scholarly journals Dyslipidaemia in Behcet's disease as a thrombotic risk factor

2006 ◽  
Vol 65 (9) ◽  
pp. 1248-1249 ◽  
Author(s):  
J M Ricart ◽  
A Vaya ◽  
M Santaolaria ◽  
F Espana ◽  
J Aznar
2020 ◽  
Vol 31 (1) ◽  
pp. 214-218
Author(s):  
Hiroaki Kato ◽  
Masaki Takeuchi ◽  
Nobuyuki Horita ◽  
Takehito Ishido ◽  
Ryuta Mizuki ◽  
...  

Author(s):  
Omayma Abdelaleem ◽  
Olfat Shaker

IntroductionBackground: The current study designed to analyze whether polymorphisms of miR-146a and miR-155 are related to Behçet’s disease (BD) in Egyptian population.Material and methodsMethods: A total of 96 unrelated BD patients and 100 healthy subjects were genotyped for miR-146a (rs2910164) and miR-155(rs767649) using real-time polymerase chain reaction.ResultsResults: the results showed significant elevation in the frequency of rs2910164 GG and CC genotypes in BD patients compared with controls (adjusted OR = 22.156, 95% CI (4.728-103.818); P < 0.001 and adjusted OR = 40.358, 95% CI (8.928 -182.440); P < 0.001, respectively). Also, rs2910164 G allele conferred a higher risk of developing BD (adjusted OR = 3.665, 95% CI (2.013-6.671); P < 0.001). MiR-146a (rs2910164) polymorphism was a risk factor for susceptibility to BD in dominant, recessive and additive models of inheritance(All P < 0.001), while, the miR-155(rs767649) polymorphism was a risk factor in recessive model only (P = 0.021). GG and CG genotypes of rs2910164 were associated with higher BDCAI activity and ocular involvement compared with CC genotype (P = 0.005 and P =0.004, respectively). Genotype AT of rs767649 was related to higher BDCAI activity (P = 0. 026) compared with TT or AA genotypes.ConclusionsConclusion: The miR-146a (rs2910164) and miR-155(rs767649) were likely to play an important role in Egyptian population to develop BD and also influence disease severity.


2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Rachel Black ◽  
Sue Lester ◽  
Emma Dunstan ◽  
Farhad Shahram ◽  
Abdolhadi Nadji ◽  
...  

2019 ◽  
Vol 78 (9) ◽  
pp. 1274-1282 ◽  
Author(s):  
Alexandre Le Joncour ◽  
Raphael Martos ◽  
Stephane Loyau ◽  
Nicolas Lelay ◽  
Antoine Dossier ◽  
...  

ObjectivesBehçet’s disease (BD) is a chronic systemic vasculitis. Thrombosis is a frequent and life-threatening complication. The pathogenesis of BD is poorly understood and evidence supporting a role for primed neutrophils in BD-associated thrombotic risk is scant. To respond to inflammatory insults, neutrophils release web-like structures, known as neutrophil extracellular traps (NETs), which are prothrombotic. We evaluated the role of NETs and markers of NETs in BD.MethodsBlood samples were collected from patients with BD, according to the International Study Group Criteria for Behçet's disease, and healthy donors (HD). NET components, including cell-free DNA (CfDNA) and neutrophil enzymes myeloperoxidase (MPO), were assessed in serum or in purified neutrophils from patients with BD and HD.ResultsPatients with active BD had elevated serum cfDNA levels and MPO-DNA complexes compared with patients with inactive BD and to HD. In addition, levels of cfDNA and MPO-DNA complexes were significantly higher in patients with BD with vascular involvement compared with those without vascular symptoms. Purified neutrophils from patients with BD exhibited spontaneous NETosis compared with HD. Thrombin generation in BD plasma was significantly increased and positively correlated with the levels of MPO-DNA complexes and cfDNA. Importantly, DNAse treatment significantly decreased thrombin generation in BD plasma but not in HD plasma. In addition, biopsy materials obtained from patients with BD showed NETs production in areas of vasculitic inflammation and thrombosis.ConclusionsOur data show that NETs and markers of NETS levels are elevated in patients with BD and contribute to the procoagulant state. Targeting NETs may represent a potential therapeutic target for the reduction or prevention of BD-associated thrombotic risk.


1994 ◽  
Vol 53 (5) ◽  
pp. 351-352 ◽  
Author(s):  
A Orem ◽  
O Deger ◽  
O Memis ◽  
K Caliskan ◽  
G Cimsit

2017 ◽  
Vol 4 (2) ◽  
pp. 109-112 ◽  
Author(s):  
Gonca Mumcu ◽  
Fatma Alibaz Oner ◽  
Sibel Yilmaz Oner ◽  
Gulsen Ozen ◽  
Pamir Atagunduz ◽  
...  

1991 ◽  
Vol 66 (03) ◽  
pp. 292-294 ◽  
Author(s):  
K K Hampton ◽  
M A Chamberlain ◽  
D K Menon ◽  
J A Davies

SummaryCoagulation and fibrinolytic activities were studied in 18 subjects with Behçet's disease and compared with results from 14 matched control patients suffering from sero-negative arthritis. Significantly higher plasma concentrations (median and range) were found in Behçet's patients for the following variables: fibrinogen 3.7 (1.7-6.9) vs 3.0 (2.0-5.1) g/1, p <0.05; von Willebrand factor antigen, 115 (72-344) vs 74 (60-119)%, p <0.002; plasminogen activator activity (106/ECLT2) 219 (94-329) vs 137 (78-197) units, p <0.002; tissue plasminogen activator inhibitor (t-PA-I) activity, 9.1 (5.5-19.3) vs 5.1 (1.8-12.0) IU/ml, p <0.002; and PAI-1 antigen, 13.9 (4.5-20.9) vs 6.4 (2.4-11.1) ng/ml, p <0.002. Protein C antigen was significantly lower: 97 (70-183) vs 126 (96-220)%, p <0.02. No differences were observed in antithrombin III activity or antigen, factor VIII coagulant activity, fibrinopeptides A and Bβ15-42, plasminogen, α-2-antiplasmin, functional and immunological tissue-plasminogen activator, thrombin-antithrombin complexes and D-dimer. Levels of tissue plasminogen activator inhibitor (activity and antigen) correlated with disease activity while fibrinogen and von Willebrand factor concentrations did not. Seven of the 18 subjects with Behçet's disease had suffered thrombotic events but it was not possible to distinguish these from the 11 patients without thrombosis using the assays performed. The results suggest the abnormal fibrinolytic activity in Behçet's disease is due to increased inhibition of tissue plasminogen activator. No abnormality of coagulation or fibrinolytic activity specific to Behçet's disease was detected.


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