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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. The majority of patients who develop HCC have underlying cirrhosis, which suggests that cirrhosis itself represents a preneoplastic condition. Nevertheless, whereas patients with cirrhosis of any origin are at increased risk of developing HCC, those with chronic hepatitis B or C infection seem to be at greatest risk. Patients with cirrhosis resulting from chronic alcohol use, hemochromatosis, autoimmune hepatitis, or alpha-1 antitrypsin deficiency have less risk of developing this cancer, and some hepatic diseases, such as primary biliary cirrhosis and Wilson's disease, do not predispose affected persons to an appreciable risk of developing HCC. Certain histological features, such as liver cell dysplasia and macroregenerative nodules, may represent preneoplastic alterations of hepatocytes, but these changes do not seem to be a necessary step in the evolution of liver cancer. The pathogenesis of HCC is unclear, but seems to involve several steps. Hepatitis B virus infection may result in the malignant transformation of hepatocytes by some directly oncogenic mechanism, whereas other necroinflammatory conditions probably predispose to the development of HCC through the introduction of genetic alterations coupled with a reduction of genetic repair functions. Screening patients at risk for the development of HCC using alpha fetoprotein measurements and ultrasonography is widely practiced despite inconclusive evidence of efficacy. If screening is performed, the program used should be tailored to the perceived risk for a particular patient.
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PMID:Preneoplastic conditions of the liver. 870 61

Hepatocellular carcinoma (HCC) is the most frequent primary cancer of the liver and the most frequent tumour in males, worldwide. The annual incidence of HCC is maximum in Asian and African countries, lower in western countries where it is close to 4/100,000 inhabitants. In 90% of the cases, HCC complicates course of liver cirrhosis, with an annual incidence in cirrhoties of 2 to 6%. Risk factors for HCC in cirrhotics are male gender (sex-ratio: 4/1), age (above 50 years old), macronodular cirrhosis and large cell dysplasia. HCC can complicate the course of cirrhosis of any cause, but might be less frequent in primary biliary cirrhosis, Wilson's disease and auto-immune hepatitis. Currently, the diagnosis of HCC is usually considered in the presence of a focal nodular lesion, during systematic ultrasonographic examination of the liver. In high incidence areas, HCC can still be diagnosed because of HCC-related symptoms. In the case of a focal lesion discovered on a cirrhotic liver, the diagnosis of HCC can be confirmed by studying the behaviour of the lesion of helical CT scan of the liver (enhancement of the tumour during the arterial phase) or MRI (hyperintensity of the tumour on T2 relaxation time); study of peritumour vessels can also be helpful. Serum alpha-foeto-protein level, when higher than 300 to 500 micrograms/L is very specific of HCC. When aggressive treatment of HCC is considered and when the diagnosis of HCC remains uncertain, HCC can be assessed by means of cytological or histological study of the tumour on samples taken by fineneedle aspiration (80% sensitivity) or liver biopsy during laparoscopic laparotomy. Forthcoming improvements in imaging technology might eliminate the need for such invasive diagnostic techniques in the future.
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PMID:[Epidemiology and diagnosis of hepatocellular carcinomas in cirrhosis]. 975

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

Although primary sclerosing cholangitis (PSC) is not a common disease, it is important in the differential diagnosis of hepatobiliary tract diseases in clinical practice. A diagnosis of PSC should be made only after the exclusion of similar diseases with well known etiologies or pathogeneses. In this review, the pathology of classical PSC and its variants or related diseases is highlighted. PSC is histologically characterized by progressive periductal fibrosis with luminal stenosis or obliteration, along with the formation of a fibrous core, as well as dilatation (cholangiectasis). Its etiology is unknown. Bacterial ascending cholangitis is superimposed on its long clinical course. Such a heterogeneous distribution of biliary lesions with biliary obliteration and cholangiectasis is responsible for the radiological demonstration of biliary abnormalities, particularly the beaded appearance. Sampling variability is common in needle or wedge biopsied specimens. As a result of biliary damage, the liver shows progressive cholestatic change followed by biliary fibrosis and cirrhosis, and this hepatic progression is divisible into four stages. There are several variants of PSC or related diseases, such as localized biliary sclerosis and stenosis, sclerosing cholangitis associated with inflammatory pseudotumor, and PSC-autoimmune hepatitis overlapping syndrome. Cholelithiasis, including secondary hepatolithiasis and, to a lesser degree, biliary carcinoma and dysplasia, are also known to develop at the perihilar bile ducts as a late complication of PSC.
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PMID:Definition and pathology of primary sclerosing cholangitis. 1066 78

Fifty three consecutive cases of chronic hepatitis C ("b" series) were considered and strictly (numerically and qualitatively) compared with the series ("a") reported by Scheuer et al. Two groups (gr.) respectively inclusive of chronic persistent hepatitis, chronic lobular hepatitis and mild/moderate chronic active hepatitis (gr. I) and severe chronic active hepatitis, developing cirrhosis and established cirrhosis (gr. II) were identified, studied and scored according to the following accessory histological parameters: "lymphoid aggregates and follicles" (LA&F), "bile duct damage" (BDD), "acidophil bodies" (AB), "lymphocytic infiltration of sinusoids" (LIS) and "fatty changes" (FC). In order to interpret the results the "b" series was further examined in relation to lobular "spotty necrosis" (SN) and subtle morphology of FC (type of vacuolarity and topography). Moreover dysplasia (in "a" and "b") and other minor accessory parameters (in "b" only) were briefly considered. In conclusion the comparison of "b" versus "a" confirms a characteristic histomorphological pattern in chronic hepatitis C. As far as the major accessory parameters are concerned the reproducibility was acceptable for BDD and FC, but inadequate for LA&F, LIS and AB. In particular the following points seem to be the most critical challenges: reassessment of the morphological criteria for LA&F, LIS and AB; improvement of the analysis of FC; elucidation of the relation between LIS, AB, SN and LA&F; ascertainment of sensibility and specificity of the accessory parameters in relation to "grading", "staging", differential diagnosis, post-therapy evaluation and non histological findings.
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PMID:[Accessory parameters in the histopthology of hepatitis C. Comparative analysis]. 1084 95

Liver biopsy interpretation continues to play an integral role in diagnosis and management of most forms of liver disease. In this review, the common histopathologic features of the more commonly encountered processes, chronic hepatitis, autoimmune hepatitis, and chronic cholestatic liver diseases, are discussed. In addition, areas of ongoing investigation and controversy, including steatohepatitis and dysplasia, are reviewed. Finally, the pathology of adult metabolic liver disease, drug-induced liver disease, and various miscellaneous disease processes, including venous outflow obstruction, acute fatty liver of pregnancy, and fulminant hepatic failure, are reviewed.
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PMID:Liver biopsy interpretation for the gastroenterologist. 1098 Oct

Two sibs with an infantile onset of hyperglycemia, recurrent hepatitis, renal insufficiency, developmental delay, and skeletal epiphyseal dysplasia are described. Clinical presentation and radiological features are suggestive of Wolcott-Rallison syndrome, a rare autosomal recessive disease. In both of our cases we found evidence of central hypothyroidism, which appears to be an associated feature of this syndrome. Hypothyroidism should be suspected and screened for in all cases of Wolcott-Rallison syndrome.
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PMID:Wolcott-Rallison syndrome in two siblings with isolated central hypothyroidism. 1221 Mar 48

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare autosomal recessive disorder, which is characterized by an immune-mediated destruction of endocrine tissues, chronic candidiasis and ectodermal disorders. In contrast to many other autoimmune diseases, APECED is associated with mutations of a single gene, designated autoimmune regulator (AIRE). We describe an APECED patient with severe deformities of the tibia with radiological signs of metaphyseal dysplasia in addition to candidiasis, hepatitis, diabetes mellitus and adrenal failure. In this patient, we identified a novel AIRE mutation in association with the C322fsX372 mutation in exon 8, which is frequently detected in Caucasian patients. The frame shift mutation G263fsX377 in exon 6 results in a protein lacking both PHD zinc-finger domains similar to the R257 X mutation. This novel mutation was not found in 50 German controls.
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PMID:A novel AIRE mutation in an APECED patient with candidiasis, adrenal failure, hepatitis, diabetes mellitus and osteosclerosis. 1278 92

Helicobacter hepaticus infection of A/JCr mice is a model of infectious liver cancer. We monitored hepatic global gene expression profiles in H. hepaticus infected and control male A/JCr mice at 3 months, 6 months, and 1 year of age using an Affymetrix-based oligonucleotide microarray platform on the premise that a specific genetic expression signature at isolated time points would be indicative of disease status. Model based expression index comparisons generated by dChip yielded consistent profiles of differential gene expression for H. hepaticus infected male mice with progressive liver disease versus uninfected control mice within each age group. Linear discriminant analysis and principal component analysis allowed segregation of mice based on combined age and lesion status, or age alone. Up-regulation of putative tumor markers correlated with advancing hepatocellular dysplasia. Transcriptionally down-regulated genes in mice with liver lesions included those related to peroxisome proliferator, fatty acid, and steroid metabolism pathways. In conclusion, transcriptional profiling of hepatic genes documented gene expression signatures in the livers of H. hepaticus infected male A/JCr mice with chronic progressive hepatitis and preneoplastic liver lesions, complemented the histopathological diagnosis, and suggested molecular targets for the monitoring and intervention of disease progression prior to the onset of hepatocellular neoplasia.
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PMID:Hepatic temporal gene expression profiling in Helicobacter hepaticus-infected A/JCr mice. 1551 11

Hepatitis C infection is associated with the development of hepatocellular carcinoma, and progress has been made in a number of areas. Transgenic mice lines expressing the hepatitis C core protein develop hepatic steatosis, adenomas, and hepatocellular carcinomas, with no significant hepatitis or fibrosis. This implies that hepatitis C can lead directly to malignant transformation. A new lesion, irregular regeneration, has been described in chronic hepatitis C infection and is associated with a 15-fold increase in the relative risk of developing hepatocellular carcinoma. A minority of patients with hepatitis C-related hepatocellular carcinoma have intense lymphocytic infiltration of the cancer, a feature associated with a better prognosis. Several studies have confirmed the association between large cell dysplasia and hepatocellular carcinoma. However, large cell dysplasia may not be a premalignant lesion and instead may be a marker for premalignant alterations elsewhere in the liver. Oral contraceptives previously have been linked to an increased risk of hepatocellular carcinoma. A large multicenter European case-control study has shown minimal increased risk of hepatocellular carcinoma with use of steroidal contraception. Tamoxifen had shown promise in the management of advanced hepatocellular carcinoma. However, a randomized placebo-controlled study of 477 patients with hepatocellular carcinoma found no benefit from tamoxifen. In a preliminary study, however, octreotide has shown improved survival and quality of life in patients with advanced hepatocellular carcinoma. Finally, interferon treatment continues to be linked to a reduced risk of hepatocellular carcinoma in patients with hepatitis C. These studies generally are not randomized, and a randomized prospective study is required to address this issue.
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PMID:Hepatocellular carcinoma. 1702 53


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