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)

Criteria for the classification of polyarteritis nodosa were developed by comparing 118 patients who had this disease with 689 control patients who had other forms of vasculitis. For the traditional format classification, 10 criteria were selected: weight loss greater than or equal to 4 kg, livedo reticularis, testicular pain or tenderness, myalgias, mononeuropathy or polyneuropathy, diastolic blood pressure greater than 90 mm Hg, elevated blood urea nitrogen or serum creatinine levels, presence of hepatitis B reactants in serum, arteriographic abnormality, and presence of granulocyte or mixed leukocyte infiltrate in an arterial wall on biopsy. The presence of 3 or more of these 10 criteria was associated with a sensitivity of 82.2% and specificity of 86.6%. A classification tree was also constructed, with 6 criteria being selected. Three of these, angiographic abnormality, biopsy-proven granulocyte or mixed leukocyte infiltrate in arterial wall, and neuropathy, were criteria used in the traditional format. The other 3 criteria used in the tree format included the patient's sex, weight loss greater than 6.5 kg, and elevated serum aspartate aminotransferase or alanine aminotransferase levels above the range of normal. The classification tree yielded a sensitivity of 87.3% and a specificity of 89.3%.
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PMID:The American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. 197 74

Infection of humans with hepatitis B virus (HBV) frequently results in suppression of hematopoiesis; in some cases this may lead to severe bone marrow failure. The mechanism whereby HBV infection affects hematopoiesis is unknown. In vitro exposure of human bone marrow to HBV results in a dose-dependent inhibition of erythroid (erythroid burst forming units, BFU-E; erythroid colony-forming units CFU-E), myeloid (colony-forming units-granulocyte macrophage CFU-GM), and lymphoid (CFU-[T-lymphocytic]-TL) hematopoietic stem cells. Inactivation or immunoabsorption of HBV from sera resulted in loss of HBV-induced inhibition of hematopoietic stem cells. De novo gamma interferon was not detectable in the supernatants of cultures of bone marrow cells with HBV. Antibodies to gamma interferon did not affect the suppression of hematopoietic stem cells by HBV. Hepatitis B surface antigen (HBsAg) was detected by immune electron microscopy in nuclei of greater than 70% of immature hematopoietic cells including myeloblasts, normoblasts, and lymphoblasts; granulocytes had mostly cytoplasmic HBsAg. Hepatitis B virus core antigen (HBcAg) was also detected in about 5% of HBV infected bone marrow cells by immunoperoxidase staining. These data indicate that HBV can infect hematopoietic cells and their progenitors, thus suggesting a wider range of tropism for HBV than previously reported. These results may provide a basis to study HBV infection in vitro, and the effects of HBV on hematopoiesis.
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PMID:In vitro hepatitis B virus infection of human bone marrow cells. 309 Jan 3

Eight patients with primary hepatocellular carcinoma (PHC) whose blood was positive for hepatitis B surface antigen (HBsAg) received treatment with cyclophosphamide, adriamycin, and 5-fluorouracil. In 4 cases, a rise in serum HBsAg titer occurred after chemotherapy. In 2 cases involving drug-related leukopenia, the rise in HBsAg titer was marked and associated with a sharp rise in the serum transaminase level (SGOT), up to 1700 in 1 case. Lower-dosage chemotherapy was safely resumed after SGOT had returned to pretreatment levels. No evidence of immunodeficiency after chemotherapy was revealed by in vitro testing of lymphocyte and granulocyte function, percentage of circulating T-cells, and immunoglobulin and complement levels. All 8 cases were negative for e antigen (eAg) and 4 were anti-positive. In 3 of 4 cases, anti-e became negative after chemotherapy, but all remained eAg negative. The negative eAg tests in these cases of PHC suggest they are not highly infectious, in spite of increased HBsAg titers in blood following chemotherapy.
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PMID:Primary hepatocellular carcinoma with hepatitis B antigenemia: effects of chemotherapy. 626 Mar 26

Many of the complications experienced by patients undergoing hemodialysis can be attributed to their altered host defenses. Increased cutaneous staphylococcal carriage along with repeated intravascular cannulation and defective mucocutaneous barriers lead to frequent invasion by infectious agents. Pathogens encounter granulocytes with subnormal locomotion, phagocytosis, and intracellular killing. Depressed cell-mediated immunity may be explained by shortened lymphocyte survival, lymphopenia, inhibition of lymphocyte transformation, and suppressor T-cell activity. This is manifested by cutaneous anergy, prolonged graft survival, altered tumor surveillance, and abnormal responses to hepatitis B and tuberculosis. Host interaction with the hemodialysis membrane leads to cellular disruption, which may induce autoantibodies. Activation of the alternate complement pathway during hemodialysis leads to granulocyte sequestration in small vessels, specifically within the lungs. These hemodialysis-induced alterations along with the manifestations of underlying chronic renal insufficiency may obscure clinical evaluation of these patients.
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PMID:Host defenses and immunologic alterations associated with chronic hemodialysis. 700 76

Cytokines, mediators of intercellular communication, penetrate as a new therapeutic group in to haematology, oncology, immunology and other disciplines. Recently two main spheres of indication of wider clinical use are in the foreground: 1. treatment of leukaemias and advanced solid tumours (interferons, interleukin-2, tumour-necrosis factor and others) and 2. treatment of impaired haematopoiesis (in clinical practice in particular erythropoietin, granulocyte-macrophage and granulocyte colonies stimulating factor). Other possibilities are offered by cytokines in the treatment of viral diseases (in addition to hepatitis B and C, perspectively also AIDS), inborn immunodeficiencies, progressive systemic sclerosis and other indications. In particular in oncological diseases, contrary to original assumptions, monotherapy with cytokines will not be greatly extended and a combination of cytokines with classical treatment will be used. The limiting factor in addition to cost is the considerable toxicity of some cytokines which calls for alternative routes of administration (local, compartmental etc).
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PMID:[Cytokine therapy]. 771 24

There is a compelling clinical need for adjuvants suitable for human use to enhance the efficacy of vaccines in the prevention of life-threatening infection. Candidate populations for such vaccine-adjuvant strategies include normal individuals at the two extremes of life, as well as the ever increasing population of immunocompromised individuals. In addition, adjuvants that would increase the efficiency of vaccination with such vaccines as those directed against hepatitis B and Streptococcus pneumoniae would have an even greater general use. Cytokines, as natural peptides intimately involved in the normal immune response, have great appeal as potential adjuvants. An increasing body of work utilizing recombinant versions of interleukin-1, -2, -3, -6, -12, gamma-interferon, tumor necrosis factor, and granulocyte-monocyte-colony stimulating factor has shown that cytokines do have vaccine adjuvant activity. However, in order to optimize adjuvant effect and minimize systemic toxicity, strategies in which the cytokine is fused to the antigen, or the cytokine is presented within liposomes or microspheres appear to be necessary to make this a practical approach suitable for human use. There is much promise in this approach, but there is much work to be accomplished in order to optimize the pharmacokinetics of cytokine administration as well as its side effect profile.
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PMID:Cytokines as potential vaccine adjuvants. 786 56

We have recently reported that administration of recombinant tumor necrosis factor alpha (TNF-alpha) to hepatitis B virus (HBV) transgenic mice reduces the hepatic steady-state content of HBV-specific mRNA by up to 80% in the absence of liver cell injury. In the current study, we analyzed the regulatory effects of several other inflammatory cytokines in the same transgenic model system. Hepatic HBV mRNA content was reduced by up to 90% following administration of a single noncytopathic dose (100,000 U) of interleukin 2 (IL-2). Comparable effects were produced by administration of alpha and beta interferons (IFN-alpha and IFN-beta), but only after multiple injections of at least 500,000 U per mouse. Importantly, the regulatory effect of IL-2 was completely blocked by the prior administration of antibodies to tumor necrosis factor alpha (TNF-alpha), which did not block the effect of IFN-alpha or IFN-beta. In contrast to these observations, recombinant IFN-gamma, IL-1, IL-3, IL-6, TNF-beta, transforming growth factor beta, and granulocyte-monocyte colony-stimulating factor were inactive in this system. These results suggest that selected inflammatory cytokines can down-regulate HBV gene expression in vivo by at least two pathways, one that is dependent on TNF-alpha and another that is not. These results imply that antigen-nonspecific products of the intrahepatic HBV-specific inflammatory response may contribute to viral clearance or persistence during HBV infection.
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PMID:Interleukin-2 and alpha/beta interferon down-regulate hepatitis B virus gene expression in vivo by tumor necrosis factor-dependent and -independent pathways. 810 92

MxA protein is interferon inducible, and its role as an antiviral mediator is being studied in various viral diseases. Several cytokines, including type 1 interferons (alpha and beta), interleukins 2 and 12, and granulocyte, macrophage, and granulocyte-macrophage colony-stimulating factors, were tested for their ability to induce human MxA protein synthesis in peripheral blood mononuclear cells from 15 chronic hepatitis B virus-infected patients and 6 healthy subjects as controls. Constitutive MxA expression was scarce in patients and controls but increased significantly in response to type I interferons. MxA responsiveness to interferon alpha was diminished significantly in chronic hepatitis B patients, compared with healthy donors (P < 0.05); this effect was more marked in patients with high viremia levels. Interleukins 2 and 12, and none of the colony-stimulating factors tested, induced low, but detectable, MxA protein levels. These results indicate that chronic infection by hepatitis B virus may impair activation of the immune cells and their capacity to respond to type 1 interferons.
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PMID:Impaired interferon induction of human MxA protein in chronic hepatitis B virus infection. 909 49

Dendritic cells (DC) derived from bone marrow precursors of BALB/c or C57BL/6 mice in low-serum cultures supplemented with granulocyte macrophage colony stimulating factor and Flt(3) ligand were pulsed in vitro with hepatitis B surface antigen (HBsAg) particles. DC processed exogenous HBsAg and presented its MHC class I-binding epitopes to cytotoxic T lymphocytes (CTL). This specific and restricted interaction of DC with CTL stimulated release of IFN-gamma and macrophage inflammatory protein (MIP)-1 alpha from the responding CTL. MIP-1 alpha enhanced the survival of DC in vitro but did not induce proliferation. Furthermore, co-delivery of MIP-1 alpha facilitated CTL priming in vivo to exogenous HBsAg in low responder C57BL/6 (H-2(b)) mice: a single injection of a low dose of HBsAg particles (without further adjuvants) successfully primed K(b)-restricted CTL responses to HBsAg only when the exogenous antigen was co-delivered with 100 ng MIP-1 alpha. These in vitro and in vivo data point to an important role of MIP-1 alpha in the DC-dependent priming of CTL to exogenous viral antigens.
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PMID:Monocyte inflammatory protein-1 alpha facilitates priming of CD8(+) T cell responses to exogenous viral antigen. 1096 32

Infections are common in systemic lupus erythematosus (SLE), and remain a source of mortality. The types of infections (such as pneumonia, urinary tract infection, cellulitis, and sepsis) in SLE patients are similar to the general population and include the same pathogens (Gram-positive and Gram-negative). SLE patients may also develop opportunistic infections, especially when treated with immunosuppressive agents. As a high-risk population, identification and treatment of chronic infections such as tuberculosis, hepatitis B, or human immunodeficiency virus (HIV), are important prior to the institution of immunosuppression to prevent reactivation or exacerbation of the infection. A common caveat is to distinguish between a lupus flare and an acute infection; judicious use of corticosteroids and cytotoxic drugs is critical in limiting infectious complications. The risk factors associated with susceptibility to disease include severe flares, active renal disease, treatment with moderate or high doses of corticosteroids and/or immunosuppressive agents, and others. Genetic factors (complement deficiencies, mannose-binding lectin, Fcgamma III, granulocyte macrophage colony-stimulating factor [GM-CSF], osteopontin) may predispose certain SLE patients to develop infections. Parameters including C-reactive protein (CRP) and adhesion molecules may help to differentiate an infectious disease from an exacerbation of the disease. Finally, the mechanism of molecular mimicry by specific microbial agents may play a role in the induction of SLE.
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PMID:SLE and infections. 1279 59


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