factor ◽  
Asian Countries ◽  
Genetic Changes ◽  
Amyloid A ◽  
Phenotype Classification ◽  
New Type ◽  
Strong Immunoreactivity

Hepatocellular adenoma (HCA) is generally a benign hepatocellular tumor arising in a nonfibrotic/cirrhotic liver, and recently four major subgroups were identified based on genotype and phenotype classification from Europe. HCA is rare in Asian countries including Japan, and there have been few studies regarding the subgroups of HCA in Japan. We surveyed subgroups of HCA in 13 patients (7 women) in Japan, based on the phenotypic classification. As results, we identified 2 hepatocyte nuclear factor (HNF) 1α-inactivated HCAs (15%), twoβ-catenin-activated HCAs (15%), 5 inflammatory HCAs (39%), and 4 unclassified HCAs (29%). The use of oral contraceptives was found only in 2 unclassified HCAs (29%). Rather low percentage of female patients and use of oral contraceptives appear to be common clinicopathological features in Japan and also East Asian countries. Furthermore, a group of possible inflammatory HCAs characterized by strong immunoreactivity for serum amyloid A (SAA) was found in patients with alcoholic cirrhosis. The inflammatory HCA/SAA-positive hepatocellular neoplasm in alcoholic cirrhosis may be a new entity of HCA, which may have potential of malignant transformation. Further studies are needed to clarify genetic changes, monoclonality, and pathogenesis of this new type of hepatocellular neoplasm.

Serum Amyloid A-Positive Hepatocellular Neoplasm: A New Type of Tumor Arising in Patients with Advanced Alcoholic Disease

2015 ◽  
Vol 33 (5) ◽  
pp. 648-654 ◽  
Author(s):  
Motoko Sasaki ◽  
Yasuni Nakanuma
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Serum Amyloid A ◽  
Hepatocellular Adenoma ◽  
Clinicopathological Features ◽  
Serum Amyloid ◽  
Amyloid A ◽  
New Type ◽  
Strong Immunoreactivity ◽  
Alcoholic Disease

This chapter reviews a new type of hepatocellular neoplasm, serum amyloid A-positive hepatocellular neoplasm (SAA-HN), which arises in patients with advanced alcoholic liver disease such as cirrhosis. SAA-HNs share histological and immunohistochemical features with inflammatory hepatocellular adenoma, for example, a strong immunoreactivity for SAA. Clinicopathological features and issues regarding SAA-HN are reviewed with emphasis regarding its potential to develop into hepatocellular carcinoma.

Isolated Gastric Varices and Use of Balloon-occlusive Retrograde Transvenous Obliteration: A Case Report and Literature Review*

2016 ◽  
Vol 25 (1) ◽  
pp. 115-117
Author(s):  
Thomas R. McCarty ◽  
Mena Bakhit ◽  
Tarun Rustagi
Keyword(s):  
Treatment Approach ◽  
Alcoholic Cirrhosis ◽  
Gastric Varices ◽  
Portosystemic Shunt ◽  
Asian Countries ◽  
End Stage Liver Disease ◽  
Intrahepatic Portosystemic Shunt ◽  
Isolated Gastric Varices ◽  
Splenic Thrombosis ◽  
End Stage

Isolated gastric varices are far less prevalent in Western countries where the rate of splenic thrombosis is much lower. However, in Asian countries the entity is more common and therefore a more robust treatment approach has been developed. Balloon-occlusive retrograde transvenous obliteration (BRTO) was first described in 1984 and then revived in 1996. The procedure, while uncommon in the U.S. and not recognized by the AASLD practice guidelines, allows for direct exclusion from the portosystemic system. Here we describe the case of a patient with alcoholic cirrhosis decompensated by bleeding gastric varices treated with BRTO. Abbrevations: BRTO: balloon-occlusive retrograde transverse obliteration; EGD: esophagogastro-duodenoscopy; HE: hepatic encephalopathy; MELD: Model for End Stage Liver Disease; TIPS: transjugular intrahepatic portosystemic shunt.

scholarly journals A case of β-catenin-activated hepatocellular adenoma with TERT promoter mutation in a young woman not taking oral contraceptives

Kanzo ◽  
2020 ◽  
Vol 61 (9) ◽  
pp. 461-469
Author(s):  
Takuo Tokairin ◽  
Yohei Koshima ◽  
Hiroyuki Yoshidome ◽  
Yurie Soejima ◽  
Akiko Adachi ◽  
...  
Keyword(s):  
Young Woman ◽  
Oral Contraceptives ◽  
Hepatocellular Adenoma ◽  
Tert Promoter Mutation ◽  
Promoter Mutation ◽  
Tert Promoter

scholarly journals The impact of hepatocyte nuclear factor-1α on liver malignancies and cell stemness with metabolic consequences

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Xue Wang ◽  
Waseem Hassan ◽  
Jing Zhao ◽  
Sahar Bakht ◽  
Yunjuan Nie ◽  
...  
Keyword(s):  
Hepatocellular Adenoma ◽  
Scientific Data ◽  
Signal Molecules ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Liver Malignancies ◽  
Future Opportunity ◽  
Important Player ◽  
Nuclear Factor 1 ◽  
The Impact

Abstract Hepatocyte nuclear factor-1 alpha (HNF-1α) is a transcription factor expressed predominantly in the liver among other organs. Structurally, it contains POU-homeodomain that binds to DNA and form proteins that help in maintaining cellular homeostasis, controlling metabolism, and differentiating cell lineages. Scientific research over the period of three decades has reported it as an important player in various liver malignancies such as hepatocellular cancers (HCCs), hepatocellular adenoma (HA), and a more specific HNF-1α-inactivated human hepatocellular adenoma (H-HCAs). Abundant clinical and rodent data have noted the downregulation of HNF-1α in parallel with liver malignancies. It is also interesting to notice that the co-occurrence of mutated HNF-1α expression and hepatic carcinomas transpires typically along with metabolic repercussion. Moreover, scientific data implies that HNF-1α exerts its effects on cell stemness and hence can indirectly impact liver malignancies and metabolic functioning. The effects of HNF-1α on cell stemness present a future opportunity to explore a possible and potential breakthrough. Although the mechanism through which inactivated HNF-1α leads to hepatic malignancies remain largely obscure, several key signal molecules or pathways, including TNF-α, SHP-1, CDH17, SIRT, and MIA-2, have been reported to take part in the regulations of HNF-1α. It can be concluded from the present scientific data that HNF-1α has a great potential to serve as a target for liver malignancies and cell stemness.

Clinicopathological characteristics of serum amyloid A-positive hepatocellular neoplasms/nodules arising in alcoholic cirrhosis

2015 ◽  
Vol 66 (6) ◽  
pp. 836-845 ◽  
Author(s):  
Motoko Sasaki ◽  
Norihide Yoneda ◽  
Yoshiyuki Sawai ◽  
Yasuharu Imai ◽  
Fukuo Kondo ◽  
...  
Keyword(s):  
Serum Amyloid A ◽  
Alcoholic Cirrhosis ◽  
Clinicopathological Characteristics ◽  
Serum Amyloid ◽  
Amyloid A

scholarly journals How Normal Is the Liver in Which the Inflammatory Type Hepatocellular Adenoma Develops?

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Jing Han ◽  
Marius C. van den Heuvel ◽  
Hironori Kusano ◽  
Koert P. de Jong ◽  
Annette S. H. Gouw
Keyword(s):  
Hepatocellular Adenoma ◽  
Normal Liver ◽  
Remnant Liver ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Amyloid A ◽  
Sinusoidal Dilatation ◽  
Lobular Architecture ◽  
Benign Liver Tumor ◽  
Benign Liver

The inflammatory type hepatocellular adenoma (IHCA) is a subtype of HCA which is a benign liver tumor, predominantly occurring in young women in an otherwise normal liver. IHCA contains either a mutation of gp130 or STAT3. Both mutations lead to a similar morphologic phenotype and to increased expression of C-reactive protein (CRP) and/or serum amyloid-A (SAA). IHCA comprised about 40% of all HCAs and is associated with obesity. We investigated the histomorphological and immunophenotypical changes of the nontumorous liver of 32 resected IHCA specimens. Similar types of changes are present in samples taken adjacent to tumor and distant ones. The lobular architecture is well preserved. Mild/moderate steatosis is found in a high frequency which is in accordance with the median BMI of 32 in our cases. Of note are the regular findings of sinusoidal dilatation, single arteries, and minute CRP foci which are all features of HCA. These distinct CRP foci are mostly found in cases of multiple IHCA which indicates that the remnant liver may also contain IHCA foci. These findings show that the nonlesional liver in IHCA does contain abnormalities, and this may have consequences for the followup, especially since it is known that obesity may stimulate malignant growth.

scholarly journals Huge Hepatocellular Adenoma

2020 ◽  
pp. 1-2
Author(s):  
Tomas Urbonas ◽  
Andrei Ryllo ◽  
Tomas Urbonas
Keyword(s):  
Hepatocellular Carcinoma ◽  
Abdominal Pain ◽  
Oral Contraceptives ◽  
Liver Tumor ◽  
Hepatocellular Adenoma ◽  
Surgical Excision ◽  
Vascular Supply ◽  
Chronic Abdominal Pain ◽  
Benign Liver Tumor ◽  
Benign Liver

Hepatocellular adenoma (HCA) is generally uncommon benign liver tumor with potential to become malignant. Its prevalence has been increasing steadily secondary to wide use of oral contraceptives and due to the increased use of imaging for a variety of unrelated reasons. Large adenomas may present with chronic abdominal pain. As HCA become larger it is prone to rupture and hemorrhage due to central necrosis because the vascular supply is limited to the surface of the tumor. If left untreated HCA can undergo transformation into hepatocellular carcinoma which can be as high as in 10% of cases1 or even higher. Surgical excision is a preferred method of treatment. Other modalities include embolization of bleeding tumors and ablative modalities in selected cases.

scholarly journals A Case of hepatocyte nuclear factor 1^|^alpha;-inactivated hepatocellular adenoma, involving anomalous portal tract, difficult to be differentiated from FNH-like lesion

Kanzo ◽  
2013 ◽  
Vol 54 (2) ◽  
pp. 135-142 ◽  
Author(s):  
Katsuhiko Ito ◽  
Fukuo Kondo ◽  
Satoru Otawa ◽  
Takayuki Ishii ◽  
Yoshiaki Shimizu ◽  
...  
Keyword(s):  
Portal Tract ◽  
Hepatocellular Adenoma ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Nuclear Factor 1
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