ArticleVascular health and risk management2018
Thromboangiitis obliterans episode: autoimmune flare-up or reinfection?
Article in Vascular health and risk management, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Exploring the oxidative and inflammatory markers landscape in Buerger's disease: A comparative analysis.Journal of education and health promotion · 2025Article
- The Role of Gut Microbiota in Thromboangiitis Obliterans: Cohort and Mendelian Randomization Study.Biomedicines · 2024Article
- Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB.Clinics (Sao Paulo, Brazil) · 2024Article
- Pathological and immunological differences of arterial thrombi and wall caused by three different periodontal bacterial injections in rat models and proposals on the pathogeneses of vascular diseases.Clinical and experimental dental research · 2021Article
- Recent Updates and Advances in Winiwarter-Buerger Disease (Thromboangiitis Obliterans): Biomolecular Mechanisms, Diagnostics and Clinical Consequences.Diagnostics (Basel, Switzerland) · 2021Review
- The Imbalance among Oxidative Biomarkers and Antioxidant Defense Systems in Thromboangiitis Obliterans (Winiwarter-Buerger Disease).Journal of clinical medicine · 2020Article
- The IL-33/sST2 Axis in Thromboangiitis Obliterans.Journal of inflammation research · 2020Article
- Assessment of T helper 17-associated cytokines in thromboangiitis obliterans.Journal of inflammation research · 2019Article
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Authors and funding
4 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe possible role of infectious pathogens in the development of thromboangiitis obliterans (TAO) was considered soon after the disease was first described. However, it is not yet known whether infectious pathogens induce thrombotic vasculitis or if they cause a type of autoimmune disease. To investigate whether TAO relapses are more likely due to reinfection or autoimmune flare, the serum levels of toll-like receptor (sTLR) 4, sTLR2, C-reactive protein (CRP), and neopterin were evaluated in TAO patients during both the acute and quiescent phases of the disease as well as in a gender-, age-, and smoking habit-matched control group.
methodsFollowing a cross-sectional study design, 28 patients in the acute phase of TAO and 23 patients in the quiescent phase participated in this study. In addition, 31 matched controls were enrolled.
resultsToll-like receptor (TLR) 4 was significantly higher in patients in the acute phase of the disease than in patients in the quiescent phase (
conclusionThese findings indicate that the trigger of TAO might be Gram-negative bacteria, which can be hidden or immunologically suppressed in the quiescent phase of TAO, leading to a lower level of TLR4 accompanying the normal level of neopterin. However, relapses might develop according to toxic or hypoxic cell injuries. Hence, TLR4 shedding will increase, and therefore, sTLR4 could become closer to the level demonstrated in the controls.
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