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)

The sex-specific and age-specific incidence rates of the major parenchymal liver diseases in a North European population were estimated using a computerized registry of all admissions to somatic hospitals in Denmark. The incidence was calculated by counting all incident cases of these diseases reported to the registry in the 5-yr period 1981 to 1985 and dividing the number of cases by the number of person-years at risk in this period. The incidence rates (per million person-years) were for men and women, respectively: infectious hepatitis, 109 and 71; toxic hepatitis, 19 and 22; chronic hepatitis, 27 and 29; alcoholic cirrhosis, 190 and 85; nonalcoholic nonbiliary cirrhosis, 110 and 82; primary biliary cirrhosis, 4 and 14. The pattern of the age-specific incidence rates was similar in men and women in infectious hepatitis, alcoholic cirrhosis, nonalcoholic nonbiliary cirrhosis and primary biliary cirrhosis. Toxic and chronic hepatitis had a higher incidence in women than in men only in older age groups. The incidence of idiopathic hemochromatosis, Wilson's disease, secondary biliary cirrhosis, portal vein thrombosis and Budd-Chiari's syndrome were less than four in both sexes.
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PMID:Incidence of parenchymal liver diseases in Denmark, 1981 to 1985: analysis of hospitalization registry data. The Danish Association for the Study of the Liver. 201 Jan 59

The various forms of chronic and acute hepatitis are today exclusively diagnosed by serological tests, since clinical criteria do not permit exact classification of a specific hepatitis type. This contribution deals with the most important serological findings relating to the acute forms of viral hepatitis "in the strict sense" - hepatitis A (HA), hepatitis B (HB), hepatitis D (HD) and hepatitis C (HC). The serological markers for chronic active hepatitis B (CAH-B), chronic hepatitis C (CAH-C), primary active biliary cirrhosis (PBC) and the auto-immune forms of chronic hepatitis (AIH) are also discussed.
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PMID:[Serological studies in acute, chronic and autoimmune hepatitis]. 204 29

Always take a full travel, drug and contact history in any patient presenting with jaundice. All drugs should be suspected as potential hepatotoxins. With hepatitis A the presence of IgM antibodies reflects recent infection, and IgG antibody indicates past infection and lifelong immunity. There is no chronic carrier state of hepatitis A and E. All patients with jaundice should be tested for hepatitis B surface antigen (HBsAg). Hepatitis B infection is usually benign and short lived, but it can be fatal if chronic hepatitis develops, which may lead later to cirrhosis and hepatocellular carcinoma. Up to 5 to 10 per cent of patients with hepatitis B will become chronic carriers (especially drug addicts and homosexuals). Such carriers are identified by persistent titres of HBsAg and possibly HBeAg, the latter indicating the presence of the whole virus and active replication and high infectivity. A raised gamma glutamyl transferase accompanied by a raised MCV is a good screening test for alcohol abuse.
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PMID:Jaundice. 204 97

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

Twenty-six patients with the Budd-Chiari syndrome were treated surgically at the Johns Hopkins Hospital. Twenty-one of the patients were female and five were male, with a median age at diagnosis of 37 years. Nine patients had polycythemia vera, 6 were receiving estrogen therapy, 5 had a previous hepatitis A or B infection, and 4 had cirrhosis. There was one case each of hepatic malignancy, paroxysmal nocturnal hemoglobinuria, and idiopathic thrombocytopenic purpura. In five cases no etiologic factors or associated disorders were identified. Ascites was the most common presenting feature in this group of patients. Hepatic function at the time of diagnosis, as measured by standard serum chemistries, was only minimally abnormal. The diagnosis of the Budd-Chiari syndrome was confirmed in all 26 patients by hepatic vein catheterization. Inferior vena cavography was also performed and revealed caval occlusion in 4 patients, significant caval obstruction in 13 patients, and a normal vena cava in 9 patients. Interpretation of the vena cavogram was helpful in selecting the appropriate surgical procedure for each patient. Twenty-three of the twenty-six patients underwent percutaneous liver biopsy before operation, with no morbidity or mortality. Four patients had well-established cirrhosis noted on biopsy. Thirty mesenteric-systemic venous shunts were performed on the 26 patients. In 11 patients a mesocaval shunt was performed and in one instance conversion to a mesoatrial shunt was required as a second procedure. In 15 patients a mesoatrial shunt was performed as the initial procedure. Graft thrombosis occurring in 2 of these 15 patients prompted one revision in 1 patient and 2 revisions in the second patient. After mesenteric-systemic venous shunt, eight of the patients (31%) died before discharge from the hospital. The remaining 18 patients in this series were discharged from the hospital alive and well with patent shunts. Patients were followed for a median of 43 months (range, 9 months to 13 years). Five late deaths occurred between 5 and 84 months after the operation. Three- and five-year actuarial survival rates were 65% and 59%, respectively.
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PMID:Current management of the Budd-Chiari syndrome. 200 20

Plasma concentrations of tissue-type plasminogen activator (t-PA), urokinase (u-PA), plasminogen activator inhibitor 1 (PAI-1) and PAI-2 were studied in 53 patients with liver deficiency caused by chronic alcoholism (n = 40), viral hepatitis (n = 10) or malignant disease of the liver (n = 3) and compared to that of a control group (n = 20) of healthy subjects. u-PA and PAI-1 levels were significantly increased in all patients with chronic alcoholism, whereas high t-PA was only observed in combination with disturbed liver function tests or with liver cirrhosis (two and six-fold above control values, respectively). A good correlation was observed between t-PA and gamma glutamyl transferase (r = 0.615; p less than 0.001). In patients with infectious hepatitis or with malignant disease of the liver t-PA was normal whereas u-PA and PAI-1 were increased. PAI-2 levels were close to or below the detection limit (15 ng/ml) in the control group and in most patients. However, in two patients with alcohol induced cirrhosis PAI-2 levels were approximately 45 ng/ml and in one patient with hepatocarcinoma even 66 ng/ml. Thus, in liver disease, marked elevations of t-PA, u-PA and PAI-1 levels may occur, with increased PAI-1 as an early marker of liver defects and t-PA a marker of severe liver defects.
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PMID:Plasminogen activators and plasminogen activator inhibitors in liver deficiencies caused by chronic alcoholism or infectious hepatitis. 251 Mar 45

We describe a 27-year-old woman who presented with infertility, and over the subsequent 7 years developed chronic Epstein-Barr virus infection, hepatitis A, cirrhosis and nasopharyngeal carcinoma. Serological evidence of chronic infection with Chlamydia, Epstein-Barr virus and hepatitis A virus was documented.
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PMID:Chronic infection with Epstein-Barr virus, Chlamydia and hepatitis A virus, terminating in cirrhosis and nasopharyngeal carcinoma. 254 39

Markers of hepatitis A and B virus were tested in 88 adult Sudanese subjects in Khartoum, Sudan. The subjects consisted of 25 control hospitalized patients, 21 volunteer blood donors, 23 patients with hepatosplenic schistosomiasis, 13 patients with liver cirrhosis and 6 patients with hepatocellular carcinoma (HCC). Antibody to hepatitis A virus was detected in 96% of the total. Hepatitis B surface antigen (HBsAg) was positive in 4, 24, 22, 31, and 67% of the subject groups, respectively. Antibody against hepatitis B core antigen (HBcAb) of undiluted serum was positive in 60, 57, 65, 77 and 83%, and there was no difference in incidence among the groups. It was positive in 200X diluted serum in 4, 24, 17, 23 and 60%. HBsAg and HBcAb (200X) were detected more often in HCC patients than in the control subjects (p less than 0.01). Hepatitis B virus is an important factor in the etiology of HCC in the Sudan.
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PMID:Hepatitis B virus markers in patients with schistosomiasis, liver cirrhosis and hepatocellular carcinoma in Khartoum, Sudan. 255 52

Hepatitis non-A, non-B (HNANB) is due to one or more transmissible agents, probably viruses. Epidemiologically, HNANB is transmitted predominantly by transfusion of blood or plasma derivatives, and percutaneous inoculation, but a non-percutaneous transmission by the fecal-oral route is also established. However, despite 10 years of intense world-wide research, the transmissible agent, or agents, have not been identified and there are no serological assays for either an antigen or an antibody that can be used to detect this infection. The clinical diagnosis of HNANB remains, therefore, a diagnosis of exclusion mainly of hepatitis A and B, Epstein-Barr virus, cytomegalovirus and drug-induced liver disease. In contrast to hepatitis A and B, the clinical and biochemical course of HNANB tends to be less severe and the proportion of asymptomatic and anicteric cases is higher, but fulminant hepatitis and fatalities also occur. Typically, there is a fluctuating waxing and waning pattern of the serum aminotransferase activities in HNANB. HNANB has a relative high tendency to progress to a chronic stage. The exact frequency of HNANB-induced liver cirrhosis and convincing evidence for an association with hepatocellular carcinoma cannot be assessed, although the persistence of the infectious agent in chronic HNANB and the existence of a chronic asymptomatic carrier state have been proved. By light microscopy there is a broad morphologic spectrum of acute and chronic viral hepatitis, but no single pathognomonic lesion exists that allows a reliable distinction to be made of HNANB from hepatitis A and B. Electron microscopy of liver biopsy specimens of chimpanzees, experimentally infected with HNANB agents, permits the visualisation of cytoplasmic changes, which appear to be specific for infection with HNANB viruses. In human liver biopsy specimens from patients with HNANB, identical ultrastructural cytoplasmic changes could not consistently be demonstrated. In contrast, intranuclear aggregates of spherical and tubular particles measuring 20-29 nm, first described in experimental HNANB in chimpanzees, have been repeatedly demonstrated in acute and chronic HNANB in man. These nuclear particles have been considered as compelling evidence of human HNANB infection. The specificity has been challenged, however, by the demonstration of identical particles in other viral and non-viral hepatopathies and in liver biopsies of healthy volunteers. By immune electron microscopy, a multiplicity of virus-like particles are described in association with HNANB.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Hepatitis non-A, non-B: epidemiologic, clinical, serologic and morphologic aspects]. 258 79


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