Scandinavian journal of gastroenterology · 1998
Small-bowel mucosal inflammation in reticulin or gliadin antibody-positive patients without villous atrophy.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kaukinen K, Collin P, Holm K, Karvonen A L, Pikkarainen P, Mäki M
Аннотация
BACKGROUND: We investigated whether individuals with positive coeliac disease antibodies but without small-bowel villous atrophy have mucosal inflammation implicating gluten-sensitivity.
METHODS: Small-bowel mucosal morphology; CD3+, alphabeta+, and gammadelta+ T-cell receptor-bearing intraepithelial lymphocytes; and mucosal HLA-DR expression were studied in 96 IgA-class antireticulin or antigliadin antibody-positive adults suspected of having coeliac disease and in 27 control subjects.
RESULTS: Villous atrophy compatible with coeliac disease was found in altogether 29 patients, in 18 of 21 (86%) patients with both antireticulin and antigliadin antibodies, in 9 of 15 (60%) patients with antireticulin antibodies only, and in 2 of 60 (3%) with antigliadin antibodies only. In 67 antibody-positive patients with normal villous architecture the densities of CD3+, alphabeta+, and gammadelta+ intraepithelial lymphocytes were significantly higher than in non-coeliac control subjects. Ten patients with initially increased densities of gammadelta+ T cells but normal villous structure underwent a follow-up biopsy after 4-18 months, which showed villous atrophy in five patients.
CONCLUSIONS: IgA-class antireticulin or antigliadin antibody-positive patients with normal small-bowel mucosal morphology frequently have immunohistochemical markers of coeliac disease latency. Together with our follow-up data this implies that they may be gluten-sensitive.
METHODS: Small-bowel mucosal morphology; CD3+, alphabeta+, and gammadelta+ T-cell receptor-bearing intraepithelial lymphocytes; and mucosal HLA-DR expression were studied in 96 IgA-class antireticulin or antigliadin antibody-positive adults suspected of having coeliac disease and in 27 control subjects.
RESULTS: Villous atrophy compatible with coeliac disease was found in altogether 29 patients, in 18 of 21 (86%) patients with both antireticulin and antigliadin antibodies, in 9 of 15 (60%) patients with antireticulin antibodies only, and in 2 of 60 (3%) with antigliadin antibodies only. In 67 antibody-positive patients with normal villous architecture the densities of CD3+, alphabeta+, and gammadelta+ intraepithelial lymphocytes were significantly higher than in non-coeliac control subjects. Ten patients with initially increased densities of gammadelta+ T cells but normal villous structure underwent a follow-up biopsy after 4-18 months, which showed villous atrophy in five patients.
CONCLUSIONS: IgA-class antireticulin or antigliadin antibody-positive patients with normal small-bowel mucosal morphology frequently have immunohistochemical markers of coeliac disease latency. Together with our follow-up data this implies that they may be gluten-sensitive.