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)

Tumor necrosis factor (TNF) was determined with ELISA in 72 patients with hepatitis C and hepatitis B virus infections. Interleukin 6 (IL-6) was determined at the same time. TNF and IL-6 were significantly increased in patients with hepatitis C virus infections when compared with normal subjects and hepatitis B patients. There was a significant positive correlation between TNF and IL-6. It is suggested that increased TNF and IL-6 may play an important role in pathogenesis of hepatitis C virus infection.
Zhonghua Nei Ke Za Zhi 1992 Jun
PMID:[Tumor necrosis factor and interleukin 6 in hepatitis C virus infection]. 128 84

In order to investigate the significance of HBV DNA in the serum of anti-HBs positive persons, the serum of 76 anti-HBs positive persons was studied for HBV DNA by means of polymerase chain reaction (PCR). The results showed that 21 (32.2%) out of 65 cases without hepatitis B vaccination were positive for HBV DNA detected with PCR (PCR-HBV DNA), but no one was positive for PCR-HBV DNA in 11 cases inoculated against hepatitis B. It was also found that 6 cases were positive for HBsAg-Ab immunocomplex in those positive for PCR-HBV DNA and the liver tissue in 2 of the 5 cases with liver-biopsy were positive for HBVAg determined with immunohistologic ABC method. We believed that persons, who acquired anti-HBs after HBV infection were different from those who were vaccinated, might carry HBV which come from the HBsAg-Ab immunocomplex and HBVAg positive hepatocytes. In addition, the study also proved that the PCR-HBV DNA positive rate correlated significantly with the anti-HBe and or anti-HBc positive rate and with the abnormal rate of liver function in the anti-HBs positive persons. It was suggested that persistent presence of HBV DNA in the bodies should be responsible for the persistent presence of anti-HBe and anti-HBc in the serum and also for the liver damage.
Zhonghua Nei Ke Za Zhi 1992 Oct
PMID:[Hepatitis B virus DNA in the serum of anti-HBs positive persons]. 130 57

Response to interferon therapy in chronic hepatitis B virus (HBV) carrier is preceded by the appearance of IgM class anti-HBc (antibody to hepatitis B core antigen). The temporal relationship and magnitude of the IgM anti-HBc response is variable, suggesting that the antibody is not directly involved in hepatocyte lysis, but is merely a marker of a changed state of immunity to the nucleocapsid proteins induced by interferon. IgG 1, 2, 3 and 4 did not change during therapy. IgG anti-HBc of all subclasses was absent in two Chinese HBV carriers. Lower than normal titres of anti-HBc (P less than 0.001) were detected in human immunodeficiency virus antibody positive (anti-HIV) carriers. These data indicate the presence of altered immunity to the nucleocapsid antigens in these two types of chronic HBV carrier that are known to respond poorly to antiviral therapy.
Zhonghua Nei Ke Za Zhi 1990 Mar
PMID:[Subclasses of antibodies to hepatitis B core antigen in chronic HBV infections: changes during treatment with interferons and predictors of response]. 169 93

The rate of micronucleus formation in lymphocytes was determined in 42 patients (including 10 acute icteric hepatitis B, 15 chronic active hepatitis B (CAH), 8 liver cirrhosis and 9 liver cancer) and 13 normal subjects. The results showed that the rate of micronucleus formation in lymphocytes in the patients with CAH (12.267 +/- 5.298%), liver cirrhosis (12.375 +/- 8.551%) or liver cancer (19.444 +/- 13.324%) was markedly higher than that in those with acute icteric hepatitis B (5.400 +/- 1.430%) or normal subjects (3.308 +/- 1.284%) (P less than 0.01). The rate of micronucleus formation in lymphocytes is higher in the liver cancer group than that in the CAH group or cirrhosis group (P less than 0.05). The rate of presence of two or more micronuclei in the lymphocytes was obviously higher in the liver cancer group (3.667 +/- 4.743%) than that in the liver cirrhosis group (1.500 +/- 1.690%), CAH group (1.467 +/- 1.807%), acute icteric hepatitis B group (0.600 +/- 1.075%) or healthy group (0.462 +/- 0.660%) (P less than 0.01 or less than 0.05). This method is much simpler than the measurement of chromosomal damage, and its reliability is as good as the latter. Measurement of micronuclei in lymphocytes can reflect the degree of liver damage in patients with the infection of hepatitis B virus. It may be used as the subclinical marker of the patients with liver cancer too.
Zhonghua Nei Ke Za Zhi 1991 May
PMID:[Determination of the rate of micronucleus formation in lymphocytes in liver diseases and its clinical significance]. 187 42

To explore the etiological agent(s) of HBsAg negative chronic active hepatitis, serum HBV DNA was tested in thirty-six of such cases with polymerase chain reaction. In total, viral DNA was detected in 24 cases (67%), including 11 of the 12 cases with positive anti-HBc alone, four of the nine cases with positive anti-HBs and nine of the 15 cases without any HBV markers. The results suggest that in cases of HBsAg-negative chronic active hepatitis, the etiology may still be hepatitis B virus, especially in cases with positive anti-HBc. Furthermore, the cause of activated histology might be due to viral replication.
Zhonghua Nei Ke Za Zhi 1991 Jan
PMID:[Identification of HBV infection in HBsAg-negative chronic active hepatitis with polymerase chain reaction]. 203 90

By using immunohistochemical techniques the deposition of HBV associated immune complexes was studied in 845 consecutive cases of renal biopsy. In 665 cases of primary glomerulonephritis the frequencies of HBsAg, HBeAg and HBcAg detection in glomeruli were 11.9%, 8.3% and 3.2% respectively with a total HBV antigen positive frequency of 12.2%. High positive rates were found in membranous glomerulonephritis (MGN, 37.1%), mesangioproliferative GN (MPGN, 26%) and IgA nephropathy (IgA-NP, 18.9%). The detection of HBV infection markers in serum were simultaneously performed in 213 cases; 31.7% of the patients with primary GN were found to be positive. In patients with positive HBV infectious markers in the serum, deposits of HBV antigens in glomeruli were found in 49.1% of the cases. The incidence was significantly different in the serum negative group (10.6%). Meanwhile, about 68.3% of the cases with HBV antigen deposits in the kidney was found to have positive HBV markers in the serum. Also the incidence was significantly different in the group without HBV antigen deposits in the kidney (20.9%). It was again confirmed that the pathogenesis of hepatitis B virus associated glomerulonephritis (HBV-GN) was related to the deposition of HBV immune complexes in kidney tissue. It was noticed that the deposition of three different types of HBV antigens was somewhat associated with the development of specific forms of HBV GN. The diagnostic criteria of HBV-GN were discussed in detail.
Zhonghua Nei Ke Za Zhi 1990 Sep
PMID:[Further study on the immunopathology of hepatitis B virus associated glomerulonephritis]. 208 24

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.
Zhonghua Nei Ke Za Zhi 1990 Feb
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.
Zhonghua Nei Ke Za Zhi 1990 Jun
PMID:[Hepatitis D virus RNA in serum from patients with hepatitis B]. 226 30

A close relationship (r = 0.186, P less than 0.025) was found between the serologic level of HBsAg/pre-S2, an envelope protein of hepatitis B virus, and the level of viral replication expressed by HBeAg. The rate of co-appearance and co-absence of both pre-S2 and HBeAg was 75.0%. Among HBeAg-positive cases, the prevalence of pre-S2 and its serologic level were significantly higher during exacerbation than resolution of chronic active hepatitis (73.3 vs 33.3%, 111.4 vs 1.4 ng/ml), and also higher than those among HBeAg-negative cases. Those the prevalence and the level were also higher in chronic active hepatitis than in chronic asymptomatic carriers (26.9 vs 11.5%, 2.95 vs 0.49 ng/ml). Pre-S2 prevalence in the group with highest scoring of histological activity was significantly higher than that in the groups with lower scoring (88.9 vs 40.0 and 36.4%) and the serologic level of pre-S2 also increased along with the scoring. Those data suggest that pre-S2 was associated with hepatic inflammatory activity as well.
Zhonghua Nei Ke Za Zhi 1989 Apr
PMID:[HBsAg/PRE-S2 expression of viral replication and hepatic inflammation in chronic hepatitis B virus infection]. 280 54

Effects of interferon (IFN) treatment on mutation of hepatitis B virus (HBV) precore were studied with a rapid polymerase chain reaction method to investigate the stop codon in the distal precore region during HBV precore mutation. 6 cases of chronic hepatitis B were treated with recombinant IFN alpha 1 3 x 10(6) U/day for 14 weeks. In 4 of them HBV DNA was undetectable after treatment. Precore mutant was detected in the remaining 2 cases whose HBV DNA was still positive. In a group of 11 cases not treated with IFN, mutants were detected in 3. HBV e antigen (HBeAg) became negative after IFN treatment in one case, the original wild strain was replaced by a status of co-existence of mutant and wild strain. These results suggest that HBeAg negative seroconversion after IFN treatment does not necessarily implicate a complete clearance of HBV and the possibility of mutation of precore still exists.
Zhonghua Nei Ke Za Zhi 1995 Apr
PMID:[Effects of interferon treatment on mutation of hepatitis B virus precore genome]. 758 99


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