Meningococcal septicaemia in a C6-deficient patient and effects of plasma transfusion on lipopolysaccharide release
Patients whose blood is deficient in the terminal component of complement have an increased susceptibility to meningococcal infection. However, mortality from meningococcal infection is lower in these patients than in immunocompetent subjects. We studied a C6-deficient patient with meningococcal sep...
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| Veröffentlicht in: | The Lancet (British edition) 1992-12, Vol.340 (8832), p.1379-1381 |
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| creator | Lehner, P.J. Cohen, J. Davies, K.A. Walport, M.I. Cape, A.P. Wurzner, R. Orren, A. Morgan, B.P. |
| description | Patients whose blood is deficient in the terminal component of complement have an increased susceptibility to meningococcal infection. However, mortality from meningococcal infection is lower in these patients than in immunocompetent subjects. We studied a C6-deficient patient with meningococcal sepsis who received fresh frozen plasma (FFP). The patient's initial plasma endotoxin, C6, and terminal-complement-complex concentrations were low, but rose sharply after treatment with FFP. Samples of the patient's serum taken shortly after admission did not cause endotoxin release from
Escherichia coli J5 in vitro, but endotoxin-releasing activity was restored in serum samples taken after infusion of FFP. It is possible that C6-deficient patients have reduced mortality from meningococcal infection because their serum cannot cause acute release of endotoxin from the invading organism and extensive tissue damage is thus avoided. |
| doi_str_mv | 10.1016/0140-6736(92)92561-S |
| format | Article |
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Escherichia coli J5 in vitro, but endotoxin-releasing activity was restored in serum samples taken after infusion of FFP. It is possible that C6-deficient patients have reduced mortality from meningococcal infection because their serum cannot cause acute release of endotoxin from the invading organism and extensive tissue damage is thus avoided.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>DOI: 10.1016/0140-6736(92)92561-S</identifier><identifier>PMID: 1360091</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adult ; Bacteremia - immunology ; Bacteremia - mortality ; Blood ; Blood Bactericidal Activity ; Blood Component Transfusion ; Complement C6 - deficiency ; Complement Membrane Attack Complex - immunology ; E coli ; Endotoxins ; Endotoxins - metabolism ; Escherichia coli - metabolism ; Female ; Humans ; Lipopolysaccharides - blood ; Medical research ; Meningitis, Meningococcal - immunology ; Meningitis, Meningococcal - mortality ; Mortality ; Neisseria meningitidis - immunology ; Plasma</subject><ispartof>The Lancet (British edition), 1992-12, Vol.340 (8832), p.1379-1381</ispartof><rights>1992</rights><rights>Copyright Lancet Ltd. Dec 5, 1992</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c299t-a9f29895cf3dded60a7fc6ddf8466b41606056dc9986992d33095597ab35250e3</citedby><cites>FETCH-LOGICAL-c299t-a9f29895cf3dded60a7fc6ddf8466b41606056dc9986992d33095597ab35250e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/014067369292561S$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1360091$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lehner, P.J.</creatorcontrib><creatorcontrib>Cohen, J.</creatorcontrib><creatorcontrib>Davies, K.A.</creatorcontrib><creatorcontrib>Walport, M.I.</creatorcontrib><creatorcontrib>Cape, A.P.</creatorcontrib><creatorcontrib>Wurzner, R.</creatorcontrib><creatorcontrib>Orren, A.</creatorcontrib><creatorcontrib>Morgan, B.P.</creatorcontrib><title>Meningococcal septicaemia in a C6-deficient patient and effects of plasma transfusion on lipopolysaccharide release</title><title>The Lancet (British edition)</title><addtitle>Lancet</addtitle><description>Patients whose blood is deficient in the terminal component of complement have an increased susceptibility to meningococcal infection. However, mortality from meningococcal infection is lower in these patients than in immunocompetent subjects. We studied a C6-deficient patient with meningococcal sepsis who received fresh frozen plasma (FFP). The patient's initial plasma endotoxin, C6, and terminal-complement-complex concentrations were low, but rose sharply after treatment with FFP. Samples of the patient's serum taken shortly after admission did not cause endotoxin release from
Escherichia coli J5 in vitro, but endotoxin-releasing activity was restored in serum samples taken after infusion of FFP. It is possible that C6-deficient patients have reduced mortality from meningococcal infection because their serum cannot cause acute release of endotoxin from the invading organism and extensive tissue damage is thus avoided.</description><subject>Adult</subject><subject>Bacteremia - immunology</subject><subject>Bacteremia - mortality</subject><subject>Blood</subject><subject>Blood Bactericidal Activity</subject><subject>Blood Component Transfusion</subject><subject>Complement C6 - deficiency</subject><subject>Complement Membrane Attack Complex - immunology</subject><subject>E coli</subject><subject>Endotoxins</subject><subject>Endotoxins - metabolism</subject><subject>Escherichia coli - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Lipopolysaccharides - blood</subject><subject>Medical research</subject><subject>Meningitis, Meningococcal - immunology</subject><subject>Meningitis, Meningococcal - 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have an increased susceptibility to meningococcal infection. However, mortality from meningococcal infection is lower in these patients than in immunocompetent subjects. We studied a C6-deficient patient with meningococcal sepsis who received fresh frozen plasma (FFP). The patient's initial plasma endotoxin, C6, and terminal-complement-complex concentrations were low, but rose sharply after treatment with FFP. Samples of the patient's serum taken shortly after admission did not cause endotoxin release from
Escherichia coli J5 in vitro, but endotoxin-releasing activity was restored in serum samples taken after infusion of FFP. It is possible that C6-deficient patients have reduced mortality from meningococcal infection because their serum cannot cause acute release of endotoxin from the invading organism and extensive tissue damage is thus avoided.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>1360091</pmid><doi>10.1016/0140-6736(92)92561-S</doi><tpages>3</tpages></addata></record> |
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| subjects | Adult Bacteremia - immunology Bacteremia - mortality Blood Blood Bactericidal Activity Blood Component Transfusion Complement C6 - deficiency Complement Membrane Attack Complex - immunology E coli Endotoxins Endotoxins - metabolism Escherichia coli - metabolism Female Humans Lipopolysaccharides - blood Medical research Meningitis, Meningococcal - immunology Meningitis, Meningococcal - mortality Mortality Neisseria meningitidis - immunology Plasma |
| title | Meningococcal septicaemia in a C6-deficient patient and effects of plasma transfusion on lipopolysaccharide release |
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