Search results for "Fulminant"

showing 10 items of 27 documents

Role of IL-17-producing lymphocytes in severity of multiple sclerosis upon natalizumab treatment.

2016

Objective: Natalizumab is known to prevent T-helper cells entering the central nervous system (CNS). We hypothesize that more pathogenic T-helper cells are present outside the CNS and a possible relationship to disease severity. Methods: Characterization and enrichment of human CD4+IL-17+ cells were performed ex vivo using peripheral blood mononuclear cells from natalizumab-treated relapsing-remitting multiple sclerosis (RRMS) patients ( n = 33), untreated RRMS patients ( n = 13), and healthy controls ( n = 33). Magnetic resonance imaging (MRI) scans were performed routinely for patients. Results: Lymphocytes were elevated in peripheral blood of natalizumab-treated patients compared to untr…

0301 basic medicineAdultCD4-Positive T-LymphocytesCentral Nervous SystemMaleMultiple SclerosisAdolescentFulminantCellCentral nervous systemPeripheral blood mononuclear cell03 medical and health sciencesYoung Adult0302 clinical medicineNatalizumabmedicineHumansbusiness.industryMultiple sclerosisNatalizumabInterleukin-17Middle Agedmedicine.disease030104 developmental biologymedicine.anatomical_structureNeurologyImmunologyLeukocytes MononuclearFemaleNeurology (clinical)Interleukin 17business030217 neurology & neurosurgeryEx vivomedicine.drugMultiple sclerosis (Houndmills, Basingstoke, England)
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Selection of a precore mutant after vertical transmission of different hepatitis B virus variants is correlated with fulminant hepatitis in infants

1995

The incidence of perinatal transmission of hepatitis B virus (HBV) depends on the HBeAg/anti-HBe status of the mother. While children of HBeAg-positive mothers have a 90% probability of acquiring a chronic hepatitis B virus carrier state, babies of anti-HBe-positive mothers are more likely to develop fulminant hepatitis within the first 3 to 4 months of life. There is evidence that precore (pre-C) mutations of the HBV can be associated with fulminant hepatitis. The pre-C region was therefore examined in sera from nine infants with fulminant hepatitis after vertical transmission, one HBeAg-positive and seven anti-HBe-positive mothers by polymerase chain reaction (PCR) and direct sequence ana…

AdultHepatitis B virusAdolescentMolecular Sequence DataPopulationmedicine.disease_causeVirusPregnancyVirologymedicineHumansHepatitis B e AntigensFulminant hepatitiseducationHepatitis B viruseducation.field_of_studyBase Sequencebiologyvirus diseasesHepatitis BHepatitis Bmedicine.diseasebiology.organism_classificationVirologyInfectious Disease Transmission Verticaldigestive system diseasesInfectious DiseasesHepadnaviridaeHBeAgDNA ViralMutationImmunologyFemaleViral diseaseSequence AnalysisJournal of Medical Virology
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Anti-hepatitis A virus seroprevalence and seroconversion in a cohort of patients with chronic viral hepatitis

2002

Abstract Background. Patients with chronic hepatitis C infected by hepatitis A virus have a substantial risk of fulminant hepatitis or death, while the course of hepatitis A virus is uncomplicated in most subjects with chronic hepatitis B. Aim. To evaluate the prevalence of anti-hepatitis A virus antibodies and the incidence of hepatitis A virus seroconversion in a nationwide sample of 530 patients with chronic hepatitis B and/or hepatitis C infection initially susceptible to this infection after a follow-up of some years. Results. The overall anti-hepatitis A virus prevalence was 85.7%, with no difference between males and females. By the age of 50 years, almost all patients were found to …

AdultMalemedicine.medical_specialtyAdolescentHepatitis C virusmedicine.disease_causeHepatitis A AntibodiesVirusHepatitis B ChronicSeroepidemiologic StudiesInternal medicinemedicineHumansSeroconversionFulminant hepatitisAgedHepatitis B virusHepatologybusiness.industryIncidenceGastroenterologyHepatitis CHepatitis BHepatitis AHepatitis C ChronicMiddle Agedmedicine.diseaseVirologyChronic liver disease; Hepatitis A virus superinfection; Hepatitis B virus; Hepatitis C virus;ItalyHepatitis A AntibodieFemalebusinessViral hepatitisHepatitis A Virus HumanHuman
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Remission of severe rheumatoid arthritis following liver transplantation.

1993

We present the case of a 32-year-old male who suffered from severe RA from the age of 21 years. After 9 years of active disease and poor response to therapy the patient developed severe hepatitis induced by the NSAID pirprofen. He went into fulminant hepatic failure necessitating emergency liver transplantation. Liver transplantation was followed by clinical and laboratory remission of his RA and he has remained virtually asymptomatic for more than 3.5 years. The possibility that this favourable clinical course was due to the immunosuppressive effect of the liver transplant rather than the ensuing immunosuppressive therapy is discussed.

AdultMalemedicine.medical_specialtyTime Factorsmedicine.medical_treatmentRemission SpontaneousArthritisLiver transplantationAsymptomaticGastroenterologyArthritis RheumatoidFulminant hepatic failureRheumatologyPirprofenInternal medicinemedicineHumansPharmacology (medical)HepatitisPhenylpropionatesbusiness.industrymedicine.diseaseSurgeryLiver TransplantationTransplantationRheumatoid arthritismedicine.symptomChemical and Drug Induced Liver InjurybusinessImmunosuppressive Agentsmedicine.drugFollow-Up StudiesBritish journal of rheumatology
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IL-28A Is a Key Regulator of T-Cell–Mediated Liver Injury via the T-Box Transcription Factor T-Bet

2006

Background & Aims: T-cell–mediated fulminant hepatitis is a potentially life-threatening event for which the underlying pathogenic mechanisms are not fully understood. Here, we demonstrate a key regulatory role of IL-28A in T-cell–mediated hepatitis. Methods: We cloned the murine IL-28A gene by reverse-transcription polymerase chain reaction, assessed the effects of recombinant IL-28A, and generated IL-28A–transgenic mice. Results: IL-28A induced TH1 cytokine production by CD4+ T lymphocytes in a T-bet–dependent manner and was up-regulated in a murine model of T-cell–mediated hepatitis upon Con A administration. In vivo, CD4+ T cells from newly created IL-28A–transgenic animals revealed an …

CD4-Positive T-Lymphocytesmedicine.medical_treatmentT cellCodon InitiatorMice TransgenicBiologyAntibodiesProinflammatory cytokineInterferon-gammaMiceT-Lymphocyte SubsetsInterferonConcanavalin AmedicineAnimalsCloning MolecularReceptors CytokineFulminant hepatitisLiver injuryHepatitisHepatologyInterleukinsGastroenterologyLiver Failure AcuteOligonucleotides Antisensemedicine.diseaseMolecular biologyMice Inbred C57BLSTAT1 Transcription FactorReal-time polymerase chain reactionCytokinemedicine.anatomical_structureInterleukin-2Interleukin-4MitogensT-Box Domain ProteinsCell DivisionSignal Transductionmedicine.drugGastroenterology
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Fulminant hepatic failure requiring liver transplantation in 22q13.3 deletion syndrome.

2010

We report on a 4-year-old girl with severe developmental delay, absent speech, and chromosome 22q13.3 deletion (Phelan-McDermid syndrome), karyotype 46,XX.ish del(22)(q13.31qter)(ARSA-,N85A-,SHANK3-). At the age of 3 years, she needed an emergency liver transplantation because of fulminant hepatic failure, most likely caused by hyperacute autoimmune hepatitis triggered by a viral infection. This is the second report of a patient with 22q13.3 deletion and fulminant liver failure. By array-CGH we identified in this patient a 5.675 Mb terminal deletion (22q13.31 --> qter; including approximately 55 genes; from NUP50 to RABL2B) and in the previous patient a 1.535 Mb deletion (22q13.32 --> qter;…

Candidate genemedicine.medical_specialtyFulminantmedicine.medical_treatmentChromosomes Human Pair 22Chromosome DisordersAutoimmune hepatitisDiseaseLiver transplantationGastroenterologyFulminant hepatic failureInternal medicineGeneticsmedicineHumansGenetics (clinical)In Situ Hybridization FluorescenceOligonucleotide Array Sequence AnalysisComparative Genomic Hybridizationmedicine.diagnostic_testbusiness.industryKaryotypeSyndromeLiver Failure Acutemedicine.diseaseLiver TransplantationChild PreschoolFemaleChromosome DeletionLiver function testsbusinessAmerican journal of medical genetics. Part A
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Parvovirus B19 nonstructural protein-induced damage of cellular DNA and resultant apoptosis.

2010

Parvovirus B19 is a widespread virus with diverse clinical presentations. The viral nonstructural protein, NS1, binds to and cleaves the viral genome, and induces apoptosis when transfected into nonpermissive cells, such as hepatocytes. We hypothesized that the cytotoxicity of NS1 in such cells results from chromosomal DNA damage caused by the DNA-nicking and DNA-attaching activities of NS1. Upon testing this hypothesis, we found that NS1 covalently binds to cellular DNA and is modified by PARP, an enzyme involved in repairing single-stranded DNA nicks. We furthermore discovered that the DNA nick repair pathway initiated by poly(ADPribose)polymerase and the DNA repair pathways initiated by …

DNA RepairDNA damageViral nonstructural proteinDNA repairPoly ADP ribose polymerasevirusesBlotting WesternParvovirus B19Viral Nonstructural ProteinsCell Linechemistry.chemical_compoundsystemic lupus erythematosusParvovirus B19 HumanHumansImmunoprecipitationPolymerasebiologyfulminant liver failureDNA damage and repairapoptosisvirus diseasesGeneral MedicineTransfectionMolecular biologyProliferating cell nuclear antigenchemistrybiology.proteinDNAautoantibodyDNA DamageResearch PaperInternational journal of medical sciences
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Fulminantes Lungenödembei Malaria tropica

2003

HISTORY AND ADMISSION FINDINGS A 54-year-old man was admitted because of intermittent fever for 2 days. Ten days earlier he had returned from Kenya. He had not taken any antimalarial drugs prophylactically. INVESTIGATIONS Initial blood smears showed Plasmodium falciparum in 10.4% of erythrocytes. Laboratory tests indicated hyponatremia and disseminated intravascular coagulation. Also, laboratory markers of infection and hemolysis were clearly positive and accompanied by a low-grade normocyticanaemia. Chest radiograph showed the heart size to be at the upper limit of normal and no signs of congestion, pleural effusion or inflammatory infiltrates. Sonography demonstrated hepatosplenomegaly wi…

Disseminated intravascular coagulationmedicine.medical_specialtymedicine.diagnostic_testPleural effusionbusiness.industryFulminantHepatosplenomegalyGeneral MedicineLung injurymedicine.diseasePulmonary edemaGastroenterologyHeart failureInternal medicineparasitic diseasesmedicinemedicine.symptombusinessChest radiographDMW - Deutsche Medizinische Wochenschrift
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Drugs and Toxins Effects on the Liver

2011

Drug induced hepatotoxicity can be defined as a liver injury caused by drug or herbal medicines leading to liver test abnormalities or to a liver dysfunction with a reasonable exclusion of the other competing aetiologies. The liver has a central function in the metabolism of the xenobiotics, and as a result it may be susceptible to its toxic or idiosyncratic effects. While the overall incidence of drug induced liver injury (DILI) is infrequent (1 in 10.000 to 100.000 persons exposed), the impact is significant in the general population, with broad implications for patients, physicians, pharmaceutical industries and governmental regulatory agencies. DILI is the principle reason for the termi…

DrugLiver injurymedicine.medical_specialtyeducation.field_of_studyPrescription drugbusiness.industrymedia_common.quotation_subjectPopulationmedicine.diseaseClinical trialFulminant hepatic failurePathognomonicmedicineIntensive care medicineeducationAdverse effectbusinessmedia_common
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Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture

2010

A clinical association between idiopathic liver disease and parvovirus B19 infection has been observed. Fulminant liver failure, not associated with other liver-tropic viruses, has been attributed to B19 in numerous reports, suggesting a possible role for B19 components in the extensive hepatocyte cytotoxicity observed in this condition. A recent report by Abe and colleagues (Int J Med Sci. 2007;4:105-9) demonstrated a link between persistent parvovirus B19 genotype I and III infection and fulminant liver failure. The genetic analysis of isolates obtained from these patients demonstrated a conservation of key amino acids in the nonstructural protein 1 (NS1) of the disease-associated genotyp…

GenotypevirusesCytotoxicityApoptosisViral Nonstructural ProteinsProtein SParvoviruschemistry.chemical_compoundLiver diseaseStructure-Activity Relationshiphemic and lymphatic diseasesGenotypemedicineParvovirus B19 HumanHumansCytotoxicitychemistry.chemical_classificationMethioninebiologyParvovirusB19Fulminant Liver Failurevirus diseasesGeneral MedicineHep G2 Cellsmedicine.diseasebiology.organism_classificationFlow CytometryVirologyAmino acidmedicine.anatomical_structurechemistryAmino Acid SubstitutionHepatocytebiology.proteinResearch PaperInternational Journal of Medical Sciences
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