Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a patient who developed a mononucleosis syndrome 6 weeks after starting phenytoin therapy for a seizure disorder. Improvement followed initial discontinuation of the phenytoin, but near-fatal hepatic necrosis resulted from intravenous phenytoin rechallenge. A serious reaction with a 18% overall mortality, phenytoin hepatitis may closely resemble infectious mononucleosis with fever, pharyngitis, lymphadenopathy, and atypical lymphocytosis. Continued administration of phenytoin or later rechallenge may increase the severity of the reaction.
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PMID:Phenytoin hypersensitivity hepatitis and mononucleosis syndrome. 309 62

The in vivo infection of neonatal dogs by the microsporidian protozoan parasite, Encephalitozoon cuniculi, was studied. Microscopic examination of tissues from infected animals showed granulomatous nephritis, meningoencephalitis, hepatitis, and pneumonitis. A large component of the inflammatory infiltrate consisted of plasma cells and lymphocytes. In addition, hyperplasia of B-lymphocyte-dependent regions of lymph nodes and erythrophagocytosis were consistently seen in infected dogs. Infected dogs developed lymphocytosis, hypergammaglobulinemia, anti-encephalitozoon antibodies, and an antigen-specific blastogenic response to E. cuniculi spores. Lymphocyte blastogenic responses to the lectin phytohemagglutinin A (PHA) were depressed compared to controls. Dogs dying during the 2-month experimental trial were bacteremic. The findings of these experiments suggest that postnatal infection results in a demonstrable although seemingly ineffective immune and inflammatory response without detectable clinical disease.
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PMID:Experimental encephalitozoonosis in neonatal dogs. 310

Cytomegalovirus-induced hepatitis presented as acute right upper quadrant pain with a cholestatic profile in a middle-aged woman. The presentation was confused by the presence of gallstones. Her course was complicated by pleuritis, atypical lymphocytosis, lymphadenopathy, and transient arthritis. Urine virus cultures grew cytomegalovirus and seroconversion of indirect immunofluorescent antibody to late cytomegalovirus antigen was demonstrated. Biopsies of the patient's liver failed to grow cytomegalovirus or to show viral inclusions. Electron micrographic studies were negative. Biopsy specimens were stained with monoclonal antibodies to cytomegalovirus by an indirect fluorescence technique. Clearly defined inclusions were specifically stained. Both nuclear and cytoplasmic inclusions were demonstrated using monoclonal antibodies CH16 and CH12, respectively. Insofar as we are aware, this is the first reported direct evidence for hepatic viral infection with this virus in a previously healthy adult.
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PMID:Cytomegalovirus hepatitis: evidence for direct hepatic viral infection using monoclonal antibodies. 631 9

Studies of data from ten cases of infantile acrodermatitis and from eight cases reported in the North American literature disclose distinctive papular dermatosis of the face and extremities, often related to virus infection. None of our eight patients who were tested had evidence of hepatitis B infections, although transaminase values were elevated in two. All five patients who were tested had lymphocytosis. Six patients had antecedent upper respiratory tract symptoms. Data from our cases and from the other previously reported cases indicate that the eruption is a virus-related response. Although the hepatitis virus has been the most frequently encountered causative agent to date, other viruses, including Epstein-Barr virus, coxsackievirus, and parainfluenza virus, may produce a similar cutaneous response.
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PMID:Gianotti-Crosti syndrome. A review of ten cases not associated with hepatitis B. 632 7

We report here on two patients with kidney allografts who had hepatitis and duodenal ulcer caused by cytomegalovirus. In one case, hepatosplenomegaly and jaundice appeared after high fever lasting for ten days. Laboratory examinations showed liver dysfunction and lymphocytosis with atypical forms. Virological studies revealed cytomegalovirus infection and we successfully treated the patient with human interferon-beta. In the other case, duodenal bleeding followed by interstitial pneumonia occurred at the 54th day after transplantation. Bleeding from the small duodenal ulcer did not stop in spite of conservative and endoscopic therapies, and gastrectomy was performed. Histologically many epithelial cells with intranuclear inclusions were found around the ulcer. Virological studies showed elevation of antibody titres to cytomegalovirus which was isolated from the urine and oropharyngeal secrete. After gastrectomy and treatment with ganciclovir, the general condition improved and graft function was maintained. Our experience with these cases suggests that aggressive diagnostic investigations for cytomegalovirus infection are essential in patients with organ allografts who present liver and gastrointestinal lesions.
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PMID:Cytomegalovirus-associated hepatitis and duodenal ulcer in kidney allograft recipients. 761 76

We report an unusual clinical presentation of toxoplasmosis. Fever and headache were the only complaints of a 48-year-old immunocompetent man who was found to have a rash, hepatitis and a pericardial effusion. Lymphadenopathy was not present. Evolving atypical lymphocytosis was the clue to the diagnosis of toxoplasmosis. Undercooked meat was the probable source of infection.
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PMID:Unusual presentation of acquired toxoplasmosis in an immunocompetent adult. 780 80

We describe the first case of an Epstein-Barr virus (EBV)-associated natural killer-large granular lymphocyte (NK-LGL) leukemia in the United States to the best of our knowledge. A 29-year-old woman of Japanese descent developed EBV infection after a blood transfusion as indicated by a rise in serum antibody titers. Peripheral blood and bone marrow aspirate smears demonstrated increased LGLs. Flow cytometry showed that these cells expressed NK-associated surface antigens. Cytogenetic analysis of the bone marrow aspirate showed two distinct but related clones with multiple copies of a modified 7 marker chromosome. Death followed colonic perforation. Findings at necropsy included bone marrow lymphocytosis and erythrophagocytosis, a mononucleosis-like lymphadenitis, atypical hepatitis with a mixed, predominantly T-cell infiltrate, interstitial pneumonitis, and multiorgan system vasculitis with perforation of the transverse colon. Epstein-Barr virus transcripts were identified in lymphocytes infiltrating liver and peripheral nerve by in situ hybridization. In addition, Southern blot analyses showed monoclonal bands superimposed on oligoclonal ladders of EBV termini in liver and lymph node. The identical episomal form of EBV was found in the bone marrow, lymph node, and liver. No immunoglobulin (Ig), T-cell receptor beta, or T-cell receptor gamma chain gene rearrangements were identified. These studies support the hypothesis that the LGL population was a neoplastic EBV-related clonal proliferation of NK cells.
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PMID:Epstein-Barr virus-associated natural killer-large granular lymphocyte leukemia. 808 73

A 56 year old patient with scrub typhus infection having unusual presentation of hepatic injury resembling acute hepatitis is described. The clinical features of fever, headache, eschar, lymphadenopathy, lymphocytosis and high Rickettsia tsutsugamushi immunofluorescence titres confirmed the diagnosis of scrub typhus. Acute hepatitis was proven by hepatic biochemical tests and liver biopsy. The patient had a complete recovery soon after antibiotic treatment. The presentation of this case suggests that scrub typhus infection should be included in the list of differential diagnosis of acute hepatitis or granulomatous hepatitis, at least in the Asian Pacific region where scrub typhus still prevails.
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PMID:Granulomatous hepatitis associated with scrub typhus. 852 19

The incidence and severity of recurrent hepatitis C virus (HCV) infection in liver transplant recipients vary widely, and the long-term sequelae of recurrent infection are not known. To better define the biology of recurrent HCV in liver transplant patients, we reviewed the histology of recurrent HCV in serial biopsies of 19 patients with pretransplant polymerase chain reaction (PCR) evidence of HCV infection. All posttransplant (post-TX) biopsies (n = 81) were reviewed, and RNA was extracted from at least one paraffin-embedded biopsy from each patient. RNA was analyzed for HCV by nested, reverse transcription-PCR (RT-PCR) using primers for the 5' non-coding region of HCV as well as for albumin (as an internal control). All post-TX biopsies tested (12-1,677 days post-TX) were positive for HCV RNA by RT-PCR, while normal control biopsies were negative. Fifteen of 19 patients developed recurrent chronic hepatitis typical of HCV. Many of these patients showed a progression from early biopsies with acute lobular hepatitis to later biopsies with chronic hepatitis with portal lymphoid aggregates. An acute lobular hepatitis typified by sinusoidal lymphocytosis, acidophil bodies, and lobular disarray was seen an average of 135 days post-TX, with a range of 39-279 days. The time post-TX between this and earlier non-hepatitis biopsies was significantly different (p < 0.0004, Student's t test). Chronic hepatitis with portal lymphoid aggregates was seen an average of 356 days post-TX, with a range of 89-1,365 days. The time post-TX was significantly longer than for acute lobular hepatitis (p < 0.03, Student's t test). Fifty-three percent of HCV TX patients progressed from acute lobular hepatitis to chronic hepatitis with lymphoid aggregates within 1 year of TX, and 79% showed these changes within 4 years. Six patients had progressive fibrosis; one die of liver failure and two became cirrhotic. Recurrent HCV appears to progress from an acute lobular hepatitis to chronic hepatitis with lymphoid aggregates in the majority of patients. Significant scarring occurred in 32% of patients and 16% developed end-stage liver disease from recurrent HCV. These later findings suggest that the long-term course of recurrent HCV in liver allografts may not be as indolent as first thought.
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PMID:Histologic progression of recurrent hepatitis C in liver transplant allografts. 865 53

A healthy 19-year-old woman had vaginal intercourse on a single occasion with an HIV-1 positive male from Gambia. Two days later she developed an acute HIV infection presenting as a fulminant multisystem disease that lasted for 35 hospital days and included: immediate immunosuppression with extreme CD4+ lymphocytopenia and combined with CD8+ lymphocytosis, neutropenia and hypogammaglobulinemia; intermittent spiking fever; pneumonitis; hepatitis; changing skin rashes; peripheral neuropathy with myopathy, and panencephalitis. P24 antigen was detected by Western blot on day 23 and seroconversion was detected by ELISA on day 25. Cultured lymphocytes from peripheral blood and cerebrospinal fluid grew HIV-1.
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PMID:Immediate immunosuppression caused by acute HIV-1 infection: a fulminant multisystemic disease 2 days post infection. 887 88


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