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)

A 55 year-old man was admitted with massive ascites. Although the laboratory data on admission were compatible with hepatic cirrhosis and remarkable esophageal varices were observed during endoscopy, the imaging findings such as computed tomography and ultrasonographic examination did not confirm hepatic cirrhosis. The patient had no history of alcohol abuse, blood transfusions or acute hepatitis. Serological markers related to viral and autoimmune hepatitis were all negative. Seven years ago, the patient had undergone an operation for colon cancer and has been taking tegafur since then for a total of 55 months. Tegafur was suspected as the causative agent for the liver dysfunction of this patient and the administration of tegafur was stopped. His laboratory data improved gradually and the ascites vanished. The first liver biopsy performed 6 months after discontinuation of tegafur still revealed chronic active hepatitis. However, at the liver biopsy performed 18 months after withdrawal of tegafur, inflammatory activity had subsided and the third liver biopsy, performed 34 months thereafter, revealed further improvement of the pathological changes that had occurred in the liver. We therefore conclude that the administration of tegafur may have caused chronic active liver injury with portal hypertension manifested as ascites and esophageal varices.
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PMID:Chronic liver failure induced by long-term administration of tegafur: a case report. 995 26

The sequential development of cirrhosis and hepatocellular carcinoma (HCC) in patients with post-transfusion hepatitis was a clue that led to the identification of hepatitis C virus (HCV) as a risk factor for HCC. The average time lag between transfusion-associated infection and cancer development was 30 years, with a range of 15-45 years. Using the polymerase chain reaction (PCR) technique, HCV-RNA has been almost invariably detected in serum and tumor tissue of anti-HCV-seropositive patients with HCC In many patients, HCV-RNA was found to belong to the more pathogenic type 1b. However, it is unlikely that HCV plays a direct role in liver tumorigenesis, 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: almost all patients with HCC have cirrhosis and up to 30% of them have coexisting serological evidence of hepatitis B virus (HBV) or alcohol abuse, further supporting the idea that both HCC and cirrhosis might result from the interplay of several risk factors. However, there are also data suggesting that HCV may interact with cellular genes regulating cell growth and differentiation independently of the onset of cirrhosis.
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PMID:The role of hepatitis C virus in hepatocellular carcinoma. 1002 14

For reasons not yet determined, chronic liver disease (CLD) has been a leading cause of excess morbidity and mortality in central Harlem. We conducted a case series and case-control analysis of demographic, clinical, epidemiological, and alcohol-intake-related information from patients with CLD and age- and sex-matched hospitalized control patients. Patients' sera were tested for markers of viral hepatitis. The presumed etiology of CLD among case-patients was as follows: both alcohol abuse and hepatitis C virus (HCV) infection, 24 persons (46% of case-patients); alcohol abuse alone, 15 (29%); HCV infection alone, 6 (12%); both alcohol abuse and chronic hepatitis B virus (HBV) infection, 3 (6%); and 1 each (2%) from: 1) schistosomiasis, 2) sarcoidosis, 3) unknown causes, and 4) alcohol abuse, chronic HBV, and HCV combined. In the case-control analysis, patients who had both alcoholism and either HBV (odds ratio [OR]: 6.3; 95% CI: 0. 5-334) or HCV (OR: 2.9; 95% CI: 1.3-6.2) were at increased risk for CLD, whereas patients who had only one of these three factors were not at increased risk for CLD. Patients who tested positive for the hepatitis G virus (HGV) did not have a significantly increased risk of CLD, and neither severity of CLD nor mortality was greater among these patients. Most patients in central Harlem who had CLD had liver damage from a combination of alcohol abuse and chronic viral hepatitis. Alcohol and hepatitis viruses appear to be synergistically hepatotoxic; this synergy appears to explain both the high rate of CLD in central Harlem and the recent reductions in this rate. Persons at risk for chronic HBV and HCV infection should be counseled about their increased risk of CLD if they consume excessive alcohol. Morbidity and mortality from liver disease could be decreased further by a reduction in alcohol consumption among persons who have chronic HBV and HCV infection, avoidance of needle sharing, and hepatitis B vaccination.
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PMID:Chronic liver disease in central Harlem: the role of alcohol and viral hepatitis. 1005 93

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

We evaluated the contribution of alcohol abuse to liver failure among patients undergoing liver transplantation by reviewing their records for alcohol consumption, hepatitis serology, and outcome. Anti-HCV was present in the serum of 42 patients (39%), while 35 had consumed more than 80 g/day of alcohol for at least 10 years, allowing patients to be divided into four groups: group I, hepatitis C alone (N = 31); group II, alcoholic liver disease alone (N = 24); group III, both hepatitis C and alcoholism (N = 11); and group IV, liver failure due to other causes (N = 41). Patients were followed for a mean of 29 months after transplantation (range 0-66). Twenty-eight (26%) died during follow up, while 11 (10%) required retransplantation. There were no other significant differences in patient or graft survival among patients in the four groups. Patients with both alcoholism and chronic hepatitis C comprise a large proportion of those undergoing liver transplantation and appear to do as well as those with other causes of liver failure, at least in the short term.
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PMID:Liver transplantation in patients with chronic hepatitis C and alcoholism. 1054 50

A 28 year old patient developed a severe bullous exanthem and enanthem combined with hepatitis, fever and blood count abnormalities after taking carbamazepine and consumption of heroin and alcohol. After discontinuing carbamazepine, prednisolone was given over a five day period accompanied by intravenous fluid and electrolyte substitution and local therapy which lead to improvement. Severe bullous skin reactions nowadays are classified into erythema exsudativum multiforme majus (EEMM), Stevens-Johnson syndrome (SJS), overlap Stevens-Johnson syndrome-toxic epidermal necrolysis (SJS/TEN), TEN with maculae and TEN on large erythema, and they are most often caused by antibiotics and anticonvulsant drugs. Heroin and alcohol abuse alters host immunity which subsequently may increase susceptibility to allergic reactions. There is a high (40%) mortality rate for TEN, and patients with organ involvement are at increased risk.
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PMID:[Stevens-Johnson syndrome with transition to toxic epidermal necrolysis after carbamazepine administration, heroin and alcohol abuse]. 1066 24

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

69 patients with alcohol addiction infected with hepatitis viruses underwent clinical, laboratory and morphological examinations using light and electron microscopic studies of liver biopsies. Light microscopy revealed three variants of liver damage: viral, alcoholic and mixed. Both etiological factors affect manifestations and course of the disease as shown by electron microscopy in spite of morphological signs of only viral or mixed lesion. The lowest index of histological activity is found in combination alcohol + HCV, the highest index being in patients with HBV + HCV and HBV + HDV. Alcohol abuse in combination with HCV infection increases histological activity of liver damage.
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PMID:[Chronic viral hepatitis and alcoholic liver: clinico-morphological correlations]. 1089 36

Persons with HIV may have previous or concurrent liver impairment as a result of injection drug use, hepatitis, alcohol abuse, and damage from medications. Additional stress is placed on the liver by low-grade opportunistic infections and hemophilia. It is especially important that persons with HIV care for their liver to help this organ remain physiologically normal during chronic and acute management of HIV infection. Although modern pharmaceutical medicine does not provide liver tonics or supportives, herbal medicines have been used to ease liver stress for ages. Readily available liver protectants and their actual mechanism of action, including thioctic acid, glycyrrhizin, and Silybum marianum, are described.
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PMID:Liver function and HIV-1 infection. 1136 18

Hepatitis due to Listeria monocytogenes is uncommon in adults. This report describes the first case observed in Senegal. The patient was a 73-year old man presenting listeria-related hepatitis presumably secondary to low-grade meningeal encephalitis. Treatment using ampicillin was unsuccessful and the patient died four days after hospitalization. The authors note that the incidence of adult listeriosis has risen constantly for the past twenty years in relation with alcohol abuse, cirrhosis, diabetes, kidney insufficiency, cancer, AIDS, and organ transplantation. However no predisposing factors were observed in the present case.
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PMID:[Cerebromeningeal listeriosis associated with a cytolytic hepatitis. First case report in Senegal]. 1143 88


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