pubmed-article:12869495 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0019425 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0376618 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C1719672 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0584960 | lld:lifeskim |
pubmed-article:12869495 | lifeskim:mentions | umls-concept:C0308269 | lld:lifeskim |
pubmed-article:12869495 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:12869495 | pubmed:dateCreated | 2003-10-21 | lld:pubmed |
pubmed-article:12869495 | pubmed:abstractText | Sepsis is associated with systemic inflammation, coagulopathy, and disrupted protein C (PC) pathway function. The effect of prothrombotic polymorphism, factor V Leiden (Arg506Gln; FV Leiden), was examined in a large clinical trial (PROWESS) of severe sepsis and a mouse endotoxemia model. In PROWESS, 4.1% (n = 65) of patients were heterozygous FV Leiden (VL+/-) carriers. The 28-day mortality was lower in VL+/- (13.9%) than in non-FV Leiden (VL-/-; 27.9%) patients (P =.013). The mortality benefit of recombinant human activated PC (rhAPC) treatment was similar in VL+/- (placebo, 15.6%; rhAPC,12.1%) and VL-/- patients (placebo, 31.0%; rhAPC, 24.7%; interaction P =.981). VL+/- status did not appear to influence baseline biomarkers of coagulopathy and inflammation or disease severity, with the exception that vasopressor usage was less in VL+/- patients (46.2% versus 63.0%; P =.009). In a median lethal dose (40 mg/kg) endotoxin mouse model, VL+/- mice had lower mortality than wild-type mice (19% versus 57%; P =.008), whereas the mortality of homozygous (VL+/+) mice was almost identical to that of wild-type mice (65% versus 57%; P =.76). The findings suggest that FV Leiden constitutes a rare example of a balanced gene polymorphism that maintains the FV Leiden mutation in the general gene pool due to a survival advantage of VL+/- in severe sepsis. | lld:pubmed |
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pubmed-article:12869495 | pubmed:language | eng | lld:pubmed |
pubmed-article:12869495 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12869495 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:12869495 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12869495 | pubmed:month | Nov | lld:pubmed |
pubmed-article:12869495 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:12869495 | pubmed:author | pubmed-author:BrandtJohn... | lld:pubmed |
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pubmed-article:12869495 | pubmed:author | pubmed-author:JoyceDavid... | lld:pubmed |
pubmed-article:12869495 | pubmed:author | pubmed-author:YanS BettySB | lld:pubmed |
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pubmed-article:12869495 | pubmed:author | pubmed-author:SoodRashmiR | lld:pubmed |
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pubmed-article:12869495 | pubmed:author | pubmed-author:IsermannBeren... | lld:pubmed |
pubmed-article:12869495 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12869495 | pubmed:day | 1 | lld:pubmed |
pubmed-article:12869495 | pubmed:volume | 102 | lld:pubmed |
pubmed-article:12869495 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12869495 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12869495 | pubmed:pagination | 3085-92 | lld:pubmed |
pubmed-article:12869495 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:12869495 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12869495 | pubmed:articleTitle | Survival advantage associated with heterozygous factor V Leiden mutation in patients with severe sepsis and in mouse endotoxemia. | lld:pubmed |
pubmed-article:12869495 | pubmed:affiliation | Blood Research Institute, Blood Center of Southeast Wisconsin and Medical College of Wisconsin, Milwaukee, WI 53226, USA. | lld:pubmed |
pubmed-article:12869495 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12869495 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12869495 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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