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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Intestinal lymphangiectasia and thymic hypoplasia.</title><author><name sortKey="Sorensen, R U" sort="Sorensen, R U" uniqKey="Sorensen R" first="R U" last="Sorensen">R U Sorensen</name></author><author><name sortKey="Halpin, T C" sort="Halpin, T C" uniqKey="Halpin T" first="T C" last="Halpin">T C Halpin</name></author><author><name sortKey="Abramowsky, C R" sort="Abramowsky, C R" uniqKey="Abramowsky C" first="C R" last="Abramowsky">C R Abramowsky</name></author><author><name sortKey="Hornick, D L" sort="Hornick, D L" uniqKey="Hornick D" first="D L" last="Hornick">D L Hornick</name></author><author><name sortKey="Miller, K M" sort="Miller, K M" uniqKey="Miller K" first="K M" last="Miller">K M Miller</name></author><author><name sortKey="Naylor, P" sort="Naylor, P" uniqKey="Naylor P" first="P" last="Naylor">P. Naylor</name></author><author><name sortKey="Incefy, G S" sort="Incefy, G S" uniqKey="Incefy G" first="G S" last="Incefy">G S Incefy</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">3971596</idno><idno type="pmc">1577180</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1577180</idno><idno type="RBID">PMC:1577180</idno><date when="1985">1985</date><idno type="wicri:Area/Pmc/Corpus">001743</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001743</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Intestinal lymphangiectasia and thymic hypoplasia.</title><author><name sortKey="Sorensen, R U" sort="Sorensen, R U" uniqKey="Sorensen R" first="R U" last="Sorensen">R U Sorensen</name></author><author><name sortKey="Halpin, T C" sort="Halpin, T C" uniqKey="Halpin T" first="T C" last="Halpin">T C Halpin</name></author><author><name sortKey="Abramowsky, C R" sort="Abramowsky, C R" uniqKey="Abramowsky C" first="C R" last="Abramowsky">C R Abramowsky</name></author><author><name sortKey="Hornick, D L" sort="Hornick, D L" uniqKey="Hornick D" first="D L" last="Hornick">D L Hornick</name></author><author><name sortKey="Miller, K M" sort="Miller, K M" uniqKey="Miller K" first="K M" last="Miller">K M Miller</name></author><author><name sortKey="Naylor, P" sort="Naylor, P" uniqKey="Naylor P" first="P" last="Naylor">P. Naylor</name></author><author><name sortKey="Incefy, G S" sort="Incefy, G S" uniqKey="Incefy G" first="G S" last="Incefy">G S Incefy</name></author></analytic><series><title level="j">Clinical and Experimental Immunology</title><idno type="ISSN">0009-9104</idno><idno type="eISSN">1365-2249</idno><imprint><date when="1985">1985</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>We have evaluated the immunological abnormalities present in a 6 year old patient with primary intestinal and generalized lymphangiectasia confirmed by intestinal, lung and lymph node biopsies. Lymphocyte loss through the gut was confirmed by the detection of lymphocytes in her stool. An increased enteric protein loss was suggested by hypoproteinaemia, peripheral oedema, and a very short half-life for i.v. immune serum globulin (3 days). Lymphocyte subpopulation analysis revealed a selective loss of T lymphocytes, with a proportionally increased loss of the OKT4 positive helper/inducer subpopulation. Functionally, there was a decrease in proliferative responses to some mitogens and to allogeneic cells, and a lack of T cell help for in vitro B lymphocyte differentiation into immunoglobulin secreting cells. Natural killer function was normal. In this patient, a concomitant thymic deficiency was documented by failure to identify thymic tissue on a thymus biopsy and by an absence or decrease of the serum thymic factor (thymulin) and thymosin alpha 1. No compensatory lymphopoiesis was detected in the bone marrow. In an attempt to increase T lymphocyte development, the patient was treated with thymosin fraction 5. Daily treatment with this preparation resulted in a transient clinical improvement which could not be sustained on a weekly thymosin treatment schedule. However, lymphocyte numbers did not increase during this treatment. The findings in this patient support the notion that T lymphocytes are needed to stimulate thymic epithelium. In situations of excessive loss of long lived T lymphocytes a secondary thymic atrophy may occur and further contribute to the development of a deficiency in cell-mediated immunity.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><label>Fig. 1</label><graphic xlink:href="clinexpimmunol00136-0228-a" xlink:role="219"></graphic></fig><fig id="F2"><label>Fig. 2</label><graphic xlink:href="clinexpimmunol00136-0228-b" xlink:role="219"></graphic></fig></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Clin Exp Immunol</journal-id><journal-title>Clinical and Experimental Immunology</journal-title><issn pub-type="ppub">0009-9104</issn><issn pub-type="epub">1365-2249</issn></journal-meta><article-meta><article-id pub-id-type="pmid">3971596</article-id><article-id pub-id-type="pmc">1577180</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Intestinal lymphangiectasia and thymic hypoplasia.</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Sorensen</surname><given-names>R U</given-names></name></contrib><contrib contrib-type="author"><name><surname>Halpin</surname><given-names>T C</given-names></name></contrib><contrib contrib-type="author"><name><surname>Abramowsky</surname><given-names>C R</given-names></name></contrib><contrib contrib-type="author"><name><surname>Hornick</surname><given-names>D L</given-names></name></contrib><contrib contrib-type="author"><name><surname>Miller</surname><given-names>K M</given-names></name></contrib><contrib contrib-type="author"><name><surname>Naylor</surname><given-names>P</given-names></name></contrib><contrib contrib-type="author"><name><surname>Incefy</surname><given-names>G S</given-names></name></contrib></contrib-group><pub-date pub-type="ppub"><month>1</month><year>1985</year></pub-date><volume>59</volume><issue>1</issue><fpage>217</fpage><lpage>226</lpage><abstract><p>We have evaluated the immunological abnormalities present in a 6 year old patient with primary intestinal and generalized lymphangiectasia confirmed by intestinal, lung and lymph node biopsies. Lymphocyte loss through the gut was confirmed by the detection of lymphocytes in her stool. An increased enteric protein loss was suggested by hypoproteinaemia, peripheral oedema, and a very short half-life for i.v. immune serum globulin (3 days). Lymphocyte subpopulation analysis revealed a selective loss of T lymphocytes, with a proportionally increased loss of the OKT4 positive helper/inducer subpopulation. Functionally, there was a decrease in proliferative responses to some mitogens and to allogeneic cells, and a lack of T cell help for in vitro B lymphocyte differentiation into immunoglobulin secreting cells. Natural killer function was normal. In this patient, a concomitant thymic deficiency was documented by failure to identify thymic tissue on a thymus biopsy and by an absence or decrease of the serum thymic factor (thymulin) and thymosin alpha 1. No compensatory lymphopoiesis was detected in the bone marrow. In an attempt to increase T lymphocyte development, the patient was treated with thymosin fraction 5. Daily treatment with this preparation resulted in a transient clinical improvement which could not be sustained on a weekly thymosin treatment schedule. However, lymphocyte numbers did not increase during this treatment. The findings in this patient support the notion that T lymphocytes are needed to stimulate thymic epithelium. In situations of excessive loss of long lived T lymphocytes a secondary thymic atrophy may occur and further contribute to the development of a deficiency in cell-mediated immunity.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><label>Fig. 1</label><graphic xlink:href="clinexpimmunol00136-0228-a" xlink:role="219"></graphic></fig><fig id="F2"><label>Fig. 2</label><graphic xlink:href="clinexpimmunol00136-0228-b" xlink:role="219"></graphic></fig></sec></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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