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1.

001-es BibID:BIBFORM071355
Első szerző:Antal-Szalmás Péter (laboratóriumi szakorvos)
Cím:Serum levels of lectin complement pathway molecules do not determine the risk of bacterial infections in patients with cirrhosis / P. Antal-Szalmás, I. Földi, D. Tornai, T. Tornai, Zs. Vitális, I. Tornai, T. Dinya, M. Papp
Dátum:2016
Megjegyzések:SE1.5Serum levels of lectin complement pathway molecules do not determine the risk of bacterial infections in patientswith cirrhosisP. Antal-Szalmás1, I. Földi2, D. Tornai1, T. Tornai2, Zs. Vitális2, I Tornai2, T. Dinya3, M. Papp21Department of Laboratory Medicine, 2Department of Internal Medicine, Division of Gastroenterology, 3Institute of Surgery, Faculty ofMedicine, University of Debrecen, Debrecen, HungaryBacterial infections are a significant cause of morbidity and mortality in cirrhosis. Lectin pathway molecules of the complement system aresynthesized in the liver and have a pivotal role in the innate host defense against infectious organisms. Mannose-binding lectin (MBL) andficolins (FCNs) act as soluble pattern recognition molecules, while mannan-binding lectin serine proteases (MASPs) are effector molecules inelimination of the pathogens. Low levels of the functional proteins increase the risk of various infectious diseases but their significance hasscarcely been investigated in cirrhosis related bacterial infections.Sera of 266 patients with cirrhosis and 160 healthy subjects were assayed for the concentrations of FCN-2, FCN-3 and MASP-2 by ELISAs.In cirrhosis, a 5-year follow-up observational study was conducted to assess a possible association between lectin levels and development ofclinically significant bacterial infections (CSI) and mortality.The FCN-2, FCN-3 and MASP-2 levels were significantly lower in cirrhosis compared to healthy controls (505 vs. 769 ng/ml, 7,301 vs.10,797 ng/ml and 212 vs. 412 ng/ml, respectively, p < 0.001 for all) and decreased according to disease severity as rated by Child-Pughstage. In Kaplan-Meier analysis time to development of CSI was associated with low level of FCN-3 ( < 4,857 ng/ml, p = 0.028) but notFCN-2 ( < 427 ng/ml, p = 0.068) or MASP-2 deficiency (p = 0.368). Combined FCN deficiency even more than individual molecules wereable to predict the development of these episodes. Patients with low level of both FCNs had a cumulative risk of an infection of 52%as compared to 31% with normal level of FCNs (p = 0.021). In multivariate Cox-regression analysis, clinical factors but not the serumlectin profile remained an independent predictor of CSI. Prior episode of CSI and in a stepwise manner, the disease severity as rated byChild-Pugh stage conferred higher risk for development of CSI (HR: 2.64, 95% CI: 1.74?3.99, p < 0.001 and 2.11, 95%CI: 1.52-2.93, p < 0.001,respectively).In the present prospective study, diseases severity and prior episode of CSI but not the serum lectin profile were major determinants ofthe risk of CSI in cirrhosis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:Clinical chemistry and laboratory medicine 54 : 10 (2016), p. 162. -
További szerzők:Földi Ildikó (1981-) (orvos) Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Tornai Tamás István (1984-) (belgyógyász) Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Dinya Tamás (1974-) (sebész szakorvos, onkológus szakorvos) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
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2.

001-es BibID:BIBFORM089479
Első szerző:Balogh Boglárka (belgyógyász)
Cím:Gut barrier failure : a piece in the puzzle of acute-on chronic liver failure syndrome development? / Boglarka Balogh, Zsuzsa Vitalis, Tamas Tornai, Istvan Tornai, David Tornai, Aniko Csillag, Peter Antal-Szalmas, Maria Papp
Dátum:2020
Megjegyzések:Introduction: Intestinal barrier dysfunction induced inflammation facilitates pathologic bacterial translocation (BT) which is a characteristic feature of liver cirrhosis (LC). BT plays a crucial role in the progression of LC leading to spontaneous bacterial peritonitis (SBP), bacteraemia and induction of proinflammatory responses causing various organ damages. Therefore, the serological hallmarksof gut barrier dysfunction in cirrhosis are able to predict the accelerated progression of liver disease. Methods: In a cohort of patients with decompensated cirrhosis (n=135) prospectively followed-up for 1 year and in healthy controls (HC) (n=50) the serological markers of functional/structural gut damage (intestinal-fatty acid binding protein, I-FABP), BT (Endotoxin core antibody, EndoCab IgA) and mucosal immune response (secretory IgA, Immunoglobulin free light chain (Ig FLC) kappa and lambda,) were investigated by means of ELISA. Results: Comparing the LC to HC group the serum concentration of all investigated markers weresignificantly higher in cirrhotic patients, although they did not show any association with the disease severity. Investigating the role of the serological markers in the development of ACLF we found that significance of the serum level of Ig FLC kappa in ACLF prediction is comparable to AD score based on AUC values. Furthermore, the ACLF rate was lower in patients with low serum concentration of Ig FLC kappa compared to the group with high serum concentration of this molecule. Conclusions: Ig FLC kappa can be a usable marker in the serological panel for the prediction of ACLF development in acute decompensated cirrhotic patients. Acknowledgements: EFOP 3.6.2-16-2017-00006 (LIVE LONGER).
Tárgyszavak:Orvostudományok Klinikai orvostudományok előadáskivonat
könyvrészlet
Megjelenés:Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project /Ed. Rakonczay Zoltán, Kiss Lóránd. - p. 62. -
További szerzők:Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai Tamás István (1984-) (belgyógyász) Tornai István (1954-) (belgyógyász, gasztroenterológus) Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Csillag Anikó (1979-) (immunológus, biológus, angol-magyar szakfordító) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:EFOP-3.6.2-16-2017-00006
EFOP
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3.

001-es BibID:BIBFORM089481
Első szerző:Csillag Anikó (immunológus, biológus, angol-magyar szakfordító)
Cím:Filamentosus-actin related molecules : are they serologic hallmark of overwhelming damage-associated molecular patterns (DAMPs) in acute decompensation? / Aniko Csillag, Zsuzsa Vitalis, Tamas Tornai, Istvan Tornai, David Tornai, Boglarka Balogh, Peter Antal-Szalmas, Maria Papp
Dátum:2020
Megjegyzések:Introduction: The actin cytoskeleton has a fundamental function in cellular motility, integrity, structure and signaling mechanisms. In acute decompensated liver cirrhosis large quantities of filamentous actin (F-actin) as a danger signal is released from damaged and necrotic hepatic cells. Recently it also has been demonstrated that the presence of IgA type anti-F-actin antibodies is associated with the disease severity, unfavorable disease outcome and intestinal damage, as well. Thus, we hypothesized that the actin-scavenging system molecules in acute decompensation are able to predict the accelerated progression of liver disease. Methods: In a cohort of patients with decompensated cirrhosis (n=135) prospectively followed-up for 1 year and in healthy controls (HC, n=50) the serum levels of gelsolin and anti-F-actin IgA were investigated by means of ELISA. Results: Serum gelsolin levels were significantly higher in patients with acute decompensated liver cirrhosis (LC-AD) compared to healthy controls (HCONT) (p<0.0001). The frequency of anti-F-actin positivity was 65.4% (n=83/127) in LC-AD group (cut off: 25 U/mL). Our results demonstrated that in LC-AD group the serum gelsolin levels did not show correlation with the different disease severity, the presence of bacterial infection or renal failure at inclusion, similarly to the presence or absence of anti-F-actin IgA positivity. However, high serum level of gelsolin (>87.7 ?g/mL) is associated with short term (30 days) mortality. Conclusions: High serum level of gelsolin is likely to predict short term mortality both in cirrhotic patients with or without acute-on-chronic liver failure at inclusion. Acknowledgements: EFOP 3.6.2-16-2017-00006 (LIVE LONGER).
ISBN:978-963-306-764-2
Tárgyszavak:Orvostudományok Klinikai orvostudományok előadáskivonat
könyvrészlet
Megjelenés:"PROCEEDINGS OF THE EFOP-3.6.2- 16-2017-00006 (LIVE LONGER) PROJECT" / Ed. Rakonczay Zoltán, Kiss Lóránd. - p. 63. -
További szerzők:Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai Tamás István (1984-) (belgyógyász) Tornai István (1954-) (belgyógyász, gasztroenterológus) Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Balogh Boglárka (1993-) (belgyógyász) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:EFOP-3.6.2-16-2017-00006
EFOP
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4.

001-es BibID:BIBFORM071451
Első szerző:Dinya Tamás (sebész szakorvos, onkológus szakorvos)
Cím:Functional polymorphisms of innate immunity receptors are not risk factors for the non-SBP type bacterial infections in cirrhosis / Dinya Tamás, Tornai Tamás, Vitális Zsuzsanna, Tornai István, Balogh Boglárka, Tornai Dávid, Antal-Szalmás Péter, Sümegi Andrea, Andrikovics Hajnalka, Bors András, Tordai Attila, Papp Mária
Dátum:2018
ISSN:1478-3223 1478-3231
Megjegyzések:Background&Aims: Pattern recognition receptors (PRRs) have a key role in the innate host defense. Functional polymorphisms of various PRRs have been established to contribute to an increased susceptibility to spontaneous bacterial peritonitis (SBP). Their role in the development of cirrhosis-associated bacterial infections (BI), beyond SBP or progressive disease course related to pathological bacterial translocation (BT) remains unknown. Methods: 349 patients with cirrhosis were genotyped for common NOD2 (R702W, G908R and L1007PfsinsC), TLR2 (-16934T>A), and TLR4 (D299G) gene variants. Incidence of BIs, decompensating events (ascites, variceal bleeding and hepatic encephalopathy) and liver-related death were assessed in a 5-year follow-up observational study. Pathological BT was assessed based on the presence of anti-microbial antibodies or lipopolysaccharide-binding protein (LBP) level. Results: In patients with ascites (n=88) only NOD2 gene variants were associated with an increased cumulative probability of SBP compared to wild-type (76.9%?19.9% vs. 30.9%?6.9%, PLogRank=0.047). Neither individual polymorphisms, nor combined PRR genetic profiles were associated with the risk of non-SBP type BI. Advanced disease stage (HR,[95%CI]: 2.11 [1.38-3.25]) and prior history of a BI episode (HR: 2.42 [1.58-3.72]) were the major clinical risk factors of a subsequent BI. The risk of a non-SBP type BI in patients with advanced disease and a prior BI was even higher (HR: 4.74 [2.68-8.39]). The frequency of anti-microbial antibodies and LBP levels did not differ between various PRR genotypes. Correspondingly, PRR genetic profile was not able to predict the long-term disease course. Conclusions: In cirrhosis, functional polymorphisms of PRRs did not improve the identification of patients with high risk of BI beyond SBP or progressive diseases course.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
pattern recognition receptors
genetic polymorphisms
cirrhosis
bacterial infection
complication
mortality
Megjelenés:Liver International. - 38 : 7 (2018), p. 1242-1252. -
További szerzők:Tornai Tamás István (1984-) (belgyógyász) Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Balogh Boglárka (1993-) (belgyógyász) Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Sümegi Andrea (1969-) (biológus) Andrikovics Hajnalka Bors András Tordai Attila Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:OTKA-115818
OTKA
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5.

001-es BibID:BIBFORM066819
Első szerző:Földi Ildikó (orvos)
Cím:Lectin-complement pathway molecules are decreased in patients with cirrhosis and constitute the risk of bacterial infections / Ildiko Foldi, Tamas Tornai, David Tornai, Nora Sipeki, Zsuzsanna Vitalis, Istvan Tornai, Tamas Dinya, Peter Antal-Szalmas, Maria Papp
Dátum:2017
ISSN:1478-3223
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Liver International 37 : 7 (2017), p. 1023-1031. -
További szerzők:Tornai Tamás István (1984-) (belgyógyász) Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Sipeki Nóra (1987-) (általános orvos) Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Dinya Tamás (1974-) (sebész szakorvos, onkológus szakorvos) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:K115818/2015/1
OTKA
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6.

001-es BibID:BIBFORM087410
Első szerző:Gatselis, Nikolaos K.
Cím:Golgi protein-73 : a biomarker for assessing cirrhosis and prognosis of liver disease patients / Nikolaos K. Gatselis, Tamás Tornai, Zakera Shums, Kalliopi Zachou, Asterios Saitis, Stella Gabeta, Roger Albesa, Gary L. Norman, Mária Papp, George N. Dalekos
Dátum:2020
ISSN:1007-9327
Megjegyzések:Abstract BACKGROUND Reliable biomarkers of cirrhosis, hepatocellular carcinoma (HCC), or progression of chronic liver diseases are missing. In this context, Golgi protein-73 (GP73) also called Golgi phosphoprotein-2, was originally defined as a resident Golgi type II transmembrane protein expressed in epithelial cells. As a result, GP73 expression was found primarily in biliary epithelial cells, with only slight detection in hepatocytes. However, in patients with acute or chronic liver diseases and especially in HCC, the expression of GP73 is significantly up-regulated in hepatocytes. So far, few studies have assessed GP73 as a diagnostic or prognostic marker of liver fibrosis and disease progression. AIM To assess serum GP73 efficacy as a diagnostic marker of cirrhosis and/or HCC or as predictor of liver disease progression. METHODS GP73 serum levels were retrospectively determined by a novel GP73 ELISA (QUANTA Lite? GP73, Inova Diagnostics, Inc., Research Use Only) in a large cohort of 632 consecutive patients with chronic viral and non-viral liver diseases collected from two tertiary Academic centers in Larissa, Greece (n=366) and Debrecen, Hungary (n=266). Aspartate aminotransferase (AST)/Platelets (PLT) ratio index (APRI) was also calculated at the relevant time points in all patients. Two hundred and three patients had chronic hepatitis B, 183 chronic hepatitis C, 198 alcoholic liver disease, 28 autoimmune cholestatic liver diseases, 15 autoimmune hepatitis, and 5 with other liver-related disorders. The duration of follow-up was 50 (57) mo [median (interquartile range)]. The development of cirrhosis, liver decompensation and/or HCC during follow-up were assessed according to internationally accepted guidelines. In particular, the surveillance for the development of HCC was performed regularly with ultrasound imaging and alpha-fetoprotein (AFP) determination every 6 mo in cirrhotic and every 12 mo in non-cirrhotic patients. RESULTS Increased serum levels of GP73 (> 20 units) were detected at initial evaluation in 277 out of 632 patients (43.8%). GP73-seropositivity correlated at baseline with the presence of cirrhosis (96.4% vs 51.5%, P < 0.001), decompensation of cirrhosis (60.3% vs 35.5%, P < 0.001), presence of HCC (18.4% vs 7.9%, P < 0.001) and advanced HCC stage (52.9% vs 14.8%, P = 0.002). GP73 had higher diagnostic accuracy for the presence of cirrhosis compared to APRI score [Area under the curve (AUC) (95%CI): 0.909 (0.885-0.934) vs 0.849 (0.813-0.886), P = 0.003]. Combination of GP73 with APRI improved further the accuracy (AUC: 0.925) compared to GP73 (AUC: 0.909, P = 0.005) or APRI alone (AUC: 0.849, P < 0.001). GP73 levels were significantly higher in HCC patients compared to non-HCC [22.5 (29.2) vs 16 (20.3) units, P < 0.001) and positively associated with BCLC stage [stage 0: 13.9 (10.8); stage A: 17.1 (16.8); stage B: 19.6 (22.3); stage C: 32.2 (30.8); stage D: 45.3 (86.6) units, P < 0.001] and tumor dimensions [very early: 13.9 (10.8); intermediate: 19.6 (18.4); advanced: 29.1 (33.6) units, P = 0.004]. However, the discriminative ability for HCC diagnosis was relatively low [AUC (95%CI): 0.623 (0.570-0.675)]. Kaplan-Meier analysis showed that the detection of GP73 in patients with compensated cirrhosis at baseline, was prognostic of higher rates of decompensation (P = 0.036), HCC development (P = 0.08), and liver-related deaths (P < 0.001) during follow-up. CONCLUSION GP73 alone appears efficient for detecting cirrhosis and superior to APRI determination. In combination with APRI, its diagnostic performance can be further improved. Most importantly, the simple GP73 measurement proved promising for predicting a worse outcome of patients with both viral and non-viral chronic liver diseases.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:World Journal of Gastroenterology. - 26 : 34 (2020), p. 5130-5145. -
További szerzők:Tornai Tamás István (1984-) (belgyógyász) Shums, Zakera Zachou, Kalliopi Saitis, Asterios Gabeta, Stella Albesa, Roger Norman, Gary L. Papp Mária (1975-) (belgyógyász, gasztroenterológus) Dalekos, George N.
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7.

001-es BibID:BIBFORM078868
035-os BibID:(PMID)31464790
Első szerző:Janka Tamás
Cím:Deleterious effect of proton pump inhibitors on the disease course of cirrhosis / Tamas Janka, Tamas Tornai, Brigitta Borbely, David Tornai, Istvan Altorjay, Maria Papp, Zsuzsanna Vitalis
Dátum:2020
Megjegyzések:OBJECTIVES: Proton pump inhibitors (PPIs) are widely prescribed to patients with liver cirrhosis. We hypothesized that long-standing PPI use is associated with spontaneous bacterial peritonitis (SBP) and accelerated development of disease-specific complications and liver-related death. METHODS: A 5-year follow-up observational cohort study assessed the impact of long-standing PPI use on the clinical course of cirrhosis in a large referral patient cohort. 350 patients with cirrhosis (males: 188, females: 162, ages: 56?6 years, alcohol: 242 [69.1%], Child-Pugh stage A/B/C: 206/108/36) were assigned to two groups: regular PPI users (n=196) and non-users (n=154). Occurrence of SBP, decompensation events (development of ascites, hepatic encephalopathy and variceal bleeding), and liver-related death were assessed. RESULTS: Regular PPI use was associated with an increased cumulative probability of SBP compared to non-users [CP: 55% vs 24.8%, HR: 4.25 (95%CI: 1.42-12.67), p=0.05], but only in patients who had no previous SBP episode (n=84). A similar association was found between regular PPI use and decompensation events. The risk of the development of a first decompensation event (ascites, HE or VB) was higher in regular PPI users compared to non-users, in patients with compensated clinical stage at enrollment (HR: 2.81, 95%CI: 1.31-6.01, p=0.008, n=146). The risk of liver-related death was also significantly increased among regular PPI users (p<0.001). In multivariate Cox-regression analysis, regular PPI use (HR: 2.81, 95%CI: 1.43-5.51, p=0.003) and MELD score (HR: 1.21, 95%CI: 1.08-1.35, p<0.001) was an independent predictor of mortality. In the present follow-up cohort study, long-term PPI use was associated with the development of SBP and a progressive disease course in patients with cirrhosis that may have been caused by enhanced pathologic BT, accelerated development of BT-dependent disease-specific complications, and liver-related death.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
proton pump inhibitors
bacterial translocation
spontaneous bacterial peritonitis
disease progression
mortality
Megjelenés:European Journal of Gastroenterology & Hepatology. - 32 : 2 (2020), p. 257-264. -
További szerzők:Tornai Tamás István (1984-) (belgyógyász) Borbély Brigitta Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Altorjay István (1954-) (belgyógyász, gasztroenterológus, onkológus) Papp Mária (1975-) (belgyógyász, gasztroenterológus) Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00048
GINOP
EFOP-3.6.1-16-2016-00022
EFOP
EFOP-3.6.2-16-2017-00006
EFOP
BO/00232/17/5
Egyéb
ÚNKP-17-4
Egyéb
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8.

001-es BibID:BIBFORM061367
035-os BibID:(scopus)84952919716 (wos)000369955100003
Első szerző:Kocsis Dorottya
Cím:Intestinalis zsírsavkötő fehérje : az enterocytakárosodás markere akut és krónikus gasztroenterológiai kórképekben / Kocsis Dorottya, Papp Mária, Tornai Tamás, Tulassay Zsolt, Herszényi László, Tóth Miklós, Juhász Márk
Dátum:2016
Megjegyzések:Az intestinalis zsírsavkötő fehérje a zsírsavkötő fehérjék családjába tartozó, a vékony- és vastagbél enterocytáinakcitoszoljában termelődő, kis molekulasúlyú fehérje. Az enterocytasejtek membránintegritásának megbomlását követőenmegjelenik a szisztémás keringésben, és a vesék glomerularis szűrőjén keresztül kiválasztódik a vizeletbe. A szerzők akut és krónikus enterocytakárosodással járó gastrointestinalis kórképekben az intestinalis zsírsavkötő fehérje biomarkerként való használatával kapcsolatos vizsgálatokat tekintik át.
Tárgyszavak:Orvostudományok Klinikai orvostudományok magyar nyelvű folyóiratközlemény hazai lapban
folyóiratcikk
intestinalis zsírsavkötő fehérje
nekrotizáló enterocolitis
akut mesenterialis ischaemia
coeliakia
gyulladásos bélbetegség
bakteriális transzlokáció
Megjelenés:Orvosi Hetilap. - 157 : 2 (2016), p. 59-64. -
További szerzők:Papp Mária (1975-) (belgyógyász, gasztroenterológus) Tornai Tamás István (1984-) (belgyógyász) Tulassay Zsolt (1944-) (belgyógyász, gasztroenterológus) Herszényi László Tóth Miklós (Budapest) Juhász Márk Félix
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9.

001-es BibID:BIBFORM072903
035-os BibID:(cikkazonosító)e0194166 (WOS)000428603100051 (Scopus)85044720189
Első szerző:Kovács György (belgyógyász, gasztroenterológus)
Cím:Significance of serological markers in the disease course of ulcerative colitis in a prospective clinical cohort of patients / Gyorgy Kovacs, Nora Sipeki, Boglarka Suga, Tamas Tornai, Kai Fechner, Gary L. Norman, Zakera Shums, Peter Antal-Szalmas, Maria Papp
Dátum:2018
ISSN:1932-6203
Megjegyzések:Background & aimsTo determine the prognostic potential of classic and novel serologic antibodies regarding unfavorable disease course in a prospective ulcerative colitis (UC) patient cohort, since few and conflicting data are available in the literature regarding this matter.Methods187 consecutive patients were studied prospectively (median follow-up: 135 months) from a single referral IBD center in Hungary. Sera were tested for different IgA/IgG type autoantibodies (anti-neutrophil cytoplasmic [ANCA], anti-DNA-bound-lactoferrin [anti-LFS], anti-goblet cell [anti-GAB] and anti-pancreatic [PAB: anti-CUZD1 and anti-GP2)]) by indirect immunofluorescence technique and for anti-microbial (anti-Saccharomyces cerevisiae [ASCA] IgG/IgA and anti-OMP Plus? IgA) antibodies by enzyme-linked immunosorbent assays.ResultsA total of 73.6%, 62.4% and 11.2% of UC patients were positive for IgA/IgG type of atypical perinuclear-ANCA, anti-LFS and anti-GAB, respectively. Occurrences of PABs were 9.6%, while ASCA IgA/IgG and anti-OMP IgA were 17.6% and 19.8%, respectively. Antibody status was stable over time. IgA type PABs were more prevalent in patients with primary sclerosing cholangitis (37.5% vs. 4.7% for anti-CUZD1 and 12.5% vs. 0% for anti-GP2, p<0.001 for both). IgA type ASCA and anti-CUZD1 antibodies were associated with higher risk of requirement for long-term immunosuppressant therapy in Kaplan-Meier analysis (pLogRank <0.01 for both). However, in multivariate Cox-regression analysis only ASCA IgA (HR: 2.74, 95%CI: 1.46?5.14, p<0.01) remained independent predictor. UC-related hospitalization due to disease activity was only associated with multiple antibody positivity (for 3 or more; HR 2.03 [95% CI: 1.16?3.56]; p = 0.013). None of the individual antibodies or their combination was associated with the risk of development of extensive disease or colectomy.ConclusionEven with low prevalence rates, present study gives further evidence to the role of certain antibodies as markers for distinct phenotype and disease outcome in UC. Considering the result of the multivariate analysis the novel antibodies investigated do not seem to be associated with poor clinical outcome in UC, only a classic antibody, IgA subtype ASCA remained an independent predictor of long-term immunosuppressive therapy.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Plos One. - 13 : 3 (2018), p. 1-18. -
További szerzők:Sipeki Nóra (1987-) (általános orvos) Suga Boglárka Tornai Tamás István (1984-) (belgyógyász) Fechner, Kai Norman, Gary L. Shums, Zakera Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:OTKA-115818
OTKA
RH/885/2013
Egyéb
BO/00426/11
Egyéb
IOIBD Research Grant (2012-2015)
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

10.

001-es BibID:BIBFORM070012
035-os BibID:e015874
Első szerző:Márta Katalin
Cím:High versus low energy administration in the early phase of acute pancreatitis (GOULASH trial) : protocol of a multicentre randomized double-blind clinical trial / Katalin Márta, Anikó Nóra Szabó, Dániel Pécsi, Péter Varjú, Judit Bajor, Szilárd Gódi, Patrícia Sarlós, Alexandra Mikó, Katalin Szemes, Mária Papp, Tamás Tornai, Áron Vincze, Zsolt Márton, Patrícia Anna Vincze, Erzsébet Lankó, Andrea Szentesi, Tímea Molnár, Roland Hagendorn, Faluhelyi Nándor, István Battyáni, Dezső Kelemen, Róbert Papp, Attila Miseta, Verzár Zsófia, Markus M. Lerch, Johan P. Neoptoleomos, Miklós Sain-Tóth, Ole H. Petersen, Peter Hegyi
Dátum:2017
ISSN:2044-6055
Megjegyzések:Introduction. Acute pancreatitis (AP) is an inflammatory disease with no specific therapy. Mitochondrial injury followed by ATP depletion in both acinar and ductal cells is a recently discovered early event in the pathogenesis. Importantly, preclinical research showed that intracellular ATP delivery restores the physiological function of the cells and protects from cell injury suggesting that restoration of energy levels in the pancreas is therapeutically beneficial. Despite several, high quality and experimental observations in this area, no randomized trials have been conducted to date to address the requirements for energy intake in the early phase of AP. Methods/Design. This is a randomized, controlled two-arms double-blind multicentre trial. Patients suffering from AP will be randomly assigned to groups A (30 kcal/kg/day energy administration starting within 24h of hospital admission) or B (low energy administration during the first 72h of hospital admission). Energy will be delivered with nasoenteric tube feeding with additional intravenous glucose supplementation or total parenteral nutrition if necessary. A combination of multi organ failure for more than 48h and mortality is defined as the primary endpoint, whereas several secondary endpoints such as length of hospitalization or pain will be determined to elucidate more detailed differences between the groups. The general feasibility, safety and quality checks required for high quality evidence will be adhered to.Ethics and Dissemination. The study has been approved by the relevant organization, The Scientific and Research Ethics Committee of the Hungarian Medical Research Council (55961- 2/2016/EKU). This study will provide evidence whether early high-energy nutritional support is beneficial in the clinical management of AP. The results of this trial will be published in an open access way and disseminated among medical doctors.Trial registration: The trial has been registered at the ISRCTN (ISRTCN 63827758).
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
acute pancreatitis
energy administration
enteral feeding
randomized clinical trial
Megjelenés:BMJ Open. - 7 : 9 (2017), p. 1-9. -
További szerzők:Szabó Anikó Nóra Pécsi Dániel Varjú Péter Bajor Judit Gódi Szilárd Sarlós Patrícia Mikó Alexandra Szemes Katalin Papp Mária (1975-) (belgyógyász, gasztroenterológus) Tornai Tamás István (1984-) (belgyógyász) Vincze Áron Márton Zsolt Vincze Patrícia Anna Lankó Erzsébet Szentesi Andrea Molnár Tímea Hágendorn Roland Faluhelyi Nándor Battyáni István Kelemen Dezső Papp Róbert Miseta Attila Verzár Zsófia Lerch, Markus M. Neoptoleomos, Johan P. Sain-Tóth, Miklós Petersen, Ole H. Hegyi Péter Jenő (belgyógyász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00015
GINOP
KH-125678
NKFI
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

11.

001-es BibID:BIBFORM099044
035-os BibID:(WoS)000784212600008 (Scopus)85118996099
Első szerző:Moran, Robert A.
Cím:Early infection is an independent risk factor for increased mortality in patients with culture-confirmed infected pancreatic necrosis / Moran Robert A., Halloran Christopher, Guo Qiang, Umapathy Chandra, Jalaly Niloofar Y., Jain Saransh, Cowzer Darren, Cuadrado Robles Enrique Perez, Quesada-Vázquez Noé, Szentesi Andrea, Papp Mária, Chua Tiffany, Márta Katalin, Sampath Kartik, Jin David X., Sahebally Shaheel Mohammad, Kuschnereit Tobias Philipp, Khashab Mouen A., Rock Clare, Darvasi Erika, Saunders Rebecca, García-Rayado Guillermo, Torrijos Yolanda Sánchez, Coady Laoise, Papachristou Georgios I., Mayerle Julia, Geoghegan Justin, Banks Peter A., Gardner Timothy B., Szabó Anikó Nóra, Stevens Tyler, Tornai Tamás, Tóth Emese, McEntee Gerry, Garg Pramod K., Hegyi Péter, Yadav Dhiraj, Hu Weiming, Neoptolemos John, Singh Vikesh K.
Dátum:2022
ISSN:1424-3903
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Infected pancreatic necrosis
Necrosectomy
Mortality
Surgery
Pancreatic necrosis
Necrotizing pancreatitis
Minimally invasive surgery
Megjelenés:Pancreatology. - 22 : 1 (2022), p. 67-73. -
További szerzők:Halloran, Christopher Guo, Qiang Umapathy, Chandra Jalaly, Niloofar Y. Jain, Saransh Cowzer, Darren Cuadrado Robles, Enrique Perez Quesada-Vázquez, Noé Szentesi Andrea Papp Mária (1975-) (belgyógyász, gasztroenterológus) Chua, Tiffany Márta Katalin Sampath, Kartik Jin, David X. Sahebally, Shaheel Mohammad Kuschnereit, Tobias Philipp Khashab, Mouen A. Rock, Clare Darvasi Erika Saunders, Rebecca García-Rayado, Guillermo Sánchez Torrijos, Yolanda Coady, Laoise Papachristou, Georgios I. Mayerle, Julia Geoghegan, Justin Banks, Peter A. Gardner, Timothy B. Szabó Anikó Nóra Stevens, Tyler Tornai Tamás István (1984-) (belgyógyász) Tóth Emese McEntee, Gerry Garg, Pramod K. Hegyi Péter Jenő (belgyógyász) Yadav, Dhiraj Hu, Weiming Neoptoleomos, Johan P. Singh, Vikesh K.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM073777
Első szerző:Pályu Eszter
Cím:Major changes of von Willebrand factor multimer distribution in cirrhotic patients with stable disease or acute decompensation / Eszter Palyu, Jolan Harsfalvi, Tamas Tornai, Maria Papp, Miklos Udvardy, Katalin Szekeres-Csiki, Lajos Pataki, Karen Vanhoorelbeke, Hendrik B. Feys, Hans Deckmyn, Istvan Tornai
Dátum:2018
ISSN:0340-6245
Megjegyzések:Background and aims: There is an unstable balance between pro- and anti-haemostatic processes in patients with cirrhosis. We hypothesized, that in patients with acute decompensation (AD) the major alterations of von Willebrand factor (VWF) could contribute to the prothrombotic situation as compared to patients with stable (ST) cirrhosis. Methods: We analyzed different parameters of VWF, including detailed multimer distribution by densitometry and platelet adhesion together with ADAMTS13 activity and antigen and C-reactive protein (CRP) levels in patients with ST (n=99), with AD (n=54) and controls (n=92). Results: VWF antigen, ristocetin cofactor as well as collagen binding activities were elevated in both cirrhotic groups in a stepwise manner. There was a decrease in high and an increase in low molecular weight multimer ratios in the majority of ST cirrhosis. However, in 24 out of 54 AD patients ultra-large VWF multimers (ULMWM) were found. ADAMTS13 activity in ST and AD patients without ULMWM was similar to controls [median, (IQR)%: 98 (67-132) and 91 (60-110) vs. 106 (88-117), respectively]. The presence of ULMWM in AD patients was associated with low ADAMTS13 activity [33 (24-49)%] and high CRP level [23 (7.1-83.6)mg/l]. Adhesion of normal platelets showed a stepwise increase in the presence of cirrhotic plasmas, reaching the highest level in AD patients with ULMWM. Conclusion: Characteristic changes of VWF parameters are seen in ST cirrhosis. In AD patients highly increased VWF and reduced ADAMTS13 activity could be found, along with the presence of ULMWM, which are possible markers and contributors of the disease progression.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cirrhosis
acute decompensation
systemic inflammation
von Willebrand factor multimers
trhombotic microangiopathy
Megjelenés:Thrombosis and Haemostasis. - 118 : 8 (2018), p. 1397-1408. -
További szerzők:Hársfalvi Jolán (1949-) (klinikai biokémikus) Tornai Tamás István (1984-) (belgyógyász) Papp Mária (1975-) (belgyógyász, gasztroenterológus) Udvardy Miklós (1947-) (belgyógyász, haematológus) Szekeres-Csiki Katalin (1979-) (orvos) Pataki Lajos Vanhoorelbeke, Karen Feys, Hendrik B. Deckmyn, Hans Tornai István (1954-) (belgyógyász, gasztroenterológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:
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