Disease relevance of Thromboangiitis Obliterans

• The mean stimulation index--the ratio of thymidine incorporation in the presence of antigen to that in its absence--with both Type I and Type III collagens used as antigens was significantly higher in patients with thromboangiitis obliterans than in patients with arteriosclerosis obliterans or in healthy male controls [1].
• The purposes of this study were to examine the TNFR2 polymorphism in Japanese patients with SLE and to investigate its association with other autoimmune diseases accompanied by vasculitis, mixed connective tissue disease, Buerger's disease, and Takayasu's arteritis [2].
• The hemorheologic abnormalities were studied in patients suffering from thromboangiitis obliterans (TAO) and compared findings with those of patients suffering from critical limb ischemia because of peripheral atherosclerotic obstructive disease (PAOD) and the healthy subjects [3].
• Twenty-seven patients (17 collagen vascular disease, four thromboangiitis obliterans, three embolism, three atherothrombosis) presenting with ischemic rest pain and/or ulcerations of the fingers received a single block with 5 mg guanethidine injected in 60 mL into the clinically more affected hand under 30 minutes of arterial arrest [4].

High impact information on Thromboangiitis Obliterans

• Trial of iloprost versus aspirin treatment for critical limb ischaemia of thromboangiitis obliterans. The TAO Study [5].
• 152 patients with thromboangiitis obliterans (Buerger's disease) and pain from critical leg ischaemia were randomly allocated to receive iloprost, a chemically stable prostacyclin analogue, or low-dose aspirin, for 28 days in a double-blind trial [5].
• The role of cocaine in the etiology of Buerger disease is questionable [6].
• Seven patients (5 with arteriosclerosis obliterans and 2 with Buerger's disease) completed a two-phase double-blind crossover trial of propranolol in intermittent claudication [7].
• Is there a role for genetic polymorphism of C677T methylenetetrahydrofolate reductase (MTHFR) in Buerger's disease [8]?

Chemical compound and disease context of Thromboangiitis Obliterans

• Successful treatment of digital ulceration in Buerger's disease with nicotine chewing gum [9].
• Amounts of coronary arterial luminal narrowing and composition of the material causing the narrowing in Buerger's disease [10].
• Enhanced platelet response to serotonin in Buerger's disease [11].
• The effect of a 5HT2 receptor antagonist sarpogrelate (MCI-9042) treatment on platelet function in Buerger's disease [12].
• The effect of a new, specific 5-HT2 receptor antagonist sarpogrelate (MCI-9042) treatment on platelet function and serotonin levels in both plasma and whole blood in Buerger's disease, was assessed in a pilot study [12].

Biological context of Thromboangiitis Obliterans

• The incidence of Thromboangiitis Obliterans in brothers and the high prevalence in some ethnic groups have led us to investigate the histocompatibility HLA-A, B and DR antigens of 46 Buerger's disease patients [13].
• Intramuscular injection of naked HGF plasmid DNA was performed in ischemic limbs of 6 CLI patients with arteriosclerosis obliterans (n=3) or Buerger disease (n=3) graded as Fontaine III or IV [14].

Anatomical context of Thromboangiitis Obliterans

• The uptake and incorporation of [I14-C] oleic acid by diseased arterial intima removed by thrombendarteriectomy in 3 patients with Thromboangiitis obliterans (TAO) was studied [15].
• Whole blood and plasma levels of serotonin (5-hydroxy-tryptamine, 5-HT) as well as its uptake and spontaneous release from blood platelets were studied in 20 patients suffering from thromboangiitis obliterans (TAO, Buerger's disease) and 20 healthy subjects matched in pairs for age [16].
• A significant favourable effect of the balneological treatment on the RFC markers of peripheral blood lymphocytes was shown, with the exception of cases of thromboangiitis obliterans [17].

Gene context of Thromboangiitis Obliterans

• The serum VEGF and M-CSF concentrations were determined in patients with arteriosclerosis obliterans (ASO) and thromboangitis obliterans (TAO) [18].
• In conclusion, Buerger's disease is associated with the endothelial derangement with increased u-PA release and decreased PAI-1 release, which does not influence the function of fibrinolytic system [19].
• Buerger's disease involving the celiac artery [20].
• The presence of antineutrophil cytoplasmic antibodies (ANCA) and their specificity to myeloperoxidase, lactoferrin and elastase were studied in 27 patients with thromboangiitis obliterans (Buerger's disease), including nine in mild stage of the disease (group I) and 18 in active or severe stage (group II) [21].
• Treatment of thromboangiitis obliterans (Buerger's disease) by intramuscular gene transfer of vascular endothelial growth factor: preliminary clinical results [22].

References