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

Acute viral hepatitis has several identifiable morphologic components but the major categories are (1) cytopathic, (2) inflammatory, and (3) regenerative. Each category has independently variable characteristics. Extreme alterations related to severity of disease, alteration of immune response, or pre-existing liver disease may result in diagnostic difficulties for the pathologist. In contrast to the usual concept, patients who survive fulminant viral hepatitis rarely, if ever, develop cirrhosis and those who have severe hepatic necrosis from hepatitis also do not usually develop serious sequelae of that disease except in the older age group where the difficulty is in impaired regeneration (IR). The usual criteria for the diagnosis of chronic active hepatitis or chronic aggressive hepatitis need a thorough review since many of the variations of acute viral hepatitis result in histologic patterns that might be considered to be chronic aggressive hepatitis using the previous definitions; yet such patients recover without developing chronic liver disease. Chronic active hepatitis, a progressive hepatic disorder, is characterized by changes in the distribution of necrosis and regeneration within the lobule from that usually observed in acute viral hepatitis. Persistent viral hepatitis, a development in 10 to 12 per cent of adult patients after icteric acute disease, is characterized by a "cobblestone" hepatocellular change that resembles continued regeneration, focal hepatocytolysis, and often portal lymphoid hyperplasia. Apparently with time, these histologic features fade and the incidence, in type B PVH, of "ground glass" HBs Ag laden cells increases. This may reflect a continued adaptation of host and virus to one another.
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PMID:Viral hepatitis: a pathologic spectrum. 17 49

In 1968, studies of infectious hepatitis in volunteers were reported. Immunologic procedures for serologic study of the hepatitis A virus were not available at that time, and only the clinical and biochemical parameters of the disease were reported. Serial serum specimens from the participants in the study were retained; these specimens had been taken before inoculation and up to more than 100 days after inoculation. When a radioimmune assay for antibody to hepatitis A virus was developed, the series of sera was analyzed retrospectively. Forty-four male volunteers were involved in a series of three studies. Twenty (46%) of the volunteers were found to be initially immune to hepatitis A virus. Eighteen susceptible volunteers (with no preexisting antibody) were challenged with infectious virus. Eight of these volunteers developed clinical hepatitis and seroconverted; one seroconverted without evidence of clinical disease; and nine neither seroconverted nor had evidence of clinical disease. The radioimmune assay provided a method for diagnosis of immune status and of the acute disease caused by hepatitis A virus.
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PMID:Serologic studies of transmission of hepatitis A in humans. 22 Mar 30

The discovery of Australian antigen (HBsAg) has led to an increasing deal of knowledges about the virus of type B hepatitis (HBV); several markers of HBV have been detected and are becoming disposable for clinical and epidemiological purposes. The HBsAg is carried by 3 types of particulate structures discovered by electron microscopy as small spherical particles having diameter around 22 nm, long filaments and spherical particles having an overall diameter of the 42 nm (Dane-particle) with an electron-dense core. Dane-particle core contains circular double-stranded DNA molecules and an enzyme, the DNA polymerase. At present, Dane-particle is thought to represent the HBV, having properties consistent with those of a complete virus. Four antigen/antibody systems related to viral type B hepatitis have been discovered; they have been designated with the following nomenclature: HBsAg/anti-HBs, HBcAg/anti-HBc, HBeAg/anti-HBe, epilon antigen/anti epilson. The availability of the HBV markers for clinical purposes will permit a better understanding of the sequence of the biological reactions as well as of the clinical and epidemiological features concerning this viral infection: incubation period, acute disease, resolution, chronic carrier state, actively or passively immunized subject, persistent or subsided infectivity, prognosis.
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PMID:[Markers of type B viral hepatitis]. 38 66

Non-A, non-B hepatitis, previously transmitted to chimpanzees by inoculation of human serum, was serially transmitted through a second and third passage to additional chimpanzees using serum drawn during acute non-A, non-B hepatitis. Sera obtained at weeks 4 and 5 after inoculation from two different chimpanzees, and from one chimpanzee at week 13 after inoculation, were shown to cause elevation of serum aminotransferase levels and abnormal liver biopsies in recipient chimpanzees, with no serologic evidence of hepatitis A or B, cytomegalovirus, or Epstein-Barr virus infection. Serum obtained 3 wk after inoculation did not cause elevation of aminotransferase levels in the recipient chimpanzee, although a single abnormal biopsy was obtained. Thus, the non-A, non-B hepatitis agent was present in serum during acute disease near the time of the first aminotransferase elevation (week 4; perhaps also week 3), and persisted at least until 1 week after the peak aminotransferase level (week 13).
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PMID:Acute non-A, non-B hepatitis. Prolonged presence of the infectious agent in blood. 42 94

Genetic study of acute and chronic mouse hepatitis virus type 3 disease was carried out in segregating generations of a cross involving a susceptible (C57BL/6) and a resistant (A/J) mouse strain. The data obtained indicate that one or two recessive genes may be involved in resistance of acute and chronic diseases but suggest that the genes involved in both diseases are different. In this cross, no correlation was observed between H-2 and acute or chronic disease. In mice of congenic lines, however, A/Sn (H-2a), A.SW (H-2s), A.BY (H-2b), and A.CA (H-2f), it appeared that the presence of the H-2f allele conferred to heterozygote as well as to homozygote animals the capacity to resist the development of chronic disease. It seems, therefore, that MHV3 sensitivity in mice is under the influence of at least two major genes: one for the acute disease and the other, H-2 linked, for the chronic disease.
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PMID:Genetic study of mouse sensitivity to MHV3 infection: influence of the H-2 complex. 44 93

Potent sheep anti-mouse interferon globulin has been used to determine the role of virus-induced interferon in mouse hepatitis virus type 3-infected susceptible (C57BL/6), semiresistant (C3H/He), and resistant (A/J) strains of mice. Injection of anti-interferon globulin accelerated the onset of death in C57BL/6 mice, induced almost 100% mortality in C3H/He mice that usually do not die of acute disease, and caused death in 4- and 6-week-old A/J mice, but not in older mice. We conclude that interferon is an important host defense factor in the initial response of different strains of mice to MHV-3 infection. Other factors, however, such as the capacity of macrophages to restrict viral multiplication probably underlie the genetically determined susceptibility or resistance of mice to MHV-3 infection.
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PMID:Role of interferon in the pathogenesis of viral diseases of mice as demonstrated by the use of anti-interferon serum. V. Protective role in mouse hepatitis virus type 3 infection of susceptible and resistant strains of mice. 65 66

329 patients with acute ouvert viral hepatitis which occurred in the Hannover area 1975 were classified according to virological data. The proportions of type A and type non A - non B hepatitis were each approximately 20 percent of the total cases (n = 60). Viral hepatitis B was the most frequent type of viral hepatitis (n = 209). 174 individuals of the 329 hepatitis patients were reexamined serologically two years after the onset of the acute disease. 7 out of 105 patients with hepatitis B (6,7%) and 5 out of 40 patients with hepatitis non A - non B (12,5%) revealed a serological pattern compatible with chronic hepatitis. In contrast none of 29 patients with hepatitis A indicated chronic liver disease. The frequency of anti-HAV was also determined in 41 patients with HBsAg positive and HBsAg negative histologically proven chronic hepatitis or liver cirrhosis. All patients were under 35 years of age. An equal proportion of anti-HAV was found in both groups. These results suggest that hepatitis A practically never results in chronic hepatitis, while hepatitis non A - non B can run a chronic course with a frequency similar to that of hepatitis B.
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PMID:[Chronic hepatitis as sequela of acute viral hepatitis A and hepatitis non A - non B (author's transl)]. 74 46

In acute cases of hepatitis, DNA polymerase activity was found 2 to 3 times more frequently than positive radioimmunoassay. For each case the DNA polymerase reactivity was shown to be associated with hepatitis B antigens. Inhibitors to this DNA polymerase, with properties of IgM and IgG antibody, were found in 13 of 34 cases of acute hepatitis but only in 1 case out of 22 of cirrhosis. During the course of the acute disease these antibodies were detected 3 times more frequently than those to HBs antigen; the two types of antibodies were almost always found separately in different patients, those to DNA polymerase were apparently transient and developed earlier since they were found as early as 3 days after the clinical onset and no later than the 6th week following the onset.
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PMID:Comparison of DNA polymerase and radioimmune assays for the detection of hepatitis B antigens and antibodies. 120 57

Synthesis rates of albumin and fibrinogen were determined in six patients with acute virus hepatitis and in nine control patients using the 14C carbonate method of McFarlane. Five patients were restudied several weeks after complete recovery. The following results were obtained. (1) The mean albumin and fibrinogen synthesis rates in the control group were 238.8 and 23.5 mg/kg/day, respectively. (2) In two patients with mild courses of hepatitis and in one patient studied during the early phase of a rapid and fatal course the albumin synthesis rate during the acute disease did not differ from controls whereas fibrinogen synthesis rate was slightly increased. (3) Three patients with severe hepatitis showed a definite decrease in albumin and fibrinogen synthesis rates, the lowest value being 76 mg/kg/day for albumin and 6.3 mg/kg/day for fibrinogen. (4) The decrease in plasma protein synthesis correlated neither with serum transaminase or bilirubin levels nor with plasma albumin or fibrinogen concentrations during the acute phase. (5) The two patients with the lowest albumin and fibrinogen synthesis rates also showed a definite decrease of the prothrombin index during the acute phase. Both patients presented very prolonged courses of the disease. (6) In all patients studied twice, plasma protein synthesis rates were normal after recovery.
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PMID:Synthesis rates of albumin and fibrinogen during and after acute hepatitis. 120 13

The extent of involvement of hepatitis C, as compared to hepatitis A and hepatitis B, virus infection in acute and chronic liver disease in the Asir Region, southwestern Saudi Arabia, was assessed in 898 patients hospitalized during the period from June 1990 to November 1991. Acute icteric hepatitis cases with severe onset were distinguished by their referral to the fever hospital while cases with milder onset and those with chronic hepatitis were followed at two general hospitals. Antibodies to the c-100-3 antigen of hepatitis C virus (anti HCV) were detected in a significant proportion of patients with chronic liver disease (chronic active hepatitis (65%), cirrhosis (44%)). Anti HCV was also detected in patients with acute hepatitis with milder onset at the general hospitals (10.9%) but proportionately much less in patients at the fever referral hospital (< 1%) where hepatitis A (52%) and, to a lesser extent hepatitis B (11%), were mostly diagnosed. These results indicate that HCV is a major identifiable infection in hospitalized patients with chronic liver disease in this region but that anti HCV antibodies (c-100-3) are not detected, at least at onset, in sporadic cases with acute manifestations. Testing for additional viral antigens or RNA and a longer follow-up period would be required before exclusion of a role for HCV in acute disease. Alternatively, other viral and non-viral agents may be sought in this illness.
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PMID:Serodiagnosis of hepatitis C in acute and chronic liver disease in southwestern Saudi Arabia. 128 Dec 39


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