Mean platelet volume and β-thromboglobulin levels in familial mediterranean fever: Effect of colchicine use?

Abanonu, Gul Babacan; Daskin, Alper; Akdoğan, Mehmet Fatih; Uyar, Seyit; Demirtunç, Refik

doi:10.1016/j.ejim.2012.04.007

Cited by 27 publications

(17 citation statements)

References 32 publications

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“…In a subgroup of 49 patients with platelet aggregation measured, there was no noted difference in platelet aggregation in response to ADP, arachadonic acid, or collagen [16]. Likewise, another study demonstrated no difference in mean platelet volume, a marker of platelet activity based on size, between patients with familial mediterranean fever on colchicine and age- and sex-matched healthy subjects [17–18]. Overall, these data suggest that colchicine may not inhibit platelet homotypic aggregation within the pharmacologically achievable range in humans.…”

Section: Discussionmentioning

confidence: 99%

Effect of Colchicine on Platelet-Platelet and Platelet-Leukocyte Interactions: a Pilot Study in Healthy Subjects

et al. 2015

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The cardioprotective mechanisms of colchicine in patients with stable ischemic heart disease remain uncertain. We tested varying concentrations of colchicine on platelet activity in vitro, and a clinically relevant 1.8 mg oral loading dose administered over one hour in 10 healthy subjects. Data are shown as median [interquartile range]. Colchicine addition in vitro decreased light transmission platelet aggregation only at supratherapeutic concentrations, but decreased monocyte- (MPA) and neutrophil-platelet aggregation (NPA) at therapeutic concentrations. Administration of 1.8 mg colchicine to healthy subjects had no significant effect on light transmission platelet aggregation but decreased the extent of MPA (28% [22–57] to 22% [19–31], p=0.05) and NPA (19% [16–59] to 15% [11–30], p=0.01), platelet surface expression of PAC-1 (370 mean fluorescence intensity (MFI) [328–555] to 333 MFI [232–407], p=0.02) and P-selectin (351 MFI [269–492] to 279 [226–364], p=0.03), and platelet adhesion to collagen (10.2% [2.5–32.6] to 2.0% [0.2–9.5], p=0.09) 2 hours post-administration. Thus, in clinically relevant concentrations, colchicine decreases expression of surface markers of platelet activity and inhibits leukocyte-platelet aggregation, but does not inhibit homotypic platelet aggregation.

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Section: Discussionmentioning

confidence: 99%

Effect of Colchicine on Platelet-Platelet and Platelet-Leukocyte Interactions: a Pilot Study in Healthy Subjects

et al. 2015

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“…The cardiovascular applications of colchicine have been evolving in the last decade. FMF patients treated with colchicine were observed to have lower markers for endothelial dysfunction and cardiovascular risk such as β-thromboglobulin and mean platelet volume [42] [43]. Colchicine inhibited intimal hyperplasia and leukocyte vascular endothelial growth factor (VEGF) expression in an angioplasty model in dogs [44].…”

Section: Resultsmentioning

confidence: 99%

Colchicine—Update on mechanisms of action and therapeutic uses

Leung

Hui

Kraus

2015

Seminars in Arthritis and Rheumatism

628

505

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Objectives To review the literature and provide an updates on the mechanisms of action and therapeutic uses of oral colchicine in arthritis and inflammatory conditions. Methods We performed PubMed database searches through June 2014 for relevant studies in the English literature published since the last update of colchicine in 2008. Searches encompassed colchicine mechanisms of action and clinical applications in medical conditions. A total of 381 articles were reviewed. Results The primary mechanism of action of colchicine is tubulin disruption. This leads to subsequent down regulation of multiple inflammatory pathways and modulation of innate immunity. Newly described mechanisms include various inhibitory effects on macrophages including the inhibition of the NACHT-LRRPYD-containing protein 3 (NALP3) inflammasome, inhibition of pore formation activated by purinergic receptors P2X7 and P2X2, and stimulation of dendritic cell maturation and antigen presentation. Colchicine also has anti-fibrotic activities and various effects on endothelial function. The therapeutic use of colchicine has extended beyond gouty arthritis and Familial Mediterranean Fever, to osteoarthritis, pericarditis and atherosclerosis. Conclusion Further understanding of the mechanisms of action underlying the therapeutic efficacy of colchicine will lead to its potential use in a variety of conditions.

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“…In addition, free from attack status, Abanonu et al found no significant difference in MPV levels between FMF patients and healthy controls (21). In contrast, Sahin et al (22) reported significantly lower MPV levels in FMF patients compared to healthy controls while there was no difference in MPV levels between FMF patients during attack and attack-free periods. In the current study, lowest MPV values were observed in patients with an acute attack and the highest MPV values were in patients with Colchicine use may suppress platelet activation (24)(25)(26), and the majority of our patients were on colchicine treatment.…”

Section: Discussionmentioning

confidence: 85%

Mean Platelet Volume in Children with Familial Mediterranean Fever and the Relationship with Attack Status, Colchicine Treatment and Gene Mutation

et al. 2014

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Mean platelet volume and β-thromboglobulin levels in familial mediterranean fever: Effect of colchicine use?

Cited by 27 publications

References 32 publications

Effect of Colchicine on Platelet-Platelet and Platelet-Leukocyte Interactions: a Pilot Study in Healthy Subjects

Effect of Colchicine on Platelet-Platelet and Platelet-Leukocyte Interactions: a Pilot Study in Healthy Subjects

Colchicine—Update on mechanisms of action and therapeutic uses

Mean Platelet Volume in Children with Familial Mediterranean Fever and the Relationship with Attack Status, Colchicine Treatment and Gene Mutation

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