Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AIM:To determine the clinical presentations, survival and prognostic factors of hepatocellular carcinoma (HCC) in Southern Thailand.METHODS:Retrospective analysis was performed on the 336 hepatocellular carcinoma patients treated at Songklanagarind hospital between 1 January 1991 and 31 January 1999.RESULTS:Of these 336 patients, 276 were males and 60 were females. The mean age was 54.4 years. The common symptoms and signs were abdominal pain and hepatomegaly. The most common presentation of tumor was a dominant mass with daughter nodules. Portal vein involvement was found in 50% of total. Extrahepatic metastasis was found in 13%, and the lung was the most common site. There were 65.4% with evidence of cirrhosis and half of them were in Child's class B. HBsAg was positive in 72.6%. Regarding a(c)Okuda's tumor staging, 15%, 61% and 24% were stage I, II and III, respectively. Overall median survival was 2.1 months (11.5 2.6 and 0.7 months for stage I, II and III respectively). Treatments of HCC improved patient survival (5.5 months vs 1.6 months for untreated patients). Most common causes of death were hepatic failure. Using multivariate analysis, the prognostic factors identified were tumor staging, alpha-fetoprotein level above 10000&mgr;gcenter dotL(-1), extrahepatic metastasis, portal vein thrombosis and treatment.CONCLUSION:HCC in Thailand is a fatal disease with poor outcome due to late presentation and high prevalence of liver cirrhosis. Early detection and proper management may improve outcome.
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PMID:Review of 336 patients with hepatocellular carcinoma at Songklanagarind Hospital. 1181 93

The factors that contribute to the effect of portal vein embolization before hepatectomy for hepatocellular carcinoma are unclear. Sixty-six patients with hepatocellular carcinoma were enrolled in the study. Changes in liver function, portal vein pressure, and liver volume after embolization were examined. A multiple linear regression analysis was performed to identify factors that independently contributed to the effects of portal vein embolization. The acceptable volume ratio of the remnant liver was calculated from liver function and compared with the volume ratio of the non-embolized liver. No postoperative deaths were observed after portal vein embolization or hepatectomy. Serum total bilirubin and prothrombin time did not change significantly after portal vein embolization. In patients who underwent arterial embolization before portal vein embolization, aminotransferase levels increased significantly. The only factor that could significantly predict the atrophy effects of portal vein embolization was previous arterial embolization. The volume ratio of the non-embolized liver was smaller than the acceptable volume ratio of the remnant liver in 18 of 40 patients and increased over the acceptable volume ratio in all cases after portal vein embolization. Portal vein embolization induced atrophy or hypertrophy of the embolized or non-embolized liver sufficiently, even when the liver was dysfunctional or cirrhotic. The atrophy effects were significant, especially when arterial embolization had been performed before portal vein embolization.
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PMID:Preoperative portal embolization in patients with hepatocellular carcinoma. 1189 42

A 49-year-old woman was admitted to our hospital because of hepatocellular carcinoma (HCC). She had no hepatitis virus. Serum AFP and PIVKA-II levels were as high as AFP 329.4 ng/ml (AFP-L3% 73.1%) and 281 AU, respectively. Portal venous thrombus was observed from the right portal branch to left portal branch and superior mesenteric vein. An extended right hemihepatectomy with extraction of portal venous thrombus was performed. On postoperative day 8, low-dose cisplatin (10 mg/day for 5 days/week) and 5-fluorouracil (250 mg/day for 5 days/week) were administered through the hepatic artery for 4 weeks. After chemotherapy, one intrahepatic metastasis appeared and RFA was performed for this tumor. At 16 months after surgery, she had multiple lymph node metastases and died at 20 months after the surgery without intrahepatic metastasis. Low-dose CDDP/5-FU intra-hepatic artery infusion chemotherapy was effective for prevention of intrahepatic recurrence after resection of HCC with portal venous thrombus.
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PMID:[A case of Vp4 hepatocellular carcinoma treated with surgical resection and continuous intrahepatic artery infusion chemotherapy of low-dose cisplatin and 5-fluorouracil]. 1461 15

The objective of this study was to demonstrate the safety of laparoscopic right hepatectomy for benign or malignant disease. Many reports document the success of minor or segmental liver resections performed laparoscopically. Major hepatic resection has rarely been reported. This report documents our experience with 12 laparoscopic right hepatectomies. Ten patients had suspected malignancy, but all had lesions well clear of the midplane of the liver. The surgery followed three distinct phases: (1). Portal dissection during which diathermy and harmonic shears are used, clips are applied to the right hepatic duct and right hepatic artery, and a vascular stapler is used to divide the right portal vein; (2). dissection of the vena cava, which is usually done by tunneling below the liver using harmonic shears, clips, and a linear stapler to divide the right hepatic vein; and (3). parenchymal division during which harmonic shears and multiple firings of linear staplers are used to divide the liver substance. In five patients the procedure was completed totally laparoscopically, five patients had a laparoscopic-assisted procedure, and two patients had to be converted to formal open hepatectomy. Four patients required blood transfusion. There were no deaths and two cases of major morbidity-bile leakage in one and wound dehiscence in one. The average hospital stay was 8 days, but for those whose operations were completed totally laparoscopically, 4 days was the average. Two of the nine patients with documented cancer have since died-one with widespread intrahepatic hepatocellular carcinoma and another with widespread metastatic melanoma after resection of a colorectal metastasis. Seven patients with colorectal cancer are alive and disease free with follow-up of 6 to 24 months. Laparoscopic right hepatectomy is feasible in selected patients. It is technically demanding but can be safely accomplished by surgeons who have experience in advanced laparoscopic procedures and open hepatic surgery.
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PMID:Laparoscopic right hepatectomy: surgical technique. 1503 98

Primary malignancies of the liver include tumors arising from the hepatocytes (hepatocellular carcinoma and the fibrolamellar variant) and the intrahepatic bile ducts (intrahepatic cholangiocarcinoma). Hepatocellular carcinoma is the most common primary cancer of the liver and is a leading cause of death from cancer worldwide. Although it is uncommon in the United States, the incidence of hepatocellular carcinoma is rising. Hepatitis, ethanol use, and cirrhosis often dominate the clinical picture and may dictate prognosis. New clinical and pathological staging systems have allowed for the more accurate stratification of patients to more appropriately identify patients for resection, transplantation, and percutaneous ablation therapies. A correlation between liver volume and surgical outcome has recently been demonstrated, with small liver remnant size being associated with increased morbidity. Portal vein embolization has therefore been proposed as one way to induce hypertrophy of the anticipated liver remnant before resection. Initial reports have shown that portal vein embolization decreases the incidence of postoperative complications. More recently, systemic chemotherapy and chemoembolization have been investigated as both primary and neoadjuvant therapy. Chemoimmunotherapy with 5-fluorouracil and interferon may be associated with a superior response rate in the fibrolamellar variant of hepatocellular carcinoma. Two recent randomized studies have also indicated improved survival after hepatic artery embolization in selected patients.
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PMID:Advances in the surgical management of liver malignancies. 1513 Feb 67

In the last ten years new techniques, such as percutaneous ethanol injection (PEI) and radiofrequency ablation (RFA), have been developed for the treatment of hepatocellular carcinoma (HCC). Portal vein involvement is a complication of HCC and the role of surgical resection for HCC with tumor thrombi in the portal veins is controversial. Here we present the case of a 58-year-old man, with Child's class A cirrhosis and a focal lesion of HCC with thrombosis of the segmental portal branch extending into the right portal vein. We treated the nodule with RFA and the portal tumor thrombosis with ethanol injection. Twenty-two months after the combined treatment, an enhanced spiral CT scan showed complete necrosis of the nodule and color/power Doppler ultrasound demonstrated the complete patency of the right portal vein.
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PMID:Radiofrequency ablation combined with percutaneous ethanol injection in the treatment of hepatocellular carcinoma and portal vein neoplastic thrombosis. 1533 Jan 93

Helicobacter hepaticus infection induces sustained inflammation and carcinoma of the liver in A/JCr mice, and serves as a model of human cancers associated with viral hepatitis and H. pylorichronic gastritis. Here we describe the pathogenesis of premalignant disease in A/JCr mice infected with H. hepaticus. We inoculated dams intragestationally and/or pups postnatally, and evaluated offspring at 3, 6, or 12 months. Mice infected at or before 3 weeks of age, but not at 12 weeks, developed disease. Male mice were most affected, but expressed a bimodal pattern of susceptibility. Males exhibited lobular necrogranulomatous and interface (chronic active) hepatitis, while females usually developed intraportal (chronic persistent) hepatitis. Portal inflammation was slowly progressive, with tertiary lymphoid nodule development by 12 months. Hepatic bacterial load and preneoplastic lesions, including clear and tigroid cell foci of cellular alteration, were correlated with lobular hepatitis severity. No extrahepatic surrogate disease marker reliably predicted individual hepatitis grade. In conclusion, gender and bacterial exposure timing are key determinants of H. hepaticus disease outcomes. Intrahepatic inflammation is driven by local signals characterized by a vigorous but nonsterilizing immune response. Continued study of chronic hepatitis progression may reveal therapeutic targets to reduce the risk of hepatocellular carcinoma.
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PMID:Progression of chronic hepatitis and preneoplasia in Helicobacter hepaticus-infected A/JCr mice. 1551 10

Molecular events preceding the development of hepatocellular carcinoma were studied in the Mdr2-knockout (Mdr2-KO) mice. These mice lack the liver-specific P-glycoprotein responsible for phosphatidylcholine transport across the canalicular membrane. Portal inflammation ensues at an early age followed by hepatocellular carcinoma development after the age of 1 year. Liver tissue samples of Mdr2-KO mice in the early and late precancerous stages of liver disease were subjected to histologic, biochemical, and gene expression profiling analysis. In an early stage, multiple protective mechanisms were found, including induction of many anti-inflammatory and antioxidant genes and increase of total antioxidant capacity of liver tissue. Despite stimulation of hepatocyte DNA replication, their mitotic activity was blocked at this stage. In the late stage of the disease, although the total antioxidant capacity of liver tissue of Mdr2-KO mice was normal, and inflammation was less prominent, many protective genes remained overexpressed. Increased mitotic activity of hepatocytes resulted in multiple dysplastic nodules, some of them being steatotic. Expression of many genes regulating lipid and phospholipid metabolism was distorted, including up-regulation of choline kinase A, a known oncogene. Many other oncogenes, including cyclin D1, Jun, and some Ras homologues, were up-regulated in Mdr2-KO mice at both stages of liver disease. However, we found no increase of Ras activation. Our data suggest that some of the adaptive mechanisms induced in the early stages of hepatic disease, which protect the liver from injury, could have an effect in hepatocarcinogenesis at later stages of the disease in this hepatocellular carcinoma model.
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PMID:Multiple adaptive mechanisms to chronic liver disease revealed at early stages of liver carcinogenesis in the Mdr2-knockout mice. 1661 19

Hepatocellular carcinoma (HCC) is usually diagnosed at an advanced stage, when little remedy could be offered. There is a need for relatively affordable, available and non-invasive tests for diagnosis, staging and detection of metastasis among individuals at risk. A clinical, chest radiographic (CXR) and abdominal ultrasonographic examination was carried out to detect and evaluate the pattern of metastasis among 53 untreated patients. One patient had clinical paraparesis with no outward evidence of metastasis. CXR revealed lung metastasis in 11 (20.8%), with multifocal deposits and bilateral involvement in 10 (18.8%), and unilateral single deposit in one. Two (3.8%) patients had perihilar lymphadenopathy and consolidation, respectively, while 18 (34%) patients had elevated right hemidiaphragm and four 17.5%) had pleural effusion. One had right basal pneumonitis, multiple cavitatory lesions in the lung fields and soft-tissue wasting. No abnormality was seen in 17 (32.1%) cases. Abdominal ultrasonograph showed probe tenderness in 22 (41.5%), hepatomegaly in 49 (92.5%), with 33 (62.3%) of these having nodularities of varying sizes. The spleen was enlarged in 10 (18.9%) cases, with four (7.5%) showing irregular outline. There were eight (15.1%) cases with para-aortic lymphadenopathy. Portal hepatic lymphadenopathy was demonstrated in two (3.8%) cases, while pleural effusion was detected in seven (13.2%). Metastasis is common in HCC at presentation, the lung is the commonest site of spread. Clinically visible metastasis appears uncommon in HCC.
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PMID:Clinicoradiologic and sonographic patterns of metastasis in hepatocellular carcinoma. 1705 52

Non-alcoholic fatty liver disease (NAFLD) is an important complication of the metabolic syndrome, which is becoming an increasingly common cause of chronic liver disease. Histological changes typically mainly affect perivenular regions of the liver parenchyma and include an overlapping spectrum of steatosis, steatohepatitis and persinusoidal or pericellular fibrosis, in some cases leading to cirrhosis. Once cirrhosis has developed, typical hepatocellular changes are often no longer conspicuous, leading to such cases being mistakenly diagnosed as 'cryptogenic'. Portal inflammation, ductular reaction and periportal fibrosis can also be seen as part of the morphological spectrum of NAFLD, particularly in the paediatric population. Hepatocellular carcinoma has also been described as a complication of NAFLD-associated cirrhosis. NAFLD is also an important cofactor in other chronic liver diseases, especially hepatitis C. Histological assessments have an important role to play in the diagnosis and management of NAFLD. These include making the potentially important distinction between simple steatosis and steatohepatitis and providing pointers to the aetiology, including cases where a dual pathology exists. A number of systems have been devised for grading and staging the severity of fatty liver disease. These require further evaluation, but have a potentially important role to play in determining prognosis and monitoring therapeutic responses.
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PMID:Histological assessment of non-alcoholic fatty liver disease. 1706 91


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