Patients with venous stasis ulceration have increased monocyte-platelet aggregation
Name:
Publisher version
View Source
Access full-text PDFOpen Access
View Source
Check access options
Check access options
Authors
Peyton, Brian D.Rohrer, Michael J.
Furman, Mark I.
Barnard, Marc R.
Rodino, Louis J.
Benoit, Stephen E.
Hechtman, Herbert B.
Valeri, C. Robert
Michelson, Alan D.
Document Type
Journal ArticlePublication Date
1998-06-01Keywords
Adenosine DiphosphateAdult
Antibodies, Monoclonal
Cell Aggregation
Chronic Disease
Female
Flow Cytometry
Humans
Male
Middle Aged
*Monocytes
Peptide Fragments
*Platelet Aggregation
Stimulation, Chemical
Tetradecanoylphorbol Acetate
Varicose Ulcer
Hematology
Oncology
Pediatrics
Metadata
Show full item recordAbstract
PURPOSE: Leukocyte activation has been implicated in the pathogenesis of venous stasis ulceration, but the involvement of activated platelets and leukocyte-platelet aggregates has not been previously investigated. The purpose of this study was to determine whether patients with venous stasis ulceration have increased platelet activation and a propensity toward formation of leukocyte-platelet aggregates. METHODS: Blood was drawn from the superficial veins of the leg just proximal to a venous stasis ulcer and from an antecubital vein in 14 patients with venous stasis ulceration. Blood was also drawn from the antecubital vein of 14 volunteers without evidence of venous disease. Whole-blood flow cytometry was used to analyze the samples before and after activation with a panel of agonists for evidence of platelet activation and the formation of leukocyte-platelet aggregates. RESULTS: Patients with venous stasis ulceration had a greater number of monocyte-platelet aggregates in both the arm and leg samples than did the control subjects (p andlt; 0.01). Furthermore, antecubital blood samples from patients with venous stasis ulceration stimulated with either thrombin-receptor agonist peptide, adenosine diphosphate, or phorbol myristate acetate formed more monocyte-platelet aggregates than did control samples (p andlt; 0.05). No differences in platelet activation or neutrophil-platelet aggregate formation were noted among the three sample groups. CONCLUSIONS: Patients with venous stasis ulceration have an increase in the number of monocyte-platelet aggregates in systemic venous blood as well as in venous blood adjacent to a venous stasis ulcer, implicating the monocyte as the leukocyte involved in the pathogenesis of venous stasis ulceration. No association was identified between the presence of a venous stasis ulcer and either neutrophil-platelet aggregation or the activation of individual platelets. Because platelet activation is necessary for the formation of monocyte-platelet aggregates, these data also suggest that monocyte-platelet aggregation is a more sensitive marker for in vivo platelet activation than is the identification of individual activated platelets.Source
J Vasc Surg. 1998 Jun;27(6):1109-15; discussion 1115-6. doi 10.1016/S0741-5214(98)70013-8DOI
10.1016/S0741-5214(98)70013-8Permanent Link to this Item
http://hdl.handle.net/20.500.14038/43372PubMed ID
9652473Related Resources
Link to article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/S0741-5214(98)70013-8