Cases reported "Focal Nodular Hyperplasia"

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1/89. MRI of intralesional hemolysis in focal nodular hyperplasia of the liver.

    A case of kasabach-merritt syndrome caused by focal nodular hyperplasia of the liver is presented with atypical magnetic resonance findings due to intratumoral hemosiderin deposition. The high sensitivity of magnetic resonance imaging for iron served to identify the site of hemolysis in this patient with kasabach-merritt syndrome. ( info)

2/89. Spontaneous hepatocellular adenoma with marked cystic degeneration.

    We report a case of spontaneous hepatocellular adenoma with marked cystic degeneration in the non-cirrhotic liver. A 36 year-old Japanese woman with neither history of liver diseases nor use of oral contraceptives and steroids, complained of a 6 kg weight loss over 6 months. barium meal study revealed an extramural compression along the fornix of the stomach. Abdominal ultrasonography (UC) and computed tomography (CT) demonstrated a mass in the left lateral segment of the liver that measured 11.6x9.5 cm with cystic lesions. Laboratory data on admission showed no significant findings. Celiac angiography revealed a hyper-vascular mass. Surgical exploration revealed a soft mass arising and protruding from the left lateral segment of the liver. Partial resection of the left lateral segment was performed. Histologically, the tumor was surrounded by a thin fibrous pseudocapsule. The neoplastic cells resembling normal hepatocytes around the tumor were large, pale and arranged in thick, irregular cords. Neither mitotic figures nor foci of dysplasia were present. The central portions of the tumor showed marked cystic degeneration. The tumor was histologically diagnosed as hepatocellular adenoma (HCA). HCA with cystic degeneration has been rarely reported. ( info)

3/89. Two cases of focal nodular hyperplasia of the liver: value of scintigraphy with Tc-99m GSA and positron emission tomography with FDG.

    focal nodular hyperplasia (FNH) of the liver is relatively rare, and can be difficult to differentiate from other benign tumors arising in the liver. We describe a 23-year-old woman and a 25-year-old man with FNH. They were hospitalized for further evaluation of a space-occupying lesion in the liver. Scintigraphy with Tc-99m diethylenetriaminepentaacetic acid galactosyl human serum albumin (Tc-99m GSA) revealed increased radioactivity in the tumor in one patient and radioactivity similar to that in the normal part of liver in the other. F-18 fluorodeoxyglucose positron emission tomography (FDG-PET) showed uptake similar to that of the normal liver in both patients. FNH was diagnosed on the basis of angiographic findings and histological findings in liver biopsy specimens. Our results show that scintigraphy with Tc-99m GSA and FDG-PET may provide information helpful in the diagnosis of FNH. ( info)

4/89. Intratumoral steatosis in focal nodular hyperplasia coinciding with diffuse hepatic steatosis: CT and MRI findings with histologic correlation.

    focal nodular hyperplasia (FNH) is a benign tumorlike condition that is thought to be a hyperplastic response to increased blood flow in an arterial malformation rather than a true neoplasm. Radiologically, FNH usually shows typical findings on unenhanced and enhanced computed tomography (CT) and magnetic resonance images (MRI), with atypical features being the exception rather than the rule. We report an unusual case of FNH with extensive fatty infiltration of the lesion illustrated on CT and MRI and proven by histopathology. ( info)

5/89. focal nodular hyperplasia contiguous with an echinococcal cyst.

    We report the first case of an Echinococcal cyst and focal nodular hyperplasia, two usually isolated hepatic lesions, in direct contiguity. The patient presented with right upper quadrant pain and subsequent imaging studies found a cystic and solid lesion. These studies suggested that this lesion was an hepatic adenoma, which had bled forming a hematoma. Pathological examination of the surgical resection showed echinococcus multilocularis with contiguous focal nodular hyperplasia. Because focal nodular hyperplasia is a benign hepatic lesion the etiology of which is thought to be abnormal arterial blood flow, we postulate that the parasitic hepatic infection by E. multilocularis may have incited the formation of this contiguous hepatic lesion. ( info)

6/89. Clinicopathological characteristics of surgically resected minute hepatocellular carcinomas.

    BACKGROUND/AIMS: The multistep development of overt hepatocellular carcinoma from very well-differentiated early hepatocellular carcinoma, and of early hepatocellular carcinoma from adenomatous hyperplasia has been strongly suggested. The clinicopathologic and immunohistochemical characteristics of solitary minute hepatocellular carcinomas smaller than 1 cm in size have yet to be clarified. METHODOLOGY: Fourteen minute hepatocellular carcinomas were divided into 2 groups consisting of: 1) hepatocellular carcinoma of hepatitis b surface antigen positive patients (B-HCC) (n = 5), and 2) hepatocellular carcinoma of hepatitis c virus antibody positive patients (C-HCC) (n = 9), then they were all analyzed histopathologically and clinicopathologically. Immunohistochemical studies were also performed using the antibodies against p53 protein. RESULTS: Six of the 14 minute hepatocellular carcinoma were demonstrated to be moderately or poorly differentiated tumors. Among the 8 well-differentiated minute hepatocellular carcinomas, 2 tumors already contained less differentiated components. B-HCC tended to be less differentiated than C-HCC (P < 0.05). Adenomatous hyperplasia was detected in only 2 cases of C-HCC. Small cell liver dysplasia was detected significantly more frequently in C-HCC than in B-HCC (P < 0.05). The prognosis of the 14 minute hepatocellular carcinomas varied considerably. Immunohistochemically, some tumor cells were positive for p53 in 3 cases. CONCLUSIONS: Our study suggests that 1) the multistep carcinogenesis through adenomatous hyperplasia may not be so frequent, 2) De novo carcinogenesis from not only well-differentiated hepatocellular carcinoma, but also from less differentiated hepatocellular carcinoma, especially B-HCC, may be present, 3) the carcinogenesis in the B-HCC cases may behave differently from that in C-HCC cases, and 4) minute hepatocellular carcinomas demonstrate varying prognoses after hepatectomy. ( info)

7/89. Multiple macroregenerative nodules in liver cirrhosis due to budd-chiari syndrome. case reports and review of the literature.

    Clinical, radiological, histological and immunohistochemical methods were used to define the nature of multiple rapidly growing hepatic nodules in 2 young patients with budd-chiari syndrome due to myeloproliferative diseases. In one patient, the arterial hyperperfusion of large nodules was demonstrated by dynamic computed tomography and angiography. The explanted livers of these patients showed multiple well-demarcated nodules up to 3 cm in diameter on the background of liver cirrhosis resulting from chronic hepatic congestion. Histologically, these nodules covered a spectrum ranging from adenoma-like lesions to nodules resembling focal nodular hyperplasia. They consisted of essentially normal hepatocytes, and variably contained fibrous septa including neoductules and large, mostly dysmorphic arteries. Sometimes, they were located close to still patent or recanalized veins. These rapidly growing hepatic nodules are best defined as macroregenerative nodules. The knowledge of this entity may help the physician to avoid misinterpretation of such nodules as carcinomas. ( info)

8/89. Nodular regenerative hyperplasia of the liver in budd-chiari syndrome: CT and MR features.

    We report the imaging findings of spiral computed tomography (CT), magnetic resonance (MR) imaging, and MR angiography in a patient with nodular regenerative hyperplasia of the liver associated with budd-chiari syndrome. Spiral CT showed multiple enhancing nodules during the hepatic arterial and portal venous phases. MR images showed multiple hyperintense nodules on T1-weighted images and hypointense or isointense nodules on T2-weighted images. MR angiography showed thrombotic occlusion of three hepatic veins, suggesting budd-chiari syndrome. ( info)

9/89. Simultaneous occurrence of focal nodular hyperplasia and primary sclerosing cholangitis in a young female.

    We report the case of a 22-year-old female with primary sclerosing cholangitis who was found, during hepatic imaging, to have a large liver mass. Imaging techniques and histological examination confirmed the mass to be focal nodular hyperplasia. A review of the literature indicates that the simultaneous occurrence of these two hepatic pathologies is unique. The differential diagnosis of hepatic masses in primary sclerosing cholangitis is discussed. focal nodular hyperplasia needs to be included in the differential diagnosis of hepatic lesions in primary sclerosing cholangitis. ( info)

10/89. Hepatic lesion differentiated from accessory spleen by a heat-damaged red blood cell scan.

    A 34-year-old woman referred for evaluation of an abdominal mass underwent a computed tomographic portagram that showed a large mass in the region of the left hepatic lobe and adjacent to the spleen. A liver-spleen scan with sulfur colloid did not clearly show whether the mass originated in the liver or the spleen. To evaluate the possibility of an accessory spleen, a selective spleen scan using Tc-99m-labeled heat-damaged red blood cells was performed and showed intense uptake in the region of the spleen only. The patient underwent surgical exploration and excision of the lesion, which proved to be focal nodular hyperplasia of the liver. Thus, the heat-damaged red blood cell scan ruled out an accessory spleen as a cause for the mass. ( info)
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