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)

Using a radioimmunoassay which detect concentrations of alpha-fetoprotein as low as 5 ng per ml, 38% of 176 patients with viral hepatitis compared with health volunteers and patients with chronic diseases not affecting the liver. When separated into two groups based on histological classification of liver biopsy specimens, differences in the degree and frequency of increased serum alpha-fetoprotein were related to the severity of the hepatic lesion. Of 75 patients with the lesion of viral subacute hepatic necrosis, in which zones of necrosis bridge adjacent portal triads or central veins, 52% had increased values, and 12% had levels ranging from 500 to 3300 ng per ml. In contrast, only 28% of the 101 patients without bridging necrosis had increased values, and none had levels that exceeded 500 ng per ml. In the patients with subacute hepatic necrosis, comparison of alpha-fetoprotein concentrations with the duration of illness indicated that the protein rose to peak levels in serum as the SGOT was declining. This was confirmed by serial observations in 10 patients. Thus, the increase of alpha-fetoprotein in the sera of patients with severe hepatitis occurs as liver necrosis is subsiding. Due to other known features of alpha-fetoprotein, it is intriguing to speculate that the increase in serum levels of this protein in viral hepatitis reflects hepatic regeneration after parenchymal damage.
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PMID:Relationship of serum alpha-fetoprotein to the severity and duration of illness in patients with viral hepatitis. 16 80

Hepatitis A antibody was detected by specific immune adherence and complement-fixation tests in a study involving 473 serum specimens from 20 patients who had viral hepatitis, Type A. In all 20 patients who had no detectable immune adherence antibody (less than 1:5) before onset of hepatitis high levels (greater than or equal to 1:1024) developed one to four weeks later, occasionally reaching peak levels exceeding greater than or equal to 1:81,920 several months thereafter. Five to 10 years later the immune adherence antibody levels ranged between 1:640 and 1:20,480. In general, the complement-fixation test was not as sensitive or as specific as the immune adherence test. These findings indicate that the immune adherence test should be a valuable tool for diagnosis, for epidemiologic surveys, for identification of susceptible and immune persons, for quantitative assays of gamma globulin and for identification of hepatitis A virus in attempts to propagate the virus in cell culture.
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PMID:Viral hepatitis, type A. Identification by specific complement fixation and immune adherence tests. 16 27

In the present study, the plasma levels of lipoproteins, triglycerides, and cholesterol were followed serially in a group of 57 patients with acute viral hepatitis. Mean plasma triglyceride levels were found elevated at the onset of the disease and gradually returned to normal, while mean plasma cholesterol values, low initially, gradually increased, alpha-lipoprotein was absent at the early stage of hepatitis in 41 out of 46 patients with mild or moderate course and reappeared gradually during the course of the disease. In 11 cases of viral hepatitis with impending or overt coma, alpha-lipoprotein was absent for the whole duration of the acute stage and never reappeared in those who eventually died, while it eventually returned to normal in those who survived. The reappearance of alpha-lipoprotein in acute viral hepatitis appears to be a sensitive index of improvement and a significant prognostic sign.
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PMID:Plasma alpha-lipoprotein pattern in acute viral hepatitis. 16 67

The hypothesis that hepatitis B infection is etiologically related to hepatoma has been investigated by studying the interrelationships between hepatitis B surface antigen (HBsAg, Australia antigen) and the fast-moving 5'-nucleotide phosphodiesterase Band V isoenzyme (5'-NPDase-V). Sera from 58 patients with viral hepatitis were tested for 5'-NPDase-V and HBsAg. The isoenzyme was found in 34 of 37 patients who were also positive for HBsAg but in only 4 of 21 hepatitis patients who were HBsAg negative. Five patients convalescing from hepatitis were negative for both HBsAg and the isoenzyme. Preparative gel electrophoresis showed that these 2 markers were different proteins. Of 34 hepatoma patients, 29 were positive for 5'-NPDase-V. Only 1 isoenzyme-positive patient was positive for HBsAg by counterimmunoelectrophoresis. However, of 16 isoenzyme-positive hepatoma patients available for radioimmunoassay, 8 were NBsAg positive (50%). None of 21 hepatoma samples tested for antibody to NBsAg was positive. Of 21 "normal" carriers of HBsAg and 10 carriers with Down's syndrome, 4 persons were detected with the isoenzyme. The results suggest that HBsAg and 5'-NPDase-V in the presence of liver damage are associated and thus provide a new marker enzyme between hepatitis B infection and hepatoma.
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PMID:5'-nucleotide phosphodiesterase isoenzyme in patients with hepatitis B infection. 16 56

Two episodes of acute viral hepatitis occurred in each of 34 patients. One episode in each patient was serologically diagnosable as type B hepatitis on the basis of tests for hepatitis B surface antigen or antibody. The other episode was classified as "non-B" on the basis of seronegativity, reinforced by seropositivity in an alternate bout. An epidemiologic background appropriate to "serum" hepatitis, either transfusion (one bout) or illicit self-injection (46 bouts), was associated just as frequently with serologically non-B episodes as with identified type B disease. The diagnosis of type B hepatitis, therefore, should be made only on the basis of serologic tests specific for hepatitis B virus infection. Other cases of sporadic diseases in adults must be labeled "viral hepatitis, type unspecifiable."
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PMID:Hepatitis types B and non-B. Epidemiologic background. 16 17

Lipoprotein electrophoresis with measurement of serum lipids was performed on 115 patients with various forms of liver disease. There was a reduction in alpha-lipoproteins and an increase in beta-lipoproteins, as well as a reduced separability of pre-beta and beta fractions in those with acute viral hepatitis. All these changes regressed completely with healing. Similar changes were shown also in chronic liver disease and were most marked in acute liver failure, but also marked in decompensated liver cirrhosis and chronic progressive hepatitis, while less marked in chronic persistent hepatitis and compensated liver cirrhosis. In patients with fatty livers there were no characteristic findings other than a slight increase in pre-beta lipoproteins. On the other hand, the lipoprotein pattern was markedly changed in cases with tumour in the region of the gallbladder, but similar changes were noted also with tumours at other sites. They are, therfore, unlikely to be liver-specific.
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PMID:[Lipoprotein pattern in acute and chronic liver disease (author's transl)]. 17 52

The susceptibility of chimpanzees to viral hepatitis type A was examined with immine electron microscopy. Of four seronegative infant chimpanzees, two were inoculated with a hepatitis A acute-phase stool filtrate rich in 27 nm virus-like hepatitis A antigen (HA Ag) particles, and two were inoculated with an HA Ag-negative preinfection stool filtrate. One of each pair of chimpanzees was inoculated intravenously, the other orally. One month later both chimpanzees that had received the HA Ag-positive filtrate developed biochemical, histologic, and clinical evidence of acute viral hepatitis. HA Ag particle (27 nm) were detected in their stools by immune electron microscopy; particle shedding followed a pattern similar to that in human volunteers. Immune electron microscopy also showed that antibody HA Ag had developed in the convalescent-phase sera of the infected chimpanzees. Control animals remained free of illness at this time but did develop hepatitis three to five weeks after exposure to the two infected chimpanzee-. The infectious inoculum was titrated in two additional seronegative chimpanzees. It was concluded that hepatitis a can be successfully transmitted to seronegative chimpanzees. Moreover, these studies provide further evidence that the 27-nm virus-like HA Ag particle is the etiologic agent of viral hepatitis type A.
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PMID:Experimental infection of chimpanzees with hepatitis A virus. 17 20

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 the majority of instances acute viral hepatitis resolves totally without sequelae. Fulminant hepatitis is a highly lethal lesion but 20 to 25 per cent of patients, principally young patients, survive. Survivors do not appear to develop chronic liver disease. Persistent viral hepatitis follows acute icteric hepatitis, both type B and non-B, in 10 to 12 per cent of patients. Six long-term HBs Ag carriers demonstrated HBs Ag clearance after 14-73 months. Chronic active viral hepatitis often progresses to cirrhosis. This progressive hepatitis appeared as a sequelae of acute icteric type B hepatitis in 3 per cent of 429 patients. In patients with chronic active type B hepatitis, low titers of HBs Ag are common.
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PMID:Viral hepatitis: clinical aspects. 17 56

Several types of viral hepatitis may exist. Hepatitis A (MS-1 type) can be transmitted to marmosets and chimpanzees. Virus-like particles, which may be parvo- or enteroviruses and which have been demonstrated in feces of this type of hepatitis, do not share cross-reacting antigens with hepatitis B but do cross-react with fecal hepatitis A antigen. Hepatitis A (GB type), which also does not cross-react with hepatitis B, is not antigenically identical with MS-1; it can be transmitted to marmosets and it may be similar to non-type A/non-type B post-transfusion hepatitis. Hepatitits B does not cross-react either with HA particles, the faecal hepatitis type A antigen or with the MS-1 or GB strains; it can be transmitted to chimpanzees and rhesus monkeys but not to marmosets.
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PMID:The mythology of various hepatitis A virus isolates. 17 1


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