Linked Life Data

10088635

Source:http://linkedlifedata.com/resource/pubmed/id/10088635

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-5-25
pubmed:abstractText
Thromboses are a serious complication in patients with sickle cell disease, paroxysmal nocturnal hemoglobinuria, beta-thalassemia major, or thalassemia intermedia. Despite prophylaxis, thrombotic events can continue and can result in severe physical or mental debilitation or death of the patient. The fact that thrombosis does not occur in all patients with hemolytic anemias suggests that multiple factors interact to cause the coagulation crisis. Genetic modifiers, associated diseases, nutritional status, infections, environment, and treatment modalities are variables implicated in thrombophilia. The complexity confounds attempts to identify single causative agents in humans with hemolytic anemias. In the past year, mutations in putative genetic modifiers of the coagulation response have been examined as risk factors in patients with a history of thromboses; red cell binding sites on endothelial cells have been identified; and mouse models of thrombogenesis that permit experimental manipulation of single factors on a defined genetic background have been described.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1065-6251
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
71-5
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Thrombosis in heritable hemolytic disorders.
pubmed:affiliation
The Jackson Laboratory, Bar Harbor, ME 04609, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review