Signs of increased leakage over the jejunal mucosa during gliadin challenge of patients with coeliac disease.
Identifieur interne : 004037 ( Istex/Curation ); précédent : 004036; suivant : 004038Signs of increased leakage over the jejunal mucosa during gliadin challenge of patients with coeliac disease.
Auteurs : B. Lavö [Suède] ; L. Knutson [Suède] ; L. Lööf [Suède] ; B. Odlind [Suède] ; R. H Llgren [Suède]Source :
- Gut [ 0017-5749 ] ; 1990-02.
Abstract
Intestinal secretion rates of albumin, hyaluronan, and beta 2-microglobulin (beta 2-micro) were determined under basal conditions and after gliadin challenge of coeliac patients and healthy controls by the use of a jejunal perfusion technique. A new tube system was used where a jejunal segment is isolated between balloons and then perfused with a balanced salt solution. Under basal conditions the secretion rate of albumin was similar in the patients and controls while the secretion rate of the glycosaminoglycan hyaluronan, a high molecular weight connective tissue component, was increased more than two times in coeliac patients. Beta 2-micro was secreted in on average three-fold rates in coeliacs compared with controls. All three substances were secreted at a higher rate in patients with active disease than in those with inactive disease defined by morphological damage in small bowel biopsies. The concentrations in jejunal perfusion fluids relative to serum levels in the coeliac patients were for albumin 0.0007, beta 2-micro 0.10, and for hyaluronan 1.94. Challenge with a single dose of gliadin into the jejunal segment gave within 60 min a significant, about two-fold, increase of the secretion rates of all three measured substances. The appearance of hyaluronan could reflect a gliadin induced mucosal oedema with an enhanced leakage from the interstitial/lymph fluid, rich in this glycosaminoglycan. The observed parallel increases in the jejunal secretion of albumin and beta 2-micro after gliadin challenge are best explained by a similar mechanism.
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DOI: 10.1136/gut.31.2.153
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Lavö</name><affiliation wicri:level="1"><mods:affiliation>Department of Internal Medicine, University Hospital, Uppsala, Sweden.</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Internal Medicine, University Hospital, Uppsala</wicri:regionArea></affiliation></author><author><name sortKey="Knutson, L" sort="Knutson, L" uniqKey="Knutson L" first="L" last="Knutson">L. Knutson</name><affiliation wicri:level="1"><mods:affiliation>Department of Internal Medicine, University Hospital, Uppsala, Sweden.</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Internal Medicine, University Hospital, Uppsala</wicri:regionArea></affiliation></author><author><name sortKey="Loof, L" sort="Loof, L" uniqKey="Loof L" first="L" last="Lööf">L. Lööf</name><affiliation wicri:level="1"><mods:affiliation>Department of Internal Medicine, University Hospital, Uppsala, Sweden.</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Internal Medicine, University Hospital, Uppsala</wicri:regionArea></affiliation></author><author><name sortKey="Odlind, B" sort="Odlind, B" uniqKey="Odlind B" first="B" last="Odlind">B. Odlind</name><affiliation wicri:level="1"><mods:affiliation>Department of Internal Medicine, University Hospital, Uppsala, Sweden.</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Internal Medicine, University Hospital, Uppsala</wicri:regionArea></affiliation></author><author><name sortKey="H Llgren, R" sort="H Llgren, R" uniqKey="H Llgren R" first="R" last="H Llgren">R. H Llgren</name><affiliation wicri:level="1"><mods:affiliation>Department of Internal Medicine, University Hospital, Uppsala, Sweden.</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Internal Medicine, University Hospital, Uppsala</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Gut</title><title level="j" type="abbrev">Gut</title><idno type="ISSN">0017-5749</idno><idno type="eISSN">1468-3288</idno><imprint><publisher>BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><date type="published" when="1990-02">1990-02</date><biblScope unit="volume">31</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="153">153</biblScope></imprint><idno type="ISSN">0017-5749</idno></series><idno type="istex">8859E4DB85CE665E9F3B813491FDA24FB473921C</idno><idno type="DOI">10.1136/gut.31.2.153</idno><idno type="href">gutjnl-31-153.pdf</idno><idno type="PMID">2179068</idno><idno type="local">gutjnl;31/2/153</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0017-5749</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Intestinal secretion rates of albumin, hyaluronan, and beta 2-microglobulin (beta 2-micro) were determined under basal conditions and after gliadin challenge of coeliac patients and healthy controls by the use of a jejunal perfusion technique. A new tube system was used where a jejunal segment is isolated between balloons and then perfused with a balanced salt solution. Under basal conditions the secretion rate of albumin was similar in the patients and controls while the secretion rate of the glycosaminoglycan hyaluronan, a high molecular weight connective tissue component, was increased more than two times in coeliac patients. Beta 2-micro was secreted in on average three-fold rates in coeliacs compared with controls. All three substances were secreted at a higher rate in patients with active disease than in those with inactive disease defined by morphological damage in small bowel biopsies. The concentrations in jejunal perfusion fluids relative to serum levels in the coeliac patients were for albumin 0.0007, beta 2-micro 0.10, and for hyaluronan 1.94. Challenge with a single dose of gliadin into the jejunal segment gave within 60 min a significant, about two-fold, increase of the secretion rates of all three measured substances. The appearance of hyaluronan could reflect a gliadin induced mucosal oedema with an enhanced leakage from the interstitial/lymph fluid, rich in this glycosaminoglycan. The observed parallel increases in the jejunal secretion of albumin and beta 2-micro after gliadin challenge are best explained by a similar mechanism.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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