Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Beta 2-Microglobulin expression on hepatocyte membrane was studied in 117 liver biopsies from patients with acute and chronic hepatitis B and in 11 subjects with normal liver function, using immunohistochemical PAP method. In normal liver beta 2-microglobulin could not be detected on hepatocyte membrane, compared with that in subjects with normal liver, in asymptomatic HBsAg carrier and in patients with chronic persistent hepatitis, there is significant enhancement of beta 2-microglobulin expression in patients with acute mild hepatitis and chronic mild active hepatitis. Beta 2-Microglobulin expression in patients with chronic active hepatitis with moderate to severe activity and cirrhosis has a significant enhancement, when compared with acute mild hepatitis and chronic mild active hepatitis. Moreover, location of beta 2-microglobulin expression on hepatocyte membrane was associated with lesion of hepatocytes. Enhanced expression of beta 2-microglobulin on hepatocyte membrane in acute and chronic hepatitis B probably reflects enhanced display of HLA-ABC antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of T cell-mediated hepatocytelysis.
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PMID:[A study of the relation of the expression of beta-microglobulin and hepatocytic lesions in hepatitis B]. 220 29

To clarify the correlation of hepatitis D virus (HDV) infection and viral replication in liver diseases, the authors detected HDV RNA and serological HDV markers in serum from 285 patients with hepatitis B and 45 asymptomatic carriers of HBsAg. With dot blot hybridization, serum HDV RNA was detected in 8.8% (29/330) of the patients with HBV infection. The positive rate of HDV RNA in fulminant hepatitis was higher than that in benign hepatitis (15/74 vs 3/47, P less than 0.05). 10 of the 139 patients with chronic active hepatitis and 1 of the 6 cases with cirrhosis were positive for HDV RNA. However, all of the 19 cases with chronic persistent hepatitis and 45 asymptomatic carriers of HBsAg were negative fo, HDV RNA. Serological HDV markers, HDAgr anti-HD and IgM-anti-HD, were determined with ELISA. HDV RNA was detected in all of the serum samples with positive HDAg and/or IgM-anti-HD, in 15 of the 26 cases with positive-anti-HD and in 8 cases without HDV markers. Our results showed that 40 of the 330 patients with HBsAg were infected by HDV. This investigation suggests that HDV is one of the etiological factors for fulminant hepatitis and chronic active hepatitis.
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PMID:[Hepatitis D virus RNA in serum from patients with hepatitis B]. 226 30

Hepatitis B virus (HBV) is a high risk factor in the frequently found liver involvement of renal transplant recipients. As in other immunosuppressed patients, these often follow a course of slight jaundice, with a progressive tendency and great replicative and infectious power. Also, in addition to an increased incidence of chronic hepatitis (CH) in transplanted when compared with hemodialized patients, specially when HBsAg is present, it is surprising the poor correlation between enzyme levels and the grade of activity of the hepatic lesion. In a retro and prospective study, we present 52 patients of the 73 transplant reviewed. There are 32 men and 20 females, with and average age of 34 years, minimum time on dialysis of 2 months and maximum of 7 years, time of renal transplant from 6 moth to 15 years (average 4.9 years). There were 31 cadaver transplants and 21 live donors. The HBsAg was + in 20 (9 seroconverted), HBeAg was + in 4 (with 2 seroconvertions), hyperbilirrubinemia in 5, hyperalkaline phosphatasemia (2 or more times) in 11 and elevated serum transaminases (SGPT) (3 times or more) in 20 cases. Positive HBsAg plus SGPT x 3 was found on 9 occasions and positive HBsAg with SGPT x 3 in 3 cases. liver biopsy (LB), in those with enzymatic changes and/or positive antigenemia, was performed in 15 instances and there were 5 autopsies. The most important histological findings were: 5 acute viral hepatitis, 2 active chronic hepatitis (CAH), 2 persistent chronic hepatitis (CPH), 5 with fat infiltration and 4 with colestasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hepatitis B virus in patients with renal transplant. Report of 52 cases]. 227 11

Two variants of dysplastic hepatocytes are revealed: small and large which are characterized by cell atypia and probably result from the disturbance of regenerative processes. The disturbance of the liver lobule architectonics is also a feature of dysplasia. The degree of hepatocyte dysplasia assessed by morphometric indices (nuclei surface, ratio of ellipticity) and its frequency increase with progression of the pathological process: chronic persistent hepatitis----chronic active hepatitis----liver cirrhosis----hepatocellular carcinoma. More frequent observation of the hepatocyte dysplasia in viral liver conditions (HBsAg in dysplastic hepatocytes) indicates the role of hepatitis B virus in the development of hepatocyte dysplasia. Increase of DNA content and nuclei polymorphism are observed in small and large dysplastic hepatocytes when the degree of dysplasia is increasing, this making these cells closer to cells of hepatocellular carcinoma and favouring the concept of hepatocellular carcinoma development in the foci of dysplastic hepatocytes, particularly in liver cirrhosis.
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PMID:[The morphological characteristics of hepatocyte dysplasia]. 228 82

A Pacific white-sided dolphin (Lagenorhynchus obliquidens) developed clinical signs, serum biochemical values, and serologic viral markers consistent with chronic persistent hepatitis caused by a hepatitis B-like virus. The hepatitis had a sporadic cyclical pattern of lethargy, inappetance, and icterus, with leukocytosis and increased serum activities of alanine transaminase, aspartate transaminase, and gamma-glutamyltransferase. The serum from this dolphin contained hepatitis B virus core antibodies, hepatitis B surface antibodies, and hepatitis B viral DNA. Supportive treatment consisted of administration of antibiotics, cimetidine, menadiol sodium diphosphate, and vitamin/dextrose supplementation. A clinically normal killer whale (Orcinus orca) housed in the same pool had serum hepatitis B surface antibodies, suggesting immunologic responsiveness and that this disease was not species-specific.
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PMID:Hepatitis B-like infection in a Pacific white-sided dolphin (Lagenorhynchus obliquidens). 229 47

Eighty-eight consecutive hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) positive, heterosexual patients of Caucasian origin presenting with chronic hepatitis were followed for 1 to 15 years (mean, 5.4 years). During the study period, 45 (51%) patients cleared HBeAg and hepatitis B virus-deoxyribonucleic acid from serum and were followed for 53 +/- 29 months (mean +/- SD) after seroconversion to antibody to hepatitis B e antigen. All patients manifested biochemical improvement. During follow-up, 10 (22%) of the 45 patients experienced spontaneous reactivation of hepatitis B replication with reappearance of serum hepatitis B virus-deoxyribonucleic acid and, in 4 patients, of hepatitis B e antigen. All patients then showed biochemical exacerbation of disease. These serologic events were transient, lasting an average of 12 months, in 8 (80%) patients. All patients were asymptomatic or minimally symptomatic. Histologic findings of liver tissue from 7 patients showed progression from chronic active hepatitis to active cirrhosis in 2 (28%) patients, while in the remaining 6 cases histology remained unchanged or improved from chronic active to chronic persistent hepatitis. These data indicate that spontaneous reactivation of hepatitis B infection occurs in heterosexual patients with chronic hepatitis B and this event is usually transient and asymptomatic, although in some patients it may be the major cause of progressive hepatic damage.
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PMID:Spontaneous reactivation of hepatitis B virus infection in patients with chronic type B hepatitis. 238 55

We have studied antibodies (anti-pol antibody) against the polymerase gene product of hepatitis B virus by solid-phase enzyme immunoassay using synthetic peptides coded for by this gene. Sera from six patients with acute hepatitis B, 112 chronic hepatitis B virus carriers and six healthy individuals with naturally acquired immunity to hepatitis B virus were tested for anti-pol antibody. In acute hepatitis B virus infection, anti-pol antibody was detected in three of six patients. In chronic hepatitis B virus infection, anti-pol antibody was detected in 17 of 29 (59%), in 23 of 33 (70%) of cirrhotic patients and in 18 of 24 (75%) patients with cirrhosis complicated by hepatocellular carcinoma, compared with 4 of 19 (21%) asymptomatic carriers and 2 of 7 (29%) patients with chronic persistent hepatitis. Titers of anti-pol antibody were higher in cirrhotic patients with and without hepatocellular carcinoma than in patients with chronic active hepatitis. The presence of anti-pol antibody, however, had no relationship with hepatitis B virus-associated DNA polymerase activities and other viral replicative markers. As for sera from six healthy individuals with naturally acquired immunity to hepatitis B virus, two (33%) were positive for anti-pol antibody. These results indicate that the immune response toward the polymerase gene product is induced during acute and chronic hepatitis B virus infection. In chronic hepatitis B virus infection, anti-pol antibody may serve as a new marker indicative of a long period of hepatitis B virus-induced hepatitis.
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PMID:Detection of antibodies against the polymerase gene product in hepatitis B virus infection. 239 Oct 62

In 44 hepatitis B virus (HBV) carriers with chronic persistent hepatitis (CPH), serial liver biopsies were available. At presentation 38 patients had HBV-DNA in their serum including 31 HBeAg positive and seven anti-HBe positive cases. The remaining six patients were anti-HBe positive and HBV-DNA negative. During a mean histologic follow-up of 4.2 years, 12 (32%) of the 38 HBV-DNA positive patients progressed to chronic active hepatitis (six cases) or to active cirrhosis (six cases), while 26 patients showed either unchanged features of CPH (21 cases), or histologic improvement to normal liver (five cases). Persistence of HBV-DNA in serum, independently of HBeAg/anti-HBe events, was significantly (p less than 0.01) associated with deterioration of liver disease, while termination of HBV replication correlated significantly (p less than 0.05) with spontaneous biochemical remission and with unchanged or improved histology. None of the six anti-HBe positive patients without serologic markers of hepatitis B virus replication showed histologic deterioration. These findings indicate that continuing HBV replication is a marker which predicts unfavourable evolution of chronic persistent hepatitis and frequent transition to chronic active hepatitis or cirrhosis.
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PMID:Chronic persistent hepatitis type B can be a progressive disease when associated with sustained virus replication. 239 64

Chronic hepatitis is defined as chronic liver disease of at least 6 months' duration. Liver biopsy is essential for diagnosis and allows classification into chronic persistent hepatitis and chronic active hepatitis. Chronic persistent hepatitis is associated with hepatitis B infection or with infection with the non A non B viruses. The prognosis is good and it requires no treatment. Autoimmune chronic active hepatitis presents a very active clinical, biochemical and immunological picture. Prednisolone therapy is of benefit in prolonging life. Steroid therapy is disappointing in hepatitis B related chronic active hepatitis. Superinfection with delta agent may affect HBsAg positive patients: it appears to cause activation of disease and progression towards cirrhosis. Hepatocarcinoma is another complication of chronic B infection. Chronic active non A non B hepatitis is diagnosed by elimination since there is no specific diagnostic test.
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PMID:[Value of puncture biopsy of the liver during diagnostic and follow-up examinations (clinical aspects, immunological markers, images) in chronic hepatitis]. 242 1

The course after hepatitis B virus infection seems to be determined by the host's immune response, which in turn may be regulated by the major histocompatibility complex. In order to find a possible relationship between the course of disease and the phenotype frequency of HLA determinants, we studied 396 Dutch subjects of northern European local race. Six groups of individuals with various courses after hepatitis B virus infection were compared to healthy controls. The hepatitis B patients were grouped according to standard criteria: 47 had recovered from acute symptomatic hepatitis B virus infection; 60 had recovered from asymptomatic hepatitis B virus infection; 26 were asymptomatic hepatitis B surface antigen carriers; 16 had chronic persistent hepatitis B; 37 had chronic active hepatitis B, and 10 had chronic active hepatitis after elimination of hepatitis B antigens. Twenty-nine Class I and 13 Class II HLA antigens were assayed by standard microlymphocytotoxicity tests. The phenotype frequency of the Class II antigen DQw1 appeared to be significantly lower in patients with chronic active hepatitis B virus infection. Some other HLA specificities showed deviations from control values, but they were not statistically significant after correction for the number of antigens tested. In conclusion, we have found no evidence that the elimination of hepatitis B virus is related to HLA phenotype. DQw1, however, may affect the morphologic type of chronic hepatitis B infection, since its presence may protect against chronic active hepatitis.
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PMID:HLA antigens in patients with various courses after hepatitis B virus infection. 243 2


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