liu.seSearch for publications in DiVA
Change search
ReferencesLink to record
Permanent link

Direct link
Enhanced platelet adhesion in essential thrombocythemia after in vitro activation
Linköping University, Department of Medicine and Health Sciences, Pharmacology . Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medicine and Health Sciences, Clinical Pharmacology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pharmacology.
Linköping University, Department of Medicine and Health Sciences, Pharmacology . Linköping University, Faculty of Health Sciences.ORCID iD: 0000-0003-3184-0427
2010 (English)In: TURKISH JOURNAL OF HEMATOLOGY, ISSN 1300-7777, Vol. 27, no 2, 82-90 p.Article in journal (Refereed) Published
Abstract [en]

Objective: Essential thrombocythemia (ET) is a chronic myeloproliferative disorder characterized by elevated platelet counts and increased risk of thrombosis. Ex vivo data suggest increased platelet reactivity in agreement with the increased thrombosis risk, while in vitro tests often detect decreased platelet activity. The present study aimed to investigate adhesion of ET-platelets in vitro, which is an aspect of platelet function that has been addressed in only a few studies on ET patients. Material and Methods: The study included 30 Er patients and 14 healthy controls. Platelet adhesion was measured with a static platelet adhesion assay. Results: The main finding was that ET-platelets were more readily activated by adhesion-inducing stimuli in vitro than control platelets. This was particularly evident in elderly patients and when using multiple stimuli, such as surfaces of collagen or fibrinogen combined with addition of adenosine 5-diphosphate or ristocetin. Such multiple stimuli resulted in adhesion above the control mean +2 standard deviations for approximately 50% of the patients. Conclusion: The results are in accordance with the concept of increased platelet activity in ET, but opposite to most other in vitro studies. We suggest that the conditions in the adhesion assay might mimic the in vivo situation regarding the presence of chronic platelet activation. (Turk J Hematol 2010; 27: 82-90)

Place, publisher, year, edition, pages
Aves Yayincilik , 2010. Vol. 27, no 2, 82-90 p.
Keyword [en]
Essential thrombocythemia; platelet activation; adhesion; thrombosis; platelet assay
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-13249DOI: 10.5152/tjh.2010.05ISI: 000278947500005OAI: diva2:18138
Available from: 2008-05-21 Created: 2008-05-21 Last updated: 2013-09-03
In thesis
1. Platelet Adhesion to Proteins in Microplates: Applications in Experimental and Clinical Research
Open this publication in new window or tab >>Platelet Adhesion to Proteins in Microplates: Applications in Experimental and Clinical Research
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Platelets are crucial for prevention of blood loss after vessel injury. Platelet adhesion to disrupted vessel walls is mediated by receptors such as the GPIb-IX-V complex that binds von Willebrand factor and the collagen-binding integrin α2β1. Also cross-linking of platelets, mediated by αIIbβ3 that binds to fibrinogen, results in platelet aggregation that further contributes to hemostasis. Platelets are also important pathophysiologically because of their role in thrombus formation following atherosclerotic plaque rupture. Pharmacological treatments aimed to prevent such events include use of platelet inhibitors such as acetylsalicylic acid (ASA) and clopidogrel. Despite the presence of several different platelet function assays, no one has so far been considered useful for clinical evaluation of the effect of anti-platelet treatment. The aim of this thesis was to evaluate possible applications in experimental as well as in clinical research for a platelet adhesion assay performed during static conditions. In principle, platelets in plasma are allowed to attach to protein coated microplates. Adhered platelets are then detected by induction of an enzymatic reaction followed by spectrophotometric measurements of the developed product. Our results show that the platelet adhesion assay is able to detect experimentally induced activation as well as inhibition of platelets. The assay also seems useful for investigation of synergistically induced platelet activation, especially when the coated surface consists of albumin. This is exemplified by the combination of lysophosphatidic acid and adrenaline, which induced a synergistically increased platelet adhesion to albumin that was dependent on αIIbβ3-receptors and on the secretion of ADP. Furthermore, secretion of ADP as well as TXA2 seems to contribute to several adhesive reactions investigated with this assay. The dependence on secretion, together with results showing that adhesion to collagen and fibrinogen is dependent on α2β1- and αIIbβ3-receptors respectively, indicate that the adhesive interactions occurring in the assay is in accordance with the general knowledge about platelet function. Regarding clinical applications, we found that platelet adhesion was increased for patients with essential thrombocythemia (ET) compared to controls. This is in line with the in vivo function of ET-platelets since a common complication for ET-patients is thrombosis. Furthermore, the assay was able to detect effects of treatment with clopidogrel in patients with unstable angina. To some extent it also measured the effects of ASA-treatment. In conclusion, our results suggest that the assay is suitable for experimental research and that further studies should be performed aimed at developing the assay into a clinically useful device.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2008. 67 p.
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1068
platelets, platelet adhesion, platelet assay, synergistic activation, thrombosis, anti-platelet treatment
National Category
Pharmacology and Toxicology
urn:nbn:se:liu:diva-11733 (URN)978-91-7393-863-1 (ISBN)
Public defence
2008-06-03, Aulan, Hälsans Hus 240, Hälsouniversitetet, Campus US, Linköpings universitet, Linköping, 13:00 (English)
Available from: 2008-05-21 Created: 2008-05-21 Last updated: 2013-09-03Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full text

Search in DiVA

By author/editor
Eriksson, Andreas CLotfi, KouroshWhiss, Per A
By organisation
Pharmacology Faculty of Health SciencesClinical Pharmacology Department of Clinical Pharmacology
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 151 hits
ReferencesLink to record
Permanent link

Direct link