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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Kings College group was the first to describe a clinical syndrome similar to autoimmune hepatitis in children and young adults transplanted for non-immune mediated liver diseases. They coined the term "de novo autoimmune hepatitis". Several other liver transplant centres confirmed this observation. Even though the condition is uncommon, patients with de novo AIH are now seen in most of the major transplant centres. The disease is usually characterized by features of acute hepatitis in otherwise stable transplant recipients. The most characteristic laboratory hallmark is a marked hypergammaglobulinaemia. Autoantibodies are common, mostly ANA. We described also a case of LKM1-positivity in a patients transplanted for Wilson's disease, however this patients did not develop clinical or histological features of AIH. Development of SLA/LP-autoantibodies is also not described. Therefore, serologically de novo AIH appears to correspond to type 1 AIH. Like classical AIH patients respond promptly to treatment with increased doses of prednisolone and azathioprine, while the calcineurin inhibitors cyclosporine or tacrolimus areof very limited value - which is not surprising, as almost all patients develop de novo AIH while receiving these drugs. Despite the good response to treatment, most patients remain a clinical challenge as complete stable remissions are uncommon and flares, relapses and chronic disease activity can often occur. Pathogenetically this syndrome is intriguing. It is not clear, if the immune response is directed against allo-antigens, neo-antigens in the liver, or self-antigens, possibly shared by donor and host cells. It is very likely that the inflammatory milieu due to alloreactive cells in the transplanted organ contribute to the disease process. Either leading to aberrant antigen presentation, or providing co-stimulatory signals leading to the breaking of self-tolerance. The development of this disease in the presence of treatment with calcineurin inhibitors supports the view held by most specialists in autoimmune hepatitis that these drugs, even though effective in acute disease, are not helpful in the long-term management of autoimmune liver diseases.
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PMID:De novo autoimmune hepatitis after liver transplantation. 1793 Dec 3

Inoculation with the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of mice results in an acute encephalitis associated with an immune-mediated demyelinating disease. During acute disease, infiltrating CD8(+) T cells secrete gamma interferon (IFN-gamma) that controls replication in oligodendrocytes, while infected astrocytes and microglia are susceptible to perforin-mediated lysis. The present study was undertaken to reveal the functional contributions of the activating NKG2D receptor in host defense and disease following JHMV infection. NKG2D ligands RAE-1, MULT1, and H60 were expressed within the CNS following JHMV infection. The immunophenotyping of infiltrating cells revealed that NKG2D was expressed on approximately 90% of infiltrating CD8(+) T cells during acute and chronic disease. Blocking NKG2D following JHMV infection resulted in increased mortality that correlated with increased viral titers within the CNS. Anti-NKG2D treatment did not alter T-cell infiltration into the CNS or the generation of virus-specific CD8(+) T cells, and the expression of IFN-gamma was not affected. However, cytotoxic T-lymphocyte (CTL) activity was dependent on NKG2D expression, because anti-NKG2D treatment resulted in a dramatic reduction in lytic activity by virus-specific CD8(+) T cells. Blocking NKG2D during chronic disease did not affect either T-cell or macrophage infiltration or the severity of demyelination, indicating that NKG2D does not contribute to virus-induced demyelination. These findings demonstrate a functional role for NKG2D in host defense during acute viral encephalitis by selectively enhancing CTL activity by infiltrating virus-specific CD8(+) T cells.
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PMID:NKG2D receptor signaling enhances cytolytic activity by virus-specific CD8+ T cells: evidence for a protective role in virus-induced encephalitis. 1816 Apr 33

Viral infection of the central nervous system (CNS) results in varied outcomes ranging from encephalitis, paralytic poliomyelitis or other serious consequences. One of the principal factors that directs the outcome of infection is the localized innate immune response, which is proceeded by the adaptive immune response against the invading viral pathogen. The role of the immune system is to contain and control the spread of virus within the CNS, and paradoxically, this response may also be pathological. Studies with a neurotropic murine coronavirus, mouse hepatitis virus (MHV) have provided important insights into how the immune system combats neuroinvasive viruses, and have identified molecular and cellular mechanisms contributing to chronic disease in persistently infected mice.
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PMID:Mouse hepatitis virus infection of the CNS: a model for defense, disease, and repair. 1850 18

Autoimmune hepatitis (AIH) is a chronic disease of unknown etiology that is characterized by the presence of circulatory autoantibodies and inflammatory histological changes in the liver. Although the pathogenesis of AIH is not known, it is thought that, in a genetically predisposed individual, environmental factors such as viruses can trigger the autoimmune process. Herpes simplex virus, Epstein-Barr virus, measles virus, and hepatitis viruses are thought to play a role in the etiology of AIH. Proteins belonging to these viruses may be similar to the amino acid chains of different autoantigens in the liver, this causes immune cross reactions and liver tissue damage. We report a case of severe AIH following varicella zoster infection in a 23-year-old man, and speculate that, based on the molecular mimicry hypothesis, the liver damage was caused by an immune cross reaction to the viral proteins. Varicella-zoster-induced AIH has not been reported previously.
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PMID:Severe autoimmune hepatitis triggered by varicella zoster infection. 1924 2

The serologic responses in hepatitis A, B, C and D have been extensively studied and a wide range of sensitive and specific serologic assays are available for detection of the antigens and antibodies of these hepatitis. Today, the correct diagnosis, the evaluation of the patient, the replicative status of the virus, the discrimination between acute and chronic disease, and the response to drugs that affect the course of the hepatitis can be assessed by using serodiagnostic tests.
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PMID:[Serological markers in viral hepatitis]. 1925 25

Chronic expression of CXC chemokine ligand 10 (CXCL10) in the central nervous system (CNS) following infection with the neurotropic JHM strain of mouse hepatitis virus (JHMV) is associated with an immune-mediated demyelinating disease. Treatment of mice with anti-CXCL10 neutralizing antibody results in limited CD4+ T cell infiltration into the CNS accompanied by a reduction in white matter damage. The current study determines the antigen-specificity of the T lymphocytes present during chronic disease and evaluates how blocking CXCL10 signaling affects retention of virus-specific T cells within the CNS. CXCL10 neutralization selectively reduced accumulation and/or retention of virus-specific CD4+ T cells, yet exhibited limited effect on virus-specific CD8+ T cells. The response of CXCL10 neutralization on virus-specific T cell subsets is not due to differential expression of the CXCL10 receptor CXCR3 on T cells as there was no appreciable difference in receptor expression on virus-specific T cells during either acute or chronic disease. These findings emphasize the importance of virus-specific CD4+ T cells in amplifying demyelination in JHMV-infected mice. In addition, differential signals are required for trafficking and retention of virus-specific CD4+ and CD8+ T cells during chronic demyelination in JHMV-infected mice.
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PMID:CXCL10 and trafficking of virus-specific T cells during coronavirus-induced demyelination. 1962 87

Alcohol is a risk factor for chronic disease burden in developed countries. Alcoholic liver disease affects 1% of the North American population and is the second most frequent indication for liver transplantation in the United States. It is a spectrum that ranges from simple hepatic steatosis to alcoholic hepatitis to steatohepatitis and eventually cirrhosis. The clinical spectrum of alcoholic hepatitis is wide and ranges from the asymptomatic patient to overt liver failure and death. Liver biopsy as a means of prognostication in alcoholic hepatitis has mostly been replaced with less invasive scoring systems. The management of alcoholic liver disease is challenging. Abstinence is the cornerstone of therapy and should include rehabilitation with a multidisciplinary approach. No specific treatment is required in mild to moderate alcoholic hepatitis. In patients with severe hepatitis, there appears to be a moderate survival benefit from the use of either corticosteroids or pentoxifylline in the absence of contraindications to their use. Nonresponders should have steroid therapy withdrawn by day 7, as persistence with therapy is not beneficial. Orthotopic liver transplantation remains the definitive therapy for decompensated alcoholic cirrhosis despite alcohol abstinence. More studies are needed to define the optimal timing of orthotopic liver transplantation and patients at risk of alcohol relapse post-transplant. Mt Sinai J Med 76:484-498, 2009. (c) 2009 Mount Sinai School of Medicine.
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PMID:Controversies in the management of alcoholic liver disease. 1978 55

Q fever is a zoonotic disease caused by the ubiquitous pathogen Coxiella burnetii responsible for acute and chronic clinical manifestations. Farm animals and pets are the main reservoirs of infection, and transmission to human beings is mainly accomplished through inhalation of contaminated aerosols. This illness is associated with a wide clinical spectrum, from asymptomatic or mildly symptomatic seroconversion to fatal disease. In humans Q fever can manifest as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. In contrast in animals, Q fever is in most cases, strikingly asymptomatic. The definite diagnosis of Q fever is made based on a significant increase in serum antibody titers, the determination of which often requires considerable time, and therefore patients must be monitored for a certain period. The treatment is effective and well tolerated, but must be adapted to the acute or chronic pattern with the tetracyclines to be considered the mainstay of antibiotic therapy. Several actions have been proposed to prevent and reduce the animal and environmental contamination. Vaccination of animals in infected flocks, as well as in uninfected ones close to them, with an efficient vaccine can prevent abortions and shedding of the bacteria.
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PMID:Q Fever. 1987 49

Viral hepatitis can be caused by the hepatitis A, B, C, D and E viruses. In the Western world, hepatitis A, B or C do not seem to influence the course of pregnancy, whereas hepatitis E infection, when contracted during the second or third trimester, seems to have a higher risk of developing into a fulminant hepatitis. Mother-to-infant transmission of hepatitis A seems to be very uncommon. The majority of HBsAg-positive and HBeAg-positive mothers can transmit the disease vertically. The timing of transmission is predominantly peripartum, and newborns of HBsAg-positive mothers should receive hepatitis B immunoglobulins within 12 h of birth, with HBV vaccine at birth and 1 and 6 months later. Hepatitis C is more often a chronic disease. Vertical transmission of hepatitis C is considered to be relatively rare but high viraemia or coinfection with HIV can increase this risk. There is currently no treatment to prevent this vertical transmission and pregnancies among HCV-positive mothers should not be discouraged. Infants should be tested for anti-HCV at 1 year and followed for the development of hepatitis. Breast feeding does not seem to play an important role in the transmission of hepatitis B and C.
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PMID:Treatment of viral hepatitis in pregnancy. 1992 3

PFAPA syndrome is a chronic disease classified in the group of autoinflammatory syndromes characterized by periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis in young children. The etiology of this disorder is still unknown, but a primary dysfunction of the innate immune system seems to be involved. According to Marshall criteria, it is not possible to diagnose PFAPA in the presence of autoimmune diseases. We present here the case report of an 8-month girl with PFAPA who developed autoimmune hepatitis type 2 at the age of 18 months. We suppose that the dysregulation in innate immunity that is typical of patients with PFAPA could trigger autoimmune disorders such as autoimmune hepatitis in susceptible subjects. The possible relationships between immune-system dysfunction peculiar to this syndrome and autoimmune hepatitis are discussed.
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PMID:Autoimmune hepatitis type 2 arising in PFAPA syndrome: coincidences or possible correlations? 2014 86


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