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1.

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
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM065752
Első szerző:Papp Mária (belgyógyász, gasztroenterológus)
Cím:Presepsin teardown : pitfalls of biomarkers in the diagnosis and prognosis of bacterial infection in cirrhosis / Maria Papp, Tamas Tornai, Zsuzsanna Vitalis, Istvan Tornai, David Tornai, Tamas Dinya, Andrea Sumegi, Peter Antal-Szalmas
Dátum:2016
Megjegyzések:AIM: Bacterial infections are frequent complications in cirrhosis with significant mortality. Early laboratory diagnosis is essential but challenging. We aimed to evaluate the diagnostic and prognostic value of presepsin in cirrhosis associated bacterial infections. METHODS: 216 patients with cirrhosis were enrolled. At admission, presence of bacterial infections and level of plasma presepsin, serum CRP and PCT were evaluated. Patients were followed for three months to assess the possible association between presepsin level and short-term mortality. RESULTS: 34.7% of patients had bacterial infection. Presepsin levels were significantly higher in patients with infection than without (median, 1002 vs. 477 pg/mL, p<0.001), increasing with the severity of infection (organ failure[OF]Yes vs. No: 2358 vs. 710 pg/mL, p<0.001). Diagnostic accuracy of presepsin for severe infections was similar to PCT and superior to CRP (AUC-ROC: 0.85, 0.85 and 0.66, respectively, p=NS for presepsin vs. PCT and p<0.01 for presepsin vs. CRP). At the optimal cut-off value of presepsin>1206 pg/mL sensitivity, specificity, PPV and NPV were as follows: 87.5%, 74.5%, 61.8% and 92.7%. The accuracy of presepsin, however, decreased in advanced stage of the disease or in the presence of renal failure, most probably because of the significantly elevated presepsin levels in non-infected patients. 28-day mortality rate was higher among patients with >1277 pg/mL compared to those with ?1277 pg/mL (46.9% vs. 11.6%, p<0.001). In a binary logistic regression analysis, however, only PCT [OR: 1.81, (95%CI: 1.09?3.01), p=0.022] but neither presepsin and nor CRP were independent risk factor for 28-day mortality after adjusting with MELD score and leukocyte count.CONCLUSION: Presepsin is a valuable new biomarker for defining severe infections in cirrhosis proving same efficacy as PCT. However, it is not a useful marker of short-term mortality.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
presepsin
cirrhosis
bacterial infection
organ failure
mortality
Megjelenés:World Journal of Gastroenterology 22 : 41 (2016), p. 1-14. -
További szerzők:Tornai Tamás István (1984-) (belgyógyász) Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Dinya Tamás (1974-) (sebész szakorvos, onkológus szakorvos) Sümegi Andrea (1969-) (biológus) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM071775
Első szerző:Satishchandran, Abhishek
Cím:MicroRNA 122, Regulated by GRLH2, Protects Livers of Mice and Patients From Ethanol-Induced Liver Disease / Abhishek Satishchandran, Aditya Ambade, Sitara Rao, Ying-Chao Hsueh, Arvin Iracheta-Vellve, David Tornai, Patrick Lowe, Benedek Gyongyosi, Jia Li, Donna Catalano, Li Zhong, Karen Kodys, Jun Xie, Shashi Bala, Guangping Gao, Gyongyi Szabo
Dátum:2018
ISSN:0016-5085
Megjegyzések:BACKGROUND & AIMS:Chronic, excessive alcohol consumption leads to alcoholic liver disease (ALD) characterized by steatosis, inflammation, and eventually cirrhosis. The hepatocyte specific microRNA 122 (MIR122) regulates hepatocyte differentiation and metabolism. We investigated whether an alcohol-induced decrease in level of MIR122 contributes to development of ALD.METHODS:We obtained liver samples from 12 patients with ALD and cirrhosis and 9 healthy individuals (controls) and analyzed them by histology and immunohistochemistry. C57Bl/6 mice were placed on a Lieber-DeCarli liquid diet, in which they were fed ethanol for 8 weeks, as a model of ALD, or a control diet. These mice were also given injections of CCl4, to increase liver fibrosis, for 8 weeks. On day 28, mice with ethanol-induced liver disease and advanced fibrosis, and controls, were given injections of recombinant adeno-associated virus 8 vector that expressed the primary miR-122 transcript (pri-MIR122, to overexpress MIR122 in hepatocytes) or vector (control). Two weeks before ethanol feeding, some mice were given injections of a vector that expressed an anti-MIR122, to knock down its expression. Serum and liver tissues were collected; hepatocytes and liver mononuclear cells were analyzed by histology, immunoblots, and confocal microscopy. We performed in silico analyses to identify targets of MIR122 and chromatin immunoprecipitation quantitative polymerase chain reaction analyses in Huh-7 cells.RESULTS:Levels of MIR122 were decreased in liver samples from patients with ALD and mice on the Lieber-DeCarli diet, compared with controls. Transgenic expression of MIR122 in hepatocytes of mice with ethanol-induced liver disease and advanced fibrosis significantly reduced serum levels of alanine aminotransferase (ALT) and liver steatosis and fibrosis, compared with mice given injections of the control vector. Ethanol feeding reduced expression of pri-MIR122 by increasing expression of the spliced form of the transcription factor grainyhead like transcription factor 2 (GRHL2) in liver tissues from mice. Levels of GRHL2 also were increased in liver tissues from patients with ALD, compared with controls; increases correlated with decreases in levels of MIR122 in human liver. Mice given injections of the anti-MIR122 before ethanol feeding had increased steatosis, inflammation, and serum levels of alanine aminotransferase compared with mice given a control vector. Levels of hypoxia-inducible factor 1 alpha (HIF1?) mRNA, a target of MIR122, were increased in liver tissues from patients and mice with ALD, compared with controls. Mice with hepatocyte-specific disruption of Hif1? developed less-severe liver injury following administration of ethanol, injection of anti-MIR122, or both.CONCLUSIONS:Levels of MIR122 decrease in livers from patients with ALD and mice with ethanol-induced liver disease, compared with controls. Transcription of MIR122 is inhibited by GRHL2, which is increased in livers of mice and patients with ALD. Expression of an anti-MIR122 worsened the severity of liver damage following ethanol feeding in mice. MIR122 appears to protect the liver from ethanol-induced damage by reducing levels of HIF1?. These processes might be manipulated to reduce the severity of ALD in patients.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
alkoholos májbetegség
Megjelenés:Gastroenterology. - 154 : 1 (2018), p. 238-252. -
További szerzők:Ambade, Aditya Rao, Sitara Hsueh, Ying-Chao Iracheta-Vellve, Arvin Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Lowe, Patrick Gyöngyösi Benedek Li, Jia Catalano, Donna Zhong, Li Kodys, Karen Xie, Jun Bala, Shashi Gao, Guangping Szabó Gyöngyi
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM102132
035-os BibID:(WoS)000810325500003 (Scopus)85131793956
Első szerző:Tornai Dávid (hepatológia, biomarker kutatás)
Cím:Serological biomarkers for management of primary sclerosing cholangitis / Tornai Dávid, Vén Péter László, Lakatos Péter László, Papp Mária
Dátum:2022
ISSN:1007-9327
Megjegyzések:Clinical manifestations and progression of primary sclerosing cholangitis (PSC) are heterogeneous, and its pathogenesis is poorly understood. The importance of gut-liver interactions in the pathogenesis has been clinically confirmed and highlighted in different theories. Recent advances regarding biomarkers of biliarygut crosstalk may help to identify clinically relevant PSC subgroups assisting everyday clinical work-up (e.g., diagnosis, disease stratification, or surveillance) and the exploration of potential therapeutic targets. Alkaline phosphatase produced by the biliary epithelium is consistently associated with prognosis. However, its level shows natural fluctuation limiting its use in individual patients. Inflammatory, cell activation, and tissue remodeling markers have been reported to predict clinical outcome. Elevated immunoglobulin (Ig) G4 level is associated with a shorter transplantation-free survival. IgG type atypical perinuclear anti-neutrophil cytoplasmic antibodies (P-ANCAs) are non-specific markers of various autoimmune liver diseases and may reflect an abnormal B-cell response to gut microbial antigens. IgG type atypical P-ANCA identifies PSC patients with particular clinical and genetic (for human leukocyte antigens) characteristics. The presence of IgA type anti-F-actin antibody (AAA) may predict a progressive disease course, and it is associated with enhanced mucosal immune response to various microbial antigens and enterocyte damage. IgA type anti-glycoprotein 2 (GP2) antibodies identify patients with a severe disease phenotype and poor survival due to enhanced fibrogenesis or development of cholangiocarcinoma. Elevated soluble vascular adhesion protein-1 (sVAP-1) level is associated with adverse disease outcomes in PSC. High sVAP-1 levels correlate with mucosal addressin cell adhesion molecule-1 (MAdCAM-1) expression in the liver that contributes to gut activated T-cell homing to the hepatobiliary tract. In the present paper, we review the evidence on these possible serological markers that could potentially help address the unmet clinical needs in PSC.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Primary sclerosing cholangitis
Hepatobiliary
Serological biomarker
Immunoglobulin
Inflammatory
Tissue remodeling
Megjelenés:World Journal of Gastroenterology. - 28 : 21 (2022), p. 2291-2301. -
További szerzők:Vén Péter László Lakatos Péter (Semmelweis Egyetem) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:OTKA-138041
OTKA
EFOP-3.6.1-16-2016-00022
EFOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM091813
035-os BibID:(cikkazonosító)94
Első szerző:Tornai Dávid (hepatológia, biomarker kutatás)
Cím:Abnormal ferritin levels predict development of poor outcomes in cirrhotic outpatients : a cohort study / David Tornai, Peter Antal-Szalmas, Tamas Tornai, Maria Papp, Istvan Tornai, Nora Sipeki, Tamas Janka, Boglarka Balogh, Zsuzsanna Vitalis
Dátum:2021
ISSN:1471-230X
Megjegyzések:Abstract Background: Both iron overload and iron deficient anemia can associate with cirrhosis. At the same time, inflammation might be continuously present in cirrhotic patients due to bacterial translocation and patients' susceptibility to infections. Ferritin is a sensitive and widely available marker of iron homeostasis, in addition it acts as an acute phase protein. Therefore, we evaluated the prognostic potential of serum ferritin in the longterm follow-up of cirrhotic outpatients. Methods: A cohort of 244 cirrhotic outpatients was recruited and followed for 2 years. We measured their serum ferritin levels in our routine laboratory unit at enrolment and investigated its association with clinical outcomes. Results: Ferritin serum level was higher in males and older patients than in females (median: 152.6 vs. 75 ?g/L, p<0.001) or younger individuals (median: 142.9 vs. 67.9 ?g/L, p=0.002). Patients who previously survived variceal bleeding had lower ferritin levels (median: 43.1 vs. 146.6 ?g/L, p<0.001). In multivariate regression models, including laboratory and clinical factors, lower (<40 ?g/L) ferritin concentration was associated with the development of decompensated clinical stage in patients with previously compensated cirrhosis (sHR: 3.762, CI: 1.616-8.760, p=0.002), while higher (>310 ?g/L) circulating ferritin levels were associated with increased risks of bacterial infections in decompensated patients (sHR: 2.335, CI: 1.193-4.568, p=0.013) and mortality in the whole population (HR: 2.143, CI: 1.174-3.910, p=0.013). Conclusion: We demonstrated usefulness of serum ferritin as a prognostic biomarker in cirrhosis, pointing out that both low and high concentrations need attention in these patients.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Bmc Gastroenterology. - 21 : 1 (2021), p. 1-13. -
További szerzők:Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Tornai Tamás István (1984-) (belgyógyász) Papp Mária (1975-) (belgyógyász, gasztroenterológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Sipeki Nóra (1987-) (általános orvos) Janka Tamás Balogh Boglárka (1993-) (belgyógyász) Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM089190
Első szerző:Tornai Dávid (hepatológia, biomarker kutatás)
Cím:Increased sTREM-1 levels identify cirrhotic patients with bacterial infection and predict their 90-day mortality / Tornai David, Vitális Zsuzsanna, Jónás Alexa, Janka Tamás, Földi Ildikó, Tornai Tamás, Sipeki Nóra, Csillag Anikó, Balogh Boglárka, Sümegi Andrea, Földesi Róza, Papp Mária, Antal-Szalmás Péter
Dátum:2021
Megjegyzések:Background & Aims: Patients with cirrhosis are susceptible to bacterial infections (BIs) that are major causes of specific complications and mortality. However, the diagnosis of BIs can often be difficult in advanced disease stage since their symptoms may overlap with the ones of acute decompensation (AD). Soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is released from monocytes/macrophages and neutrophils during activation and has been reported to correlate with activity of various inflammatory processes. We investigated its diagnostic and prognostic performance in patients with cirrhosis and BI. Methods: Sera of 269 patients were assayed for sTREM-1 by ELISA (172 outpatients and 97 patients with AD of whom 56 had BI). We investigated capacity of sTREM-1 to identify patients with BI and conducted a 90-day follow-up observational study to assess its possible association with short-term mortality. Results: sTREM-1 levels were significantly higher in patients with more severe liver disease, BI, and acute-on-chronic liver failure than in patients without these conditions. sTREM-1 had similar accuracy to CRP identifying BI [sTREM-1: AUROC (95%CI) 0.804 (0.711-0.897), p<0.0001, CRP: 0.791 (0.702-0.881) p<0.0001)] among AD patients. The combination of these two molecules and the presence of ascites into a composite score significantly increased their discriminative power (AUROC:0.878, 95%CI:0.812-0.944, p<0.0001). High sTREM-1 level (>660 pg/mL) was an independent predictor of 90-day mortality in patients with BI [HR: 2.941, (95%CI: 1.009-8.573), p=0.048] in our multivariate model. Conclusions: Use of sTREM-1 could increase the recognition of BIs in cirrhosis and help clinicians in mortality risk assessment of these patients.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
sTREM-1
bacterial infection
cirrhosis
acute decompensation
mortality
Megjelenés:Clinics and Research in Hepatology and Gastroenterology. - 45 : 5 (2021), p. 1-12. -
További szerzők:Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Jónás Alexa Janka Tamás Földi Ildikó (1981-) (orvos) Tornai Tamás István (1984-) (belgyógyász) Sipeki Nóra (1987-) (általános orvos) Csillag Anikó (1979-) (immunológus, biológus, angol-magyar szakfordító) Balogh Boglárka (1993-) (belgyógyász) Sümegi Andrea (1969-) (biológus) Földesi Róza (1967-) (klinikai laboratóriumi kutató, PhD hallgató) Papp Mária (1975-) (belgyógyász, gasztroenterológus) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos)
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
ÚNKP-19-4
ÚNKP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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7.

001-es BibID:BIBFORM069781
Első szerző:Tornai Tamás István (belgyógyász)
Cím:Gut barrier failure biomarkers are associated with poor disease outcome in patients with primary sclerosing cholangitis / Tamas Tornai, Eszter Palyu, Zsuzsanna Vitalis, Istvan Tornai, David Tornai, Peter Antal-Szalmas, Gary L. Norman, Zakera Shums, Gabor Veres, Antal Dezsofi, Gabriella Par, Alajos Par, Peter Orosz, Ferenc Szalay, Peter L. Lakatos, Maria Papp
Dátum:2017
ISSN:1007-9327
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:World Journal of Gastroenterology. - 23 : 29 (2017), p. 5412-5421. -
További szerzők:Pályu Eszter (1983-) Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Norman, Gary L. Shums, Zakera Veres Gábor (orvos) Dezsőfi Antal Pár Gabriella Pár Alajos Orosz Péter (Miskolc) Szalay Ferenc (belgyógyász) Lakatos Péter (Semmelweis Egyetem) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:OTKA-115818
OTKA
MTA-Bolyai János Kutatási Ösztöndíj
Egyéb
ÚNKP-16-3
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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