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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

History of the concept and definition of hepatitis is briefly reviewed. The landmarks of progress are based on better understanding of liver structure and introduction of biopsy techniques to follow the pathologic alterations in acute and chronic hepatitis, cirrhosis, dysplasia and hepatoma. Modern achievements are recognition of the etiologic agents of viral hepatitis A through G, viral nucleic acid sequencing, viral genome and gene products leading to development of immunologic tests to etiologic diagnosis. Viral particles are visualized by electron microscopy. In tissue, localization of viral products is obtained by histochemical, immunologic and by in situ hybridization methods. Diagnostic criteria for each of the viral etiologic agents is reviewed, as is cirrhosis and its occurrence in viral hepatitis and alcohol abuse.
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PMID:Progress in diagnosis of hepatitis and the cirrhotic liver. 1021 95

Cirrhosis, a condition whose diagnosis is dependent on histology, is characterized by a combination of two main lesions, namely fibrosis and regeneration nodules. Alcohol abuse and viral infections are the two most common causes of cirrhosis. Symptoms and laboratory test abnormalities appear when hepatic failure and portal hypertension occur as a result of the cirrhosis. Ascites, gastrointestinal bleeding, encephalopathy, and bacterial infections are the main clinical manifestations. Hepatocellular carcinoma is a common and dreaded complication of cirrhosis. Serum albumin, serum bilirubin, and the prothrombin time are the most useful laboratory parameters. In combination with clinical criteria they allow determination of the Child-Pugh stage, which is largely used to evaluate the severity of cirrhosis, and evaluation of the prognosis. Recently, the early detection of cirrhosis has been shown to benefit from assays of serum markers for fibrosis, most notably hyaluronate. Quantitative tests evaluating the functional liver mass are helpful for monitoring cirrhosis and for selecting patients for liver transplantation, which is the only available treatment for end-stage cirrhosis.
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PMID:[Cirrhosis]. 1060 69

Generally, 0.4-2.5% of patients with chronic hepatitis C virus (HCV) infection develop hepatocellular carcinoma (HCC). HCC occurs more often in patients with cirrhosis and in those with increased liver cell proliferation. HCV-related tumors occur in older patients and often have a less aggressive course than HCC, related to other etiological factors. Many HCV-related HCC are multifocal in origin. However, many tumors grow as a single hepatic nodule for years before generating satellite or distant tumor nodules. The growth pattern varies from one tumor to another, with tumor volume doubling times ranging from 1 to 20 months. Tumor progression and hepatic failure are the leading causes of death in most patients. Using the polymerase chain reaction technique, HCV-RNA has been almost invariably detected in serum and tumor tissue of anti-HCV patients with HCC. In many patients, HCV-RNA was found to belong to the possibly more pathogenic type 1b. However, it is unlikely that HCV plays a direct role in liver tumorogenesis, since no reverse transcriptase activity has been found in infected livers. One current opinion is that HCV may promote cancer through cirrhosis, which is per se an important risk factor for this tumor. In HCV carriers, the risk of developing HCC and having more severe tumor disease may be increased by coexisting hepatitis B virus (HBV) or alcohol abuse, further supporting the idea that both HCC and cirrhosis might be a result of the interplay of several risk factors. HCC could also be the consequence of HCV interacting with cellular genes that regulate cell growth and differentiation, independent of the effect of cirrhosis.
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PMID:Natural history and pathogenesis of hepatitis C virus related hepatocellular carcinoma. 1062 56

Hepatitis C, transmitted through body fluid exchange, affects approximately 1.8% of the U.S. population, roughly 3.9 million persons. Transfusion of blood and blood products was once an important source of hepatitis C transmission. Since the initiation of the hepatitis C screening program in 1985, however, injection drug use has become a major route. Hepatitis C is a leading cause of chronic liver disease. In 80% to 85% of those infected with the virus, chronic hepatitis C eventually develops, which can lead to cirrhosis and hepatocellular carcinoma, with alcohol abuse and coinfection with hepatitis B as additional risk factors. Screening for hepatitis C can be achieved with serologic assays. Molecular assays are helpful in confirming the diagnosis, assessing viral load, and characterizing the genetic nature of the viruses. Interferon alpha (IFN-alpha) and a combination of IFN-alpha 2B and ribavirin are therapies available in treatment of hepatitis C, but sustained response to the treatment has been unsatisfactory. Further studies are indicated to obtain more effective therapies for eradication of the disease. Hepatitis C is preventable, and clinicians should use every opportunity possible in their practice to assess those at risk and actively engage them in risk factor reductions.
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PMID:Hepatitis C infection: a review. 1071 Nov 35

The purpose of this investigation was to determine the role of alcohol in development of progressive liver disease. For this purpose, 41 alcoholic patients were followed up for 5 years. Criteria for alcohol abuse was that the patients were enjoying 20 g alcohol daily in a period of 5 years for females and respectively 60 g daily for males. In the same time a group of 51 nonalcoholic patients with histologically proven chronic liver disease were investigated. In all 92 patients chronic liver disease and progression of the disease was proven by liver biopsy during a 5-years follow-up. In sera of all patients the markers of hepatitis viruses B, D and C were continuously determined and chronic viral hepatitis was excluded. Also, autoimmune chronic hepatitis was excluded. The results of the investigation showed that alcoholics develop cirrhosis hepatitis, in most cases 78.04%. The most progressive chronic liver diseases--cirrhosis and hepatocellular carcinoma--are significantly present among nonalcoholics (p < or = 0.05). In the mentioned investigation a large group of 51 patients with severe chronic hepatitis without a proven etiology of disease was found and it deserves priority in future research.
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PMID:Prognosis for the patients with alcoholic and nonalcoholic liver disease. 1089 52

Fatty acids are ligands for the peroxisome proliferator-activated receptor alpha (PPAR alpha). Fatty acid levels are increased in liver during the metabolism of ethanol and might be expected to activate PPAR alpha. However, ethanol inhibited PPAR alpha activation of a reporter gene in H4IIEC3 hepatoma cells expressing alcohol-metabolizing enzymes but not in CV-1 cells, which lack these enzymes. Ethanol also reduced the ability of the PPAR alpha ligand WY14,643 to activate reporter constructs in the hepatoma cells or cultured rat hepatocytes. This effect of ethanol was abolished by the alcohol dehydrogenase inhibitor 4-methylpyrazole and augmented by the aldehyde dehydrogenase inhibitor cyanamide, indicating that acetaldehyde was responsible for the action of ethanol. PPAR alpha/retinoid X receptor extracted from hepatoma cells exposed to ethanol or acetaldehyde bound poorly to an oligonucleotide containing peroxisome proliferator response elements. This effect was also blocked by 4-methylpyrazole and augmented by cyanamide. Furthermore, in vitro translated PPAR alpha exposed to acetaldehyde failed to bind DNA. Thus, ethanol metabolism blocks transcriptional activation by PPAR alpha, in part due to impairment of its ability to bind DNA. This effect of ethanol may promote the development of alcoholic fatty liver and other hepatic consequences of alcohol abuse.
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PMID:The transcriptional and DNA binding activity of peroxisome proliferator-activated receptor alpha is inhibited by ethanol metabolism. A novel mechanism for the development of ethanol-induced fatty liver. 1102 51

It has been suggested that excess iron may facilitate the occurrence of cancer. Patients with hereditary hemochromatosis (HH) are at high risk of developing liver cancer, and studies of limited series reported a high frequency of nonhepatic cancers. To verify whether patients with HH are at higher risk of liver cancer and other malignancies as compared with patients with non-iron-related chronic liver disease (CLD), we analyzed the occurrence of neoplasms in 230 patients with HH and 230 with non-iron-related CLD. The patients were matched by sex, age, duration of follow-up (+/-5 years), and severity of liver disease. On enrollment, the following variables were considered: hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, alcohol abuse, smoking, and a family history of cancer (first-degree relatives). The diagnosis of primary cancers was confirmed by histology. During the follow-up, hepatocellular carcinoma (HCC) developed in 49 and 29 patients (all cirrhotic patients) with HH and non-iron-related CLD, respectively, with a relative risk of 1.8 (95% confidence interval [CI] 1.1-2.9); nonhepatic cancers occurred in 20 and 11 patients, respectively, with a relative risk of 1.8 (95% CI 0.8-4). Four patients with HH and 1 with non-iron-related CLD developed 2 different primary cancers during follow-up. The risk of cancer after adjustment for alcohol abuse, smoking, and family history of cancer was 1.9 (95% CI 1.1-3.1) in the patients with HH. In conclusion, patients with HH are at high risk of both liver cancer and other malignancies, which should be carefully sought during follow-up.
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PMID:Increased cancer risk in a cohort of 230 patients with hereditary hemochromatosis in comparison to matched control patients with non-iron-related chronic liver disease. 1123 Jul 45

Many transplant centres are reluctant to accept alcoholic patients because of their supposed potential for alcoholic recidivism, resulting in graft failure and recurrence of alcoholic liver cirrhosis. From May 1982 to January 1993 80 patients received orthotopic liver transplantation (OLT) at our institution either for alcoholic cirrhosis exclusively (n = 58) or for a hepatoma in an alcoholic cirrhosis (n = 22). The outcome of these patients was analysed with particular attention to recurrence of liver disease. Overall survival in this group was 67% and 49% at 1 and 5 years, respectively, with a median follow-up of 45 months. Actuarial survival of patients transplanted since January 1989 (n = 46) and 84% and 82% at 1 and 2 years (median follow-up 31 months). Non-fatal clinical endpoints were analysed in those patients surviving for at least 3 months (n = 61). Return to alcohol abuse was documented in 16 patients at routine short-term out patient check-ups. All patients except one admitted to taking alcohol and showed changes in their laboratory test results. A specific pattern of liver function test values related to alcohol abuse was not detected and at the end of a relapse the liver function values usually returned to pre-event values. Only in one case was toxic injury of the liver related to alcoholic recidivism diagnosed on percutaneous liver needle biopsy or post-mortem examination. Compliance with the required immunosuppressive regimen and social rehabilitation after OLT were excellent. Unwillingness to offer OLT to individuals with alcoholic liver disease because of failure to demonstrate 100% long-term abstinence appears difficult to defend in the face of results showing good survival, compliance and social rehabilitation. The hypothesis of a higher sensitivity of the transplanted liver to a drinking episode and the redevelopment of alcoholic diesease in the new liver was not confirmed in our study population.
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PMID:Transplantation for alcoholic cirrhosis: how does recurrence of disease harm the graft? 1127 Nov 84

Laparoscopy with laparoscopic ultrasound (L-LUS) has proved to be superior to conventional CT imaging in the staging of hepatocellular carcinoma (HCC). The aim of our prospective study was to evaluate the efficacy of L-LUS as compared with currently available imaging techniques (spiral CT or Lipiodol CT) in patients with HCC and liver cirrhosis. From January 1998 to May 2000, 70 consecutive patients (50 men and 20 women; mean age 67 +/- 7 years) were enrolled. Liver cirrhosis was related to chronic hepatitis C virus infection in 55, hepatitis B virus infection in seven, and alcohol abuse in eight patients. Preoperative diagnostic workup included the following: 70 ultrasound examinations of the liver, 23 CT scans after Lipiodol arteriography, and 53 spiral CT scans. A single lesion was found in 39 patients, two lesions in 20 patients, and three lesions in 11 patients. L-LUS was performed in all patients under general anesthesia using a two- to three-trocar technique. The examination was completed in 68 patients (97%); in two cases extensive adhesions prevented the L-LUS examination. L-LUS yielded additional information in 39 patients (57%). New histologically proved HCC lesions were detected in 14 patients (in the same liver segment in 4 cases and in different liver segments in 10 cases), and an adrenal metastasis was seen in one patient. In 23 patients, benign nodules were identified as regenerative macronodules, low-grade dysplastic nodules, or small hemangiomas. In 10 patients, correct localization of the primary lesion was detected by L-LUS in comparison with the preoperative liver location. In our experience, L-LUS is a safe and reliable procedure. It provides superior information (intraoperative histologic confirmation) for the diagnosis and pretreatment staging of HCC in patients with cirrhosis when compared with current radiologic imaging techniques.
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PMID:Laparoscopy with laparoscopic ultrasound for pretreatment staging of hepatocellular carcinoma: a prospective study. 1136 55

Alcohol abuse is accompanied by a high prevalence of hepatitis C virus (HCV) infection, which arise in the Great La Plata up to 20%. This condition worsen the histological necro-inflamatory activity of HCV chronic hepatitis patients, accelerating the evolution to liver cirrhosis, to cirrhosis decompensation, and surely facilitating the development of hepatocellular carcinoma. Besides of that, active alcohol abuse implies severe decrease in therapeutic response and yet more, a real contraindication for IFN mono-drug or combined treatment. All of that remarks the need for a correct investigation of alcohol consumption in HCV infected patients through a careful clinical examination, routine use of biological markers and incorporation of specialized systematic questionnaires, submitting the patient as early as possible to a special treatment (mental health team, self-help groups, naltrexone or similar trials). Alcohol abuse suppression is the first great therapeutic gesture in chronic hepatitis C patients to allow specific combined treatment and eventually a more successful liver transplant.
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PMID:[Hepatitis C and alcohol: notes for consensus]. 1137 Jan 79


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