Circulating anti‐glomerular basement membrane antibodies in coeliac disease and epidermolysis bullosa acquisita
Identifieur interne : 002F81 ( Main/Exploration ); précédent : 002F80; suivant : 002F82Circulating anti‐glomerular basement membrane antibodies in coeliac disease and epidermolysis bullosa acquisita
Auteurs : J. A. Savige ; C. Baker ; M. Gallicchio ; G. VarigosSource :
- Australian and New Zealand Journal of Medicine [ 0004-8291 ] ; 1991-12.
English descriptors
- Teeft :
- Acquisita, Antibody, Antibody binding, Assay, Aust, Basement membrane, Biol chem, Bullosa, Chem, Clin, Coeliac, Coeliac disease, Collagen, Collagen type, Dermatology, Direct immunofluorescence, Elisa, Epidermolysis, Epidermolysis bullosa acquisita, Further hour, Glomerular, Glomerular basement membrane, Glomerulonephritis, Goodpasture, Goodpasture antigen, Hereditary nephritis, Immunofluorescence, Immunological, Immunological mediators, Laboratory worker, Lamina propria, Lockwood, Melbourne, Membrane, Monoclonal, Monoclonal antibody, Noncollagenous domain, Normal range, Positive results, Progressive scarring, Renal, Renal function, Royal melbourne hospital, Savige, Small intestine, Subepidermal basement membrane, Syndrome, Western blots, Wieslander.
Abstract
Abstract The demonstration of circulating anti‐glomerular basement membrane (GBM) antibodies is almost diagnostic for anti‐GBM disease and Goodpasture's syndrome. These antibodies are, however, occasionally present in SLE and diabetes, in association with IgA disease and membranous nephropathy and after transplantation in Alport's syndrome. In addition, we describe circulating anti‐GBM antibodies in a research worker who handled GBM and in whom coeliec disease later developed, and in an individual with epidermolysis bullosa acquisita. Neither patient had impaired renal function nor an abnormal urinary sediment, suggesting either that these antibodies were of low affinity, or that additional factors are required for the pathogenesis of an aggressive glomerular lesion when circulating anti‐GBM antibodies are present. In at least one of these individuals anti‐GBM antibodies may have developed after the exposure of basement membrane collagen type IV to activated immunological mediators and cells. (Aust NZ J Med 1991; 21: 867–870.)
Url:
DOI: 10.1111/j.1445-5994.1991.tb01409.x
Affiliations:
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A." last="Savige">J. A. Savige</name><affiliation></affiliation><affiliation><wicri:noCountry code="subField">MRC.</wicri:noCountry></affiliation></author><author><name sortKey="Baker, C" sort="Baker, C" uniqKey="Baker C" first="C." last="Baker">C. Baker</name><affiliation><wicri:noCountry code="subField">Vic.</wicri:noCountry></affiliation></author><author><name sortKey="Gallicchio, M" sort="Gallicchio, M" uniqKey="Gallicchio M" first="M." last="Gallicchio">M. Gallicchio</name><affiliation><wicri:noCountry code="subField">Vic.</wicri:noCountry></affiliation></author><author><name sortKey="Varigos, G" sort="Varigos, G" uniqKey="Varigos G" first="G." last="Varigos">G. Varigos</name><affiliation><wicri:noCountry code="subField">Vic.</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Australian and New Zealand Journal of Medicine</title><title level="j" type="alt">AUSTRALIAN AND NEW ZEALAND JOURNAL OF MEDICINE</title><idno type="ISSN">0004-8291</idno><idno type="eISSN">1445-5994</idno><imprint><biblScope unit="vol">21</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="867">867</biblScope><biblScope unit="page" to="870">870</biblScope><biblScope unit="page-count">4</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1991-12">1991-12</date></imprint><idno type="ISSN">0004-8291</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0004-8291</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acquisita</term><term>Antibody</term><term>Antibody binding</term><term>Assay</term><term>Aust</term><term>Basement membrane</term><term>Biol chem</term><term>Bullosa</term><term>Chem</term><term>Clin</term><term>Coeliac</term><term>Coeliac disease</term><term>Collagen</term><term>Collagen type</term><term>Dermatology</term><term>Direct immunofluorescence</term><term>Elisa</term><term>Epidermolysis</term><term>Epidermolysis bullosa acquisita</term><term>Further hour</term><term>Glomerular</term><term>Glomerular basement membrane</term><term>Glomerulonephritis</term><term>Goodpasture</term><term>Goodpasture antigen</term><term>Hereditary nephritis</term><term>Immunofluorescence</term><term>Immunological</term><term>Immunological mediators</term><term>Laboratory worker</term><term>Lamina propria</term><term>Lockwood</term><term>Melbourne</term><term>Membrane</term><term>Monoclonal</term><term>Monoclonal antibody</term><term>Noncollagenous domain</term><term>Normal range</term><term>Positive results</term><term>Progressive scarring</term><term>Renal</term><term>Renal function</term><term>Royal melbourne hospital</term><term>Savige</term><term>Small intestine</term><term>Subepidermal basement membrane</term><term>Syndrome</term><term>Western blots</term><term>Wieslander</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract The demonstration of circulating anti‐glomerular basement membrane (GBM) antibodies is almost diagnostic for anti‐GBM disease and Goodpasture's syndrome. These antibodies are, however, occasionally present in SLE and diabetes, in association with IgA disease and membranous nephropathy and after transplantation in Alport's syndrome. In addition, we describe circulating anti‐GBM antibodies in a research worker who handled GBM and in whom coeliec disease later developed, and in an individual with epidermolysis bullosa acquisita. Neither patient had impaired renal function nor an abnormal urinary sediment, suggesting either that these antibodies were of low affinity, or that additional factors are required for the pathogenesis of an aggressive glomerular lesion when circulating anti‐GBM antibodies are present. In at least one of these individuals anti‐GBM antibodies may have developed after the exposure of basement membrane collagen type IV to activated immunological mediators and cells. (Aust NZ J Med 1991; 21: 867–870.)</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Baker, C" sort="Baker, C" uniqKey="Baker C" first="C." last="Baker">C. Baker</name><name sortKey="Gallicchio, M" sort="Gallicchio, M" uniqKey="Gallicchio M" first="M." last="Gallicchio">M. Gallicchio</name><name sortKey="Savige, J A" sort="Savige, J A" uniqKey="Savige J" first="J. A." last="Savige">J. A. Savige</name><name sortKey="Varigos, G" sort="Varigos, G" uniqKey="Varigos G" first="G." last="Varigos">G. Varigos</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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