A 54-year-old man with hypertension, dyslipidemia, diabetes mellitus and fatty liver was referred to our institution for accurate diagnosis of a 4-cm space-occupying lesion in subsegment 6 of the liver, identified on ...A 54-year-old man with hypertension, dyslipidemia, diabetes mellitus and fatty liver was referred to our institution for accurate diagnosis of a 4-cm space-occupying lesion in subsegment 6 of the liver, identified on ultrasonography as an iso-to hypointense lesion with clear margins. Dynamic computed tomography disclosed light accumulation of contrast medium at the margins of the space-occupying lesion from the arterial phase through to the venous phase. Sonazoid-enhanced ultrasonography showed staining of the tumor margins in the vascular phase, disappearing in the post-vascular phase. Hepatic arteriography identified the space-occupying lesion as hypervascular. Since accurate diagnosis by imaging was difficult, tumor resection was performed to exclude hepatocellular carcinoma, after obtaining consent from the patient. Histological examination revealed steatohepatitis and sinusoidal dilatation, representing socalled peliosis hepatis, in the surroundings, while the tumor showed mild hepatocellular atypia. On immunohistochemistry, tumor cells were positive for liver fatty acid-binding protein, glutamine synthetase and serum amyloid A, and negative for β-catenin and glypican 3. Glutamine synthetase, in particular, showed strong diffuse staining. Inflammatory hepatocellular adenoma was thus considered the most likely diagnosis. The pathogenesis and outcome of inflammatory hepatocellular adenoma are not fully understood, and this case with concomitant steatohepatitis was considered worth reporting.展开更多
We present a rare case of rapidly enlarging inflamematory hepatocellular adenoma (IHCA) in a 60-year-old Japanese man. Screening abdominal computed tomography (CT) for the fatty liver patient revealed a 1.7-cm liver m...We present a rare case of rapidly enlarging inflamematory hepatocellular adenoma (IHCA) in a 60-year-old Japanese man. Screening abdominal computed tomography (CT) for the fatty liver patient revealed a 1.7-cm liver mass in the anterior segment of the liver. After 19 months, the lesion had rapidly enlarged to 6 cm in diameter and the patient was referred to our hospital. On perflubutane microbubble contrast-enhanced ultrasonography, the tumor showed a characteristic centripetal filling pattern in the vascular phase. We performed hepatic anterior segment resection because we could not rule out malignant tumor. Histopathological examination showed hyperplasia of mildly atypical hepatocytes and sinusoidal dilatation with marked inflammatory cell infiltration. Immunohistological staining revealed positive staining for serum amyloid A and C-reactive protein;therefore, we diagnosed this tumor as IHCA. The patient remains alive 42 months after operation without evidence of recurrence.展开更多
This practical atlas aims to help liver and non liver pa-thologists to recognize benign hepatocellular nodules on resected specimen. Macroscopic and microscopic views together with immunohistochemical stains illustrat...This practical atlas aims to help liver and non liver pa-thologists to recognize benign hepatocellular nodules on resected specimen. Macroscopic and microscopic views together with immunohistochemical stains illustrate typical and atypical aspects of focal nodular hyperplasia and of hepatocellular adenoma, including hepatocel-lular adenomas subtypes with references to clinical and imaging data. Each step is important to make a correct diagnosis. The specimen including the nodule and the non-tumoral liver should be sliced, photographed and all different looking areas adequately sampled for par-affin inclusion. Routine histology includes HE, trichrome and cytokeratin 7. Immunohistochemistry includes glu-tamine synthase and according to the above results ad-ditional markers such as liver fatty acid binding protein, C reactive protein and beta catenin may be realized to differentiate focal nodular hyperplasia from hepatocel-lular adenoma subtypes. Clues for differential diagnosis and pitfalls are explained and illustrated.展开更多
Studies that compare tumor genotype with phenotype have provided the basis of a new histological/molecular classification of hepatocellular adenomas. Based on two molecular criteria (presence of a TCF1/HNF1α or β-ca...Studies that compare tumor genotype with phenotype have provided the basis of a new histological/molecular classification of hepatocellular adenomas. Based on two molecular criteria (presence of a TCF1/HNF1α or β-catenin mutation), and an additional histological criterion (presence or absence of an inflammatory infiltrate), subgroups of hepatocellular adenoma can be defined and distinguished from focal nodular hyperplasia. Analysis of 96 hepatocellular adenomas performed by a French collaborative network showed that they can be divided into four broad subgroups: the fi rst one is defi ned by the presence of mutations in TCF1 gene inactivating the hepatocyte nuclear factor 1 (HNF1α); the second by the presence of β-catenin activating mutations; the category without mutations of HNF1α or β-catenin is further divided into 2 subgroups depending on the presence or absence of in? ammation. Therefore, the approach to the diagnosis of problematic benign hepatocytic nodules may be entering a new era directed by new molecular information. It is hoped that immunohistological tools will improve significantly diagnosis of liver biopsy in our ability to distinguish hepatocellular adenoma from focal nodular hyperplasia (FNH), and to delineate clinically meaningful entities within each group to define the best clinical management. The optimal care of patients with a liver nodule will benefit from the recent knowledge coming from molecular biology and the combined expertise of hepatologists, pathologists, radiologists, and surgeons.展开更多
文摘A 54-year-old man with hypertension, dyslipidemia, diabetes mellitus and fatty liver was referred to our institution for accurate diagnosis of a 4-cm space-occupying lesion in subsegment 6 of the liver, identified on ultrasonography as an iso-to hypointense lesion with clear margins. Dynamic computed tomography disclosed light accumulation of contrast medium at the margins of the space-occupying lesion from the arterial phase through to the venous phase. Sonazoid-enhanced ultrasonography showed staining of the tumor margins in the vascular phase, disappearing in the post-vascular phase. Hepatic arteriography identified the space-occupying lesion as hypervascular. Since accurate diagnosis by imaging was difficult, tumor resection was performed to exclude hepatocellular carcinoma, after obtaining consent from the patient. Histological examination revealed steatohepatitis and sinusoidal dilatation, representing socalled peliosis hepatis, in the surroundings, while the tumor showed mild hepatocellular atypia. On immunohistochemistry, tumor cells were positive for liver fatty acid-binding protein, glutamine synthetase and serum amyloid A, and negative for β-catenin and glypican 3. Glutamine synthetase, in particular, showed strong diffuse staining. Inflammatory hepatocellular adenoma was thus considered the most likely diagnosis. The pathogenesis and outcome of inflammatory hepatocellular adenoma are not fully understood, and this case with concomitant steatohepatitis was considered worth reporting.
文摘We present a rare case of rapidly enlarging inflamematory hepatocellular adenoma (IHCA) in a 60-year-old Japanese man. Screening abdominal computed tomography (CT) for the fatty liver patient revealed a 1.7-cm liver mass in the anterior segment of the liver. After 19 months, the lesion had rapidly enlarged to 6 cm in diameter and the patient was referred to our hospital. On perflubutane microbubble contrast-enhanced ultrasonography, the tumor showed a characteristic centripetal filling pattern in the vascular phase. We performed hepatic anterior segment resection because we could not rule out malignant tumor. Histopathological examination showed hyperplasia of mildly atypical hepatocytes and sinusoidal dilatation with marked inflammatory cell infiltration. Immunohistological staining revealed positive staining for serum amyloid A and C-reactive protein;therefore, we diagnosed this tumor as IHCA. The patient remains alive 42 months after operation without evidence of recurrence.
基金Supported by Association pour la Recherche sur le Cancer,No.3194
文摘This practical atlas aims to help liver and non liver pa-thologists to recognize benign hepatocellular nodules on resected specimen. Macroscopic and microscopic views together with immunohistochemical stains illustrate typical and atypical aspects of focal nodular hyperplasia and of hepatocellular adenoma, including hepatocel-lular adenomas subtypes with references to clinical and imaging data. Each step is important to make a correct diagnosis. The specimen including the nodule and the non-tumoral liver should be sliced, photographed and all different looking areas adequately sampled for par-affin inclusion. Routine histology includes HE, trichrome and cytokeratin 7. Immunohistochemistry includes glu-tamine synthase and according to the above results ad-ditional markers such as liver fatty acid binding protein, C reactive protein and beta catenin may be realized to differentiate focal nodular hyperplasia from hepatocel-lular adenoma subtypes. Clues for differential diagnosis and pitfalls are explained and illustrated.
文摘Studies that compare tumor genotype with phenotype have provided the basis of a new histological/molecular classification of hepatocellular adenomas. Based on two molecular criteria (presence of a TCF1/HNF1α or β-catenin mutation), and an additional histological criterion (presence or absence of an inflammatory infiltrate), subgroups of hepatocellular adenoma can be defined and distinguished from focal nodular hyperplasia. Analysis of 96 hepatocellular adenomas performed by a French collaborative network showed that they can be divided into four broad subgroups: the fi rst one is defi ned by the presence of mutations in TCF1 gene inactivating the hepatocyte nuclear factor 1 (HNF1α); the second by the presence of β-catenin activating mutations; the category without mutations of HNF1α or β-catenin is further divided into 2 subgroups depending on the presence or absence of in? ammation. Therefore, the approach to the diagnosis of problematic benign hepatocytic nodules may be entering a new era directed by new molecular information. It is hoped that immunohistological tools will improve significantly diagnosis of liver biopsy in our ability to distinguish hepatocellular adenoma from focal nodular hyperplasia (FNH), and to delineate clinically meaningful entities within each group to define the best clinical management. The optimal care of patients with a liver nodule will benefit from the recent knowledge coming from molecular biology and the combined expertise of hepatologists, pathologists, radiologists, and surgeons.
