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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
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001-es BibID:BIBFORM010925
Első szerző:Papp Mária (belgyógyász, gasztroenterológus)
Cím:Anti-microbial antibodies in celiac disease : trick or treat? / Maria Papp, Ildiko Foldi, Istvan Altorjay, Eszter Palyu, Miklos Udvardy, Judit Tumpek, Sandor Sipka, Ilma Rita Korponay-Szabo, Eva Nemes, Gabor Veres, Tamas Dinya, Attila Tordai, Hajnalka Andrikovics, Gary L. Norman, Peter Laszlo Lakatos
Dátum:2009
ISSN:1007-9327 (Print)
Megjegyzések:To determine the prevalence of a new set of anti-glycan and anti-outer membrane protein (anti-OMP) antibodies in a Hungarian cohort of adult Celiac disease (CD) patients. METHODS: 190 consecutive CD patients [M/F: 71/119, age:39.9 (SD:14.1) years], 100 healthy, and 48 gastrointestinal controls were tested for glycan anti-Saccharomyces cerevisiae (gASCA), anti-laminaribioside (ALCA), anti-chitobioside, anti-mannobioside, anti-OMP antibodies and major NOD2/CARD15 mutations. Thirty out of 82 CD patients enrolled at the time of diagnosis were re-evaluated for the same antibodies after longstanding gluten-free diet (GFD). RESULTS: 65.9% of the CD patients were positive for at least one of the tested antibodies at the time of the diagnosis. Except anti-OMP and ALCA, anti-microbial antibodies were exclusively seen in untreated CD; however, the overall sensitivity was low. Any glycan positivity (LR+: 3.13; 95% CI: 2.08-4.73) was associated with an increased likelihood ratio for diagnosing CD. Significant correlation was found between the levels of anti-glycan and anti-endomysial or anti-transglutaminase antibodies. Anti-glycan positivity was lost after longstanding GFD. Anti-glycan antibody titers were associated with symptoms at presentation, but not the presence of NOD2/CARD15 mutations. Patients with severe malabsorption more frequently had multiple antibodies at diagnosis (P = 0.019). CONCLUSION: The presence of anti-glycan antibodies in CD seems to be secondary to the impaired small bowel mucosa which can lead to increased antigen presentation. Furthermore, anti-glycan positivity may be considered an additional marker of CD and dietary adherence.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:World Journal of Gastroenterology 15 : 31 (2009), p. 3891-3900. -
További szerzők:Földi Ildikó (1981-) (orvos) Altorjay István (1954-) (belgyógyász, gasztroenterológus, onkológus) Pályu Eszter (1983-) Udvardy Miklós (1947-) (belgyógyász, haematológus) Tumpek Judit (1944-) (orvosi laboratóriumi szakorvos) Sipka Sándor (1945-) (laboratóriumi szakorvos) Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nemes Éva (1957-) (csecsemő- és gyermekgyógyász, gasztroenterológus) Veres Gábor (1969-2020) (csecsemő- és gyermekgyógyász, gasztroenterológus) Dinya Tamás (1974-) (sebész szakorvos, onkológus szakorvos) Tordai Attila Andrikovics Hajnalka Norman, Gary L. Lakatos Péter (Semmelweis Egyetem)
Internet cím:DOI
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