Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent advances in epidemiology, virology, of clinical of hepatitis are presented in the paper. The authors pointed out that hepatitis A never becomes chronic. On the other hand, with hepatitis B or B and D, evolution to chronicity is possible. Two distinct forms of non-A non-B hepatitis are now distinguished: parenterally transmitted non-A non-B hepatitis, mainly due to hepatitis C virus; enterically transmitted non-A non-B hepatitis mainly due to hepatitis E virus. C virus hepatitis is characterized by a frequent course to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Chronic forms are associated with the presence of anti-HC antibodies in the serum. These antibodies are rarely present in the acute stage of the disease. Hepatitis E is almost exclusively encountered in developing countries. Like with A virus hepatitis, chronicity never occurs. However, fulminant hepatitis is possible in pregnant women in the third trimester of pregnancy. There is no routine serological test. Development of vaccines against A, E and C viruses can be expected very soon. There is no specific treatment of acute viral hepatitis.
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PMID:[Acute viral hepatitis--present status and perspectives]. 136 29

Two distinct forms of non A non B viral hepatitis are now distinguished: (a) parenterally transmitted non A non B hepatitis, mainly due to hepatitis C virus, (b) enterically transmitted non A non B hepatitis, mainly due to hepatitis E virus. Hepatitis C virus is an enveloped, 50 to 60 nm in diameter, single stranded RNA virus. Its transmission is essentially parenteral and resembles that of hepatitis B virus. Individuals at risk are those in contact with blood products. Sexual transmission is uncommon. C virus hepatitis is characterized by a frequent course to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Fulminant hepatitis is rare. Chronic forms are associated with the presence of anti-HCV antibodies in the serum. These antibodies are rarely present in the acute stage of the disease. Hepatitis E virus is a non-enveloped, 30 nm in diameter, single stranded RNA virus. Its transmission is faecal-oral, thus similar to that of hepatitis A virus. The disease is almost exclusively encountered in developing countries. It is not observed in France, apart from imported cases. Like A virus hepatitis, chronicity never occurs. Fulminant hepatitis is possible in pregnant women in the third trimester of pregnancy. There is no routine serological test. Development of vaccines against these two viruses can be expected.
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PMID:[Non-A non-B acute hepatitis]. 211 1

Hepatitis may be caused by hepatitis A virus, hepatitis B virus, hepatitis C virus (classic non-A non-B viral hepatitis), hepatitis D virus (delta agent), and hepatitis E virus (epidemic non-A non-B viral hepatitis). Cytomegalovirus, Epstein-Barr virus, and herpes simplex virus may also occasionally cause hepatitis. Some forms of hepatitis carry the risks of chronic infection, cirrhosis, or hepatocellular carcinoma. Treatment options for viral hepatitis are limited and, in many cases, still under investigation. Prophylaxis is available for many forms of hepatitis and should be offered to those at risk.
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PMID:Viral hepatitis. The new ABC's. 212 Jun 86

A total of 200 consecutive patients bearing histologically confirmed primary hepatocellular carcinoma (PHC) were studied at University of Calabar Teaching Hospital (CTH), Calabar, Nigeria in 5 years and compared with 150 patients with metastatic hepatic carcinoma (MHC). Four hundred symptomless non-icteric nontumor-bearing individuals were noncontemporaneous controls. Sera (a total of 750) were assayed for markers of hepatitis B virus (HBV) infection; hepatitis B surface antigen (HBsAg), hepatitis B core antibody (anti-HBc), and hepatitis B surface antibody (anti-HBs). Specimens which were positive for HBsAg also were examined for hepatitis E antigen (HBeAg) and antibody (anti-HBe). The results show that PHC was associated with HBV seropositivity in 80% of patients, and postnecrotic (macronodular) cirrhosis of the liver in 90% clearly indicating a strong association between primary liver cancer and HBV infections and liver cirrhosis. The main factor associated with seropositivity among normal controls was a large number of therapeutic injections. Seropositives received over twice as many injections as seronegatives. Public health measures are urgently required to prevent parenteral transmission of HBV in Nigeria.
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PMID:Hepatocellular carcinoma, hepatic cirrhosis, and hepatitis B virus infection in Nigeria. 282 23

The association between viral hepatitis and pregnancy is not common, nevertheless it has been described that hepatitis is the most frequent cause of jaundice in pregnant women. In this article the current knowledge on the perinatal repercussions of the different types of viral hepatitis are reviewed. Hepatitis A is rare during pregnancy and is not associated with perinatal risk. Hepatitis B virus (HBV) can be transmitted transplacentally, 20 per cent of the children infected by this route will develop liver cirrhosis or carcinoma in the adult age, so the infants of HBsAg carrier mothers must be immunized at born. The perinatal transmission of hepatitis C virus has been proved but the repercussion in the fetus or newborn is unknown. Hepatitis D virus can only be transmitted from mother to child together with HBV. Hepatitis E has been associated with a mortality of 10 to 40 per cent in pregnant women.
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PMID:[The behavior and perinatal impact of viral hepatitis in pregnancy]. 771 69

Viral causes of acute or chronic hepatitis are the hepatitis A virus [HAV], the hepatitis B virus [HBV], the hepatitis C virus [HCV], the hepatitis delta virus [HDV], and the hepatitis E virus [HEV]. These viruses haven been characterized in great detail and can be detected by specific and sensitive serological or molecular assays. While HAV and HEV cause only acute hepatitis, infection with HBV, HCV or HDV frequently takes a chronic course. With time chronic viral hepatitis can progress to liver cirrhosis and its clinical sequelae as well as to hepatocellular carcinoma [HCC]. Apart from prophylactic measures aimed at the prevention of these viral infections, for those chronically infected natural or recombinant alpha-interferon may be a therapeutic option with the potential to prevent the development of liver cirrhosis and HCC.
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PMID:[Viral hepatitis A to E--diagnosis, clinical aspects and therapy]. 794 Apr 9

The prevalence of serum antibodies to hepatitis C virus was assessed by an enzyme-linked immunosorbent assay in patients with epidemic non-A, non-B hepatitis (14), sporadic non-A, non-B hepatitis (42), chronic hepatitis (14) and cirrhosis (26). None of the patients with epidemic non-A, non-B hepatitis (14) and acute self-limiting sporadic non-A, non-B hepatitis without prior parenteral exposure (38) tested positive for hepatitis C virus antibody. Based on epidemiologic features, hepatitis E virus is presumably the etiologic agent for both these entities. Hepatitis C virus (HCV) antibody was positive in none of the patients with cryptogenic chronic hepatitis (11) and in 2(8%) patients with cryptogenic cirrhosis (25). It was concluded that cryptogenic chronic hepatitis and cirrhosis in India may be caused by alternative viral agents of the non-A, non-B type or by hepatotoxins to which the population may be exposed. Of 8 patients with prior parenteral exposure (transfusions 6, needle pricks 2) 5 (62.5%) patients tested positive for HCV antibody. HCV antibody was detected in 1 (25%) patient with acute self-limiting, parenterally transmitted non-A, non-B hepatitis and in 4 (100%) patients with chronic parenterally transmitted non-A, non-B hepatitis.
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PMID:Hepatitis C virus antibodies in acute and chronic liver disease in India. 838 58

Thanks to progress in serologic techniques evidence was obtained in 1980 showing that acute hepatitis epidemics observed in India were due to neither virus A nor virus B. The presence of another virus was confirmed and its genome was cloned and sequenced in 1991. Hepatitis virus E is a small RNA virus that differs from other known human viruses. Man and probably a few animal species maintain dissemination by the fecal route. Subjects not previously contaminated are susceptible and produce protective antibodies. Contamination occurs by the fecal-oral route general from water or tainted food. Direct contamination is rare. Vertical transmission from mother to fetus can also be observed. Outbreaks of the disease are characterized by epidemic proportions, preferential involvement of adolescent and young adults, and high incidence of fulminant cases especially in pregnant women. Outbreaks have been observed in endemic settings in southern Asia, Africa, and Mexico where sporadic cases are observed. Endemic areas are found in all developing countries. Hepatitis E is not clinically different from other acute viral hepatitis. Asymptomatic forms are common especially in children. The course of the disease is usually benign with little risk of development of chronic symptoms and cirrhosis. However hepatitis E is associated with a high incidence of severe cases with a mortality of 1 to 2% from icteric forms which occur in 15 to 20% of cases involving women contaminated during the last three months of pregnancy. Diagnosis can be made using either synthetic proteins or recombinant peptides. for the epitopes of the virus. Prevention depends on protection of the water supply and proper sewage disposal. Successful active immunization of monkeys holds promise for development of a vaccine. Due to its magnitude and high mortality rate hepatitis E is a major health problem for numerous regions around the world including Southeast Asia.
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PMID:[Viral hepatitis E]. 902 99

Subacute hepatic failure has been a controversial diagnosis ever since it was first identified more than 15 years ago. The Working Committee on Subacute Hepatic Failure has attempted to redefine this entity in which exclusion of preexisting cirrhosis on liver biopsy has been emphasized. Acute viral hepatitis in a patient with asymptomatic chronic liver disease (e.g., hepatitis B or C, Wilson's disease) can be misdiagnosed as subacute hepatic failure in the absence of a liver biopsy. This situation is common in developing countries where the prevalence of feco-orally transmitted (hepatitis A [<20 years] and hepatitis E [>20 years]) and parenterally transmitted (hepatitis B) viruses is high. To obtain and interpret liver biopsy specimens in such a situation is difficult and hazardous, and hence rarely performed. Acute viral hepatitis in a patient with asymptomatic chronic liver disease should be carefully looked for and excluded, especially in developing countries, before a diagnosis of subacute hepatic failure is confirmed.
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PMID:Subacute hepatic failure: diagnosis of exclusion? 956 18

Acute viral hepatitis is the most common cause of jaundice in pregnancy. The course of acute hepatitis is unaffected by pregnancy, except in patients with hepatitis E and disseminated herpes simplex infections, in which maternal and fetal mortality rates are significantly increased. Chronic hepatitis B or C infections may be transmitted to neonates; however, hepatitis B virus transmission is effectively prevented with perinatal hepatitis B vaccination and prophylaxis with hepatitis B immune globulin. Cholelithiasis occurs in 6 percent of pregnancies; complications can safely be treated with surgery. Women with chronic liver disease or cirrhosis exhibit a higher risk of fetal loss during pregnancy. Preeclampsia is associated with HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome, acute fatty liver of pregnancy, and hepatic infarction and rupture. These rare diseases result in increased maternal and fetal mortality. Treatment involves prompt delivery, whereupon the liver disease quickly reverses. Therapy with penicillamine, trientine, prednisone or azathioprine can be safely continued during pregnancy.
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PMID:Liver disease in pregnancy. 1006 7


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