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)

Insulin suppresses hepatitis B surface antigen (HBsAg) gene expression and stimulates cell proliferation in human hepatoma Hep3B cells. 12-O-tetradecanoyl phorbol-13-acetate, TPA, has been demonstrated to mimic insulin actions in these cells. We examined the role of phosphatidylinositol 3-kinase (PI 3-kinase) in the signaling pathways of insulin and TPA towards these two biological phenomena in Hep3B cells. The pre-treatment of 5 microM of wortmannin diminished insulin suppressed HBsAg production and completely abolished insulin stimulated cell proliferation. However, wortmannin had no effect on TPA actions in both HBsAg suppression and cell growth stimulation. We further investigated the effect of wortmannin in mitogen-activated protein kinases (MAPKs) activation induced by insulin or TPA. After the pretreatment of wortmannin, insulin activated MAPKs was completely blocked, but TPA was still capable to activate MAPKs. These results suggest that PI 3-kinase is involved in insulin actions but not in TPA effects, and allow us to dissociate the signaling pathways of insulin and TPA in human hepatoma Hep3B cells.
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PMID:Phosphatidylinositol 3-kinase is required for the regulation of hepatitis B surface antigen production and mitogen-activated protein kinase activation by insulin but not by TPA. 960 88

Insulin stimulates cellular oncogenic activators such as c-jun, c-fos, and c-myc; and hepatitis B virus (HBV) X, a viral transactivator, is known to induce liver cancer in transgenic mice. In this respect, the effect of insulin on the expression of HBx protein was investigated in HepG2 cells. Insulin-stimulated transcription from the HBV X promoter in a dose-dependent manner was assessed by chloramphenicol acetyltransferase (CAT) assay. A mutation preventing AP-1 binding to the E element abolished the activation of the HBV X promoter by insulin. In addition, insulin stimulated the minimal thymidine kinase (tk) gene promoter activity through both the HBV E element and the consensus AP-1 binding site in HepG2 cells. An electrophoretic mobility shift assay (EMSA) using insulin-treated HepG2 nuclear extracts showed that insulin actually enhanced the binding of nuclear proteins to the HBV E element as well as to the consensus AP-1 binding site. Both HBV E and AP-1 oligonucleotides were effective competitors for this binding. These results showed that insulin elevated the expression of HBx protein through the AP-1 binding site of HBV EnI. We suggest that insulin can augment the role of HBx in the development of hepatocellular carcinoma (HCC) in HBV-infected liver, probably through interaction with other cellular oncogenes.
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PMID:Insulin activates the hepatitis B virus X gene through the activating protein-1 binding site in HepG2 cells. 983 4

Non-insulin-dependent diabetes mellitus (NIDDM) may be associated with chronic hepatitis C virus (HCV) infection. This was studied further in two parts. First, 1,151 patients with HCV-related cirrhosis and 181 patients with hepatitis B virus (HBV)-related cirrhosis, well matched for age, sex, and severity of cirrhosis, were reviewed retrospectively. The prevalence of diabetes mellitus was higher in HCV-related cirrhosis (23.6%) than in HBV-related cirrhosis (9.4%; odds ratio [OR], 2.78; 95% confidence interval [CI], 1.6-4.79; P =.0002). The prevalence of diabetes mellitus was associated closely with the Child-Pugh score (OR, 3.83; 95% CI, 2. 38-6.17; P <.0001) and increasing age (OR, 1.02; 95% CI, 1.00-1.03; P =.0117). Second, 235 patients with biopsy confirmed chronic HBV or HCV underwent an oral glucose tolerance test. Only 1 of 70 patients with chronic viral hepatitis without cirrhosis was diabetic. However, 31 of 127 patients with HCV-related cirrhosis (24.4%) were diabetic compared with 3 of 38 patients with HBV-related cirrhosis (7.9%, P =.0477). The major variables associated with NIDDM were cirrhosis (OR, 14.39; 95% CI, 1.91-108; P =.0096) and male sex (OR, 4.64; 95% CI, 1. 32-16.18; P =.0161). Fasting insulin levels in 30 patients with HCV-related cirrhosis and diabetes mellitus were elevated significantly, which was consistent with insulin resistance. However, acute insulin responsiveness was reduced in all patients with HCV infection and diabetes suggesting concomitant B-cell dysfunction. This study confirms an association between HCV and NIDDM.
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PMID:Further evidence for an association between non-insulin-dependent diabetes mellitus and chronic hepatitis C virus infection. 1049 60

Vast changes are taking place in vaccinology consequent to the introduction of new technologies. Amongst the vaccines included in the Expanded Programme of Immunization (EPI), the pertussis vaccine has been replaced by acellular purified fractions devoid of side-effects. Non-pathogenic but immunogenic mutants of tetanus and diptheria toxins are likely to replace the toxoids. An effective vaccine against hepatitis B prepared by recombinant technology is in large-scale use. Conjugated vaccines against Haemophilus influenzae b, S. pneumococcus and meningococcus are now available, as also vaccines against mumps, rubella and measles. Combination vaccines have been devised to limit the number of injections. Vaccine delivery systems have been developed to deliver multiple doses of the vaccine at a single contact point. A genetically-engineered oral vaccine for typhoid imparts better and longer duration of immunity. Oral vaccines for cholera and other enteric infections are under clinical trials. The nose as a route for immunization is showing promise for mucosal immunity and for anti-inflammatory experimental vaccines against multiple sclerosis and insulin-dependent diabetes mellitus. The range of vaccines has expanded to include pathogens resident in the body such as Helicobacter pylori (duodenal ulcer), S. mutans (dental caries), and human papilloma virus (carcinoma of the cervix). An important progress is the recognition that DNA alone can constitute the vaccines, inducing both humoral and cell-mediated immune responses. A large number of DNA vaccines have been made and shown interesting results in experimental animals. Live recombinant vaccines against rabies and rinderpest have proven to be highly effective for controlling these infections in the field, and those for AIDS are under clinical trial. Potent adjuvants have added to the efficacy of the vaccines. New technologies have emerged to 'humanize' mouse monoclonals by genetic engineering and express these efficiently in plants. These recombinant antibodies are opening out an era of highly specific and safe therapeutic interventions. Human recombinant antibodies would be invaluable for treating patients with terminal tetanus and rabies. Antibodies are already in use for treatment of cancer, rheumatoid arthritis and allergies. An advantage of preformed antibodies directed at a defined target and given in adequate amounts is the certainty of efficacy in every recipient, in contrast to vaccines, where the quality and quantum of immune response varies from individual to individual.
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PMID:The impact of new technologies on vaccines. 1073 30

Hepatitis C virus (HCV) infection has recently been suggested to be a risk factor for the development of diabetes mellitus. The aim of our study was to investigate whether the prevalence of diabetes is increased among liver transplant recipients infected with HCV. We compared the prevalence of diabetes among 278 liver transplant recipients whose original cause of liver failure was HCV infection (110 patients), hepatitis B virus infection (HBV; 53 patients), and cholestatic liver disease (CLD; 115 patients). The pretransplantation prevalence of diabetes was higher in the HCV group (29%) compared with the HBV (6%) and CLD (4%) groups (P <.001). The prevalence of diabetes remained higher in the HCV group 1 year after transplantation: 37%, 10%, and 5% in the HCV, HBV, and CLD groups, respectively (P <.001). The cumulative steroid dose during the first year of transplantation was significantly lower in the HCV group compared with the CLD group. Multivariate analysis revealed that HCV-related liver failure (P =.002), pretransplantation diabetes (P <.0001), and male sex (P =.019) were independent predictors of the presence of diabetes 1 year after transplantation. The high prevalence of diabetes persisted in the HCV group, with 41% diabetic at 5 years. The majority of patients with diabetes mellitus (89%) required insulin therapy after transplantation. Patient and graft survival rates were similar among patients with and without diabetes. In conclusion, our study shows that there is a high prevalence of diabetes among liver transplant recipients infected with HCV both before and after transplantation.
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PMID:Hepatitis C-related cirrhosis: a predictor of diabetes after liver transplantation. 1086 93

Post-transplant diabetes mellitus (PTDM) is a common complication after orthotopic liver transplantation (oLT). In our study, we investigated the prevalence and risk factors one year after transplantation in 618 patients who underwent oLT between 1990 and 1996 in a single center. The influence of steroid medication and hepatitis B or C (HBV/HCV) was also studied. Before oLT 66 of the 618 patients were diabetic. After transplantation 37 of these 66 (56%) patients showed no further signs of DM. Of the 552 patients without DM before transplantation 39 (7.2%) developed new onset PTDM. There was no influence of steroid medication on the presence of PTDM (steroids 10.4% PTDM, no steroids 12.5% PTDM). In addition we found no influence of HBV or HCV-infection on PTDM development. Analysis for risk factors showed no significant influence of the diagnosis leading to oLT, of FK506 or Cyclosorin A medication, age, gender or Child-Pugh class. Five year patient survival was not influenced by the presence of PTDM, especially patients with a preexisting DM showed no reduced survival. However, a subgroup of patients with new onset insulin-requiring PTDM showed significantly reduced 5 year survival (p<0.05). In conclusion we found new onset PTDM in 7.2% of patients undergoing oLT one year after the operation. On the other hand in more than 50% of patients with preexisting DM, the disease was no longer present post-transplant. This could be an indication that DM is dependent on liver function in these patients. Patients with preexisting DM should not be excluded from transplantation if indicated. Development of new onset insulin-requiring PTDM could be an important prognostic factor for patient survival after oLT. Further investigations are necessary to evaluate the prognostic meaning of PTDM and the pathophysiologic mechanisms.
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PMID:Liver transplantation and diabetes mellitus. 1102 53

A 68-year old mildly obese Caucasian man underwent hepatic resection for multinodular hepatocellular carcinoma which had developed in the left lobe of a non-cirrhotic liver. The only risk factors found were heavy drinking, smoking, and serum markers of hepatitis B virus without virus genome in hepatocytes. The non tumoral liver was mildly fibrotic and iron overloaded (hepatic iron index: 1.6) with three types of iron-free lesions: (i) periportal clear hepatocyte foci, (ii) hyperplastic nodules and (iii) dysplastic or neoplastic nodules with well to moderately-differentiated hepatocellular carcinoma. The genetic investigation was negative for the C282Y and the H63D mutations of the HFE gene. This observation illustrates the multistep process of carcinogenesis in the non-cirrhotic liver and raises the question of i) the origin of this iron overload possibly linked to insulin resistance syndrome and ii) the role of iron as a co-carcinogen.
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PMID:[Premalignant lesions and hepatocellular carcinoma on non cirrhotic liver overloaded with iron]. 1108 32

From 1991 to 1998 we vaccinated 4835 neonates against hepatitis B virus (HBV) and monitored their humoral response to the recombinant vaccine. In a sample of 184 of these babies we studied the association between HLA class I and II genomic polymorphisms and humoral response to the vaccine and the association between the response and immune-mediated diseases. A subgroup of 96 babies also underwent HLA class III (C4A and C4B) typing. Four levels of humoral response were identified, each with a peculiar MHC restriction. Different HLA products seem to act as agonists (C4AQ0 and HLA-DQB1(*)02) or antagonists (C4AQ0, HLA-DQB1(*)02, and HLA-DRB1(*)11, DQB1(*)0301) in lowering humoral response to HBV vaccine. The group of responders was characterized more for lacking "nonresponder" alleles than for having specific "responder" ones. Tolerance to HBV peptides may have clinical implications, possibly being a marker for babies with a genetic risk of immunopathologies. In fact, many of the poor responders carried from two to four HLA-DQ alpha beta heterodimers predisposing to insulin-dependent diabetes mellitus and celiac disease. Two true nonresponders suffered from allergies and two slow responders had transient episodes of hyperglycemia.
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PMID:Humoral response to recombinant hepatitis B virus vaccine at birth: role of HLA and beyond. 1111 62

The incidence and significance of hepatocellular carcinoma (HCC) in non-alcoholic steatohepatitis (NASH) has not been previously evaluated in detail. We recently experienced a case of NASH with multicentric HCC in a female patient. At the age of 58 years, the patient was diagnosed with non-insulin-dependent diabetes mellitus, treated by insulin therapy. The patient did not drink alcohol. She was negative for all serological markers of hepatitis B and C virus infection. Because of liver dysfunction, a needle biopsy was performed at the age of 62 years, and pathological findings, such as fatty change, Mallory's body, nuclear glycogen and pericellular fibrosis, suggested a diagnosis of NASH. Subsequently, four nodules were detected in the liver by imaging. Liver biopsies were performed from each nodule. One nodule was pathologically diagnosed as a pseudolymphoma, while three other nodules were moderately differentiated HCC (10 years after the diagnosis of non-alcoholic steatohepatitis), well-differentiated HCC (11 years later) and dysplastic nodule (11 years later), suggesting multicentric occurrence of HCC. This case suggests that HCC could be a late complication of NASH.
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PMID:Hepatocellular carcinoma arising in non-alcoholic steatohepatitis. 1116 53

The adverse effects of vaccines include local reactions and systemic symptoms or illnesses. Local reactions are frequent, most often presenting as transient pain, redness, edema and/or nodule. Fever of short duration is the main systemic symptom, generally occurring within 24-48 hours following vaccination. Some vaccines have recognized specific adverse effects such as thrombocytopenic purpura for the measles-mumps-rubella vaccine, and febrile convulsions for the pertussis vaccine. Hepatitis B vaccine and Haemophilus influenzae type b vaccine have been respectively suspected to be responsible for neurological demyelinating disease and insulin-dependent diabetes mellitus, but large-scale epidemiological studies have failed to confirm these allegations.
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PMID:[Secondary effects of vaccinations]. 1127 Feb 59


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