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001-es BibID:BIBFORM044303
Első szerző:Korponay-Szabó Ilma (gyermekgyógyász)
Cím:Elevation of IgG antibodies against tissue transglutaminase as a diagnostic tool for coeliac disease in selective IgA deficiency / Korponay-Szabó I. R., Dahlbom I., Laurila K., Koskinen S., Woolley N., Partanen J., B. Kovács J., Mäki M., Hansson T.
Dátum:2003
ISSN:0017-5749
Megjegyzések:BACKGROUND:IgA serum autoantibodies against tissue transglutaminase (tTG) have an established diagnostic value in coeliac disease, and high efficacy tests are widely available for their detection. However, serological evaluation of IgA deficient subjects is still difficult.AIMS:To evaluate the diagnostic potential of IgG class anti-tTG autoantibodies measured quantitatively using an enzyme linked immunosorbent assay (ELISA) compared with immunofluorescent detection of coeliac autoantibodies.PATIENTS:We tested serum samples from 325 IgA deficient subjects, including 78 patients with coeliac disease, 73 disease controls, and 174 blood donors.METHODS:IgG antibodies against human recombinant tTG were measured with an ELISA. IgG antiendomysium antibodies (EMA) were assayed by indirect immunofluorescence on human jejunum and appendix sections.RESULTS:The IgG anti-tTG ELISA had a sensitivity of 98.7% and a specificity of 98.6%, and the correlation with IgG EMA titres was high (r(s)=0.91). One coeliac patient, initially negative in all autoantibody tests, displayed both IgG anti-tTG antibodies and IgG EMA during later gluten exposure. IgG anti-tTG antibodies and EMA titres showed significant decreases (p<0.001) in treated patients. The frequency of IgG anti-tTG autoantibody positivity was 9.8% among IgA deficient blood donors and 11 of the 12 positive subjects with known HLA-DQ haplotypes carried DQ2 or DQ8 alleles.CONCLUSIONS:IgG anti-tTG and IgG EMA autoantibody tests are highly efficient in detecting coeliac disease in IgA deficient patients. The high prevalence of coeliac antibodies among symptom free IgA deficient blood donors who also carry coeliac-type HLA-DQ genes indicates that all IgA deficient persons should be evaluated for coeliac disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Gut. - 52 : 11 (2003), p. 1567-1571. -
További szerzők:Dahlbom, Ingrid Laurila, Kaija Koskinen, Seppo Woolley, Nina Partanen, Jukka B. Kovács Judit Mäki, Markku Hansson, Tony
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2.

001-es BibID:BIBFORM042703
035-os BibID:PMID:15082580
Első szerző:Korponay-Szabó Ilma (gyermekgyógyász)
Cím:In vivo targeting of intestinal and extraintestinal transglutaminase 2 by coeliac autoantibodies / I. R. Korponay-Szabo, T. Halttunen, Z. Szalai, K. Laurila, R. Király, J. B. Kovács, L. Fésüs, M. Mäki
Dátum:2004
ISSN:0017-5749
Megjegyzések:BACKGROUND: IgA class serum autoantibodies against type 2 (tissue) transglutaminase (TG2) bind to both intestinal and extraintestinal normal tissue sections in vitro, eliciting endomysial, reticulin, and jejunal antibody reactions. It is not known whether similar binding also occurs in coeliac patients in vivo, and may thereby contribute to disease manifestations. AIMS: To investigate intestinal and extraintestinal coeliac tissues for the presence of in vivo bound TG2 specific IgA and its relation to small intestinal mucosal atrophy. PATIENTS: We investigated jejunal samples with normal villous morphology from 10 patients with developing coeliac disease who subsequently progressed to a flat lesion, from 11 patients with dermatitis herpetiformis, and from 12 non-coeliac controls. Six extrajejunal biopsy samples (liver, lymph node, muscle, appendix), obtained based on independent clinical indications from patients with active coeliac disease, were also studied. METHODS: Double colour immunofluorescent studies for in situ IgA, TG2, and laminin were performed. IgA was eluted from tissue sections and tested for TG2 specificity by enzyme linked immunosorbent assay and indirect immunofluorescence. RESULTS: IgA (in one IgA deficient case IgG) deposition on extracellularly located TG2 was detected in jejunal and extrajejunal specimens of all coeliac patients, and also in seven of 11 dermatitis herpetiformis patients, of whom two had no circulating endomysial antibodies. IgA eluted from extraintestinal coeliac tissues was targeted against TG2. CONCLUSIONS: Coeliac IgA targets jejunal TG2 early in disease development even when endomysial antibodies are not present in the circulation. Extraintestinal target sites of coeliac IgA further indicate that humoral immunity may have a pathogenetic role.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Gut. - 53 : 5 (2004), p. 641-648. -
További szerzők:Halttunen, Tuula Szalai Zoltán Laurila, Kaija Király Róbert (1975-) (biológus) Kovács J. Béla Fésüs László (1947-) (orvos biokémikus) Mäki, Markku
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3.

001-es BibID:BIBFORM028773
Első szerző:Korponay-Szabó Ilma (gyermekgyógyász)
Cím:Missing endomysial and reticulin binding of coeliac antibodies in transglutaminase 2 knockout tissues / I. R. Korponay-Szabó, K. Laurila, Zs. Szondy, T. Halttunen, Z. Szalai, I. Dahlbom, I. Rantala, J. B. Kovács, L. Fésüs, M. Mäki
Dátum:2003
ISSN:0017-5749
Megjegyzések:Autoantibodies against transglutaminase 2 (TG2) are thought to be responsible for the endomysial (EMA), reticulin (ARA), and jejunal antibody (JEA) tissue binding of serum samples from coeliac patients but the exclusive role of TG2 in these staining patterns has not yet been established. AIMS: To evaluate whether antigens other than TG2 contribute to EMA/ARA/JEA reactions. PATIENTS: Serum samples from 61 EMA/ARA/JEA positive untreated patients with coeliac disease, 40 dermatitis herpetiformis patients, and 34 EMA/ARA/JEA negative non-coeliac controls were tested. METHODS: TG2 knockout (TG2-/-) and wild-type mouse oesophagus, jejunum, liver, and kidney sections, and TG2-/- sections coated with human recombinant TG2 were used as substrates in single and double immunofluorescent studies for patient IgA binding and tissue localisation of TG2, fibronectin, actin, and calreticulin. RESULTS: None of the patient serum samples elicited EMA, ARA, or JEA binding in TG2-/- morphologically normal tissues. In contrast, 96 of 101 gluten sensitive patient samples (95%) reacted with wild-type mouse tissues and all 101 reacted in EMA/ARA/JEA patterns with TG2-/- mouse tissues coated with human TG2. Serum IgA binding to TG2-/- smooth muscle cells was observed in low titres in 31.1%, 27.5%, and 20.5%, and to TG2-/- epithelium in 26.3%, 5.0%, and 8.8% of coeliac, dermatitis herpetiformis, and control samples, respectively. These positivities partly colocalised with actin and calreticulin but not with TG2 or fibronectin. CONCLUSIONS: EMA/ARA/JEA antibody binding patterns are exclusively TG2 dependent both in coeliac and dermatitis herpetiformis patients. Actin antibodies are responsible for some positivities which are not part of the EMA/ARA/JEA reactions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Gut 52 : 2 (2003), p. 199-204. -
További szerzők:Laurila, Kaija Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Halttunen, Tuula Szalai Zoltán Dahlbom, Ingrid Rantala, I. Kovács B. J. Fésüs László (1947-) (orvos biokémikus) Mäki, Markku
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4.

001-es BibID:BIBFORM077350
035-os BibID:(WoS)000442465300008 (Scopus)85047308664
Első szerző:Ludvigsson, Jonas F.
Cím:Outcome measures in coeliac disease trials : the Tampere recommendations / Jonas F. Ludvigsson, Carolina Ciacci, Peter H. R. Green, Katri Kaukinen, Ilma R. Korponay-Szabo, Kalle Kurppa, Joseph A. Murray, Knut Erik Aslaksen Lundin, Markku J. Maki, Alina Popp, Norelle R. Reilly, Alfonso Rodriguez-Herrera, David S. Sanders, Detlef Schuppan, Sarah Sleet, Juha Taavela, Kristin Voorhees, Marjorie M. Walker, Daniel A. Leffler
Dátum:2018
ISSN:0017-5749
Megjegyzések:Objective A gluten-free diet is the only treatment option of coeliac disease, but recently an increasing number of trials have begun to explore alternative treatment strategies. We aimed to review the literature on coeliac disease therapeutic trials and issue recommendations for outcome measures. Design Based on a literature review of 10 062 references, we (17 researchers and 2 patient representatives from 10 countries) reviewed the use and suitability of both clinical and non-clinical outcome measures. We then made expert-based recommendations for use of these outcomes in coeliac disease trials and identified areas where research is needed. Results We comment on the use of histology, serology, clinical outcome assessment (including patient-reported outcomes), quality of life and immunological tools including gluten immunogenic peptides for trials in coeliac disease. Conclusion C areful evaluation and reporting of outcome measures will increase transparency and comparability of coeliac disease therapeutic trials, and will benefit patients, healthcare and the pharmaceutical industry.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Gut. - 67 : 8 (2018), p. 1410-1424. -
További szerzők:Ciacci, Carolina Green, Peter H. R. Kaukinen, Katri Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kurppa, Kalle Murray, Joseph A. Lundin, Knut Erik Aslaksen Mäki, Markku Popp, Alina Reilly, Norelle R. Rodriguez-Herrera, Alfonso Sanders, David S. Schuppan, Detlef Sleet, Sarah Taavela, Juha Voorhees, Kristin Walker, Marjorie M. Leffler, Daniel A.
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5.

001-es BibID:BIBFORM048569
Első szerző:Romanos, Jihane
Cím:Improving coeliac disease risk prediction by testing non-HLA variants additional to HLA variants / Jihane Romanos, Anna Rosén, Vinod Kumar, Gosia Trynka, Lude Franke, Agata Szperl, Javier Gutierrez-Achury, Cleo C. van Diemen, Roan Kanninga, Soesma A. Jankipersadsing, Andrea Steck, Georges Eisenbarth, David A. van Heel, Bozena Cukrowska, Valentina Bruno, Maria Cristina Mazzilli, Concepcion Núñez, Jose Ramon Bilbao, M. Luisa Mearin, Donatella Barisani, Marian Rewers, Jill M. Norris, Anneli Ivarsson, H. Marieke Boezen, Edwin Liu, Cisca Wijmenga, PreventCD Group
Dátum:2014
ISSN:0017-5749
Megjegyzések:BACKGROUND:The majority of coeliac disease (CD) patients are not being properly diagnosed and therefore remain untreated, leading to a greater risk of developing CD-associated complications. The major genetic risk heterodimer, HLA-DQ2 and DQ8, is already used clinically to help exclude disease. However, approximately 40% of the population carry these alleles and the majority never develop CD.OBJECTIVE:We explored whether CD risk prediction can be improved by adding non-HLA-susceptible variants to common HLA testing.DESIGN:We developed an average weighted genetic risk score with 10, 26 and 57 single nucleotide polymorphisms (SNP) in 2675 cases and 2815 controls and assessed the improvement in risk prediction provided by the non-HLA SNP. Moreover, we assessed the transferability of the genetic risk model with 26 non-HLA variants to a nested case-control population (n=1709) and a prospective cohort (n=1245) and then tested how well this model predicted CD outcome for 985 independent individuals.RESULTS:Adding 57 non-HLA variants to HLA testing showed a statistically significant improvement compared to scores from models based on HLA only, HLA plus 10 SNP and HLA plus 26 SNP. With 57 non-HLA variants, the area under the receiver operator characteristic curve reached 0.854 compared to 0.823 for HLA only, and 11.1% of individuals were reclassified to a more accurate risk group. We show that the risk model with HLA plus 26 SNP is useful in independent populations.CONCLUSIONS:Predicting risk with 57 additional non-HLA variants improved the identification of potential CD patients. This demonstrates a possible role for combined HLA and non-HLA genetic testing in diagnostic work for CD.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Gut 63 : 3 (2014), p. 415-422. -
További szerzők:Rosen, Anna Kumar, Vinod Trynka, Gosia Franke, Lude Szperl, Agata Gutierrez-Achury, Javier van Diemen, Cleo C. Kanninga, Roan Jankipersadsing, Soesma A. Steck, Andrea Eisenbarth, Georges Heel, David A., van Cukrowska, Bozena Bruno, Valentina Mazzilli, Maria Cristina Núnez, Concepción Bilbao, Jose Ramon Mearin, Maria Luisa Barisani, Donatella Rewers, Marian Norris, Jill M. Ivarsson, Anneli Boezen, H. Marieke Liu, Edwin Wijmenga, Cisca Korponay-Szabó Ilma (1959-) (gyermekgyógyász) PreventCD Group
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6.

001-es BibID:BIBFORM019942
Első szerző:Salmi, T. T.
Cím:Endomysial antibody-negative coeliac disease : clinical characteristics and intestinal autoantibody deposits / T. T. Salmi, P. Collin, I. R. Korponay-Szabó, K. Laurila, J. Partanen, H. Huhtala, R. Király, L. Lorand, T. Reunala, M. Mäki, K. Kaukinen
Dátum:2006
ISSN:0017-5749
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Gut. - 55 : 12 (2006), p. 1746-1753. -
További szerzők:Collin, P. Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Laurila, Kaija Partanen, Jukka Huhtala, Heini Király Róbert (1975-) (biológus) Lorand, L. Reunala, T. Mäki, Markku Kaukinen, Katri
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