Cases reported "Carcinoma, Hepatocellular"

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1/36. Generalized intraperitoneal seeding of hepatocellular carcinoma after microwave coagulation therapy: a case report.

    We first describe a case of generalized intraperitoneal seeding of hepatocellular carcinoma (HCC) after microwave coagulation therapy (MCT). A 61 year-old man underwent operative MCT for an exophytic HCC, 60 mm in diameter, in segment IV of his cirrhotic liver. Despite successful tumor ablation, the serum alpha-fetoprotein levels continuously rose after MCT. Five months later, radiographic examinations delineated several perihepatic masses with hypervascularity, and the patient presented with constipation. At the second laparotomy, there were numerous small peritoneal metastases involving the entire peritoneal cavity and slightly bloody ascites. An omental mass, 50 mm in diameter, involved the transverse colon. Most of these intraabdominal masses were removed together with the involved colon. Histologically, the initial tumor was a moderately differentiated HCC, and the peritoneal masses were poorly differentiated HCCs. The patient died of rapid tumor progression and bleeding 2 months later. In conclusion, we should be aware of the possible occurrence of peritoneal seeding after MCT for HCC. Every effort should be made to prevent this serious complication, particularly in cases of superficial, large, and less differentiated HCCs.
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2/36. Case studies in orthotopic liver transplantation for hepatitis B: a panel discussion.

    Five cases that were referred to the Division of Transplantation at NYU School of medicine for consideration for liver transplantation were discussed among a panel of hepatitis B and liver transplant experts. Opinions were obtained on the management at every stage of treatment of patients with the following initial information: Case one: young Asian woman in stage IV hepatic coma; intubated; prothrombin time (PT): 30 s; serum glutamic oxaloacetic transaminase (SGOT): 8,000 IU; total bilirubin: 25 mg/dL; hepatitis B surface antigen (HBsAg) positive. Case two: 70-yr-old woman, native of greece; decompensated cirrhosis with encephalopathy; child-Pugh Class C; HBsAg positive; hepatitis B surface antibody (HBsAb) negative; hepatitis B e antigen (HBeAg) positive; hepatitis B e antibody (HBeAb) negative; hepatitis b virus (HBV) dna titer: 10,000. Case three: Muscular detective working full-time; cirrhosis; child Pugh Class B; ascites controlled with spironolactone and furosemide; PT: 19s; HBsAg positive; HBsAb negative; HBV dna titer: 50,000; low platelet count. Case four: 45-yr-old baker; cirrhosis and resectable 4-cm hepatoma; child-Pugh Class B; PT: 16 s; Blood type O; United Network for Organ Sharing (UNOS) 2B; HBV dna titer: 3,000. Case five: 40-yr-old Indian man; 300 pounds with massive ascites; child Pugh Class C; PT: 17 s; HBsAg positive; HBV dna titer: 22,000; transplanted with intra-operative hypotension; tacrolimus; graft functioning; HBIg 10,000 IU intra-operative and around the clock during the first post-operative week; required huge doses of hepatitis B immune globulin (HBIg) to maintain adequate HBsAb level; daily loss of 5 6 L of ascites fluid; post-operative day 8: anuric, blood urea nitrogen (BUN) 127, creatinine 3, mental status changes.
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3/36. Combination radiotherapy for hepatocellular carcinoma with intraductal tumor thrombus: a case report.

    We report the successful treatment of hepatocellular carcinoma (HCC) associated with an intraductal tumor thrombus in a 67-year-old male. Abdominal ultrasonography (US) and computed tomography (CT) revealed intrahepatic biliary dilatation in the left hepatic lobe and an intraductal tumor thrombus. The main tumor lesion was not clearly visualized on abdominal US, dynamic CT, and hepatic angiography. We biopsied the intraductal tumor thrombus under US guidance. Histologically the biopsy specimen was a poorly differentiated HCC We thus diagnosed HCC with intraductal tumor thrombus. The total serum bilirubin level gradually rose to 3.1 mg/dl. This tumor was inoperable because of severe hepatic dysfunction. We chose to treat the patient with radiotherapy aimed only at the intraductal tumor thrombus because the main tumor was unclear. A percutaneous transhepatic biliary drainage (PTBD) tube was inserted into the common bile duct beyond the tumor thrombus and the tube was dilated. Once total serum bilirubin had reached the normal range, a combination of external beam radiation therapy (EBRT) plus an intraluminal brachytherapy, 192Ir boost was administered. The intraductal tumor thrombus was found to have vanished and the PTBD tube was removed. After this treatment, transcatheter hepatic arterial embolization was performed at the point of tumor appearance. This patient had a relatively long survival, approximately 30 months, with no clinical evidence of recurrent disease and biliary drainage was not necessary.
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4/36. Synchronous hepatocellular carcinoma and cholangiocarcinoma arising in two different dysplastic nodules.

    We present the first reported case of explant cirrhotic liver that had synchronous cholangiocarcinoma and hepatocellular carcinoma arising in two different high-grade dysplastic nodules. The patient was a 55-year-old woman who had hepatitis b virus-associated liver cirrhosis for 3 years. The moderately differentiated cholangiocarcinoma occurred in high-grade dysplastic nodule with a 1.7-fold cell density compared with that of cirrhotic nodule. The hepatocellular carcinoma arose in a nodule-in-nodule pattern within a peripherally low-grade and centrally high-grade dysplastic nodule and had a 2.7-fold cell density compared with that of cirrhotic nodule. By immunohistochemistry, the tumor cells of the cholangiocarcinoma as well as bile ductular cells in dysplastic nodule were diffusely positive for cytokeratin 7, whereas hepatocellular carcinoma cells and dysplastic hepatocytes were negative for cytokeratin 7. The c-kit-positive hepatic progenitor cells were singly scattered between hepatocytes, and their number was highest in cirrhotic nodule and decreased in dysplastic nodule, whereas they were absent in cholangiocarcinoma and hepatocellular carcinoma arising in dysplastic nodules. Proliferation indices were progressively increased in cirrhotic nodule, dysplastic nodule, and cholangiocarcinoma or hepatocellular carcinoma, sequentially. These observations indicate that cholangiocarcinoma as well as hepatocellular carcinoma can develop in dysplastic nodule and that hepatic progenitor cells might play a role in the early stage of cholangiocarcinogenesis and hepatocarcinogenesis.
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5/36. Solid adenoma with exclusive hepatocellular differentiation: a new variant among pancreatic benign neoplasms?

    We report a unique, previously unreported pancreatic tumor with hepatoid differentiation associated with serous microcystic adenoma in a 70-year-old man. These two lesions localized, respectively, at the body and the tail of the pancreas, were found incidentally on abdominal ultrasonography. serum alpha-fetoprotein was not increased and no hepatic lesion was displayed on computed tomography. A subtotal pancreatectomy with splenectomy was performed. The patient is alive and well 12 months after resection. Pathological examination showed a very unusual encapsulated solid tumor with hepatocytic differentiation, bile production and immunoreactivity for hepatocyte paraffin-1 antibody. The tumor cells were negative for endocrine (neuron-specific enolase, chromogranin a, synaptophysin) and acinar (amylase, trypsin) markers. Ultrastructurally, zymogen and neurosecretory granules were absent. The features of the tumor were almost indistinguishable from those of hepatocellular adenoma; therefore, we believe that this solid hepatoid tumor may represent a variant of pancreatic adenoma. Recognition of this entity is important because the only reported pancreatic hepatoid tumors to date have been malignant. The main differential diagnoses include hepatoid ductal adenocarcinoma, hepatoid acinar cell carcinoma, primitive hepatoid endocrine tumor, and metastatic hepatocellular carcinoma.
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6/36. Severe bone marrow depression induced by an anticancer herb Cantharanthus roseus.

    We report a 67-yr-old woman with hepatitis c-related liver cirrhosis and hepatoma who had developed severe bone marrow suppression after taking Cantharanthus roseus as an alternative anticancer treatment. The patient developed severe pancytopenia with initial presentations of vomiting, diarrhea, oral ulcer, and fever about 1 week after taking 5-days' course of Cantharanthus roseus. bone marrow biopsy showed autolysis, which indicated massive necrosis of the hematopoietic cells. There was no malignant cell infiltration. The patient also had severe gastrointestinal disturbances, bacteremia, urinary tract infection, and impaired renal and liver function. Supportive care with broad-spectrum antibiotics, granulocyte colony-stimulating factor, repeated blood transfusions, and albumin supplement was given. She recovered and was discharged after 48 days hospitalization. Coadministration of Cantharanthus roseus and cisapride was noted, and these two drugs are both substrates of cytochrome P450 3A4 enzymes (CYP 3A4). Because the vinca alkaloids are extensively metabolized by the liver cytochrome P450 enzymes, poor hepatic function and drug-herb interaction might predispose the patient to develop the bone marrow toxicity. This case report demonstrated possible effect of oral dose of vinca alkaloids and also hinted that all the substrates and inhibitors of CYP 3A4 have propensity to interfere with metabolism of vinca alkaloids.
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7/36. Markedly elevated alpha-fetoprotein levels without hepatocellular carcinoma.

    Although low-grade elevations of AFP are associated with benign liver disease including acute and chronic hepatitis and cirrhosis, AFP values above 400 ng/mL are often used as a surrogate marker for HCC. The case of a 45-year-old Caucasian woman, who while receiving interferon therapy for HCV, was found to have a marked elevation of her serum AFP level, is reported. Her baseline AFP of 7.0 ng/mL increased progressively over three months to a peak value of 734.5 ng/mL. Initial imaging was normal. Three months later, a CT scan detected two focal lesions in the dome of the liver. A post-ethiodol hepatic CT scan revealed persistent uptake at this site but fluoroscopy-guided liver biopsy failed to identify a HCC. Normalization of her AFP level occurred while she continued to receive IFN for HCV. The patient has remained stable over more than three years of follow-up. While others have reported AFP elevations in cirrhotics with HCV without evidence of HCC, to our knowledge there are no reports of an individual receiving IFN treatment for hepatitis c with AFP levels that rose over several months in the absence of a HCC.
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8/36. Hepatocellular carcinoma with an unusual neuroendocrine component.

    We report a rare case of hepatocellular carcinoma (HCC) with an unusual neuroendocrine component. During a follow-up study for chronic hepatitis c in a 71-year-old man, a nodular lesion showed rapid growth from 1 cm to 4 cm in diameter within 3 months. Histologically, the tumor was consistent with moderately differentiated HCC, but was intermingled with nests of small round cells with scarce cytoplasm, which resembled those found in small cell carcinoma. This population formed small solid nests among the trabecular structures. Immunohistochemically the small round cell component of the tumor was strongly positive for neuron-specific enolase (NSE), chromogranin a and synaptophysin, but hepatocyte paraffin-1 (HP-1) and alpha-fetoprotein (AFP) were negative. In contrast, HP-1 and AFP were positive, and NSE, chromogranin a and synaptophysin were negative in moderately differentiated HCC tissues. Electron microscopy revealed many intracytoplasmic neurosecretory granules in the small round cells. The labeling indexes of p53 and Ki-67 were significantly higher in the small round cell component than in the moderately differentiated HCC component. overall, we conclude that this nodule was HCC with neuroendocrine differentiation.
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9/36. 131I-rose bengal therapy in hepatoblastoma patients.

    If conventional treatment modalities have failed in hepatoblastoma patients and no distant metastases can be demonstrated therapy with radionuclide agents can be considered. In 6 patients diagnostic technetium-99m (99mTc)-disofenin and two iodine-131 (131I)-rose bengal scans were made. 2 patients demonstrated specific uptake of disofenin. One of these had a positive scintigram with radiolabelled rose bengal. This patient was subsequently treated with 1.1 GBq 131I-rose bengal. No toxicity was observed. A clear decrease in the level of alpha-fetoprotein indicated a response and demonstrated that this radiopharmaceutical can be used for tumour targeted radiation therapy in selected patients with therapy resistant tumours.
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10/36. prevalence of cardiac tumours at autopsy in Ibadan.

    The post mortem specimens, protocols, slides and hospital case notes of 6064 necropsies carried out in the University College Hospital, Ibadan over a seven year period were reviewed. Cardiac tumours were found in 64 subjects (1.06%) of all autopsies and in 8.5% of all 752 malignancies that came to autopsy during the same period. Only two of these tumours arose primarily in the heart whilst the remaining were metastatic tumours. The right side of the heart was more often involved than any other part (31.38%). The tumour with the highest cardiac involvement was Burkitt's lymphoma with an incidence of 30 cases i.e. 8.24% of all malignancies; 0.48% of all necropsies studied; 53.6% of all Burkitt's lymphoma autopsied. The risk of associating the rate of cardiac involvement of any tumour with its index of higher frequency was emphasized in the light of the paucity of involvement in a more frequent malignancy (hepatocellular) carcinoma in this environment. Routine medical examination coupled with an awareness of the possible susceptibility of the heart to secondary involvement by Burkitt's lymphoma would aid ante-mortem diagnosis of intracardiac malignancy particularly in patients of Burkitt's lymphoma age group.
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