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

In order to evaluate the pathogenesis of galactosamine hepatitis, the action of galactosamine on mast cells, and alteration in the complement system suring the course of this experimental injury were studied. It has been previously demonstrated that rat livers after colectomy are refractory to galactosamine-induced liver cell necrosis and inflammation. For this reason colectomized animals were used to see whether the biochemical alterations produced by this aminosugar and thought to be responsible for cell death developed. Results showed: 1. galactosamine potently degranulates mast cells in vivo and in vitro, 2. the complement system is a) activated during the course of galactosamine hepatitis, probably by circulating endotoxins, and b) is essential for liver cell death in galactosamine hepatitis, and 3. colectomy does not prevent biochemical changes known to occur during galactosamine metabolism. It is concluded that death of galactosamine-injured liver cells is triggered by extrahepatocellular mechanisms, which lead ultimately to an activated complement system by endotoxins. It is postulated that related mechanism may also occur in viral hepatitis and in fulminant hepatic failure in man.
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PMID:On the pathogenesis of galactosamine hepatitis. Indications of extrahepatocellular mechanisms responsible for liver cell death. 41 92

Seven patients with cardiovascular disease had clinical episodes and marked transaminase elevations that suggested viral hepatitis, but all had morphologic evidence (from liver biopsy or autopsy specimens) that documented centrilobular necrosis (ischemic hepatitis) with no evidence of viral or drug injury. Several also had moderate or marked passive congestion of the liver so the liver biopsies of 15 additional patients were retrospectively reviewed. In this latter group congestion alone was associated with normal or minimal elevation in transaminases while all patients with notable (greater than 5 times normal) transaminase elevations had centrilobular necrosis. Congestion alone, no matter how severe or prolonged, seems to do little if any damage to the liver. Centrilobular necrosis, or ischemic hepatitis, correlates with significant hypertransaminasemia, appears to result from failure of hepatic perfusion (with or without preceding hypotension), and presents with clinical and laboratory manifestations that suggest viral hepatitis.
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PMID:Ischemic hepatitis. 42 1

The clinical course, persistance of HBs antigen, and the liver biopsy morphological picture were evaluated in 40 patients with acute viral hepatitis, type B. In 34 cases, the disease ran a satisfactory course and clinical cure was corroborated histologically. In 4 cases, onset was particularly severe and the disease ran a long course. Here the immunological test for HBs antigen was still positive 8 weeks after the disease began, while a biopsy at 4 months showed a morphological picture similar to that of acute hepatitis. Lastly, two cases with a protracted clinical course displayed persistent HBs antigen positivity one year after the acute episode, with a histological finding of persistent hepatitis and cirrhosis of the liver respectively.
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PMID:[Prognosis of acute hepatitis B]. 43 75

The behaviour of LCAT was examined in acute viral hepatitis and post-hepatic cirrhosis. In the former case, the enzyme was also investigated during remissions. The influence of cholestasis on LCAT activity was evaluated. Depression was noted in cirrhosis and the acute stage of hepatitis, whereas enhanced values were observed during remissions. Depression of the enzyme by cholestasis is explained in a variety of ways.
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PMID:[The behavior of lecithin cholesterol acyltransferase (LCAT) in acute viral hepatitis and post-hepatitis cirrhosis]. 44 Jun 18

Experience with the clinical use and hepatitis risks of factor IX concentrate (Proplex) in cardiac surgical patients is presented in this report. Seventy-five patients received the concentrate for severe intraoperative or postoperative hemorrhage and 75 patients constituted matched controls. The incidence of probable type B viral hepatitis in patients receiving factor IX concentrate was 13.8 percent (four of 29) versus zero percent (zero of 29) in control patients (difference not significant). However, there was a greater incidence (p less than 0.05) of anti-HBs in patients receiving factor IX concentrate as compared to control subjects. No hepatitis-associated deaths or major morbidity were noted in these patients. It is confirmed that factor IX concentrate carries an associated significant risk of hepatitis. However, its use is justified in certain severe, acquired coagulopathies in which conventional platelet and fresh-frozen plasma therapy is inadequate.
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PMID:Hepatitis risk in cardiac surgery patients receiving factor IX concentrates. 45 27

A transversal and longitudinal epidemiological follow up was undertaken of the viral hepatitis cases occurring in two types of children communities (kindergartens and schools). The role of organized communities in the spread of hepatitis viruses and the contribution of external factors to the maintenance of hepatitis endemicity are discussed.
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PMID:Epidemiological investigations on viral hepatitis in preschool and school communities. Note I. Prevalence and incidence of viral hepatitis and the role of the community in transmission. 46 94

Hepatitis A is spread by fecal-oral transmission and accounts for 25% of the cases of sporadic hepatitis in this country; fatal cases have been documented but are unusual, and chronic hepatitis A has not been documented. Hepatitis B is spread by varied routes of transmission, fecal-oral being the least important, and accounts for half the cases of sporadic hepatitis in this country; fatal cases are well documented and chronic hepatitis B is common. The only documented route of transmission of non-A, non-B hepatitis is parenteral; fatal and chronic cases have been documented, and a quarter of the cases of sporadic hepatitis are non-A, non-B. Diagnosis of the etiology of viral hepatitis cannot be determined on clinical grounds but must be made through serologic tests.
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PMID:Viral hepatitis: prevention and prophylaxis. 46 61

With the finding of HBV and HAV, it is possible at the present time to recognize according to its etiology three types of viral hepatitis: type A, Type B and type non-A-non-B. In this paper we have proved that a low socioeconomic status plays a very important role in the spreading of this disease. In a community with a low socioeconomic status, of forty children attending the fourth grade of a primary school, 97 percent were found to have anti-HA: while in a similar group of children with a higher socioeconomic background, we found only 40 per cent of positive cases. A positive sero convertion to anti-HA was found in 90 per cent of the 73 children with acute hepatitis; the remaining 10 per cent were non-A-non-B. A group of 61 children admitted to the L. Calvo Mackenna Children's Hospital with acute or chronic non hepatic disease were studied for anti-HA. We found 77% positive cases in the group of infants under 4 months old; in older infants, a low incidence of anti-HA was observed, but a notorious increase of positive cases was seen after the age of two years, reaching 100 percent of positive cases in children above four years of age. In ten patients studied with prolonged hepatitis, five of them could be possibly classified as having a non-A-non-B hepatitis.
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PMID:[Hepatitis A antibodies in children]. 46 72

Chronic hepatitis is one of liver diseases with arguments from the clinical and histopathological aspects. Histopathological examinations were made on 687 biopsy cases clinically diagnosed as chronic hepatitis. Histopathological classification was based on our own criteria by referring to discussions in the series of Inuyama symposia on hepattis and others. The correlation between histological diagnosis and clinical data was also examined. Histopathological diagnoses made of the 687 cases were classified as follows; normal liver or liver with no pathognomonic changes of 77 cases (11.2%), non-specific reactive hepatitis of 56 cases (8.0%), viral hepatitis of 488 cases (71.0%), alcoholic hepatitis of 25 cases (3.6%), fatty liver of 23 cases (3.3%), massive liver necrosis of 3 cases, liver fibrosis of 2 cases, congestive liver of 1 case, and unclassified 12 cases due to inadequate specimens or other reasons. Among 488 viral hepatitis cases, histological stages were as follows; acute hepatitis (38 cases, 7.8%), persistent hepatitis (23 cases, 4.7%), chronic inactive hepatitis (142 cases, 29.1%), chronic active hepatitis (165 cases, 33.8%), chronic hepatitis with subloblar necrosis (33 cases, 6.8%), precirrhosis (51 cases, 10.5%), cirrhosis (27 cases, 5.5%). The relationship between histological aspects and clinical features was discussed by sex, age, and others. Of 41 follow up cases, significant values of histological type, presence of HB ag., or alcoholic were discussed as for the causative factors evolving liver cirrhosis.
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PMID:[Chronic hepatitis--clinicopathological studies of 687 cases (author's transl)]. 46 98

From September 1976 through March 1978, we investigated 11 outbreaks of non-B viral hepatitis associated with Louisiana day-care centers. The outbreaks included 168 cases, most of which were erroneously considered "sporadic" cases of non-B viral hepatitis prior to the investigations. Thirteen percent of all non-B viral hepatitis cases reported in the New Orleans metropolitan area during 1977 were associated with one of the outbreaks. Most of the cases in each outbreak and 85% overall were in older, usually adult, contacts of children attending the day-care centers. Within the household, parents appeared to be at greatest risk, particularly those who had 1- to 2-year-old children in the day-care center. Day-care center outbreaks of non-B hepatitis are easily overlooked and may be more widespread than is currently appreciated.
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PMID:Viral hepatitis associated with day-care centers. 47 89


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