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

The author summarizes the experience of many years (1956-1989) gained with studies into the relationship between the gravity of viral hepatitides in the pregnant and etiology of disease. Virus A hepatitis runs a favourable course in the pregnant, i.e. without severe and fulminant forms. In virus B hepatitis, the pregnant women are threatened with the development of hepatic coma associated with a high maternal lethality. The latter one has noticeably been decreasing over the recent years (from 1.79% in 1956-1965 to 0.29% in 1966-1980 and to 0.21% in 1981-1989, which is not so much related to the perfection of the treatment methods as to the diminution of the share of virus B hepatitis. Virus E hepatitis may be of the greatest mortal danger for mothers in conditions of water epidemic. In that case the lethality among pregnant women may reach 12.1% (in the Turkmenian SSR) and 15.6% (in the Kirghiz SSR). The aggravating influences of virus C and D hepatitides on the pregnancy outcomes and maternal lethality have not been studied much. Estimation of etiological factors in viral hepatitis occurring in the pregnant is an important prerequisite for organization of the rational preventive and treatment measures.
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PMID:[Viral hepatitis in pregnant women--the relationship of the severity of the disease to the etiology of the infection]. 209 99

We have evaluated the clinical and epidemiological features of hepatic cirrhosis in a retrospective study of 200 patients admitted to our Area Hospital from 1984 to 1987. 77% of patients were 40-69 years old and 74% were males, with a M/F ratio of 2.84. 56% were caused by high alcohol intake, 25% were cryptogenic and 13% post-hepatitis. 29.2% were diagnosed in a compensated stage of the disease. 52.2% presented with ascites, and 30.5% with upper gastrointestinal hemorrhage. We found superimposed hepatocellular carcinoma in 4.5% of patients, all of them males, with a mean age of 63.5 years. 18% died during their hospital admission, 50% from hepatic coma, 19.4% from hypovolemic shock and 16.6% from hepatorenal syndrome. Survival from the time of diagnosis in the patients who died was shorter than one year in 41.5%.
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PMID:[Clinical and epidemiological features of hepatic cirrhosis. Analysis of 200 patients]. 251 71

Intestinal microflora were studied in 62 patients with cirrhosis, 14 with hepatitis and 30 normal subjects. The fecal anaerobes, total viable organisms, E.coli, enterococcus, bifidobacterium, lactobacillus and clostridium were significantly greater in number in cirrhotic patients than in normal subjects and hepatitis. Significant increase in fecal enterococcus and clostridium was observed in the patients recently recovered from hepatic coma as compared with the patients without hepatic coma. Bifidobacterium was increased in cirrhotic patients between patients with or without LLT (+). These data suggest that there was a tendency of the intestinal microorganisms to be increased in cirrhotic patients and the existence of possible relationship between the severity of liver function impairment and quantity of intestinal flora.
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PMID:[Preliminary study on intestinal microflora in patients with cirrhosis]. 261 70

The changes in O2-uptake (VO2) during 110 liver transplantations (LTX) were studied using Fick's principle (O2-uptake = cardiac index x arteriovenous O2-content difference). During each of the three operative periods [a dissecting period before clamping of the hepatic vessels (1), the anhepatic phase (2), and after reperfusion of the new liver (3)], two measurements (A and B) were taken. After removal of the liver (2A) the VO2 decreased about 11.4%, and increased after reperfusion (3A) about 44.0%; these changes were significant (P less than 0.001). To evaluate the influence of the various indications for LTX on the course of intraoperative VO2, the following patient groups were compared: patients with hepatic tumors (n = 17), patients with cirrhosis following hepatitis (n = 14), patients with primary biliary cirrhosis (n = 17), patients with cirrhosis plus tumor (n = 11), and patients in a hepatic coma (n = 20), regardless of the underlying liver disease. Groups with less than ten subjects were not considered. The drop of VO2 in the anhepatic period (1B----2A) was between -26.7% (patients with tumors) and -7.3% (patients with cirrhosis plus tumor). The patients with cirrhosis following hepatitis showed a special feature: their VO2 increased about 13.4% after cross-clamping the hepatic vessels. After revascularization, the VO2 increased in all groups between +37.2% and +69.8%. In all groups the level of VO2 was higher after reperfusion (3A) than in the dissecting period (1B), ranging from +5.3% in patients with tumors to +61.6% in patients with cirrhosis following hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in intraoperative total oxygen consumption in patients during liver transplantation]. 284 84

The indications for cortisone administration as well as of its derivatives in the treatment of viral hepatitis (VH) have been discussed on the base of personal experience and literature data. It has been concluded that cortisone has lost its role in the treatment of VH because of its numerous negative effects, recurrences, steroid diabetes, ulcers, hemorrhages, liability to infections, and most important--the liability to chronification and long-term carriership in VHB. Manifested intoxication phenomena and impeding and present endogenic hepatic coma, remain for the present, the main indications for cortisone treatment in VH. In VHA and VH non A--non B it is not necessary and in VHB it could even by admitted to be contraindicated due to the risk of chronification and long-term carriership. It has been emphasized that post-transfusion hepatitis are with the severest course, responsible for the lethality, hence the main treatment in them remains the prophylaxis with passive and active immunization.
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PMID:[Treatment of acute viral hepatitis with cortisone]. 309 52

Clinical profiles, serological markers, and antibody responses to antigens of hepatitis B virus (HBV) were studied in patients with fulminant viral hepatitis. Whereas hepatitis A and B were found to be uncommon causes (6.9% and 12.2%, respectively), non-A, non-B (NANB) hepatitis was found to be the most common cause of fulminant hepatitis (80.9%). As against this, the incidence of hepatitis B and NANB hepatitis was very similar in nonfulminant acute viral hepatitis in adults (41.2% and 51.9%, respectively). Pregnancy with labour was an important precipitating factor for development of fulminant hepatitis of the NANB type only; 32% of fulminant NANB hepatitis patients were pregnant women and 22.6% had a history of labour preceding hepatic coma. Only 0.8% of nonfulminant NANB hepatitis cases were pregnant women. Another major precipitating factor for the development of the fulminant form of NANB hepatitis was concomitant chronic HBV carrier state. A total of 38.6% of fulminant NANB hepatitis patients were HBV carriers, whereas only 19.2% of nonfulminant acute NANB hepatitis cases were HBV carriers. Sera of 32 chronic HBV carriers with fulminant NANB hepatitis and 10 cases of fulminant hepatitis B were tested for delta antibody, and all were nonreactive. The antibody responses of the fulminant hepatitis B patients to the antigens of HBV were found to be greater compared to those of patients with nonfulminant acute hepatitis B. Antibody responses of chronic HBV carriers with fulminant NANB hepatitis to antigens of HBV were found to be depressed in comparison with those of chronic asymptomatic carriers.
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PMID:Virological markers and antibody responses in fulminant viral hepatitis. 311 69

The spontaneous course of the galactosamine-hepatitis in the guinea-pig (750 and 1000 mg/kg GalN iv respectively) is characterized by a terminal hypoglycemia together with hypothermia and arterial hypotension fifty-nine hours on average after GalN-application. Preventing hypoglycemia and hypothermia by continuous intravenous infusion of a glucose solution and by increasing room temperature, the animals do not develop hepatic coma, but show an increasing disturbance of the righting reflex and survive at least seventy-two hours. Plasma biochemical tests and liver histology reflect severe hepatic damage. A twofold increase of the liver weight is caused by raised water and lipid content combined with a concomitant depletion of liver glycogen. Pharmacological studies with 14C-Pentobarbital result in a distinctly diminished clearance and in a prolonged half life while the cytochrome P-450 content of the liver shows a moderate decrease. In animal models of acute liver failure the possible incidence of hypoglycemia, arterial hypotension and hypothermia should be considered.
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PMID:[Galactosamine-induced acute liver failure in the guinea pig--spontaneous course and controlled study conditions]. 371 20

A 43-year-old woman was initially seen because of icterus. Clinical investigations revealed severe hepatic damage probably due to non-A, non-B hepatitis. She was treated with extracorporeal charcoal-column perfusion but died two weeks later in a hepatic coma. At autopsy, the brain showed kernicterus with typical discoloration of the hippocampus, the subthalamic nuclei, and the cerebellar dentate nuclei. Kernicterus in an adult is very rare. In this case, extracorporeal charcoal-column perfusion treatment led repeatedly to severe depletion of fibrinogen, with extensive hemorrhages. Overload of the already reduced hepatic glucuronyl-transferase capacity resulted in high serum levels of unconjugated bilirubin, an apparent prerequisite for the development of bilirubin encephalopathy.
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PMID:Kernicterus in an adult. 372 14

To evaluate the alterations of plasma catecholamines in chronic and acute liver diseases and their complications: hepatic encephalopathy (grade 1-4), ascites, deranged metabolism, and circulatory alterations, we measured the concentrations of norepinephrine, epinephrine, and dopamine in plasma in 49 patients with cirrhosis of the liver, in 2 patients with fulminant hepatitis B, in 2 patients with acute gestational fatty liver, and in 11 patients with fatty liver. We examined 21 healthy controls. The norepinephrine concentrations in patients with cirrhosis were raised and reached the highest values in hepatic coma grade 4. As well patients with fulminant hepatitis B had excessive high norepinephrine concentrations. The epinephrine concentrations were not significantly raised in patients with toxic cirrhosis and in patients with posthepatitic cirrhosis without encephalopathy. In hepatic coma grade 4 in patients with cirrhosis and fulminant hepatitis they reached again the highest values. Patients with acute gestational fatty liver had only slightly increased, and patients with fatty liver had normal catecholamine concentrations in plasma.
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PMID:[Plasma catecholamine levels in liver disease]. 406 Aug 3

A 34-year-old male presented with fulminant hepatitis A associated with acute renal failure. The patient was admitted four days after flu-like symptoms developed. Physical examination was unremarkable except for icteric sclerae. Laboratory studies showed SGOT 10719 U/l, SGPT 5780 U/l, prothrombin time 22%, BUN 25.5 mg/dl, and creatinine 2 mg/dl. Serum complements were within normal ranges, and circulating immune complexes were not detected. Anti-HAV IgM was positive. He developed hepatic coma on the fourth hospital day, and his renal function deteriorated progressively. He was treated with hemodialysis, but there was no improvement in consciousness. Although acute liver failure improved, he died on the 74th hospital day of subendocardial infarction. Autopsy examination showed acute renal tubular necrosis. The liver was enlarged and was in the residual stage of acute hepatitis without submassive necrosis. The development of fulminant hepatitis in hepatitis A has been rare, but in recent years acute renal failure in hepatitis A has been reported. Although the mechanisms responsible for renal failure in liver diseases are uncertain but could be multifactorial, immune complex-mediated nephritis and/or endotoxemia have been considered.
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PMID:Report of a case with fulminant hepatitis A associated with acute renal failure. 407 29


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