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| 1 | Immune dysfunction in cirrhosis显示文摘Innate and adaptive immune dysfunction,also referred to as cirrhosis-associated immune dysfunction syndrome,is a major component of cirrhosis,and plays a pivotal role in the pathogenesis of both the acute and chronic worsening of liver function.During the evolution of the disease,acute decompensation events associated with organ failure(s),so-called acute-on chronic liver failure,and chronic decompensation with progression of liver fibrosis and also development of disease specific complications,comprise distinct clinical entities with different immunopathology mechanisms.Enhanced bacterial translocation associated with systemic endotoxemia and increased occurrence of systemic bacterial infections have substantial impacts on both clinical situations.Acute and chronic exposure to bacteria and/or their products,however,can result in variable clinical consequences.The immune status of patients is not constant during the illness;consequently,alterations of the balance between pro-and anti-in-flammatory processes result in very different dynamic courses.In this review we give a detailed overview of acquired immune dysfunction and its consequences for cirrhosis.We demonstrate the substantial influence of inherited innate immune dysfunction on acute and chronic inflammatory processes in cirrhosis caused by the pre-existing acquired immune dysfunction with limited compensatory mechanisms.Moreover,we highlight the current facts and future perspectives of how the assessment of immune dysfunction can assist clinicians in everyday practical decision-making when establishing treatment and care strategies for the patients with end-stage liver disease.Early and efficient recognition of inappropriate performance of the immune system is essential for overcoming complications,delaying progression and reducing mortality. | Nora Sipeki Peter Antal-Szalmas Peter L Lakatos Maria Papp | 2014 | World Journal of Gastroenterology2014，20，10： | 10 |
| 2 | Interaction of the major inflammatory bowel disease susceptibility alleles in Crohn’s disease patients显示文摘AIM:To investigate the interaction of interleukin-23 receptor(IL23R)(rs1004819 and rs2201841),autophagy-related 16-like 1(ATG16L1)(rs2241880), caspase recruitment domain-containing protein 15 (CARD15)genes,and IBD5 locus in Crohn's disease(CD) patients. METHODS:A total of 315 unrelated subjects with CD and 314 healthy controls were genotyped.Interactions and specific genotype combinations of a total of eight variants were tested.The variants of IBD5locus(IGR2198a_1 rs11739135 and IGR2096a_1 rs12521868),CARD15(R702W rs2066845 and L1007fs rs2066847),ATG16L1(rs2241880)and IL23R (rs1004819,rs2201841)genes were genotyped by PCR-RFLP,the G908R(rs2066844)in CARD15 was determined by direct sequencing. RESULTS:The association of ATG16L1 T300A with CD was confirmed[P=0.004,odds ratio(OR)=1.69, 95%CI:1.19-2.41],and both IL23R variants were found to represent significant risk for the disease(P= 0.008,OR=2.05,95%CI:1.20-3.50 for rs1004819 AA;P<0.001,OR=2.97,95%CI:1.65-5.33 for rs2201841 CC).Logistic regression analysis of pairwise interaction of the inflammatory bowel disease (IBD)loci indicated that IL23R,ATG16L1,CARD15 and IBD5(IGR2198a_1)contribute independently to disease risk.We also analysed the specific combina- tions by pair of individual ATG16L1,IL23R rs1004819, rs2201841,IGR2198a_1,IGR2096a_1 and CARD15 genotypes for disease risk influence.In almost all cases,the combined risk of susceptibility pairs was higher in patients carrying two different risk-associated gene variants together than individuals with just one polymorphism.The highest OR was found for IL23R rs2201841 homozygous genotype with combination of positive CARD15 status(P<0.001,OR=9.15,95% CI:2.05-40.74). CONCLUSION:The present study suggests a cumulative effect of individual IBD susceptibility loci. | Veronika Csngei Luca Járomi EnikSáfrány Csilla Sipeky Lili Magyari Bernadett Faragó Judit Bene Noémi Polgár Lilla Lakner Patrícia Sarlós Márta Varga Béla Melegh | 2010 | World Journal of Gastroenterology2010，16，2： | 2 |
| 3 | Protein kinase C modulates negatively the hepatocyte growth factor-induced migration,integrin expression and phosphatidylinositol 3-kinase activation显示文摘 | Annamaria G Sipeki S Bander E | 2004 | Cellular Signalling2004，16，5： | 1 |
| 4 | High prevalence of CYP2C19'2 allele in Roma samples: study on Roma and Hungarian population samples with review of the literature 显示文摘 | Sipeky C Weber A Szabo M | 2013 | Mol Biol Rep2013，40，8： | 1 |
| 5 | High prevalence of IgA class anti-neutrophil cytoplasmic antibodies (ANCA) is associated with increased risk of bacterial infection in patients with cirrhosis显示文摘 | Maria Papp Nora Sipeki Zsuzsanna Vitalis Tamas Tornai Istvan Altorjay Istvan Tornai Miklos Udvardy Kai Fechner Silvia Jacobsen Bianca Teegen Andrea Sumegi Gabor Veres Peter Laszlo Lakatos Janos Kappelmayer Peter Antal-Szalmas | 2013 | Journal of Hepatology2013，，： | 1 |
| 6 | Interethnic differences of CYP2C9 alleles in healthy Hungarian and Roma population samples: relationship to worldwide allelic frequencies显示文摘 | Sipeky C Lakner L Szabo M | 2009 | Blood Cells Mol Dis2009，43，3： | 1 |
| 7 | High prevalence of IgA class anti-neutrophil cytoplasmic antibodies (ANCA) is associated with increased risk of bacterial infection in patients with cirrhosis显示文摘 | Papp M Sipeki N Vitalis Z | 2013 | J Hepatol2013，59，3： | 1 |
| 8 | Genetic variability and haplotype profile of MDR1 ( ABCBI ) in Roma and Hungarian population samples with a review of the literature显示文摘 | Sipeky C Csongei V Jaromi L | 2011 | Drug Metab Pharmacokinet2011，26，： | 1 |
| 9 | Preisach-type stress-dependent magnetic vector hysteresis model显示文摘 | Sipeky A Ivanyi A | | 0，，： | 1 |
| 10 | Risk matrix for predic- tion of disease progression in a referral cohort of patients with Crohn's disease显示文摘 | Lakatos PL Sipeki N Kovacs G | 2015 | J Crohns Colitis2015，9，10： | 1 |
| 11 | Phosphatidylinositol3-kinase contributes to Erk1/Erk2 MAP kinase activation associated with hepatocyte growth factor-induced cell scattering显示文摘 | Sipeki S Bander E Buday L | 1999 | Cell Signal1999，11，12： | 1 |
| 12 | Phosphatidylinositol 3-kinase contributes to Erkl/Erk2 MAP kinase activation associated with hepatocyte growth factor-induced cell scattering显示文摘 | Sipeki S Bander E Buday L | 1999 | Cell Signal1999，11，12： | 1 |
| 13 | Magnetic hysteresis under applied stress显示文摘 | Sipeky A Ivanyi A | 2006 | Physica B2006，372，1： | 1 |
| 14 | Increased prevalence of functional minor allele variants of drug metabolizing CYP2B6 and CYP2D6 genes in Roma population samples显示文摘 | WEBER A SZALAI R SIPEKY C | 2015 | Pharmacol Rep2015，67，3： | 1 |
| 15 | High prevalence of IgA class anti-neutrophil cytoplasmic antibodies (ANCA) is associated with increased risk of bacterial infection in patients with cirrhosis<!-- Doctopic: CIRR -->显示文摘 | Maria Papp Nora Sipeki Zsuzsanna Vitalis Tamas Tornai Istvan Altorjay Istvan Tornai Miklos Udvardy Kai Fechner Silvia Jacobsen Bianca Teegen Andrea Sumegi Gabor Veres Peter Laszlo Lakatos Janos Kappelmayer Peter Antal-Szalmas | 2013 | Journal of Hepatology2013，，： | 1 |
| 16 | Prevalence of SLC22A4 1672T and SLC22A5 ?207C combination defined TC haplotype in Hungarian ulcerative colitis patients显示文摘 | Lili Magyari Judit Bene Katalin Komlósi Gábor Talián Bernadett Faragó Veronika Cs?ngei Luca Járomi Enik? Sáfrány Csilla Sipeky Lilla Lakner Márta Varga Beáta Gasztonyi Béla Melegh | 2007 | Pathology & Oncology Research2007，，1： | 1 |
| 17 | Prevalence, significance and predictive value of antiphospholipid antibodies in Crohn's disease显示文摘AIM: To assess the prevalence and stability of different antiphospholipid antibodies(APLAs) and their association with disease phenotype and progression in inflammatory bowel diseases(IBD) patients.METHODS: About 458 consecutive patients [Crohn's disease(CD): 271 and ulcerative colitis(UC): 187] were enrolled into a follow-up cohort study in a tertiary IBD referral center in Hungary. Detailed clinical phenotypes were determined at enrollment by reviewing the patients' medical charts. Disease activity, medical treatment and data about evolvement of complications or surgical interventions were determined prospectively during the follow-up. Disease course(development f complicated disease phenotype and need for surgery),occurrence of thrombotic events, actual state of diseaseactivity according to clinical, laboratory and endoscopic scores and accurate treatment regime were recorded during the follow-up,(median, 57.4 and 61.6 mo for CD and UC). Sera of IBD patients and 103 healthy controls(HC) were tested on individual anti-β2-Glycoprotein-I(anti-β2-GPI IgA/M/G), anti-cardiolipin(ACA IgA/M/G)and anti-phosphatidylserine/prothrombin(anti-PS/PT IgA/M/G) antibodies and also anti-Saccharomyces cerevisiae antibodies(ASCA IgA/G) by enzyme-linked immunosorbent assay(ELISA). In a subgroup of CD(n = 198) and UC patients(n = 103), obtaining consecutive samples over various arbitrary timepoints during the disease course, we evaluated the intraindividual stability of the APLA status. Additionally,we provide an overview of studies, performed so far, in which significance of APLAs in IBD were assessed.RESULTS: Patients with CD had significantly higher prevalence of both ACA(23.4%) and anti-PS/PT(20.4%) antibodies than UC(4.8%, p < 0.0001 and10.2%, p = 0.004) and HC(2.9%, p < 0.0001 and15.5%, p = NS). No difference was found for the prevalence of anti-β2-GPI between different groups(7.2%-9.7%). In CD, no association was found between APLA and ASCA status of the patients.Occurrence of anti-β2-GPI, ACA and anti-PS/PT was not different between the group of patients with active vs inactive disease state according to appropriate clinical, laboratory and endoscopic scores in CD as well as in UC patients. All subtypes of anti-β2-GPI and ACA IgM status were found to be very stable over time, in contrast ACA IgG and even more ACA IgA status showed significant intraindividual changes.Changes in antibody status were more remarkable in CD than UC(ACA IgA: 49.9% vs 23.3% and ACA IgG:21.2% vs 5.8%). Interestingly, 59.1% and 30.1% of CD patients who received anti-TNF therapy showed significant negative to positive changes in ACA IgA and IgG antibody status respectively. APLA status was not associated with the clinical phenotype at diagnosis or during follow-up, medical therapy, or thrombotic events and it was not associated with the probability of developing complicated disease phenotype or surgery in a Kaplan-Meier analysis.CONCLUSION: The present study demonstrated enhanced formation of APLAs in CD patients. However,presence of different APLAs were not associated with the clinical phenotype or disease course. | Nora Sipeki Laszlo Davida Eszter Palyu Istvan Altorjay Jolan Harsfalvi Peter Antal Szalmas Zoltan Szabo Gabor Veres Zakera Shums Gary L Norman Peter L Lakatos Maria Papp | 2015 | World Journal of Gastroenterology2015，21，22： | 1 |
| 18 | Location-based prediction model for Crohn’s disease regarding a novel serological marker,anti-chitinase 3-like 1 autoantibodies显示文摘BACKGROUND Defective neutrophil regulation in inflammatory bowel disease(IBD)is thought to play an important role in the onset or manifestation of IBD,as it could lead to damage of the intestinal mucosal barrier by the infiltration of neutrophils in the inflamed mucosa and the accumulation of pathogens.Like neutrophils in the context of innate immune responses,immunoglobulin A(IgA)as an acquired immune response partakes in the defense of the intestinal epithelium.Under normal conditions,IgA contributes to the elimination of microbes,but in connection with the loss of tolerance to chitinase 3-like 1(CHI3L1)in IBD,IgA could participate in CHI3L1-mediated improved adhesion and invasion of potentially pathogenic microorganisms.The tolerance brake to CHI3L1 and the occurrence of IgA autoantibodies to this particular target,the exact role and underlying mechanisms of CHI3L1 in the pathogenesis of IBD are still unclear.AIM To determine the predictive potential of Ig subtypes of a novel serological marker,anti-CHI3L1 autoantibodies(aCHI3L1)in determining the disease phenotype,therapeutic strategy and long-term disease course in a prospective referral cohort of adult IBD patients.METHODS Sera of 257 Crohn’s disease(CD)and 180 ulcerative colitis(UC)patients from a tertiary IBD referral center of Hungary(Division of Gastroenterology,Department of Internal Medicine,Faculty of Medicine,University of Debrecen)were assayed for IgG,IgA,and secretory IgA(sIgA)type aCHI3L1 by enzyme-linked immunosorbent assay using recombinant CHI3L1,along with 86 healthy controls(HCONT).RESULTS The IgA type was more prevalent in CD than in UC(29.2%vs 11.1%)or HCONT(2.83%;P<0.0001 for both).However,sIgA subtype aCHI3L1 positivity was higher in both CD and UC patients than in HCONT(39.3%and 32.8%vs 4.65%,respectively;P<0.0001).The presence of both IgA and sIgA aCHI3L1 antibodies was associated with colonic involvement(P<0.0001 and P=0.038,respectively)in patients with CD.Complicated disease behavior at sample procurement was associated with aCHI3L1 sIgA positivity(57.1%vs 36.0%,P=0.009).IgA type aCH3L1 was more prevalent in patients with frequent relapse during the disease course in the CD group(46.9%vs 25.7%,P=0.005).In a group of patients with concomitant presence of pure inflammatory luminal disease and colon involvement at the time of diagnosis,positivity for IgA or sIgA type aCH3L1 predicted faster progression towards a complicated disease course in time-dependent models.This association disappeared after merging subgroups of different disease locations.CONCLUSION CHI3L1 is a novel neutrophil autoantigenic target in IBD.The consideration of antibody classes along with location-based prediction may transform the future of serology in IBD. | Nora Sipeki Patricia Julianna Kovats Claudia Deutschmann Peter Schierack Dirk Roggenbuck Maria Papp | 2023 | World Journal of Gastroenterology2023，29，42： | 0 |
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