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

Viral infections are a common complication of pregnancy and in some cases, can have profound effects for the unborn fetus. The human herpesvirus family is composed of large, enveloped DNA viruses that have close structural similarity. The family includes the herpes simplex viruses types 1 and 2, varicella zoster virus, Epstein Barr virus, cytomegalovirus (CMV), and human herpes viruses types 6, 7 and 8. These viruses all share the ability to establish latency and reactivate at a later time. Structural fetal abnormalities can result from intrauterine infection and transmission of the infection during the pregnancy or at the time of delivery can result in important neonatal disease. Human parvovirus B19 is a DNA virus with strong tropism for erythroid precursors and infection during pregnancy can result in fetal hydrops and stillbirth. The causative agents of hepatitis are hepatotropic viruses termed hepatitis A, B, C, D (deltavirus) and E. All except hepatitis B virus are RNA viruses. Vertical transmission of maternal infection with hepatitis B and C can result in significant long term sequelae.
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PMID:Viral infections in pregnancy. 1750 58

We describe a 26-year-old female referred to us because of recurrent bacterial pneumonia. Her immunoglobulin profile on admission was; IgG 1920 mg/l, IgA 60 mg/l, IgM 260 mg/l, IgD below 20 mg/l, IgE below 1 kU/l. Antinuclear antibodies, EBV VCA IgM, anti-parvovirus B19 IgM antibodies and hepatitis infection markers were all negative. Bone marrow aspiration revealed normal cellularity without abnormal cells, especially plasma cell proliferation. No rearrangement for IgH and TCR was observed as determined by Southern blot analysis. By the given data, a diagnosis of common variable immunodeficiency (CVID) was made. The genesis of this disease remained unclear. In this study, proliferation and immunoglobulin production with or without several stimulators were examined. Proliferation stimulated by PHA, Con-A, LPS, or IL-2 was decreased compared to that of healthy individuals. Immunoglobulin production after stimulation with several agents was quite low. Interestingly, however, IL-2 or IL-4 could increase IgM production on 6 days culture significantly. These results indicate that IL-2 or IL-4 possibly restore T cell responses to several antigens and induce B cell differentiation.
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PMID:Partial restoration of immunoglobulin production by cytokines in common variable immunodeficiency. 1782 53

Antiphospholipid antibodies show a close association to a variety of infections. Recent data implicate that parvovirus B19 may be used as a model-system for studying the interaction of viral infection and the development of these autoantibodies. B19-related diseases commonly associated with the acute infection show flu-like symptoms, transient arthralgias, leukopenia and thrombocytopenia, and, in pregnant women, spontaneous abortion and hydrops fetalis. Hepatitis, myocarditis, meningitis, encephalitis, as well as pure red cell anemia may occur occasionally. In addition, parvovirus B19 infections have been frequently described as the cause or trigger of various forms of autoimmune diseases affecting all blood cell lines, joints, connective tissue, uvea, and large and small vessels. Molecular mimicry may be one major contribution to the appearance of autoimmune antibodies, for example, antiphospholipid and antineutrophil cytoplasmic antibodies as well as antinuclear antigens. These mechanisms implicated in the pathogenesis of parvovirus B19-triggered autoimmune diseases, especially focused on the development of antiphospholipid antibodies, will be discussed in this mini review.
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PMID:Are antiphospholipid antibodies an essential requirement for an effective immune response to infections? 1789 22

Several viruses have been associated with the development of inflammatory arthritis, including the hepatitis viruses (hepatitis B virus and hepatitis C virus), HIV, the parvovirus B19, the human T-cell lymphotropic virus-I, and the alphaviruses. Here, we review the epidemiology, the pathophysiological mechanisms, the pertinent clinical and laboratory findings as well as the principles of therapy of the most common virus-associated arthritides. We believe that the knowledge of these key diagnostic and therapeutic features of virus-associated arthritides is important for the rheumatologist of the 21st century.
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PMID:Virally associated arthritis 2008: clinical, epidemiologic, and pathophysiologic considerations. 1882 83

Parvovirus B19 has been associated with liver dysfunction and has been considered a potential aetiological agent of fulminant hepatitis and hepatitis-associated aplastic anaemia. The possible effects of B19 virus infection on the liver have been investigated using HepG2 hepatocellular carcinoma cells as a model system, but the reported results are inconsistent. To investigate this relationship further, this study followed the course of B19 virus infection of HepG2 cells in terms of viral DNA, RNA and protein production by quantitative PCR, RT-PCR and immunofluorescence assays. The data showed that B19 virus is able to bind and possibly enter HepG2 cells, but that viral genome replication or transcription is not supported and that viral proteins are not produced. As far as HepG2 cells can be considered a representative model system, any possible pathogenic role of B19 virus on the liver cannot be ascribed to infection or to a direct cytopathic effect on hepatocytes.
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PMID:HepG2 hepatocellular carcinoma cells are a non-permissive system for B19 virus infection. 1900 90

Few studies have evaluated the impact of viral infections on the daily management of patients with systemic lupus erythematosus (SLE). We analyzed the etiology and clinical features of acute viral infections arising in patients with SLE and their influence on the diagnosis, prognosis, and treatment of SLE. Cases occurring within the last 5 years were selected from the databases of 3 large teaching hospitals. Acute viral infections were confirmed by the identification of specific antiviral IgM antibodies and subsequent seroconversion with detection of specific IgG antibodies. In autopsy studies, macroscopic findings suggestive of viral infection were confirmed by direct identification of the virus or viruses in tissue samples. We performed a MEDLINE search for additional cases reported between January 1985 and March 2008. We included 88 cases (23 from our clinics and 65 from the literature review) of acute viral infections in patients with SLE. Twenty-five patients were diagnosed with new-onset SLE (fulfillment of the 1997 SLE criteria) associated with infection by human parvovirus B19 (n = 15), cytomegalovirus (CMV; n = 6), Epstein-Barr virus (EBV; n = 3), and hepatitis A virus (n = 1). The remaining 63 cases of acute viral infections arose in patients already diagnosed with SLE: in 18 patients, symptoms related to infection mimicked a lupus flare, 36 patients, including 1 patient from the former group who presented with both conditions, presented organ-specific viral infections (mainly pneumonitis, colitis, retinitis, and hepatitis), and 10 patients presented a severe, multiorgan process similar to that described in catastrophic antiphospholipid syndrome-the final diagnosis was hemophagocytic syndrome in 5 cases and disseminated viral infection in 5. Twelve patients died due to infection caused by CMV (n = 5), herpes simplex virus (n = 4), EBV (n = 2), and varicella zoster virus (n = 1). Autopsies were performed in 9 patients and disclosed disseminated herpetic infection in 6 patients (caused by herpes simplex in 4 cases, varicella in 1, and CMV in 1) and hemophagocytic syndrome in 3. A higher frequency of renal failure (54% vs. 19%, p = 0.024), antiphospholipid syndrome (33% vs. 6%, p = 0.023), treatment with cyclophosphamide (82% vs. 37%, p = 0.008), and multisystemic involvement at presentation (58% vs. 8%, p < 0.001); and a lower frequency of antiviral therapy (18% vs. 76%, p < 0.001) were found in patients who died, compared with survivors. The most common viral infections in patients with SLE are parvovirus B19 (predominantly mimicking SLE presentation) and CMV (predominantly presenting in severely immunosuppressed patients). CMV infection may mimic a lupus flare or present with specific organ involvement such as gastrointestinal bleeding or pulmonary infiltrates. Other herpesviruses are common in immunosuppressed SLE patients and may produce a wide range of manifestations. Physicians should examine the pharynx, eyes, skin, and genitalia and should conduct serologic and molecular studies to improve early detection of viral infection in patients with SLE.
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PMID:Acute viral infections in patients with systemic lupus erythematosus: description of 23 cases and review of the literature. 1901 2

Human parvovirus B19 is responsible for a wide variety of clinical syndromes, including erythema infectiosum, or fifth disease, polyarthritis, aplastic crisis in patients with hemolytic anemia, and chronic anemia in immunocompromised persons. Liver enzyme abnormalities are an infrequently reported association of parvovirus B19 infection in adults. We present a case of an acute transient hepatitis in the setting of parvovirus B19 infection, associated with arthralgias and an erythematous, edematous rash on the hands and leg.
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PMID:Parvovirus b19 infection associated with acute hepatitis, arthralgias, and rash. 1907 35

A 59-year-old previously healthy man had flulike symptoms of fever and diarrhea for a week, which worsened despite treatment with antibiotics. After admission, his medical condition rapidly deteriorated with renal failure, heart failure, and a marked increase of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. The patient died of a cardiac arrhythmia 3 days after the admission. The autopsy showed diffuse myocarditis with a granulocytic and monocytic infiltrate, necrotizing arteritis of the coronary arteries, and fulminant hepatitis, with microvesicular steatosis and necrosis. Cell-free serum showed high copies of human herpesvirus 6 B variant DNA by polymerase chain reaction. Human herpesvirus 6 B was identified in the heart, liver, lung, and spleen by immunohistochemistry. No parvovirus B19 was evident in the heart by immunohistochemistry. Human herpesvirus 6 is increasingly found in association with myocarditis in immunocompromised patients; however, histopathologic features and the clinical severity of this disease have not yet been clearly defined. Only 4 to 5 cases of human herpesvirus 6 fulminant myocarditis have been reported, all in young children or immunosuppressed patients. To the best of our knowledge, this is the first case in the English literature of human herpesvirus 6 fulminant myocarditis and hepatitis in an immunocompetent adult with a fatal outcome. In addition, several pathologic features of our case have not been previously reported.
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PMID:Human herpesvirus 6-related fulminant myocarditis and hepatitis in an immunocompetent adult with fatal outcome. 1976 69

A 5-year-old male, drowsy, jaundiced child presented with fulminant hepatitis and had HAV and HEV infection. He had hepatic encephalopathy grade 1, fever, pallor, hypotension, crepitations in his right lung base and hepatosplenomegaly with dyspnoea. He had highly raised liver enzymes and hypoalbuminemia (2.8 g/dl) but anemia (hemoglobin of 7.7 g/dl and 5.7 g/dl 2 days later), reticulocytopenia and severe thrombocytopenia (44 x 10(9)/l) were unexplained. Parvovirus B19-specific IgM antibodies and B19 DNA were found in the serum of the child. Chest X-ray showed pleural effusion and bronchopneumonia, while blood culture isolated coagulase-negative staphylococci (BACTEC 9120) and he had low oxygen saturation. Hence, he was treated with IV amoxicillin+ clavulinic acid and oxygen inhalation. He had seizures and cardiac arrest but was revived. On the third day his condition worsened and the child died despite intensive care. Hence it is concluded that his anemia and thrombocytopenia were B19 induced and this might have aggravated or caused fulminant hepatitis.
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PMID:Parvovirus B19-induced thrombocytopenia and anemia in a child with fatal fulminant hepatic failure coinfected with hepatitis A and E viruses. 1920 89

Cytomegalovirus (CMV) is a virus that infects both normal and compromised hosts. In normal hosts, CMV presents most often as an "infectious mononucleosis-like" illness, but less commonly may present as community-acquired pneumonia (CAP), colitis, hepatitis, or fever of unknown origin. In compromised hosts, CMV often presents as CAP, encephalitis, retinitis, adrenalitis, hepatitis, or colitis. Not unlike parvovirus B19, CMV is an immunomodulatory virus that may cause or exacerbate rheumatic/inflammatory disorders, particularly systemic lupus erythematosus (SLE). Acute CMV infection may result in de novo SLE or more commonly may precipitate an SLE flare. In patients with SLE who are taking immunosuppressives, CMV increases the degree of immunosuppression of cell-mediated immunity. We present the case of a 40-year-old woman with SLE who presented with severe CMV CAP. CMV infection was suspected because of 2 nonspecific laboratory findings: increased serum transaminases and atypical lymphocytes in the peripheral smear. SLE is a multisystem autoimmune disorder that spares the liver. Therefore, in a patient with SLE who experiences an SLE flare, increased serum transaminases should suggest the possibility of CMV. In patients with SLE with flare, the likelihood of CMV is further increased if serum transaminases are elevated with atypical lymphocytes and should prompt specific testing for CMV. This patient's severe CMV CAP was treated successfully with oral valganciclovir, and she made a slow but complete recovery.
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PMID:Severe cytomegalovirus (CMV) community-acquired pneumonia (CAP) precipitating a systemic lupus erythematosus (SLE) flare. 1948 95


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