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1.

001-es BibID:BIBFORM044485
Első szerző:Dezsőfi Antal
Cím:Az egyes HLA-DQ allélok gyakorisága 1-es típusú diabetesben és coeliakiában szenvedő gyermekekben / Dezsőfi Antal, Krikovszky Dóra, Kapitány Anikó, Szebeni Beáta, Veres Gábor, Sipka Sándor, Körner Anna, Madácsy László, Korponay-Szabó Ilma, Arató András
Dátum:2006
Tárgyszavak:Orvostudományok Klinikai orvostudományok magyar nyelvű folyóiratközlemény hazai lapban
Megjelenés:Gyermekgyógyászat. - 57 : 3 (2006), p. 287-291. -
További szerzők:Krikovszky Dóra Kapitány Anikó (1979-) (molekuláris biológus) Szebeni Beáta Veres Gábor (1969-2020) (csecsemő- és gyermekgyógyász, gasztroenterológus) Sipka Sándor (1945-) (laboratóriumi szakorvos) Körner Anna Madácsy László (Szeged) Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Arató András
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM040844
Első szerző:Dezsőfi Antal
Cím:Frequencies of Genetic Polymorphisms of TLR4 and CD14 and of HLA-DQ Genotypes in Children With Celiac Disease, Type 1 Diabetes Mellitus, or Both / Dezsőfi, A., Szebeni, B., Hermann, CS., Kapitány, A., Veres, G., Sipka, S., Körner, A., Madácsy, L., Korponay-Szabó, I., Rajczy, K., Arató, A.
Dátum:2008
ISSN:0277-2116
Megjegyzések:OBJECTIVES: Besides the central role of the adaptive immune system, a disturbance of innate immunity is also involved in the pathogenesis of celiac disease (CD). Inasmuch as CD and type 1 diabetes mellitus (T1DM) frequently coexist because of a common genetic predisposition, our aim was to study the frequency of CD14 C-260T and TLR4 A+896G single nucleotide polymorphisms (SNPs) and the distribution of HLA-DQ genotypes in children affected by CD, T1DM, or both. PATIENTS AND METHODS: TLR4 and CD14 SNPs were tested by polymerase chain reaction, followed by restriction fragment length polymorphism analysis in 80 children with T1DM, 100 children with CD, and 47 children with both CD and T1DM. Determination of HLA-DQ alleles was done by sequence-specific polymerase chain reaction. Frequencies were compared with those of healthy control children. RESULTS: The prevalence of the homozygous CD14 C-260TT genotype was significantly (P = 0.0081) lower in children with T1DM but not in those with CD and T1DM, compared with control children. No difference was found in the genotype and allele frequencies of TLR4 between the studied groups. In patients with T1DM, the frequency of the homozygous HLA-DQ8 genotype was significantly higher than in CD, whereas the frequency of homozygous or heterozygous HLA-DQ2 genotypes did not differ from that in control children. In patients with CD, both homozygous and heterozygous HLA-DQ2 genotypes were significantly more frequent than in the control and T1DM groups, and no elevation in the frequency of the HLA-DQ8 genotypes was observed. In patients with T1DM and those with CD and T1DM, the occurrence of HLA-DQ2/8 heterozygosity was significantly higher than in children with CD only and in control children. CONCLUSIONS: Our results suggest that in patients with T1DM, the CD14 C-260TT homozygous genotype increases the risk for the development of CD. The distribution of HLA-DQ genotype is different in children with CD and T1DM than in children with CD or T1DM only. Determination of the HLA-DQ genotype in children with T1DM may help in estimating the risk for the development of CD.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Pediatric Gastroenterology And Nutrition. - 47 : 3 (2008), p. 283-287. -
További szerzők:Szebeni Beáta Hermann, CS. Kapitány Anikó (1979-) (molekuláris biológus) Veres Gábor (1969-2020) (csecsemő- és gyermekgyógyász, gasztroenterológus) Sipka Sándor (1945-) (laboratóriumi szakorvos) Körner Anna Madácsy László (Szeged) Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Rajczy Katalin Arató András
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM096523
Első szerző:Szebeni Beáta
Cím:Increased Expression of Serum- and Glucocorticoid-regulated Kinase-1 in the Duodenal Mucosa of Children With Coeliac Disease / Szebeni Beáta, Vannay Ádám, Sziksz Erna, Prókai Ágnes, Cseh Áron, Veres Gábor, Dezsőfi Antal, Győrffy Hajnalka, Korponay-Szabó I. R., Arató András
Dátum:2010
ISSN:0277-2116
Megjegyzések:Objectives: Enterocyte apoptosis induced by activated intraepithelial lymphocytes is increased in coeliac disease (CD). Serum- and glucocorticoid-regulated kinase-1 (SGK1) is a serine/threonine protein kinase that may inhibit apoptosis and compensate for the excessive death of surface epithelial cells. The significance of SGK1 in CD is elusive so far. The aim of this study was to characterise the expression and localisation of SGK1 in duodenal biopsy samples taken from children with untreated CD, children with treated CD, and controls. Patients and methods: Duodenal biopsy specimens were collected from 16 children with untreated CD, 9 children with treated CD, and 10 controls. The mRNA expression of SGK1 was determined by real-time reverse transcription-polymerase chain reaction. SGK1 and phosphorylated (P)-SGK1 protein levels and their localisation were determined by Western blot and immunofluorescent staining, respectively. Results: We found increased SGK1-mRNA expression as well as higher SGK1 and P-SGK1 protein levels in the duodenal mucosa of children with untreated CD compared with controls. In the duodenal mucosa of children with treated CD, SGK1-mRNA expression was decreased and SGK1 and P-SGK1 protein levels were lower than in untreated CD. SGK1 and P-SGK1 staining intensity was stronger in duodenal villous enterocytes of children with untreated CD compared with treated CD. Conclusions: Our results of increased expression of SGK1 in untreated CD may suggest its contribution to the enterocyte survival in this disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
coeliac disease
serum-and glucocorticoid-regulated kinase-1
children
duodenal biopsies
Megjelenés:Journal Of Pediatric Gastroenterology And Nutrition. - 50 : 2 (2010), p. 147-153. -
További szerzők:Vannay Ádám Sziksz Erna Prokai Ágnes Cseh Áron Veres Gábor (1969-2020) (csecsemő- és gyermekgyógyász, gasztroenterológus) Dezsőfi Antal Győrffy Hajnalka Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Arató András
Pályázati támogatás:71730
OTKA
T046082
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM002288
Első szerző:Szebeni Beáta
Cím:Increased mucosal expression of toll-like receptor (TLR)2 and TLR4 in coeliac disease / Szebeni Beáta, Veres Gábor, Dezsőfi Antal, Rusai Krisztina, Vannai Ádám, Bokodi Géza, Vásárhelyi Barna, Korponay-Szabó Ilma, Tulassay Tivadar, Arató András
Dátum:2007
Megjegyzések:The dysregulation of adaptive immunity is extensively investigated in celiac disease (CD). Recent data also suggest, however, the implication of innate immunity in CD. Toll-like receptors (TLRs) play a central role in the initiation or maintenance of innate immune responses. The aim of this study was to characterise the expression of TLR2, TLR3, and TLR4 in duodenal biopsy samples taken from children with CD and from controls. Patients and Methods: Duodenal biopsy specimens were collected from 16 children with untreated CD, 9 children with treated CD, and 10 controls. The mRNA expression of TLR2, TLR3, and TLR4 was determined by semiquantitative reverse transcription-polymerase chain reaction. Protein levels of TLRs were determined by Western blot. Results: We found higher TLR2 and TLR4 mRNA expression and protein levels in the duodenalmucosa of children with treated CD and untreated CD compared with controls. TLR2 and TLR4 mRNA expression and protein levels were even higher in the duodenal mucosa of children with treated CD than in untreated CD. TLR3 mRNA expression was increased in the duodenal mucosa of children with treatedCD compared with untreated CD and controls. We were able to detect TLR3 protein only in the biopsy specimens of treated patients with CD. Conclusions: The alteration of TLR2 and TLR4 expression in the duodenal mucosa of patients with CD supports the potential implication of innate immune system in the pathomechanism of this disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Children-Coeliac disease
Toll-like receptor 2
Toll-like receptor 3
Toll-like receptor 4
Megjelenés:Journal of Pediatric Gastroenterology and Nutrition 45 : 2 (2007), p. 187-193. -
További szerzők:Veres Gábor (1969-2020) (csecsemő- és gyermekgyógyász, gasztroenterológus) Dezsőfi Antal Rusai Krisztina Vannai Ádám Bokodi Géza Vásárhelyi Barna Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Tulassay Tivadar Arató András
Internet cím:elektronikus változat
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5.

001-es BibID:BIBFORM025027
Első szerző:Veres Gábor (csecsemő- és gyermekgyógyász, gasztroenterológus)
Cím:Duodenal ulceration in a patient with celiac disease and plasminogen I deficiency : coincidence or cofactors? / Veres, G., Korponay-Szabo, I., Maka, E., Glasz, T., Mamula, P., Papp, M., Dezsofi, A., Arato, A.
Dátum:2011
ISSN:0031-4005
Megjegyzések:Celiac disease (CD) is a gluten-dependent inflammatory disease of the small bowel that affects up to 1% of the worldwide population. Despite severe mucosal abnormalities including total villous atrophy and autoantibody deposition, duodenal ulcer is not a feature of CD. However, a recent study found an elevated rate of peptic ulcer disease in patients with CD. Plasminogen deficiency (PLD) is an autosomal recessive disease that causes pseudomembranous lesions in different organs, but gastrointestinal involvement is rare. Here we report the case of a 6-year-old girl who had a sudden onset of hematemesis caused by duodenal ulcer. On the basis of mucosal atrophy, elevated celiac antibody levels, decreased plasminogen serum activity, and homozygous missense mutation R216H in the plasminogen gene, CD and PLD were diagnosed. This report is, to our knowledge, the first description of the 2 entities, and results of our double-immunofluorescent studies also suggest that both diseases may have a role in the ulceration process. Excessive amounts of fibrin deposition due to PLD caused the distortion of the vessels and was responsible for the unusual celiac immunoglobulin A and tissue transglutaminase 2 in vivo binding pattern. On the basis of this result, patients with CD and unknown cause of gastrointestinal ulcer may require investigation for PLD.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Pediatrics. - 128 : 5 (2011), p. e1301-1307. -
További szerzők:Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Maka Erika Glasz Tibor Mamula, Petar Papp Mária (1975-) (belgyógyász, gasztroenterológus) Dezsőfi Antal Arató András
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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