title: Role of the retention test Homburg in evaluating platelet hyperactivity and in monitoring therapy with antiplatelet drugs.
abstract: Decreased retention in the retention test Homburg (RTH) indicates a loss of platelet function; increase is associated with an increased activation of platelets, for example, in patients with vascular diseases. Compared with other materials (e.g., collagen, glass pearls, etc.) the filter surface in the retention tubes is nonthrombogenic. Therefore, the RTH seems to be well suited for measuring an in vivo over-reactivity of platelets. In a pilot study using the RTH we evaluated the postoperative over-reactivity of platelets in 14 patients and observed a significant heterogeneity of the platelet population concerning size and stickiness. Reliable platelet function tests are also necessary for "drug monitoring," since they deliver important clinical laboratory parameters for efficient control of a therapy with antiplatelet drugs. Therefore, we evaluated in vitro how, after administration of platelet aggregation-inhibiting medications (such as acetylsalicylic acid, Prostaglandin and ReoPro in various concentrations, the adenosine diphosphate (ADP), collagen, ristocetin, or suprarenin increased retention can be reduced. The reaction of the platelets in platelet-rich plasma of different patients or donors to the addition of ADP is variable. The platelet function inhibitor effect is dose dependent. In a clinical pilot study, a significant platelet-inhibiting effect of clopidogrel using the RTH has been shown.
authors.affiliation: Department of Neurosurgery, Philipps University Marburg, Germany. krischek@med.uni-marburg.de
authors.forename: Boris
authors.initials: B
authors.lastname: Krischek
authors.forename: Werner
authors.initials: W
authors.lastname: Brannath
authors.forename: Ute
authors.initials: U
authors.lastname: Klinkhardt
authors.forename: Jochen
authors.initials: J
authors.lastname: Graff
authors.forename: Ulrich
authors.initials: U
authors.lastname: Wieding
authors.forename: Amah
authors.initials: A
authors.lastname: Nemeh
authors.forename: Walter
authors.initials: W
authors.lastname: Heinrich
authors.forename: Jochen
authors.initials: J
authors.lastname: Schenk
authors.forename: Thomas
authors.initials: T
authors.lastname: Wenzel
authors.forename: Ernst
authors.initials: E
authors.lastname: Wenzel
mesh_terms: D000077284:Abciximab; D000244:Adenosine Diphosphate / Q000378:metabolism; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000166:cytology*; D048430:Cell Shape; D000077144:Clopidogrel; D003094:Collagen / Q000097:blood; D016903:Drug Monitoring / Q000379:methods*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology; D019007:P-Selectin / Q000097:blood; D010865:Pilot Projects; D010949:Plasma / Q000378:metabolism; D010974:Platelet Aggregation; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D010976:Platelet Count; D010979:Platelet Function Tests / Q000379:methods*; D011453:Prostaglandins / Q000494:pharmacology; D012310:Ristocetin / Q000097:blood; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D011453:Prostaglandins; D012310:Ristocetin; D000244:Adenosine Diphosphate; D003094:Collagen; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab