Plasminogen activators and plasminogen activator inhibitor 1 before and after venous occlusion of the upper limb in thromboangiitis obliterans (Buerger's disease)

Choudhury, N.A.; Pietraszek, M.H.; Hachiya, Takashi; Baba, Satoshi; Sakaguchi, Shukichi; Takada, Yumiko; Takada, Akikazu

doi:10.1016/0049-3848(92)90282-f

Cited by 25 publications

(10 citation statements)

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“…Choudhury and colleagues [8] demonstrated that the level of urokinase-plasminogen activator was twofold higher and that of free plasminogen activator inhibitor I was 40% lower in patients with TAO than in healthy volunteers. An increased platelet response to serotonin is described in patients with Buerger's disease [9].…”

Section: Etiology and Pathogenesismentioning

confidence: 99%

Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices

Vijayakumar

Tiwari

Prabhuswamy

2013

International Journal of Inflammation

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Thromboangiitis obliterans (TAO) is a nonatherosclerotic, segmental inflammatory disease that most commonly affects the small and medium-sized arteries and veins in the upper and lower extremities. Cigarette smoking has been implicated as the main etiology of the disease. In eastern parts of the world TAO forms 40–60% of peripheral vascular diseases. Clinical features and angiographic finding are the basis of early diagnosis of TAO. Abstinence from smoking is the only definitive treatment to prevent disease progression. Medical management in form of aspirin, pentoxyfylline, cilostazol, and verapamil increase pain-free walking distance in intermittent claudication, but long term usage fails to prevent disease progression in patients who continue to smoke. Surgical treatment in form of revascularization, lumbar sympathectomy, omentopexy, and Ilizarov techniques help reduce pain and promote healing of trophic changes. Newer treatment modalities like spinal cord stimulation, prostacyclin, bosentan, VEGF, and stem cell therapy have shown promising results. Latest treatment options include peripheral mononuclear stem cell, and adipose tissue derived mononuclear stem cells have been shown to be effective in preventing disease progression, decrease major amputation rates, and improving quality of life.

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Section: Etiology and Pathogenesismentioning

confidence: 99%

Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices

Vijayakumar

Tiwari

Prabhuswamy

2013

International Journal of Inflammation

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“…It is assumed that an impaired endogenous fibrinolysis may contribute to a prothrombotic state which enhances the risk of thrombus formation in the affected vessels. Choudhury et al [11] demonstrated no difference in basal t-PA antigen levels between patients and controls, but a diminished increase of t-PA antigen after the venous occlusion test (one of the classical stimuli for an increased release of t-PA from the endothelial cells) and decreased basal free PAI-1 antigen levels in BD patients. This is somewhat contradictory to recent results of studies of endothelial dysfunction, which showed an increased release of t-PA and PAI-1 from the damaged endothelial cells [7,12].…”

Section: Introductionmentioning

confidence: 98%

Endothelial dysfunction in Buerger's disease and its relation to markers of inflammation

Joras

Poredoš

Fras

2006

Eur J Clin Investigation

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“…It was demonstrated that all alone or combined effect of this gene deletion was impacted deep venous thrombosis (DVT), in studies [16]. Choudhury and friends detected that the free PAI-1 levels can be significant venous occlusion in TAO patients [17]. This gene mutation accused in Turkish DVT patients [18].…”

Section: Discussionmentioning

confidence: 99%

Association of the plasminogen activator inhibitor-1(PAI-1) gene 4G/5G promoter polymorphism in Buerger's disease (Tromboangiitis obliterans)

Manduz¹,

Katrancioglu²,

Karahan³

et al. 2010

Health

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Thromboangiitis obliterans (TAO) is an unusual tobacco-associated vasculopathy that is a non- atherosclerotic inflammatory disorder of unkn- own etiology that affects small and medium- sized vessels of the extremities. The single guanosine nucleotide deletion/insertion polym- orphism (4G/5G) at -675 bp in promoter region of the PAI-1 gene is the major genetic determi- nant of PAI-1 expression. Plasma PAI-1 level is higher in people with the homozygous 4G genotype than in those with the 5G/5G genotype and renders higher transcription activity. The aim of this study was to determine the status and the role of PAI-1 gene 4G/5G promoter polymorphism in patients with Buerger's disease (Thromboangiitis obliterans—TAO). The current case-control study included 30 consecutive pat- ients with Buerger's disease (mean age 42.9 ± 14.3 years, 28 men and 2 women), and 30 healthy volunteers (mean age 40.9 ± 4.79 years, 27 men and 3 women) between January 2006 and September 2009. Patients and control cases were genotyped for the 4G/5G polymorphism using the multiplex PCR based stripassay reverse hybridisation technique. It was found that heterozygote PAI-1 gene polymorphisms (p < 0.05) was significantly more frequent in patients with TAO in the current results. There was a significant difference in genotype distribution between the two groups (P < 0.001). The 4G allele occurred more frequently in the patient group of heavy smokers (P = 0.05). The current study shows the higher prevalence of of 4G allele in TAO patients in Sivas population means gene may predispose to TAO

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Plasminogen activators and plasminogen activator inhibitor 1 before and after venous occlusion of the upper limb in thromboangiitis obliterans (Buerger's disease)

Cited by 25 publications

References 10 publications

Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices

Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices

Endothelial dysfunction in Buerger's disease and its relation to markers of inflammation

Association of the plasminogen activator inhibitor-1(PAI-1) gene 4G/5G promoter polymorphism in Buerger's disease (Tromboangiitis obliterans)

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