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001-es BibID:	BIBFORM023715
Első szerző:	Nemes Éva (csecsemő- és gyermekgyógyász, gasztroenterológus)
Cím:	Gluten intake interferes with the humoral immune response to recombinant hepatitis B vaccine in patients with celiac disease / Nemes É., Lefler É., Szegedi L., Kapitány A., B. Kovács J., Balogh M., Szabados K., Tumpek J., Sipka S., Korponay-Szabó I. R.
Dátum:	2008
ISSN:	0031-4005
Megjegyzések:	Patients with celiac disease, who often carry human leukocyte antigen-DR3;DQ2, are prone to inadequate response to hepatitis B immunization. We evaluated vaccine response in relation to disease activity and whether previous treatment with a gluten-free diet influences the achievement of protective antibody titers. PATIENTS AND METHODS: We studied 128 children and adolescents with celiac disease and 113 age-matched control subjects. Twenty-two patients with celiac disease were prospectively immunized after diagnosis during dietary treatment (group 1). A total of 106 (group 2) and the control subjects received vaccination by mass immunization in schools at 14 years of age regardless of diet status and when celiac disease was still undiagnosed in 27 of these children. Diet compliance and celiac disease activity were monitored by measurement of antibodies against transglutaminase and endomysium. Vaccine response was determined by measuring antihepatitis B antibodies from serum. RESULTS: The seroconversion after hepatitis B vaccination was 95.5% in group 1. All of these patients carried human leukocyte antigen DQ2. The response rate in group 2 was 50.9% and correlated with gluten intake (untreated patients: 25.9%, non-strict diet: 44.4%, strict diet: 61.4%). Treated and compliant patients did not significantly differ from control subjects (75.2%). Thirty-seven antihepatitis B-negative patients with celiac disease received a booster during a controlled gluten-free diet, and 36 (97.3%) seroconverted, irrespective of the presence of human leukocyte antigen DQ2. CONCLUSIONS: Nonresponse to recombinant hepatitis B surface antigen may be a sign of undiagnosed celiac disease. However, there is a good vaccine response in adequately treated patients. Human leukocyte antigen DQ alleles do not seem to have a primary role. Revaccination is recommended during a controlled gluten-free diet.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Pediatrics. - 121 : 6 (2008), p. e1570-e1576. -
További szerzők:	Lefler Éva Szegedi László Kapitány Anikó (1979-) (molekuláris biológus) B. Kovács Judit Balogh Márta Szabados Katalin Tumpek Judit (1944-) (orvosi laboratóriumi szakorvos) Sipka Sándor (1945-) (laboratóriumi szakorvos) Korponay-Szabó Ilma (1959-) (gyermekgyógyász)
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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
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