Cases reported "Liver Cirrhosis"

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1/20. Giant hyperplasia of the caudate lobe of the cirrhotic liver: correlation with an anomaly of the caudate portal branch.

    Different imaging appearances of giant hyperplastic change of the caudate lobe of the liver are presented in a patient with liver cirrhosis. The mass like caudate lobe was isoechoic on ultrasound, hypodense on postcontrast computed tomography (CT), hyperintense on T1-weighted magnetic resonance, images and isointense on T2-weighted images. These imaging findings are similar to those of dysplastic nodule in cirrhotic liver. The caudate lobe received normal portal flow on CT during arterial portography, but superior mesenteric arteriography showed precocious or early division of the caudate portal branch. We suspect that caudate hyperplastic change may be correlated to anomalous caudate portal vein branch.
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2/20. A case of giant cell hepatitis recurring after liver transplantation and treated with ribavirin.

    A patient who underwent orthotopic liver transplantation for giant cell hepatitis with cirrhosis and in whom giant cell hepatitis recurred twice after orthotopic liver transplantation is reported. He was treated with ribavirin with an excellent result. The literature on this subject is reviewed. This observation clearly confirms the efficacy of ribavirin for the treatment of giant cell hepatitis, thus providing evidence for its viral origin.
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3/20. Highly well differentiated hepatocellular carcinoma and benign hepatocellular lesions. Can they be distinguished on fine needle aspiration biopsy?

    OBJECTIVE: To determine whether highly well differentiated hepatocellular carcinoma can be distinguished from benign hepatocellular lesions on fine needle aspiration biopsy (FNAB). STUDY DESIGN: Ninety-five FNABs from 88 patients with hepatic masses/diffuse conditions were reviewed according to new cytologic criteria established by Takenaka et al. They were classified into well-, moderately and poorly differentiated hepatocellular carcinomas (W-, M- and P-HCC) and benign aspirates and histologically verified. RESULTS: There were 21 W-HCC, 39 M-HCC, 10 P-HCC, 3 problematic and 22 benign aspirates. The most useful criteria for diagnosing highly W-HCC were architectural features on the smears/cell block sections, including hypercellularity; arborescent, cohesive clusters; broad trabeculae; transgressing and peripheral endothelium; and cytologic details of small, monotonous hepatocytes with nuclear crowding, decreased cytoplasm, increased nuclear/cytoplasmic ratio, atypical naked nuclei and tumor giant cells. Well-defined cytoplasmic borders, abundant thick and monotonous cytoplasm, eccentric nuclei, thick nuclear membranes, irregular nuclear contours, increased chromatin density, irregular chromatin distribution and macronucleoli were not always detectable in highly W-HCC. In fact, some of them were seen in dysplastic hepatocytes. Deficient reticulin patterns and diffuse sinusoidal CD34 reactivity were helpful. CONCLUSION: Experience, attention to architectural and cytologic details in smears/cell blocks and clinicopathologic correlation should reduce the number of indeterminate reports. However, there will always remain some cytohistologically challenging cases.
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4/20. Combined hepatocellular and cholangiocarcinoma with marked squamous cell carcinoma components arising in non-cirrhotic liver.

    We report a surgical case of liver tumor, 40 x 35 mm in size, with squamous cell carcinoma (SCC) and hepatocellular carcinoma (HCC) components in a 60-year-old Japanese man with steatohepatitis. Most of the SCC component showed typical intercellular bridge and keratinization, while most of the HCC components showed a thick trabecular pattern with mild to moderate nuclear atypia. Both components transit each other without undifferentiated foci; however, a small foci showing glandular structure was intermediated. No cyst formation was found in the liver. The primary site of the squamous cell carcinoma was not detected in general clinical and radiological examination. Immunohistochemical analysis revealed that part of the HCC components neighboring the SCC showed patchy and weak expression of cytokeratin 7. There are several possibilities for the origin of squamous cell carcinoma in this case: marked squamous metaplastic change of cholangiocarcinoma and/or HCC, and carcinoma originating from pleuripotential stem cells. Irregular fatty changes, scattered giant mitochondria and acellular fibrosis with bridging were seen in the liver; however, this patient had no episode of hepatitis-associated viral infection. This is an interesting case of combined hepatocellular and cholangiocarcinoma with marked SCC components arising in a non-cirrhotic fibrotic liver.
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5/20. Familial occurrence of giant cell hepatitis in infancy.

    The repeated occurrence within one family or giant cell hepatitis terminating in death is reported. The familial form of giant cell hepatitis has a poorer prognosis than that occuring sporadically. In the first case, reported earlier, primary liver cancer developed within a short time. In the second case, reported here, the progression of the course of the disease which terminated in cirrhosis was followed in a series of histological examinatons made at five different points of time. Electronmicroscopic examination were also conducted.
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6/20. Endovascular treatment of giant splenic aneurysm that developed after liver transplantation.

    splenic artery aneurysms (SAAs) are not uncommon in patients with portal hypertension. They are usually diagnosed in preliminary examinations prior to orthotopic liver transplantation (OLT) and are treated surgically at the time of transplantation. In our case, the patient developed a giant SAA after liver transplantation. This was detected incidentally upon routine ultrasound follow-up, and the diagnosis was confirmed on magnetic resonance (MR) angiography. The patient was treated by endovascular embolization because it is believed that this minimally invasive approach is beneficial in an immunocompromised patient following OLT. After coil embolization, to achieve complete and immediate blood flow exclusion of the sac, it was decided to inject some glue ( N-butyl-2-cyanoacrylate) directly into the aneurysm. The aneurysm was successfully obliterated. To the best of our knowledge the use of cyanoacrylate glue in an SSA has never been reported.
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7/20. Accessory splenectomy with gastroesophageal devascularization for recurrent hypersplenism and refractory bleeding varices in a patient with liver cirrhosis: report of a case.

    We report a case of recurrent thrombocytopenia associated with symptomatic enlargement of an accessory spleen, 2 years after splenectomy, in a 36-year-old man with posthepatitic liver cirrhosis. The patient suffered three episodes of variceal bleeding, but the esophageal varices were not eradicated by two sessions of endoscopic injection sclerotherapy and endoscopic band ligation. Abdominal ultrasonography and computed tomography showed a giant accessory spleen (6 x 6 x 5 cm), gallbladder stones, and complete postsplenectomy splenomesoportal thrombosis. Subsequent 99mTc scintigraphy confirmed the presence of a functioning residual splenic nodule. Thus, we performed gastroesophageal devascularization (Hassab-Paquet procedure) with accessory splenectomy and cholecystectomy, after which the platelet count normalized and no further variceal bleeding occurred during 17 months of follow-up. To our knowledge, this is the first report in the English medical literature of accessory splenectomy for recurrent thrombocytopenia in a patient with liver cirrhosis.
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8/20. azygos vein varix mimicking mediastinal mass in a patient with liver cirrhosis: a case report.

    A giant venous varix of the azygos arch is a very rare cause of a mediastinal mass. The usual diagnosis of a mediastinal mass by mediastinoscopy or percutaneous fine-needle aspiration or biopsy is very hazardous if there is a venous varix. Noninvasive thoracic CT scanning is a safe and better choice for diagnosis. We describe the case of a woman with a posterior mediastinal mass caused by a giant azygos vein varix. Thoracic CT documented the diagnosis. The etiology of the azygos varix was portal hypertension secondary to liver cirrhosis.
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9/20. Giant cell hepatocellular carcinoma.

    A terminal case of giant cell hepatocellular carcinoma, subsequent to hepatitis b-associated macronodular cirrhosis is presented, illustrated and discussed. The uncommon finding of malignant ascites, in itself atypical of hepatocellular carcinoma, with an almost exclusive content of giant cells as the cellular component, was a feature of this unusual variant of hepatocellular carcinoma.
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10/20. giant lymph node hyperplasia (Castleman's disease): a clinical study of eight patients.

    We report on 8 patients with giant lymph node hyperplasia (GLNH), diagnosed over a 10-year period. The age of the patients at diagnosis, the clinical presentation and the histological subtype varied, indicating that GNLH is a heterogeneous condition. One case was associated with liver cirrhosis, and in another patient bacterial endocarditis was diagnosed post mortem. Our study shows that GLNH is localized and benign in the young, and diffuse and aggressive in the elderly. It is concluded that GLNH should be separated into 3 clinical entities--namely, localized, systemic and reactive GLNH--defined by their clinical presentation and course, and correlated or not correlated with the histological findings.
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