Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The identification of the Hepatitis C virus using molecular cloning techniques, besides making the term Non-A Non-B Hepatitis obsolete, enables the development of specific assays for the detection of antibodies in HCV-infected individuals, thus making it possible to obtain sero-epidemiological data of the disease. The carriage of Hepatitis C antibody varies worldwide. The disease is most prevalent in intravenous drug abusers or haemophiliacs. Parenteral transmission is the most important route of transmission. Sexual, intra-familial and perinatal transmissions are uncommon. About 40% could be community-acquired (sporadic). Diagnostic tests include enzyme-linked immunosorbant (ELISA) anti-HCV assay, recombinant immunoblot assay, HCV-RNA by polymerase chain reaction and HCV-Ag. More than 50% of acute cases becomes chronic and runs a benign and indolent course. About 20% progress to cirrhosis and some of these develop hepatocellular carcinoma. Several published trials have consistently shown that treatment with interferon in some patients is useful. There is however a relapse rate of 50%. Further trials with interferon and other anti-viral agents like ribavirin are awaited for more effective treatment.
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PMID:Hepatitis C: an update. 128 40

Alpha-fetoprotein (AFP) is a specific glycoprotein which is synthesised in the fetal liver and released into the blood stream together with the closely related protein, albumin. It has been proposed that AFP functions as a carrier of essential fatty acids to certain developing cells and as a possible immunosuppressor. In man its synthesis is under the strict and complicated control of transcription of a single gene on chromosome 4. The concentration of AFP in fetal serum is greatest at about 13 weeks gestation and then decreases up to birth. During pregnancy AFP passes into the amniotic fluid and also across the placenta, so that the concentration of AFP in maternal serum increases during pregnancy in a characteristic way. Greater than normal increases may indicate certain pathological states in the fetus. Serum concentrations of AFP in the newborn infant decrease rapidly to reach levels typical for adults (< 10 micrograms/L) usually by the end of the first year. Raised concentrations of serum AFP appear in a large proportion of patients with primary hepatoma and in a smaller percentage of patients with other malignant diseases (tumours of the testis, ovary, bronchi, gastrointestinal tract). In addition, increases in serum AFP are found in other illnesses accompanied by damage to hepatocytes in the liver (hepatitis, cirrhosis etc.). Certain differences in the structure of the oligosaccharide portion of the molecule have been shown between AFP synthesized by benign or by malignant cells and between AFP synthesised by hepatocytes or by cells of endodermal origin. These differences have been used as an aid in the diagnosis of liver diseases where serum AFP is elevated. Since AFP is not strictly specific for a certain type of carcinoma, its determination is primarily used in medicine for monitoring the effects of therapy and surgery on the course of malignant conditions which initially showed increased levels of serum AFP.
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PMID:[Synthesis, structure and function of alpha-fetoproteins and their importance in medicine]. 128 28

Since the detection of hepatitis B virus (HBV) in the 1960s and hepatitis A virus in the 1970s, a considerable proportion of infections of (probably viral) hepatitis could not be classified. About 90% of transfusion-related hepatitis was identified as non-A/non-B. In 1988 investigators from the Chiron Company (USA) detected the non-A, non-B agent and named it hepatitis C virus (HCV). An anti-HCV antibody assay (ELISA) and subsequently confirmation tests (immunoblot and polymerase chain reaction) were developed. HCV infection results in a chronic carrier state of the virus in about 80%. Almost all HCV carriers have, irrespective of their liver function tests, histologic signs of chronic hepatitis and/or liver cirrhosis. Chronic HCV infection is, like HBV, also associated with the development of hepatocellular carcinoma. Most HCV carriers are infected by parenteral routes (intravenous drug use, blood transfusion, tattooing). Intravenous drug users and haemophilia patients have the highest risk (80-90%) of becoming infected. Sexual and perinatal transmission does not play an important role in spreading the infection. Antiviral therapy (alpha-interferon) in patients with chronic hepatitis C will normalize liver function tests in about 25% of the cases, but it is unclear if the HCV carrier state will disappear and if liver cirrhosis will be prevented. At present no specific immunoglobulin or vaccine preparations are available to prevent the HCV infection.
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PMID:New developments in hepatitis C. 129 54

Many tests for hepatitis C virus (HCV) infection have been developed and have proved useful for prevention of post-blood transfusion hepatitis C. However, there are at least 4 genotypes of HCV and the predominant type is different among countries. None of the tests using antigens from one genotype are sensitive in detecting the antibodies against another genotype. More sensitive tests using a more stable part of the HCV RNA sequences such as 5'-noncoding region must be developed for clinical use. Automated PCR methods and DNA sandwich hybridization methods using branched DNA amplification multimers may be candidates. Recently a hepatocyte growth factor test has been developed in Japan. Multicenter trials of this test reveal that it is useful for assessment of acute severe hepatitis. Tests for collagen type IV, fibronectin receptor, and prolyl hydroxylase have been reported useful for assessment of liver fibrosis. However, serum prolyl hydroxylase is prone to increase in response to hepatocellular damage as well as fibrotic processes. Enzymatic methods for determination of branched amino acids and tyrosine have been developed. The molar ratio of branched amino acids to tyrosine seems to have same pathophysiological meaning as the ratio of branched amino acids to aromatic amino acids (Fischer ratio) in assessment of liver cirrhosis. Lidocaine test is reported to be useful for predicting survival of transplanted liver and also assessing the function of the cirrhotic liver. Profiles of alpha-fetoprotein subfractions based on lectin-reactivity and galactosyl transferase II isoenzyme have been reported to be useful for detecting hepatocellular carcinoma but this remains to be proved.
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PMID:[Recent advances in laboratory tests for liver diseases]. 130 30

To evaluate the role of hepatitis C virus (HCV) in Chinese patients with hepatocellular carcinoma (HCC), the antibodies to HCV (anti-HCV) were detected by enzyme immunoassay in 41 (12.6%) of the 326 patients with HCC. However, none of 35 patients with metastatic carcinoma of the liver had detectable anti-HCV. The prevalence of anti-HCV was significantly higher in patients with hepatitis B surface antigen (HBsAg)-negative HCC than those with HBsAg-positive HCC (37.3% versus 4.1%, P less than 0.0001). However, the prevalence of anti-HCV was much higher in patients with HCC with negative results for HBsAg and antibody to hepatitis B core antigen (54.5%). The mean age of patients with HCC with positive results for anti-HCV was significantly greater than that of patients with HBsAg-positive HCC (65.1 versus 55.5 years, P less than 0.0001). Alpha-fetoprotein levels greater than 20 ng/ml were found in 70.7% of patients with HCC with positive results for anti-HCV and in 73.3% of patients with HBsAg-positive HCC. Of the Chinese patients with HCC, 74.5% had HBsAg-positive results and 96.6% had positive results for antibody to hepatitis core antigen. These data indicate that, although HCV may play an etiologic role in HCC, hepatitis B virus is still the most important causal agent among most Chinese patients with HCC.
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PMID:The prevalence of anti-hepatitis C virus among Chinese patients with hepatocellular carcinoma. 130 28

We compared four primer sets from conserved regions of the hepatitis C virus (HCV) genome for their ability to detect HCV RNA in a "nested" cDNA polymerase chain reaction assay on sera from 114 anti-HCV antibody-positive individuals from around the world. The different primer sets had equivalent sensitivity, detecting less than 1 chimpanzee ID50 (dose that infects 50%) when tested against reference strain H of HCV. We tested equal amounts of RNA extracted from the serum of each individual with the four primer sets. The set derived from two highly conserved domains within the 5' noncoding (NC) region of the HCV genome, which also share significant similarity with Pestivirus 5' NC sequences, was the most effective at detecting HCV RNA. All samples positive for HCV RNA with any other primer set were also positive with the primer set from the 5' NC region, and the latter was at least 3 times more likely to detect HCV infection than a primer set from within the nonstructural protein 3-like gene region (P less than 0.001). We had no false positive results in greater than 500 negative controls interspersed among the test samples. The 5' NC region primer set detected HCV-specific RNA, verified by high-stringency Southern blot hybridization and DNA sequencing, in 100% of 15 acute and 33 chronic non-A, non-B hepatitis patients from the United States, Europe, and Asia and 10 hepatocellular carcinoma patients from Africa and Asia that tested negative for the hepatitis B virus-encoded surface antigen. In conclusion, use of an appropriate primer set is crucial for detecting HCV RNA in the serum of infected individuals.
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PMID:Importance of primer selection for the detection of hepatitis C virus RNA with the polymerase chain reaction assay. 130 4

Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas from southern Africa and Qidong in China. To test this hypothesis, nine tumors induced by aflatoxin B1 in nonhuman primates were analyzed for mutations in the p53 gene. These included four hepatocellular carcinomas, two cholangiocarcinomas, a spindle cell carcinoma of the bile duct, a hemangioendothelial sarcoma of the liver, and an osteogenic sarcoma of the tibia. None of the tumors showed changes at the third position of codon 249 by cleavage analysis of the HaeIII enzyme site at codon 249. A point mutation was identified in one hepatocellular carcinoma at the second position of codon 175 (G to T transversion) by sequencing analysis of the four conserved domains (II to V) in the p53 gene. These data suggest that mutations in the p53 gene are not necessary in aflatoxin B1 induced hepatocarcinogenesis in nonhuman primates. The occurrence of mutation in codon 249 of the p53 gene in selective samples of human hepatocellular cancers may indicate involvement of environmental carcinogens other than aflatoxin B1 or that hepatitis B virus-related hepatitis is a prerequisite for aflatoxin B1 induction of G to T transversion in codon 249.
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PMID:Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates. 131 Jun 37

To clarify the relationship between hepatitis C virus (HCV) infection and hepatocellular carcinoma (HCC), frozen serum samples from 213 patients with histologically proven liver cirrhosis alone (96 alcoholics, 59 HBsAg positive, 29 non-A, non-B hepatitis, 29 cryptogenic) and 40 patients with liver cirrhosis and HCC (12 alcoholics, 7 HBsAg positive, 7 non-A, non-B hepatitis, 14 cryptogenic) were analyzed for antibodies to hepatitis C virus (anti-HCV) with the ortho-HCV-ELISA. The results were as follows. 50 of 253 (20%) patients were anti-HCV positive. The prevalence of anti-HCV was significantly higher in patients with HCC than in patients without HCC (14 of 40 [35%] vs 36 of 213 [17%]; p less than 0.001). In anti-HCV-positive patients HCC were significantly more frequent than in anti-HCV-negative patients (14 of 50 [28%] vs 26 of 203 [13%]; p less than 0.001). The significantly higher occurrence of HCC in anti-HCV-positive patients was not related to other known risk factors such as alcoholism or chronic hepatitis B virus (HBV) infection. Patients with HCV infection as the only risk factor also had a significantly higher occurrence of HCC (12 of 38 [32%] vs 26 of 203 [13%]; p less than 0.001). Our data suggest that chronic HCV infection plays an important role in the pathogenesis of HCC, in particular in patients with cirrhosis unrelated to alcohol or HBV infection.
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PMID:[Hepatitis-C virus and hepatoma]. 131 Nov 25

A 57 year old man with auto-immune chronic active hepatitis, regularly treated with immunosuppressive therapy, had hepatocellular carcinoma (HCC) 10 years after diagnosis of the hepatitis. Assays of the hepatitis C virus antibodies against capsid and non-structural proteins revealed seronegativity in serial serum samples of this patient stored in the previous 10 years during follow up. The seronegative hepatitis C antibodies excluded hepatitis C virus as the cause of the HCC. The occurrence of HCC in this case suggests the necessity of surveillance for early detection of liver cancer in patients with auto-immune chronic active hepatitis undergoing long-term immunosuppressive therapy.
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PMID:Development of hepatocellular carcinoma in a man with auto-immune chronic active hepatitis. 131 68

Serum and urinary neopterin levels were measured by radioimmunoassay in 120 healthy controls, 16 asymptomatic HBsAg carriers, 12 patients with acute hepatitis, 13 with chronic inactive hepatitis, 35 with chronic active hepatitis, 46 with liver cirrhosis, 18 with hepatocellular carcinoma, and 6 with alcoholic liver disease. Serum and urinary neopterin levels were significantly higher in almost all patients than in normal subjects. Neopterin levels were highest in acute hepatitis and correlated with the results of liver function tests, but did not show this correlation in chronic liver disease. In chronic liver disease, the levels of serum neopterin in non-A non-B viral patients was significantly increased, compared with those in B viral and alcoholic patients. The rate of abnormal urinary neopterin levels in chronic liver disease was higher than the rate of abnormal serum neopterin levels, but no difference was observed between the rates of abnormal serum and urinary levels in acute hepatitis and asymptomatic HBsAg carriers. These results indicate that serum and urinary neopterin levels may be useful markers for cell-mediated immunity in liver disease, and that the immune system response in chronic liver disease may be different for different pathogens.
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PMID:Clinical significance of serum and urinary neopterin levels in patients with various liver diseases. 131 6


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