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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
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

2.

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
Borító:
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