Consumer attitudes towards and satisfaction with emergency contraception counselling: experience from clinic and retail pharmacy settings.

OBJECTIVE: To collectively assess consumer attitudes towards and satisfaction with emergency contraception (EC) counselling by student pharmacists in two different locations: an academic healthcare clinic and a retail pharmacy. METHODS: EC counselling was provided by trained student pharmacists utilizing a standardized education toolkit. Participants were asked to rate the counselling at the end of the knowledge survey. In addition to descriptive statistics, we compared the self-reported attitudes and satisfaction with the counselling between the two sites. KEY FINDINGS: The majority of participants from both settings rated 'strongly agree' on the attitude and satisfaction statements for the EC counselling. Participants from the clinic setting rated higher in two of the four statements than the participants from the retail setting. CONCLUSIONS: Participants had positive attitudes towards and were highly satisfied with the EC counselling in both settings. EC counselling should be encouraged in practice settings.

Regulation of CD40L (CD154) and CD62P (p-selectin) surface expression upon GPIIb-IIIa blockade of platelets from stable coronary artery disease patients.

INTRODUCTION: The aim of this study was to further characterize the effect of the antiplatelet agents, aspirin and eptifibatide, on the surface expression of CD40L and CD62P on platelets from patients with stable coronary artery disease. MATERIALS AND METHODS: Platelet function was evaluated using standard light transmission aggregometry. Measurements of CD62P and CD40L were carried out by flow cytometry and ELISA assays. RESULTS: All patients had the expected level of platelet aggregation inhibition in response to 20 muM ADP in the presence of increasing eptifibatide concentrations. Platelet activation by adenosine diphosphate (ADP) or thrombin agonist peptide (TRAP) increased CD62P and CD40L surface density in the presence of aspirin by 1.9 - 2.8 -fold. Aspirin treatment did not prevent either CD62P or CD40L expression. Eptifibatide pretreatment at pharmacologically relevant concentrations blocked agonist-induced increases in CD62P platelet surface density. A marked percentage of platelets still expressed low levels of surface CD62P suggesting slight platelet activation even with potent platelet inhibition. Eptifibatide also blocked agonist-induced increases in CD40L surface expression and decreased the percent of platelets positive for surface CD40L. Decreased expression of CD40L was due to an inhibition of CD40L translocation and not caused by enhanced shedding from the surface, as soluble CD40L (sCD40L). Eptifibatide concentrations that effectively blocked platelet aggregation correlated with total inhibition of increased CD62P and CD40L surface density. CONCLUSION: Blockade of the GPIIb-IIIa receptor on platelets from coronary artery disease patients may have significant bearing on reducing proinflammatory and procoagulant events mediated by CD62P and sCD40L.

Platelets undergo phosphorylation of Syk at Y525/526 and Y352 in response to pathophysiological shear stress.

Atherosclerotic plaques can lead to partial vascular occlusions that produce abnormally high levels of arterial wall shear stress. Such pathophysiological shear stress can promote shear-induced platelet aggregation (SIPA), which has been linked to acute myocardial infarction, unstable angina, and stroke. This study investigated the role of the tyrosine kinase Syk in shear-induced human platelet signaling. The extent of Syk tyrosine phosphorylation induced by pathophysiological levels of shear stress (100 dyn/cm(2)) was significantly greater than that resulting from physiological shear stress (10 dyn/cm(2)). With the use of phospho-Syk specific antibodies, these data are the first to show that key regulatory sites of Syk at tyrosines 525/526 (Y525/526) and tyrosine 352 (Y352) were phosphorylated in response to pathophysiological shear stress. Increased phosphorylation at both sites was attenuated by pharmacological inhibition of Syk using two different Syk inhibitors, piceatannol and 3-(1-methyl-1H-indol-3-yl-methylene)-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide (OXSI-2), and by inhibition of upstream Src-family kinases (SFKs). Shear-induced response at the Syk 525/526 site was ADP dependent but not contingent on glycoprotein (GP) IIb-IIIa ligation or the generation of thromboxane (Tx) A(2). Pretreatment with Syk inhibitors not only reduced SIPA and Syk phosphorylation in isolated platelets, but also diminished, up to 50%, the platelet-mediated thrombus formation when whole blood was perfused over type-III collagen. In summary, this study demonstrated that Syk is a key molecule in both SIPA and thrombus formation under flow. Pharmacological regulation of Syk may prove efficacious in treating occlusive vascular disease.

The use of the point of care Helena ICHOR/Plateletworks and the Accumetrics Ultegra RPFA for assessment of platelet function with GPIIB-IIIa antagonists.

OBJECTIVE: To evaluate a newly modified rapid platelet function analysis system (ICHOR/ Plateletworks) and to compare the results obtained with those of traditional light transmission aggregometry (LTA), and the Ultegra/RPFA system. BACKGROUND: Anti-platelet therapy is standard of care for patients as an adjunct to percutaneous coronary intervention (PCI) or for medical management of non-ST elevation acute coronary syndromes (NSTE ACS). Recent clinical trial results suggest that the three currently approved platelet GPIIb-IIIa receptor antagonists, eptifibatide, tirofiban and abciximab, may vary in extent of inhibition of platelet aggregation (IPA) at the approved doses. Thus, pharmacodynamic evaluations of these agents to determine the extent of platelet function inhibition, especially during the periprocedural time of a cardiac intervention, are necessary. A rapid measurement method as a surrogate for LTA, the current gold standard, would be ideal in order to have the option for dose monitoring or adjustment prior to or during an intervention. The Helena ICHOR/ Plateletworks may be useful for point of care testing. METHODS: Blood samples collected in D-Phe-Pro-Arg-chloromethyl ketone dihydrochloride (PPACK) anticoagulant were treated with increasing concentrations of eptifibatide, tirofiban or abciximab. LTA was carried out in conjunction with the ICHOR/Plateletworks, using a modified method, and Accumetrics Ultegra with RPFA cartridges. RESULTS: This study demonstrated that platelet inhibition measured by the ICHOR/Plateletworks mirrored the level of IPA obtained with LTA. In contrast, the Ultegra system had less correlation when compared to LTA at inhibition levels < 90%. CONCLUSIONS: Based on these data, the ICHOR/ Plateletworks utilized under modified guidelines may serve as a surrogate for LTA when rapid measurements are necessary.A rapid platelet function measurement method as a surrogate for light transmission aggregometry (LTA), the current gold standard, is ideal in order to have the option for GPIIb-IIIa antagonist dose monitoring or adjustment prior to or during a coronary intervention. A newly modified rapid platelet function analysis system (ICHOR/Plateletworks was evaluated and compared to the results obtained with traditional light transmission aggregometry (LTA), and the Ultegra/RPFA system. Blood samples collected in D-Phe-Pro-Arg-chloromethyl ketone dihydrochloride (PPACK) anticoagulant were treated with increasing concentrations of eptifibatide, tirofiban or abciximab. LTA was carried out in conjunction with the ICHOR/Plateletworks, using a modified method, and Accumetrics Ultegra with RPFA cartridges. Based on these data, the ICHOR/Plateletworks utilized under modified guidelines may serve as a surrogate for LTA when rapid measurements are necessary.