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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-12-1
pubmed:abstractText
Increased vascular permeability and vascular leakage are characteristic pathological changes in hemorrhagic fever with renal syndrome (HFRS). Vascular endothelial cells are the main targets of Hantaan virus, the etiological agent of the severe form of HFRS. Hantaan virus can induce extensive damage of small blood vessels and capillaries. In vitro infection of human umbilical vein endothelial cells by Hantaan virus can induce the expression of intercellular adhesion molecule-1 (ICAM-1). The involvement of this molecule is implied in human HFRS. In the present study, serum-soluble ICAM-1 (sICAM-1) levels were determined and their relationships with the clinical course and disease severity were investigated in 112 HFRS patients and 30 healthy controls. The results showed that the serum levels of sICAM-1 in HFRS patients at fever, hypotensive, oliguric, and polyuric phases were significantly higher than those in controls (p?<?0.001). However, no significant differences between the serum concentrations of sICAM-1 in the milder and more severe groups of patients were observed (p?>?0.05). It is suggested that sICAM-1 was involved in the progression of HFRS. Time-dependent determinations of sICAM-1 levels may be indicators for the progression of disease, and elevated levels of sICAM-1 were not suggested to be correlated to disease severity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1435-4373
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1507-11
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Elevated sICAM-1 levels in patients with hemorrhagic fever with renal syndrome caused by Hantaan virus.
pubmed:affiliation
Department of Infectious Diseases, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an 710061 Shaanxi Province, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't