Enhanced platelet response to serotonin in Buerger's disease

Pietraszek, M.H.; Choudhury, N.A.; Koyano, Keiko; Sakaguchi, S; Kamiya, T.; Urano, Tetsumei; Takada, Yoichi; Takada, Akikazu

doi:10.1016/0049-3848(90)90186-g

Cited by 15 publications

(3 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

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.

show abstract

Section: Etiology and Pathogenesismentioning

confidence: 99%

Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices

Vijayakumar

Tiwari

Prabhuswamy

2013

International Journal of Inflammation

View full text Add to dashboard Cite

show abstract

“…Increased platelet response to serotonin has been described in TAO patients compared to healthy male controls. About half of the controls in this study were smokers [13].…”

Section: Complete Blood Count (Cbc)mentioning

confidence: 88%

Recent Updates and Advances in Winiwarter-Buerger Disease (Thromboangiitis Obliterans): Biomolecular Mechanisms, Diagnostics and Clinical Consequences

et al. 2021

View full text Add to dashboard Cite

Thromboangiitis obliterans (TAO) or Buerger’s disease is a segmental inflammatory, thrombotic occlusive peripheral vascular disease with unknown aetiology that usually involves the medium and small-sized vessels of young male smokers. Due to its unknown aetiology and similarities with atherosclerosis and vasculitis, TAO diagnosis is still challenging. We aimed to review the status of biomolecular and laboratory para-clinical markers in TAO compared to atherosclerosis and vasculitis. We reported that, although some biomarkers might be common in TAO, atherosclerosis, and vasculitis, each disease occurs through a different pathway and, to our knowledge, there is no specific and definitive marker for differentiating TAO from atherosclerosis or vasculitis. Our review highlighted that pro-inflammatory and cell-mediated immunity cytokines, IL-33, HMGB1, neopterin, MMPs, ICAM1, complement components, fibrinogen, oxidative stress, NO levels, eNOS polymorphism, adrenalin and noradrenalin, lead, cadmium, and homocysteine are common markers. Nitric oxide, MPV, TLRs, MDA, ox-LDL, sST2, antioxidant system, autoantibodies, and type of infection are differential markers, whereas platelet and leukocyte count, haemoglobin, lipid profile, CRP, ESR, FBS, creatinine, d-dimer, hypercoagulation activity, as well as protein C and S are controversial markers. Finally, our study proposed diagnostic panels for laboratory differential diagnosis to be considered at first and in more advanced stages.

show abstract

“…Patients with TAO have significantly greater plasma concentrations of free serotonin and their platelet response to serotonin might also be enhanced. 60,61 Increased levels of serotonin may also lead to platelet activation via the 5-hydroxytryptamine (5-HT) receptors on the platelet surface. 62 In time, the platelets of chronic smokers lose sensitivity to prostaglandin I2 (PGI2) and NO generated by the vascular endothelium.…”

Section: Responsible Triggersmentioning

confidence: 99%

A review on thromboangiitis obliterans pathophysiology: thrombosis and angiitis, which is to blame?

Fazeli¹,

Rezaee

2011

Vascular

View full text Add to dashboard Cite

A century has passed since thromboangiitis obliterans (TAO), or Buerger's disease, was first described, but the etiology remains unclear. It is still uncertain as to whether thrombosis or vascular inflammation is the first event. TAO is an episodic inflammatory and thrombotic-occlusive vascular disease of unknown origin. The involvement of the distal vessels and nerves within the neuro-vascular bundles occurs almost always in legs and occasionally in arms. The cumulative data demonstrate that at the cellular and molecular levels, at least four main components of inflammatory reactions, including endothelial cells, platelets, leukocytes and sensory neurons, might be involved in TAO pathogenesis. The interactions among these cells in an altered microenvironment of small- and medium-sized vessels may also orchestrate the onset of TAO events. In this review, the factors that may promote thrombosis and angiitis are reconsidered at three levels: (1) host characteristics such as male gender and genetic background; (2) probable triggers including cigarette smoking and infectious agents; and (3) environmental factors such as chronic anxiety and mental stress as a consequence of low socioeconomic status. At each level, the interactions among vascular endothelium, platelets, leukocytes and sensory neurons are discussed.

show abstract

Enhanced platelet response to serotonin in Buerger's disease

Cited by 15 publications

References 6 publications

Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices

Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices

Recent Updates and Advances in Winiwarter-Buerger Disease (Thromboangiitis Obliterans): Biomolecular Mechanisms, Diagnostics and Clinical Consequences

A review on thromboangiitis obliterans pathophysiology: thrombosis and angiitis, which is to blame?

Contact Info

Product

Resources

About