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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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001-es BibID:BIBFORM006783
Első szerző:Papp Mária (belgyógyász, gasztroenterológus)
Cím:Haptoglobin polymorphism : a novel genetic risk factor for celiac disease development and its clinical manifestations / Papp, M., Foldi, I., Nemes, E., Udvardy, M., Harsfalvi, J., Altorjay, I., Mate, I., Dinya, T., Varvolgyi, C., Barta, Z., Veres, G., Lakatos, P. L., Tumpek, J., Toth, L., Szathmari, E., Kapitany, A., Gyetvai, A., Korponay-Szabo, I. R.
Dátum:2008
ISSN:0009-9147
Megjegyzések:Haptoglobin (Hp) alpha-chain alleles 1 and 2 account for 3 phenotypes that may influence the course of inflammatory diseases via biologically important differences in their antioxidant, scavenging, and immunomodulatory properties. Hp1-1 genotype results in the production of small dimeric, Hp2-1 linear, and Hp2-2 cyclic polymeric haptoglobin molecules. We investigated the haptoglobin polymorphism in patients with celiac disease and its possible association to the presenting symptoms. METHODS: We studied 712 unrelated, biopsy-proven Hungarian celiac patients (357 children, 355 adults; severe malabsorption 32.9%, minor gastrointestinal symptoms 22.8%, iron deficiency anemia 9.4%, dermatitis herpetiformis 15.6%, silent disease 7.2%, other 12.1%) and 384 healthy subjects. We determined haptoglobin phenotypes by gel electrophoresis and assigned corresponding genotypes. RESULTS: Hp2-1 was associated with a significant risk for celiac disease (P = 0.0006, odds ratio [OR] 1.54, 95% CI 1.20-1.98; prevalence 56.9% in patients vs 46.1% in controls). It was also overrepresented among patients with mild symptoms (69.2%) or silent disease (72.5%). Hp2-2 was less frequent in patients than in controls (P = 0.0023), but patients having this phenotype were at an increased risk for severe malabsorption (OR 2.21, 95% CI 1.60-3.07) and accounted for 45.3% of all malabsorption cases. Celiac and dermatitis herpetiformis patients showed similar haptoglobin phenotype distributions. CONCLUSIONS: The haptoglobin polymorphism is associated with susceptibility to celiac disease and its clinical presentations. The predominant genotype in the celiac population was Hp2-1, but Hp2-2 predisposed to a more severe clinical course. The phenotype-dependent effect of haptoglobin may result from the molecule's structural and functional properties.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Clinical Chemistry. - 54 : 4 (2008), p. 697-704. -
További szerzők:Földi Ildikó (1981-) (orvos) Nemes Éva (1957-) (csecsemő- és gyermekgyógyász, gasztroenterológus) Udvardy Miklós (1947-) (belgyógyász, haematológus) Hársfalvi Jolán (1949-) (klinikai biokémikus) Altorjay István (1954-) (belgyógyász, gasztroenterológus, onkológus) Máté István Dinya Tamás (1974-) (sebész szakorvos, onkológus szakorvos) Várvölgyi Csaba (1958-) (belgyógyász, gasztroenterológus) Barta Zsolt (1964-) (belgyógyász, gasztroenterológus) Veres Gábor (1969-2020) (csecsemő- és gyermekgyógyász, gasztroenterológus) Lakatos Péter (Semmelweis Egyetem) Tumpek Judit (1944-) (orvosi laboratóriumi szakorvos) Tóth László (1971-) (patológus) Szathmári Erzsébet Kapitány Anikó (1979-) (molekuláris biológus) Gyetvai Ágnes Korponay-Szabó Ilma (1959-) (gyermekgyógyász)
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