H1- antihistamines and activated blood platelets

Petríková, M.; Jančinová, Viera; Nosáľ, R; Májeková, Magdaléna; Holománová, D

doi:10.1007/s00011-005-0038-9

Cited by 8 publications

(4 citation statements)

References 8 publications

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“…Finally, all above processes with their actions and interactions occurring during platelet activation lead to a conformational change in the GP IIb/IIIa receptor, converting the receptor into a form that can bind fibrinogen and link with other platelets thus resulting in platelet It must be pointed out that platelet activation in human plasma induced by thrombin or adenosine diphosphate can be significantly inhibited by H1-antihistamine dithiaden as it has been shown experimentally (23,24).…”

Section: Why Stents Are Prone To Thrombosismentioning

confidence: 99%

Thrombotic responses to coronary stents, bioresorbable scaffolds and the Kounis hypersensitivity-associated acute thrombotic syndrome

et al. 2017

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Percutaneous transluminal coronary angioplasty with coronary stent implantation is a lifesaving medical procedure that has become, nowadays, the most frequent performed therapeutic procedure in medicine. Plain balloon angioplasty, bare metal stents, first and second generation drug-eluting stents, bioresorbable and bioabsorbable scaffolds have offered diachronically a great advance against coronary artery disease and have enriched our medical armamentarium. Stented areas constitute vulnerable sites for endothelial damage, endothelial dysfunction, flow turbulence, hemorheologic changes, platelet dysfunction, coagulation changes and fibrinolytic disturbances. Implant surface attracts several proteins such as albumin, fibronectin, fibrinogen, and complement that lead to complement system activation. Macrophages recognize the implant as foreign substance due to protein adsorption and its continuous presence results in macrophage differentiation and fusion into foreign body giant cells. Polymer coating, stent metallic platforms and the released drugs can act as strong antigenic complex that apply continuous, repetitive, persistent and chronic hypersensitivity irritation to the coronary intima. The concomitant administration of oral antiplatelet drugs and environmental exposures can induce hypersensitivity inflammation. A class of platelets, activated via high-affinity and low-affinity IgE hypersensitivity receptors FCγRI, FCγRII, FCεRI and FCεRII, can induce Kounis hypersensitivity-associated thrombotic syndrome inside the stented coronaries. Type III variant of this syndrome is diagnosed when coronary artery stent thrombosis is associated with thrombus infiltrated by eosinophils or mast cells and/or when coronary intima, media and adventitia adjacent to stent, is infiltrated by eosinophils or mast cells. Careful history of hypersensitivity reactions to all implanted materials and concomitant drugs with monitoring of inflammatory mediators as well as lymphocyte transformation studies to detect hypersensitivity must be undertaken in order to avoid disastrous consequences. Food and Drug Administration recommendations for coronary stent implantation should be applied also to bioresorbable scaffolds. Further studies with inert and non-allergenic implants are necessary.

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Section: Why Stents Are Prone To Thrombosismentioning

confidence: 99%

Thrombotic responses to coronary stents, bioresorbable scaffolds and the Kounis hypersensitivity-associated acute thrombotic syndrome

et al. 2017

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“…Specifically, platelet aggregation may be decreased by beta-blockers, 46 statins 47,48 and antihistamines. 49,50 Despite venous hypertension appearing to be a common underlying risk factor for most variants of PPD, some variants do not seem to be associated with venous disease. This is particularly more relevant in generalised eruptions involving the trunk.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, platelet aggregation may be decreased by beta-blockers, 46 statins 47,48 and antihistamines. 49,50…”

Section: Discussionmentioning

confidence: 99%

Chronic venous disease, platelet and haemostatic abnormalities contribute to the pathogenesis of pigmented purpuric dermatoses

et al. 2022

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Background To investigate the aetiology of pigmented purpuric dermatoses (PPD). Methods 63 patients with a provisional diagnosis of PPD were assessed. Skin biopsies were performed to confirm the clinical diagnosis. Haemostasis was assessed using platelet function analyser-100 (PFA-100), light transmission aggregometry (LTA), impedance aggregometry (Multiplate) and measurement of clotting times and clotting factors. Chronic venous disease (CVD) was assessed by duplex ultrasound. When not contraindicated, patients were advised to discontinue haemostatic-modifying drugs or supplements for 4 weeks after which the laboratory measurements were repeated and the clinical resolution of PPD was assessed. Subsequently, a cohort of patients identified with CVD underwent endovenous interventions and further resolution of PPD was assessed. Results CVD was found in 48 patients (76.2%) while haemostatic abnormalities were found in 36 (57.1%). 30 patients (47.6%) had concurrent CVD and haemostatic abnormalities. Modifiable risk factors such as the intake of platelet inhibitors or other drugs and supplements such as fish oil were identified in 53 patients (84.1%). These could be ceased in 35 patients of whom 28 (80.0%) achieved either complete or partial resolution of PPD. Treatment of the underlying CVD was performed in 18 patients resulting in complete or partial resolution in 17 (94.4%). In seven patients (11.1%), no CVD or haemostatic abnormalities were identified, and the risk factors included dietary factors such as excessive caffeine or soft drink consumption. Conclusion Haemostatic abnormalities and CVD contribute to the pathogenesis of PPD. Resolution of PPD in the vast majority of patients may be achieved by cessation of modifiable risk factors and in particular platelet-modifying drugs or supplements and treatment of the underlying venous disease.

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“…Aspirin inhibits the action of thromboxane A2 by its effect on cyclooxygenase 1, prasugrel, clopidogrel, triflusal and ticlopidine prevent the binding of adenosine diphosphate to its receptor and antithrombins such as unfractionated or low molecular-weight heparin, hirudin and bivalirudin interfere with thrombin-induced platelet activation and coagulation. Experiments have shown that platelet activation in human plasma induced by thrombin or adenosine diphosphate can be significantly inhibited by H1-antihistamine Dithiaden [52,53].…”

Section: Pathophysiology Of Stent Thrombosismentioning

confidence: 99%

Eosinophilic responses to stent implantation and the risk of Kounis hypersensitivity associated coronary syndrome

Kounis¹,

Giannopoulos

Tsigkas

et al. 2012

International Journal of Cardiology

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H1- antihistamines and activated blood platelets

Cited by 8 publications

References 8 publications

Thrombotic responses to coronary stents, bioresorbable scaffolds and the Kounis hypersensitivity-associated acute thrombotic syndrome

Thrombotic responses to coronary stents, bioresorbable scaffolds and the Kounis hypersensitivity-associated acute thrombotic syndrome

Chronic venous disease, platelet and haemostatic abnormalities contribute to the pathogenesis of pigmented purpuric dermatoses

Eosinophilic responses to stent implantation and the risk of Kounis hypersensitivity associated coronary syndrome

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