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)

Sera of 173 patients with various forms of liver disease along with serum precipitates produced by polyethylene glycol were screened for the presence of a microsomal antigen referred to as ubiquitous tissue antigen (UTA) and its antibody by double diffusion precipitation in agarose gel. UTA was detected in 7 or 26 patients with chronic active hepatitis, 1 of 5 with alcoholic hepatitis, 2 of 14 with alcoholic cirrhosis and 18 of 98 with hepatoma. Antibodies to UTA were found only in 2 patients with chronic active hepatitis, 1 with alcoholic cirrhosis and 1 with hepatoma. No UTA or its antibody were noted in sera of 5 patients with alcoholic fatty liver, 10 patients with hepatitis B, and 15 asymptomatic carriers of HBsAg. Positivity for the UTA or its antibody was restricted to severe, chronic cases irrespective of diagnosis, indicating that persistent tissue destruction might be necessary for antigen release or antibody formation.
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PMID:Detection of a microsomal antigen and its antibody in human liver diseases. 22 26

A recent case-control study on 577 lichen planus (LP) patients and 1008 controls confirmed that LP patients may significantly associate with a chronic liver disease (CLD) which is independent from drug or alcohol intake and has some connection with hepatitis B virus (HBV) infection. The study, however, failed to define the nature of CLD. This has been investigated through the clinical and laboratory features of 50 patients with LP and impaired liver function tests. Overall, the laboratory signs of cell necrosis prevailed over those of cholestasis and a good relationship with the HBV and HCV infections was found. Ninety percent of patients with LP and CLD had antibodies to one or another of the major viruses involved in infectious hepatitis. No patient had anti-liver kidney microsomal antibodies type 1. Liver biopsies were done in 12 cases and mostly revealed a chronic active hepatitis evolving into cirrhosis. No evident cases of primary biliary cirrhosis were found. It appears that LP associated CLD is post-viral in nature.
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PMID:Clinical and laboratory presentation of lichen planus patients with chronic liver disease. 132 93

Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B1 or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiation-promotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with CCl4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of alpha-fetoprotein or ferritin, nor was there a correlation with alpha-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal EH in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.
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PMID:Serum epoxide hydrolase (preneoplastic antigen) in human and experimental liver injury. 133 49

The Hepatitis Delta Virus (HDV) is a small RNA virus which replicates only in patients who are concurrently infected with hepatitis B virus (HBV). Delta hepatitis is endemic particularly in countries in the Mediterranean basin. In other parts of the world, HDV infection occurs among intravenous drug addicts and persons who receive multiple blood transfusion. HDV superinfection in a chronic HBV carrier often leads to severe chronic hepatitis and cirrhosis, whereas acute HDV and HBV co-infection is frequently associated with fulminant hepatitis. Diagnosis is usually based on the detection of HDV antigen in liver tissue and antibody to HDV (anti-HD) in serum. Nowadays, HDV antigen can also be detected in serum using immunoblot assay. The presence of HDV-RNA can now be confirmed by molecular biology techniques including polymerase chain reaction (PCR). Interestingly, up to 50% of patients with chronic HDV infection have in the serum autoantibodies against microsomal antigens of the human liver and kidney (LKM) and antibodies against the basal cell layer of the rat forestomach. Therapeutic approaches including interferon therapy and liver transplantation are still under discussion. This review discusses in detail some of the main features of chronic HDV infection.
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PMID:Chronic hepatitis delta virus (HDV) infection. 202 85

Enlarged abdominal, mainly periportal, lymph nodes were detected by real time ultrasonography in 19% (42 of 227) of patients with chronic liver disease who had no evidence of tumor, upper gastrointestinal carcinoma, or lymphoproliferative disorder. Computed tomography, performed in 15 cases, always confirmed the sonographic findings. Lymph node biopsies from two patients showed reactive hyperplasia. Lymphadenopathy occurred more frequently in autoimmune (primary biliary cirrhosis, autoimmune, and liver-kidney microsomal antibody-positive chronic hepatitis: 33, 25, and 22% of cases, respectively) than nonautoimmune disease (cryptogenic, alcoholic, and hepatitis B virus-related chronic hepatitis: 16, 12, and 10% of cases, respectively) (p less than 0.005). Four of five patients with mixed polyclonal cryoglobulinemia or monoclonal gammopathy had lymphadenopathy. In 125 patients, including 25 with lymphadenopathy, who were monitored for a median period of 25 months, the ultrasonographic pattern remained unchanged. Abdominal, presumably benign, lymphadenopathy may accompany chronic liver disease, especially when prominent immunological features coexist. This should be kept in mind for the correct interpretation of such an ultrasound finding.
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PMID:Prevalence and significance of abdominal lymphadenopathy in patients with chronic liver disease: an ultrasound study. 240 31

The major hepatitis B virus (HBV) core protein is a viral structural protein involved in nucleic acid binding. Its coding sequence contains an extension of 29 codons (the "precore" region) at the amino terminus of the protein which is present in a fraction of the viral transcripts. This region is evolutionarily conserved among mammalian and avian HBVs, suggesting it has functional importance, although at least for duck HBV it has been shown to be nonessential for replication of infectious virions. Using in vitro assays for protein translocation across the endoplasmic reticulum membrane, we found that the precore region of the HBV genome encodes a signal sequence. This signal sequence was recognized by signal recognition particle, which targeted the nascent precore protein to the endoplasmic reticulum membrane with efficiencies comparable to those of other mammalian secretory proteins. A 19-amino acid signal peptide was removed by signal peptidase on the lumenal side of the microsomal membrane, generating a protein similar to the HBV major core protein, but containing 10 additional amino acids from the precore region at its amino terminus. Surprisingly, we found that 70-80% of this signal peptidase-cleaved product was localized on the cytoplasmic side of the microsomal vesicles and was not associated with the membranes. We conclude that translocation was aborted by an unknown mechanism, then the protein disengaged from the translocation machinery and was released back into the cytoplasm. Thus, a cytoplasmically disposed protein was created whose amino terminus resulted from signal peptidase cleavage. The remaining 20-30% appeared to be completely translocated into the lumen of the microsomes. A deletion mutant lacking the carboxy-terminal nucleic acid binding domain of the precore protein was similarly partitioned between the lumen of the microsomes and the cytoplasmic compartment, indicating that this highly charged domain is not responsible for the aborted translocation. We discuss the implications of our findings for the protein translocation process and suggest a possible role in the virus life cycle.
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PMID:Targeting of the hepatitis B virus precore protein to the endoplasmic reticulum membrane: after signal peptide cleavage translocation can be aborted and the product released into the cytoplasm. 328 45

The gene encoding the major core protein P22c of hepatitis B virus is preceded by a precore sequence. Expression of the core gene with the precore in Escherichia coli results in a membrane protein of HBe antigenicity. Expression in mammalian cells generates secreted HBeAg. To study the biosynthetic pathway of HBeAg and the function of precore in this process, we translated mRNAs for core proteins with and without precore using reticulocyte lysates and microsomal vesicles. The precore sequence was cleaved cotranslationally as a signal peptide, probably at alanine 19. The processed product P23e was partially translocated to the lumen of the microsomes. The arginine-rich carboxy-terminal domain of P23e was however not translocated and susceptible to trypsin. Clusters of positive-charged amino acids seem to act as a novel type of translocation stop signal. Trypsin generated a P16e which no longer had a transmembraneous configuration. The findings may explain the biosynthesis and potential function of HBeAg in hepatitis B virus-infected hepatocytes.
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PMID:Formation of transmembraneous hepatitis B e-antigen by cotranslational in vitro processing of the viral precore protein. 335 97

The concentrations of triiodothyronine (T3), thyroxine (T4), T3/T4 ratio, free thyroxine index, and thyroxine-binding globulin were investigated in 114 viral hepatic disease patients and 36 controls. The T3/T4 ratio in healthy hepatitis B virus carriers was significantly greater than those in the controls and fulminant, acute, or chronic active hepatitis patients. The T3/T4 ratio in the fulminant hepatitis patients was significantly less than those in the controls and other liver disease patients. The correlation coefficient between the T3/T4 ratio and microsomal arylamidase activity in liver tissue from 30 patients was 0.78 (p less than 0.001). The correlation coefficient between the T3/T4 ratio and the content of cholinesterase was 0.64 (p less than 0.001). These results suggest that the T3/T4 ratio represents a marker of microsomal function and is useful for estimation of prognosis of fulminant hepatitis or differentiation of various viral hepatic diseases.
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PMID:Serum thyroid hormone, triiodothyronine, thyroxine, and triiodothyronine/thyroxine ratio in patients with fulminant, acute, and chronic hepatitis. 370 63

We report the case of a patient with liver-kidney microsomal antibody (LKM) positive chronic active hepatitis (CAH) which was followed-up for 12 years. Besides LKM the patient's serum was positive for thyroid microsomal antibodies, but negative for antinuclear, liver membrane and smooth muscle antibodies as well as hepatitis B virus markers. The patient was HLA B 8 negative. The disease of the 23 year old female patient began as an acute hepatitis which progressed to CAH. Immuno-suppressive therapy with a combination of prednisone and azathioprine led to a long lasting normalization of transaminases, gammaglobulin levels, and finally liver histology. Despite a normal liver histology after more than six years of continuous treatment the discontinuation of therapy was followed by a relapse. The presented case with LKM-positive CAH demonstrates that discontinuation of immuno-suppressive therapy may be followed by a relapse even if normal liver histology has been achieved under treatment.
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PMID:[Chronic active hepatitis: recurrence after long-term immunosuppressive therapy in spite of normal liver histology]. 666 86

Integrated hepatitis B virus DNA derived from hepatocellular carcinomas can express, in one third of the cases investigated so far, a transcriptional activator encoded from 3' terminal truncated surface (preS/S) genes resulting in a C-terminally truncated middle surface protein (MHBst). Since MHBst, in contrast to the secreted MHBs, is retained in the secretory pathway at the ER, the question as to whether the retention generates the transcriptional activator function was investigated. Through fusion of MHBs to the ER-retention signal KDEL, it was shown that the intracellular retention does not generate the transcriptional activator function. Tryptic digestions of microsomal vesicles revealed that the amino terminal domain of MHBst directs into the cytoplasmic compartment, whereas in MHBs this domain directs into the lumen of the ER. This structural difference appears to be why transcriptional activator function arises. Through deletion analysis it was shown that non-membrane-associated MHBst proteins are also functional activators. Nonmembrane associated MHBst proteins represent a second class of MHBst proteins. These MHBst-proteins are homogenously distributed all over the cell and show no difference in functionality as compared to the membrane-associated MHBst proteins. MHBst53 (truncated at aa53) was shown to be a minimal activator of this class. Both classes of MHBst proteins were found to form dimers; an which is involved in mediating the dimerization. The integrity of this domain was also revealed to be a prerequisite for the functionality of the activator, suggesting a linkage between dimerization and functionality.
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PMID:Characterization of essential domains for the functionality of the MHBst transcriptional activator and identification of a minimal MHBst activator. 747 25


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