Buerger's disease pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]
Overview
Buerger's disease or thromboangiitis obliterans is a segmental vascular disease that causes occlusion and inflammation of the small and medium-sized vessels. Buerger's disease vasculitis is unique in having features of hypercellularity with intraluminal thrombi in the vessel wall, but sparing the elastic internal laminae of the vessel wall. The details of pathogenesis are still largely unknown.
Pathophysiology
Buerger's disease or thromboangiitis obliterans is a segmental vascular disease that causes occlusion and inflammation of the small and medium-sized vessels. Buerger's disease vasculitis is unique in having hypercellularity with intraluminal thrombi within the vessel wall that spares the elastic internal laminae of the vessel wall. The details of pathogenesis are still largely unknown.[1][2][3][4][5][6][7][8][9][10][11][12]
- In the acute phase the following occurs:
- The external lamina of the vessels of the distal extremities are usually affected first by inflammatory thrombi.
- The thrombi cause vessel occlusion whilst leukocytes and giant cells infiltrate the vessel margins.
- Fibrinoid necrosis is not a feature of Buerger's disease, however, microabscesses may be present.
- Superficial veins in particular may show evidence of thrombophlebitis, and this is characteristic and diagnostic of the acute phase.
- The subacute or intermediate phase is characterized by progressive organization of thrombi with the vessel.
- The chronic phase is characterized by the continued presence of organized thrombi with fibrosis, ending with the resolution of inflammation.
- In the chronic phase, the diseased vessels are not distinct from other vascular diseases.
- Obliteration of the supplying vessels of the extremities suffer severe ischemia and this may lead to gangrene and superimposed infection, mostly of the digits and toes.
- Tibial, popliteal and radial arteries are most often involved.
- The development of Buerger's disease may be the result of an immunologic phenomenon that leads to vascular dysfunction and the development of inflammatory thrombi.
- Patients with Buerger's disease have been identified to have a hypersensitivity against tobacco extracts that are injected intradermally.
- Evidence has demonstrated that upon exposure to tobacco there is an increased cellular response against collagen type I and III with increased levels of circulating anti-endothelial cell antibody.
- This increased cellular sensitivity leads to an impaired relaxation mechanism of the peripheral vessels.
- Cytokines are also thought to be produced in large quantities and may lead to the activation of inflammatory signals.
- The presence of elevated anti-cardiolipin antibodies is thought to be indicative of prognosis and severity.
- Rickettsial infection has been proposed to be involved in the pathogenesis of Buerger's disease.[13]
Genetics
- Genes that have been identified to be associated with tobacco hypersensitivity in patients with Buerger's disease include DRBl*0405, DQAl *03, DQBl*0401, DPBl*0501, HLA-A54, HLA-A9,and HLA-B54.[14]
Smoking
- Smoking tobacco is critical to the initiation, progression and recurrence of Buerger's disease. [4][5][6]
- It is not understood how smoking leads to the development of thromboangiitis, however, it has been hypothesized that chemical compounds within the tobacco smoke leads to a delayed hypersensitivity and may directly cause a toxic angiitis.
Gross Pathology
- On gross pathology, ischemia, cyanosis, rubor, ulceration, or dry or wet gangrene with or without autoamputation are characteristic findings of Buerger's disease.[11]
Microscopic Pathology
- On microscopic histopathological analysis, an occluding thrombus, microabscesses, leukocytes and giant cells are characteristic findings of Buerger's disease.[12]
References
- ↑ Lie JT (May 1990). "Diagnostic histopathology of major systemic and pulmonary vasculitic syndromes". Rheum. Dis. Clin. North Am. 16 (2): 269–92. PMID 1971725.
- ↑ Leu HJ (1975). "Early inflammatory changes in thromboangiitis obliterans". Pathol Microbiol (Basel). 43 (2-O): 151–6. PMID 1228574.
- ↑ Małecki R, Zdrojowy K, Adamiec R (October 2009). "Thromboangiitis obliterans in the 21st century--a new face of disease". Atherosclerosis. 206 (2): 328–34. doi:10.1016/j.atherosclerosis.2009.01.042. PMID 19269635.
- ↑ 4.0 4.1 Lie JT (1988). "Thromboangiitis obliterans (Buerger's disease) revisited". Pathol Annu. 23 Pt 2: 257–91. PMID 3060814.
- ↑ 5.0 5.1 Papa M, Bass A, Adar R, Halperin Z, Schneiderman J, Becker CG, Brautbar H, Mozes E (May 1992). "Autoimmune mechanisms in thromboangiitis obliterans (Buerger's disease): the role of tobacco antigen and the major histocompatibility complex". Surgery. 111 (5): 527–31. PMID 1598672.
- ↑ 6.0 6.1 Adar R, Papa MZ, Halpern Z, Mozes M, Shoshan S, Sofer B, Zinger H, Dayan M, Mozes E (May 1983). "Cellular sensitivity to collagen in thromboangiitis obliterans". N. Engl. J. Med. 308 (19): 1113–6. doi:10.1056/NEJM198305123081901. PMID 6835334.
- ↑ Lee T, Seo JW, Sumpio BE, Kim SJ (May 2003). "Immunobiologic analysis of arterial tissue in Buerger's disease". Eur J Vasc Endovasc Surg. 25 (5): 451–7. doi:10.1053/ejvs.2002.1869. PMID 12713785.
- ↑ Kobayashi M, Ito M, Nakagawa A, Nishikimi N, Nimura Y (March 1999). "Immunohistochemical analysis of arterial wall cellular infiltration in Buerger's disease (endarteritis obliterans)". J. Vasc. Surg. 29 (3): 451–8. PMID 10069909.
- ↑ Guzel E, Topal E, Yildirim A, Atilla P, Akkus M, Dagdeviren A (January 2010). "Targeting novel antigens in the arterial wall in thromboangiitis obliterans". Folia Histochem. Cytobiol. 48 (1): 134–41. doi:10.2478/v10042-008-0104-6. PMID 20529829.
- ↑ Edo N, Miyai K, Ogata S, Nakanishi K, Hiroi S, Tominaga S, Aiko S, Kawai T (2010). "Thromboangiitis obliterans with multiple large vessel involvement: case report and analysis of immunophenotypes". Cardiovasc. Pathol. 19 (1): 59–62. doi:10.1016/j.carpath.2008.10.004. PMID 19135391.
- ↑ 11.0 11.1 Eichhorn J, Sima D, Lindschau C, Turowski A, Schmidt H, Schneider W, Haller H, Luft FC (January 1998). "Antiendothelial cell antibodies in thromboangiitis obliterans". Am. J. Med. Sci. 315 (1): 17–23. PMID 9427570.
- ↑ 12.0 12.1 Hus I, Sokolowska B, Walter-Croneck A, Chrapko M, Nowaczynska A, Dmoszynska A (March 2013). "Assessment of plasma prothrombotic factors in patients with Buerger's disease". Blood Coagul. Fibrinolysis. 24 (2): 133–9. doi:10.1097/MBC.0b013e32835b7272. PMID 23358197.
- ↑ Fujii Y, Soga J, Nakamura S, Hidaka T, Hata T, Idei N, Fujimura N, Nishioka K, Chayama K, Kihara Y, Higashi Y (August 2010). "Classification of corkscrew collaterals in thromboangiitis obliterans (Buerger's disease): relationship between corkscrew type and prevalence of ischemic ulcers". Circ. J. 74 (8): 1684–8. PMID 20534945.
- ↑ Aerbajinai, Wulin; Tsuchiya, Terumasa; Kimura, Akinori; Yasukochi, Yukio; Numano, Fujio (1996). "HLA class II DNA typing in Buerger's disease". International Journal of Cardiology. 54: S167–S172. doi:10.1016/0167-5273(96)02681-2. ISSN 0167-5273.
- ↑ http://www.rayur.com/wp-content/uploads/2012/08/Buergers-Disease.jpg
- ↑ https://medical-dictionary.thefreedictionary.com/_/viewer.aspx?path=MosbyMD&name=thromboangiitis-obliterans.jpg&url=https%3A%2F%2Fmedical-dictionary.thefreedictionary.com%2Fthromboangiitis%2Bobliterans
