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Celiac disease diagnosis in clinical practice: ESPGHAN quality of care survey from 129 pediatric hospitals across 28 countries
A. Litwin, TG. Le Thi, N. El-Lababidi, A. Kindermann, R. Pancheva, K. Gerasimidis, CC. Goncalves, PC. Escobar, T. Niseteo, K. Ikrath, S. Koletzko, Quality‐of‐Care Network
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
Grantová podpora
ESPGHAN
Ludwig Maximilians Universität Munich
PubMed
40621676
DOI
10.1002/jpn3.70143
Knihovny.cz E-zdroje
- MeSH
- autoprotilátky krev MeSH
- celiakie * diagnóza krev MeSH
- dětské nemocnice MeSH
- dítě MeSH
- gastroenterologie normy MeSH
- imunoglobulin A krev MeSH
- kvalita zdravotní péče * MeSH
- lékařská praxe - způsoby provádění * statistika a číselné údaje MeSH
- lidé MeSH
- průzkumy a dotazníky MeSH
- průzkumy zdravotní péče MeSH
- směrnice pro lékařskou praxi jako téma MeSH
- transglutaminasy imunologie MeSH
- Check Tag
- dítě MeSH
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Evropa MeSH
OBJECTIVES: European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) guidelines recommend first-line serology for suspected celiac disease (CeD), measuring only transglutaminase antibodies (TGA-immunoglobulin A [IgA]) plus total IgA. If TGA-IgA is ≥10 times the normal value, pediatric gastroenterologists (pedGI) may diagnose CeD without biopsies if autoantibodies against endomysial antibodies (EMA-IgA) are positive in a 2nd blood sample. This Quality-of-Care (QoC) project benchmarked diagnostic workup in clinical practice using ESPGHAN CeD guidelines as reference. METHODS: A pseudonymized survey on CeD practices was sent to 141 hospitals within the ESPGHAN QoC-network in 28 countries. RESULTS: Questionnaires were completed by 129/141 (91.5%) hospitals, with 121 (94%) having pedGI staff. As reasons conflicting with good QoC for CeD in their setting, responders assumed knowledge deficits among the public (57%), primary care providers (64%), non-GI physicians (16%), and pedGIs (0%). For initial testing, 66% of physicians ordered only total IgA and TGA-IgA, 7% did not use this combination, and 29% ordered additional serology (TGA-IgG, EMA, antibodies against deaminated gliadin peptide, or native gliadin). Regarding conflicting results for TGA-IgA and histopathology in IgA-sufficient children, 61% incorrectly classified negative TGA-IgA with Marsh 2 and 57% with Marsh 3 lesions as "potential CeD," while 49% excluded CeD in the case of villous atrophy and negative TGA-IgA. Routine practice did not align with the ESPGHAN recommendations regarding performance of duodenal biopsies (27%), EMA-testing (34%), and diagnosis of CeD in IgA-deficient children (32%). CONCLUSIONS: We identified areas for improving QoC regarding both effectiveness and efficacy, in pediatric patients with suspected CeD, and consequently developed easy-to-use tools to improve guideline implementation.
Central Lisbon University Hospital Centre Lisbon Portugal
The European Society for Paediatric Gastroenterology Hepatology and Nutrition Geneva Switzerland
Unit of Nutrition and Obesity Hospital Recoletas Campo Grande Valladolid Spain
Citace poskytuje Crossref.org
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- $a OBJECTIVES: European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) guidelines recommend first-line serology for suspected celiac disease (CeD), measuring only transglutaminase antibodies (TGA-immunoglobulin A [IgA]) plus total IgA. If TGA-IgA is ≥10 times the normal value, pediatric gastroenterologists (pedGI) may diagnose CeD without biopsies if autoantibodies against endomysial antibodies (EMA-IgA) are positive in a 2nd blood sample. This Quality-of-Care (QoC) project benchmarked diagnostic workup in clinical practice using ESPGHAN CeD guidelines as reference. METHODS: A pseudonymized survey on CeD practices was sent to 141 hospitals within the ESPGHAN QoC-network in 28 countries. RESULTS: Questionnaires were completed by 129/141 (91.5%) hospitals, with 121 (94%) having pedGI staff. As reasons conflicting with good QoC for CeD in their setting, responders assumed knowledge deficits among the public (57%), primary care providers (64%), non-GI physicians (16%), and pedGIs (0%). For initial testing, 66% of physicians ordered only total IgA and TGA-IgA, 7% did not use this combination, and 29% ordered additional serology (TGA-IgG, EMA, antibodies against deaminated gliadin peptide, or native gliadin). Regarding conflicting results for TGA-IgA and histopathology in IgA-sufficient children, 61% incorrectly classified negative TGA-IgA with Marsh 2 and 57% with Marsh 3 lesions as "potential CeD," while 49% excluded CeD in the case of villous atrophy and negative TGA-IgA. Routine practice did not align with the ESPGHAN recommendations regarding performance of duodenal biopsies (27%), EMA-testing (34%), and diagnosis of CeD in IgA-deficient children (32%). CONCLUSIONS: We identified areas for improving QoC regarding both effectiveness and efficacy, in pediatric patients with suspected CeD, and consequently developed easy-to-use tools to improve guideline implementation.
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