Temporal arteritis pathophysiology

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Temporal Arteritis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2]

Overview

Temporal arteritis is caused by transmural inflammation of elastic arteries. It is understood that temporal arteritis is the result of cell mediated immunity which arises as a response to endothelial injury and is antigen-driven disease with T-cell and macrophage activation in the elastic tissue in the arterial walls. The adventitia of the vessel is the initial site of immunologic injury. The activation of dendritic cells in the adventitia causes a production of chemokines that recruit CD4+ T helper cells. The CD4+ T helper cell convert in to Th17 cells which produce interleukin 17 and Th1 cells which produce interferon gamma. Giant cell are one of many inflammatory cells that are recruited and produce growth factor which narrows and obstructs the vessels. The concentric inflammation occurs in segments. Macrophages in the adventitia produce interleukin 6. While in the intima and media of the vessel, macrophages produce vascular endothelial growth factor (VEGF) and metalloproteinases which destroy the internal elastic lamina. An increased activated platelets express P-selectin which may cause vessel inflammation and thromboembolic events. Temporal arteritis arises from giant cells, which are fused monocytes cells that are normally involved in the body immune response. Because the disease involves only arteries with internal elastic lamina, the aortic arch and its branches are often involved. Intracranial arteries do not have internal elastic lamina and are not involved.

Pathophysiology

Pathogenesis

Commonly involved sites:[9][10][11][12]

  • External vertebral arteries: It is less common though for the disease to extend more than 5 mm beyond the dural penetration.

Less commonly involved sites:[11]

Genetics

Associated Conditions

Microscopic Pathology

Giant cell arteritis-low mag Source: Case courtesy of By Nephron [CC BY-SA 3.0, from Wikimedia Commons


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References

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  2. Pache M, Kaiser HJ, Haufschild T, Lübeck P, Flammer J (2002). "Increased endothelin-1 plasma levels in giant cell arteritis: a report on four patients". Am J Ophthalmol. 133 (1): 160–2. PMID 11755863.
  3. Patel SJ, Lundy DC (2002). "Ocular manifestations of autoimmune disease". Am Fam Physician. 66 (6): 991–8. PMID 12358224.
  4. 4.0 4.1 Wang AL, Raven ML, Surapaneni K, Albert DM (2017). "Studies on the Histopathology of Temporal Arteritis". Ocul Oncol Pathol. 3 (1): 60–65. doi:10.1159/000449466. PMC 5318845. PMID 28275606.
  5. Samson, Maxime; Corbera-Bellalta, Marc; Audia, Sylvain; Planas-Rigol, Ester; Martin, Laurent; Cid, Maria Cinta; Bonnotte, Bernard (2017). "Recent advances in our understanding of giant cell arteritis pathogenesis". Autoimmunity Reviews. 16 (8): 833–844. doi:10.1016/j.autrev.2017.05.014. ISSN 1568-9972.
  6. 6.0 6.1 Eberhardt RT, Dhadly M (2007). "Giant cell arteritis: diagnosis, management, and cardiovascular implications". Cardiol Rev. 15 (2): 55–61. doi:10.1097/01.crd.0000218853.05856.b6. PMID 17303991.
  7. Diaz, Vicente A.; DeBroff, Brian M.; Sinard, John (2005). "Comparison of Histopathologic Features, Clinical Symptoms, and Erythrocyte Sedimentation Rates in Biopsy-Positive Temporal Arteritis". Ophthalmology. 112 (7): 1293–1298. doi:10.1016/j.ophtha.2005.02.016. ISSN 0161-6420.
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  9. Waldman, Corey W.; Waldman, Steven D.; Waldman, Reid A. (2013). "Giant Cell Arteritis". Medical Clinics of North America. 97 (2): 329–335. doi:10.1016/j.mcna.2012.12.006. ISSN 0025-7125.
  10. Pineles, Stacy L.; Arnold, Anthony C. (2007). "Giant Cell Arteritis". International Ophthalmology Clinics. 47 (4): 105–119. doi:10.1097/IIO.0b013e318157fb08. ISSN 0020-8167.
  11. 11.0 11.1 Liozon, E.; Ly, K.-H.; Robert, P.-Y. (2013). "Manifestations ophtalmologiques de la maladie de Horton". La Revue de Médecine Interne. 34 (7): 421–430. doi:10.1016/j.revmed.2013.02.030. ISSN 0248-8663.
  12. Wilkinson IM, Russell RW (1972). "Arteries of the head and neck in giant cell arteritis. A pathological study to show the pattern of arterial involvement". Arch Neurol. 27 (5): 378–91. PMID 5078894.
  13. Liozon E, Ouattara B, Rhaiem K, Ly K, Bezanahary H, Loustaud V; et al. (2009). "Familial aggregation in giant cell arteritis and polymyalgia rheumatica: a comprehensive literature review including 4 new families". Clin Exp Rheumatol. 27 (1 Suppl 52): S89–94. PMID 19646354.
  14. Palomino-Morales R, Torres O, Vazquez-Rodriguez TR, Morado IC, Castañeda S, Callejas-Rubio JL; et al. (2009). "Association between toll-like receptor 4 gene polymorphism and biopsy-proven giant cell arteritis". J Rheumatol. 36 (7): 1501–6. doi:10.3899/jrheum.081286. PMID 19531762.
  15. Caylor TL, Perkins A (2013). "Recognition and management of polymyalgia rheumatica and giant cell arteritis". Am Fam Physician. 88 (10): 676–84. PMID 24364483.
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  19. Gilden, Don; Nagel, Maria (2015). "Varicella Zoster Virus in Temporal Arteries of Patients With Giant Cell Arteritis". Journal of Infectious Diseases. 212 (suppl 1): S37–S39. doi:10.1093/infdis/jiu542. ISSN 0022-1899.
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