Monitoring survival and function of transfused platelets in Bernard‐Soulier syndrome by flow cytometry and a cone and plate(let) analyzer (Impact‐R)

Panzer, Simon; Eichelberger, Beate; Koren, Daniela; Kaufmann, Karin; Male, Christoph

doi:10.1111/j.1537-2995.2007.01070.x

Cited by 39 publications

(31 citation statements)

References 7 publications

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“…23,27 In brief, 130 mL of lithium heparin-anticoagulated whole blood were placed on the polystyrene plate. Shear stress was immediately applied (2050 s 21 ) using an acrylnitril-butadien-styrene cone.…”

Section: Impact-rmentioning

confidence: 99%

The Influence of Proton Pump Inhibitors on the Antiplatelet Potency of Clopidogrel Evaluated by 5 Different Platelet Function Tests

Gremmel¹,

Steiner²,

Seidinger³

et al. 2010

Journal of Cardiovascular Pharmacology

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Proton pump inhibitors (PPIs) are metabolized by the cytochrome P450 enzyme system to a variable degree and may therefore interact with the metabolism of clopidogrel to its active form. The conflicting data on this potential interaction may be due to the use of different PPIs and platelet function tests in recent studies. We therefore evaluated the influence of different PPIs on the antiplatelet effect of clopidogrel by 5 platelet function tests in the same population. Adenosine diphosphate (ADP)-inducible platelet reactivity was assessed in 230 patients on dual antiplatelet therapy after angioplasty and stenting for cardiovascular disease by the light transmission aggregometry, VerifyNow P2Y12 assay, vasodilator-stimulated phosphoprotein phosphorylation assay, multiple electrode aggregometry, and Impact-R. ADP-inducible platelet reactivity showed no significant differences between patients without (n = 95, 41.3%) and with PPI therapy (n = 135, 58.7%) in each test system (all P > 0.05). Furthermore, we observed no significant differences of ADP-inducible platelet reactivity between patients without PPIs and patients with pantoprazole (n = 95, 70.4%), esomeprazole (n = 22, 16.3%), omeprazole (n = 9, 6.65%), or lansoprazole (n = 9, 6.65%) (all P > 0.3). High on-treatment residual ADP-inducible platelet reactivity occurred to a similar extent in patients without and with PPI therapy in each assay (all P > 0.05). In conclusion, concomitant treatment with PPIs did not attenuate the antiplatelet effect of clopidogrel in patients on dual antiplatelet therapy irrespective of the type of PPI and the used test system.

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Section: Impact-rmentioning

confidence: 99%

The Influence of Proton Pump Inhibitors on the Antiplatelet Potency of Clopidogrel Evaluated by 5 Different Platelet Function Tests

Gremmel¹,

Steiner²,

Seidinger³

et al. 2010

Journal of Cardiovascular Pharmacology

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“…It has been shown that the enhancing effect of thrombin on the glycoprotein GPIb interaction with von Willebrand factor can be abolished by hirudin [15]. Similar to the absence of active glycoprotein GPIb in Bernard-Soulier patients [16], inhibition of the glycoprotein GPIb-thrombin binding site is likely to result in decreased platelet adherence under high shear conditions. Adhesion, however, was similar in the presence of heparin and lepirudin, and both anticoagulants inhibited thrombin-inducible platelet activation.…”

Section: Discussionmentioning

confidence: 96%

Thrombin-inducible platelet adhesion and regulation of the platelet seven-transmembrane thrombin receptor-1 (PAR-1): Effects of unfractionated heparin and lepirudin

Reiter¹,

Eichelberger²,

Kaider

et al. 2009

Platelets

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Heparin may induce platelet activation and even heparin-induced thrombocytopenia. Lepirudin has been approved for HIT treatment. We speculated that lepirudin inhibits platelet function under high shear and the platelet thrombin receptor PAR-1 better than heparin. Thrombin-inducible platelet adherence under high shear conditions and the expression of PAR-1 were studied after samples from healthy donors were exposed in vitro to increasing concentrations of unfractionated heparin or lepirudin. Compared to baseline and to lepirudin, heparin induced platelet P-selectin expression (p = 0.04). Platelet adherence increased slightly in the presence of lepirudin, but not heparin (p = 0.04). Thrombin-inducible platelet aggregate formation and consecutive adherence under high shear conditions was inhibited by both anticoagulants (p = 0.004). Further, heparin and lepirudin inhibited thrombin-inducible cleavage and internalization of PAR-1 at a dosage of 1.0 U/ml and 1.6 microg/ml, respectively (p = 0.004). Thus, heparin and lepirudin inhibit thrombin-inducible platelet activation in vitro to a similar extent.

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“…Furthermore, only two reports described the anesthetic and perioperative management of the patient in depth [16,17]. As yet, allogeneic platelet transfusions are the only treatment with proven efficacy for BSS patients [18]. We estimated the demand for platelet units based on the monitoring of the bleeding time, resulting in the transfusion of 20 units the day before and 30 units on the date of surgery.…”

Section: Discussionmentioning

confidence: 99%

Successful perioperative management for a breast cancer patient with Bernard–Soulier syndrome

Okita¹,

Hihara²,

Konishi³

et al. 2010

Breast Cancer

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We herein report the first case of a Bernard-Soulier syndrome (BSS) patient undergoing a surgical procedure for breast cancer. BSS is a rare hereditary thrombocytopathy associated with defects of the platelet glycoprotein complex glycoprotein Ib/V/IX and characterized by large platelets, thrombocytopenia, and severe bleeding symptoms. Because of the rarity of BSS, there are as yet no defined protocols for the perioperative management, which can be very complex and challenging in patients with coagulopathies, in particular BSS. In this case we successfully performed both an interventional examination as well as mastectomy with axillary lymph node dissection, under the preventive and intermittent transfusion of platelets. No intra- or postoperative bleeding complications occurred. Unfortunately, the patient was diagnosed as having metastatic disease involving liver, lungs, and bones 10 months after the surgery. She had received 1st, 2nd, and 3rd line chemotherapy without severe adverse events. However, gastrointestinal bleeding appeared after she was treated with 4th line chemotherapy. Finally, she succumbed 22 months after the breast surgery.

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Monitoring survival and function of transfused platelets in Bernard‐Soulier syndrome by flow cytometry and a cone and plate(let) analyzer (Impact‐R)

Abstract: Transfused PLTs were detectable by flow cytometry, and their functional activity was demonstrated by the Impact.

Cited by 39 publications

References 7 publications

The Influence of Proton Pump Inhibitors on the Antiplatelet Potency of Clopidogrel Evaluated by 5 Different Platelet Function Tests

The Influence of Proton Pump Inhibitors on the Antiplatelet Potency of Clopidogrel Evaluated by 5 Different Platelet Function Tests

Thrombin-inducible platelet adhesion and regulation of the platelet seven-transmembrane thrombin receptor-1 (PAR-1): Effects of unfractionated heparin and lepirudin

Successful perioperative management for a breast cancer patient with Bernard–Soulier syndrome

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