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Results for “HEPATITIS, INFECTIONS”

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At least 433 records · Page 24Linked to original sources

PubMed2005

Cerebral ischemic attack secondary to hepatitis C virus infection.

Hepatitis virus C (HCV) is worldwide a health problem, which may lead to serious complications. The aim of this study was to correlate the onset of the cerebral ischemic attack accompanied by mixed cryoglobulinemia, with the chronic hepatitis C virus infection. These studies were carried out in 12 patients with serologic/virusologic confirmed chronic HCV infection associated with ischemic stroke. Ischemic stroke occurred in equal proportion in women and men. The patients did not know of HCV infection diagnosis at that moment. All patients had type II mixed monoclonal cryoglobulinemia, hypergammaglobulinemia with polyclonal IgG and monoclonal IgM, blood hyperviscosity, high level of cryocrit, positive rheumatoid factor, normal levels of serum transaminases, negative serum hepatitis B surface antigen (HBs Ag), negative anti HBc antibodies, positive HCV antibodies, positive serum RNA HCV, decreased serum C3 and C4 levels, antinuclear antibodies-false positive. Immunological tests for autoantibodies, namely, anti-Sm antibody, anti-RNP antibody, anti-SS-A and -B antibodies, and anti-Scl antibody were not detectable due to high level serum cryoglobulin. Cryoglobulin was washed several times with an isotonic chloride solution for purification, then subject to immunological analyses. The purified cryoglobulin contained monoclonal IgM-kappa, polyclonal IgG. Cryoglobulinemia is a risk factor for ischemic stroke, as it causes arterial thrombosis.

Brain Ischemia↗

PubMed2004

Central nervous system involvement in hepatitis C virus infection.

Hepatic encephalopathy is the most obvious neurological consequence of chronic hepatitis C virus (HCV) infection. There are also case reports of HCV-associated cerebral vasculitis. This review is concerned with the possibility of an effect of HCV on cerebral dysfunction, occurring at an early stage of chronic infection, prior to the development of cirrhosis and unrelated to vasculitis. There is emerging evidence of mild, but significant neurocognitive impairment in HCV infection, which cannot be attributed to substance abuse, coexistent depression, or hepatic encephalopathy. In vivo magnetic resonance spectroscopy and neurophysiological studies have suggested that a biological mechanism may underlie these cognitive findings. The recent detection of HCV genetic sequences in postmortem brain tissue raises the intriguing possibility that HCV infection of the central nervous system may be related to the reported neuropsychological symptoms and cognitive impairment.

Cognition Disorders↗

PubMed1986

Interferons in the treatment of chronic hepatitis B virus infection.

Hepatitis B virus offers several properties that may help to determine how antiviral substances, such as interferon, work. A description of the phases of chronic hepatitis B virus infection is presented, as well as the rationale for interferon therapy as treatment.

Chronic Disease↗

PubMed2004

[Extrahepatic manifestations of hepatitis C virus infection].

Hepatitis C virus predominantly affects the liver, although it may also produce a number of extrahepatic manifestations, such as mixed cryoglobulinemia, salivary and lacrimal gland dysfunction, and several types of kidney disease. The pathogenesis of these conditions is not completely understood, but immunologic mechanisms are involved in many cases. In some patients with hepatitis C virus infection, the extrahepatic manifestations predominate and their proper diagnosis and management is very important.

Antiphospholipid Syndrome↗

PubMed2005

A case of acute hepatitis with positive autoantibodies who actually had hepatitis E virus infection.

Hepatitis E virus (HEV) is one of the major causative agents of acute hepatitis in many developing countries. On the other hand, recent intensive investigation has revealed the existence of non-imported cases in industrialized countries. We encountered a sporadic patient with hepatitis E in 1999, who had had no recent travel abroad. He was a 67-year-old Japanese, and his laboratory data were negative for serum markers of hepatitis A, B and C virus infection and positive anti-nuclear antibody, anti-smooth muscle antibody and high level of serum immunoglobulin G. He scored as probable autoimmune hepatitis (AIH) with the scoring system by the international AIH group. He was given a diagnosis of acute cryptogenic hepatitis including acute onset AIH in those days, but the recent retrospective examination with frozen stocked serum revealed his exact diagnosis. In conclusion, we must take HEV infection into consideration for the diagnosis of cryptogenic acute hepatitis even in the developed countries, and some patients with hepatitis E could demonstrate positive for autoantibodies similar to clinical features of AIH. This case demonstrated the needs for further studies about clinical feature of acute hepatitis E virus infection.

Journal Article↗

PubMed2005

Host genetics and the outcome of hepatitis B viral infection.

Hepatitis B Virus (HBV) infection can result in numerous different clinical outcomes. A complex combination of environment, and viral and host genetic factors play a critical role in determining both susceptibility to HBV persistence and the course of infection. Evidence is presented that suggests that host genetic factors play an important role in determining the outcome of HBV infection. This data from various groups demonstrates that multiple genes play a role in determining hepatitis B viral clearance or persistence. However, to identify all the relevant variants that affect the outcome of infection, alternative strategies such as genome-wide association studies with large sample sizes will be required to define the majority of the relevant polygenes.

Animals↗

PubMed1999

[Antiviral treatment of hepatitis C virus infection].

Hepatitis C virus infection is common and almost always chronic and can lead to cirrhosis and hepatocellular cancer. The primary goal of the treatment is virus eradication and the secondary is to reduce inflammation and liver cell damage. Interferon is the only effective therapy but disappearance of the virus is sustained in only 10 to 15%. The factors most closely associated with a response to treatment are absence of cirrhosis, low serum hepatitis C virus RNA level and genotype other than type 1. Recent studies have suggested that interferon treatment may reduce the subsequent risk of hepatocellular carcinoma in responders. The combination of interferon and oral ribavirin therapy increase the sustained response rate to about 40% in initial treatment and 50% for the treatment of relapse. The other therapeutic combination are less well documented. New agents such as hepatitis C virus-specific anti-protease may be available in the next future and treatment is evolving toward multiple-drug regimens.

Antiviral Agents↗

PubMed2006

Possible contribution of serum activin A and IGF-1 in the development of hepatocellular carcinoma in Egyptian patients suffering from combined hepatitis C virus infection and hepatic schistosomiasis.

OBJECTIVES: The present study evaluated the role of activin A, insulin-like growth factor 1 (IGF-1) and insulin-like growth factor binding protein 3 (IGFBP-3) in Egyptian patients suffering from combined hepatitis C virus (HCV) infection and hepatic schistosomiasis. DESIGN AND METHODS: Four groups were included in the present study. Group I: 30 healthy subjects were included as controls; Group II (HCV): 30 patients with chronic liver disease due to HCV infection without evidence of schistosomiasis; Group III (SHF + HCV): 30 patients with combined disease, chronic schistosomal hepatic fibrosis (SHF) and chronic hepatitis C infection; Group IV (HCC): 30 patients with hepatocellular carcinoma associated with chronic hepatitis C virus and schistosomal infection. RESULTS: Patients with HCV, HCV + SHF and those with HCC had a significantly higher serum activin A compared with the control group (P < 0.001). Serum activin A level (mean +/- SD) was 5.7 +/- 2.76, 10.59 +/- 3.59, 15.39 +/- 4.61 and 19.93 +/- 5.43 ng/mL in controls, HCV patients, HCV + SHF patients and HCC patients, respectively. Serum IGF-1 was significantly lower in HCV patients, HCV + SHF patients and HCC patients compared to the control group (P < 0.001). Serum IGF-1 was 121.7 +/- 73.4, 76.7 +/- 23.5, 35.7 +/- 17.6 and 39.9 +/- 25.9 ng/mL in controls, HCV patients, HCV + SHF patients and HCC patients, respectively. Similarly, serum IGFBP-3 was significantly lower in HCV patients, HCV + SHF patients and HCC patients compared to the control group (P < 0.001). Furthermore, serum insulin-like growth factor binding protein 3 (IGFBP-3) was significantly lower in patients with HCC compared to patients with HCV or those with HCV + SHF (P < 0.01 and P = 0.024, respectively). The median (range) of serum IGFBP-3 was 4452 (352.2-8965), 3457 (1114-6000), 2114 (867-5901) and 1202 (576-3994) ng/mL in controls, HCV patients, HCV + SHF patients and HCC patients, respectively. Serum activin A correlated positively with Child-Pugh scoring in patients with HCV, HCV + SHF and those with HCC. The correlation coefficient was significant, at 0.001, in total cases. CONCLUSIONS: We conclude that patients with HCV, HCV + SHF and those with HCC have a significantly higher serum activin A when compared with controls. Serum activin A level was significantly higher in patients with HCV + SHF compared to those with HCV alone (P < 0.01) with a significant positive correlation between the serum activin A level and Child-Pugh scoring in patients with HCV, HCV + SHF and those with HCC. Furthermore, serum IGF-1 and IGFBP-3 levels were significantly reduced in patients with HCV, HCV + SHF and those with HCC compared to the control group. We suggest that this pattern (high activin A and low IGF-1 and its binding protein 3) may play a role in development of HCC in Egyptian patients suffering from combined hepatitis C virus infection and hepatic schistosomiasis.

Activins↗

PubMed2005

[Immune dysregulation mediated by hepatitis C virus infection].

Hepatitis C virus, which is non-cytopathic, establishes persistent infection in majority of patients after acute infection, causing various degrees of clinical liver disease. To escape and survive, hepatitis C virus may take ingenious strategies. Hepatitis C virus gene products interact host proteins to evade host immune responses in addition to the appearance of quasispecies. Against hepatitis C virus infection, host may avoid extensive tissue damage by inducing the activity of regulatory T cells. Insights into this mechanism of immune regulation may help to future development of novel therapies against hepatitis C virus.

Animals↗

PubMed2001

Experimental and emerging therapies for chronic hepatitis C virus infection.

Hepatitis C virus infection is prevalent throughout the world and is associated with substantial morbidity, mortality and health economic burden. No effective preventative measure, including vaccination, is currently available. Incremental and substantial progress in the rate of viral eradication using interferon-based therapies has been made over the past decade. The most recent advance has been related to the development of a pegylated form of IFN-alpha by two independent pharmaceutical companies. Pegylation of IFN-alpha appears to prolong its half-life, allowing for less frequent dosing. Reports have suggested that pegylated interferons are also associated with better efficacy for viral eradication in patients with hepatitis C virus. Slower progress also has been made in developing non-interferon-based therapeutic agents against hepatitis C virus, including protease inhibitors, helicase inhibitors, ribozymes, antisense therapies, cytokine-based therapies and T-cell-based therapeutic vaccines.

Animals↗

PubMed2006

Immunopathogenesis of hepatitis B virus infection.

Hepatitis B virus (HBV) infection is a non-cytopathic hepatotropic virus that can lead to severe liver disease including acute hepatitis, cirrhosis and hepatocellular carcinoma. Successful clearance of the virus as well as the establishment of liver disease is largely driven by a complex interaction between the virus and the host immune response. In this review, the immunological events, including both the innate and adaptive immune response are discussed in the setting of both acute and chronic HBV infection and liver disease.

Acute Disease↗

PubMed2000

Current Views on Hepatitis C Virus Infection.

Hepatitis C virus infection affects more than 4 million people in the United States and is a leading cause of liver failure necessitating transplantation. Effective combination therapies are now available for subgroups of patients at risk for progression to cirrhosis. The benefits of therapy in immunosuppressed hosts, such as HIV-infected patients and liver transplant recipients, are less well established.

Journal Article↗

PubMed1993

Hepatitis B virus replication in diverse cell types during chronic hepatitis B virus infection.

Hepatitis B virus-specific nucleic acid sequences and proteins have been detected in extrahepatic tissues of acutely and chronically infected patients. However, apart from peripheral blood mononuclear cells and bone marrow cells, little is known about the specific cell types that permit viral replication. In this study, we assessed the extrahepatic tissues of four patients who died with chronic hepatitis B virus infection and two uninfected controls by means of in situ hybridization and immunohistochemical study. Three of these patients had diffuse extrahepatic distribution of the virus. Hepatitis B virus nucleic acid sequences and proteins were detected in the lymph nodes, spleen, bone marrow, kidney, skin, colon, stomach, testes and periadrenal ganglia. The following cell types were found to be positive for hepatitis B virus: endothelial cells, macrophages/monocytes, hematopoietic precursors, basal keratinocytes, mucosal epithelial cells, stromal fibroblasts and sustentacular and neuronal cells. It is probable that these cells could support viral replication because hepatitis B virus DNA replicative intermediates, viral transcripts and HBsAg and HBcAg proteins were detected in most. These findings may be relevant to the initiation of extrahepatic syndromes associated with chronic hepatitis B virus infection such as vasculitis, glomerulonephropathy, neuropathy and dermatitis.

Adult↗

PubMed1998

Hepatosplenic gamma delta T-cell lymphoma associated with hepatitis B virus infection.

Hepatitis B virus (HBV) infection has been implicated in the development of hepatocellular and hematopoietic malignancies. We describe a patient with chronic hepatitis B who developed hepatosplenic gamma delta T-cell lymphoma. A 45-year-old woman presented with marked hepatosplenomegaly and hepatic failure during the course of chronic hepatitis B. Peripheral blood examination revealed 57% abnormal lymphoid cells which expressed the gamma delta T-cell receptor. The cytogenetic analysis of tumor cells showed an abnormal karyotype; 47, XX, -13, +2mar in all 20 metaphases examined. A clonal rearrangement of the T-cell receptor genes was demonstrated by Southern blot analysis, showing monoclonal expansion of tumor cells. A liver biopsy specimen showed fibrosis of the portal areas and sinusoidal infiltration of tumor cells. HBV infection was documented by the presence of IgG anti-HBc and anti-HBs antibodies in serum. Although HBV-DNA was not detected in tumor cells by polymerase chain reaction analysis, there is a possibility that proliferation of gamma delta T cells in response to HBV infection played a role in the pathogenesis of hepatosplenic gamma delta T-cell lymphoma.

Chronic Disease↗

PubMed1998

Extranodal lymphomas associated with hepatitis C virus infection.

Hepatitis C virus (HCV) infection may be complicated by non-Hodgkin's lymphoma. We describe eight cases of B-cell extranodal non-Hodgkin's lymphoma occurring during the course of chronic HCV-related hepatic disease (low-grade of mucosa-associated lymphoid tissue [MALT]-type; diffuse large cell; Burkitt; diffuse small cell). Some were localized to the liver (2), liver and spleen (1), spleen (1), peritoneal cavity (1), parotid gland (1); others manifested in the nasopharynx (1) and eyelid (1) but were accompanied by nodal disease. Four lymphomatous specimens available for molecular analysis exhibited clonal immunoglobulin gene rearrangements, lacked bcl-2, bcl-6, c-myc genes and p53 alterations, and did not contain replicative intermediate HCV RNA, as documented by a strand-specific reverse transcriptase-polymerase chain reaction. Low levels of positive-strand HCV RNA were detected in a single hepatic lymphoma, suggesting the presence of the virus in residual hepatocytes. The antigen-driven properties of HCV-associated B-cell malignant neoplasms may be considered for hepatic MALT-type lymphoma, which probably originated from lymphoid tissue acquired during long-standing HCV infection.

Adult↗

PubMed2004

Reduced numbers and impaired ability of myeloid and plasmacytoid dendritic cells to polarize T helper cells in chronic hepatitis C virus infection.

Hepatitis C virus (HCV) infection induces a wide range of chronic liver injuries. The mechanism by which HCV evades the immune surveillance system remains obscure. Blood dendritic cells (DCs) consist of myeloid and plasmacytoid subsets that play distinct roles in the regulation of antivirus immune responses; however, their roles in the pathogenesis of HCV infection are yet to be determined. We compared the numbers and functions of myeloid and plasmacytoid DCs between 43 patients with chronic hepatitis and 26 age-matched healthy volunteers. Absolute numbers of myeloid DCs, plasmacytoid DCs, and DC progenitors in the periphery were significantly lower in patients with chronic hepatitis than in healthy volunteers. Myeloid and plasmacytoid DCs from the patients had impaired abilities to stimulate allogeneic CD4 T cells and to produce interleukin (IL)-12 p70 and interferon- alpha , compared with those from healthy volunteers. After exposure to naive CD4 T cells, myeloid DCs from the patients were less able to drive the T helper type 1 response, whereas myeloid and plasmacytoid DCs from the patients primed more IL-10-producing cells than did those from healthy volunteers. In conclusion, in chronic HCV infection, both types of blood DCs are reduced and have an impaired ability to polarize T helper cells.

Cells, Cultured↗

PubMed2001

Previous or occult hepatitis B virus infection in hepatitis C virus-associated hepatocellular carcinoma without hepatic fibrosis.

We investigated the role of hepatitis B virus infection in development of hepatocellular carcinoma in hepatitis C virus-infected patients without hepatic fibrosis. Of 253 patients, 8 lacked hepatic fibrosis (group 1); group 2 included the remaining 245 patients. Clinicopathologic findings were compared between the groups. Hepatitis B x gene was sought in cancers and adjoining noncancerous liver. Group 1 showed better liver function parameters and milder active hepatitis than group 2. The proportion of patients with anti-hepatitis B virus antibody tended to be higher in group 1 than in group 2. The proportion of patients with hepatitis B x RNA in cancers was significantly higher in group 1 than in group 2. All group 1 patients had previous or occult hepatitis B virus infection. Previous or occult hepatitis B virus infection may be critical in development of hepatocellular carcinomas in hepatitis C virus-infected patients without hepatic fibrosis.

Aged↗

PubMed2006

Immune therapy including dendritic cell based therapy in chronic hepatitis B virus infection.

Hepatitis B virus (HBV) infection is a global public health problem. Of the approximately 2 billion people who have been infected worldwide, more than 400 million are chronic carriers of HBV. Considerable numbers of chronic HBV carriers suffer from progressive liver diseases. In addition, all HBV carriers are permanent source of this virus. There is no curative therapy for chronic HBV carriers. Antiviral drugs are recommended for about 10% patients, however, these drugs are costly, have limited efficacy, and possess considerable side effects. Recent studies have shown that immune responses of the host to the HBV are critically involved at every stage of chronic HBV infection: (1) These influence acquisition of chronic HBV carrier state, (2) They are important in the context of liver damages, (3) Recovery from chronic HBV-related liver diseases is dependent on nature and extent of HBV-specific immune responses. However, induction of adequate levels of HBV-specific immune responses in chronic HBV carriers is difficult. During the last one decade, hepatitis B vaccine has been administered to chronic HBV carriers as a therapeutic approach (vaccine therapy). The present regimen of vaccine therapy is safe and cheap, but not so effective. A dendritic cell-based therapeutic vaccine has recently been developed for treating chronic HBV infection. In this review, we will discuss about the concept, scientific logics, strategies and techniques of development of HBV-specific immune therapies including vaccine therapy and dendritic cell-based vaccine therapy for treating chronic HBV infection.

Antiviral Agents↗