Temporal arteritis pathophysiology: Difference between revisions

Jump to navigation Jump to search
Line 9: Line 9:
===Pathogenesis===
===Pathogenesis===
*Temporal arteritis is the result of [[Cell-mediated immunity|cell mediated immunity]] which arises as a response to [[Endothelium|endothelial]] injury and is an antigen-driven disease with local [[T cell|T-cell]] and [[macrophage]] activation in the [[Elastic artery|elastic]] tissue of [[Artery|arterial]] walls with an important role of the [[Inflammation|proinflammatory]] [[Cytokine|cytokines]].<ref name="SalvaraniPipitone2007">{{cite journal|last1=Salvarani|first1=C.|last2=Pipitone|first2=N.|last3=Boiardi|first3=L.|last4=Hunder|first4=G. G|title=Do we need treatment with tumour necrosis factor blockers for giant cell arteritis?|journal=Annals of the Rheumatic Diseases|volume=67|issue=5|year=2007|pages=577–579|issn=0003-4967|doi=10.1136/ard.2007.086330}}</ref><ref name="pmid11755863">{{cite journal| author=Pache M, Kaiser HJ, Haufschild T, Lübeck P, Flammer J| title=Increased endothelin-1 plasma levels in giant cell arteritis: a report on four patients. | journal=Am J Ophthalmol | year= 2002 | volume= 133 | issue= 1 | pages= 160-2 | pmid=11755863 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11755863  }} </ref><ref name="pmid12358224">{{cite journal| author=Patel SJ, Lundy DC| title=Ocular manifestations of autoimmune disease. | journal=Am Fam Physician | year= 2002 | volume= 66 | issue= 6 | pages= 991-8 | pmid=12358224 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12358224  }} </ref>
*Temporal arteritis is the result of [[Cell-mediated immunity|cell mediated immunity]] which arises as a response to [[Endothelium|endothelial]] injury and is an antigen-driven disease with local [[T cell|T-cell]] and [[macrophage]] activation in the [[Elastic artery|elastic]] tissue of [[Artery|arterial]] walls with an important role of the [[Inflammation|proinflammatory]] [[Cytokine|cytokines]].<ref name="SalvaraniPipitone2007">{{cite journal|last1=Salvarani|first1=C.|last2=Pipitone|first2=N.|last3=Boiardi|first3=L.|last4=Hunder|first4=G. G|title=Do we need treatment with tumour necrosis factor blockers for giant cell arteritis?|journal=Annals of the Rheumatic Diseases|volume=67|issue=5|year=2007|pages=577–579|issn=0003-4967|doi=10.1136/ard.2007.086330}}</ref><ref name="pmid11755863">{{cite journal| author=Pache M, Kaiser HJ, Haufschild T, Lübeck P, Flammer J| title=Increased endothelin-1 plasma levels in giant cell arteritis: a report on four patients. | journal=Am J Ophthalmol | year= 2002 | volume= 133 | issue= 1 | pages= 160-2 | pmid=11755863 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11755863  }} </ref><ref name="pmid12358224">{{cite journal| author=Patel SJ, Lundy DC| title=Ocular manifestations of autoimmune disease. | journal=Am Fam Physician | year= 2002 | volume= 66 | issue= 6 | pages= 991-8 | pmid=12358224 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12358224  }} </ref>
*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.
*The [[adventitia]] of the [[Blood vessel|vessel]] is the initial site of [[Immunology|immunologic]] injury. The activation of [[Dendritic cell|dendritic cells]] in the [[adventitia]] causes a production of [[Chemokine|chemokines]] that recruit [[CD4]]+ [[T helper cell|T helper cells]]. The [[CD4|CD4+]] [[T helper cell]] convert in to [[T helper 17 cell|Th17]] cells which produce [[interleukin 17]] and [[T helper cell|Th1]] cells which produce [[Interferon gamma|interferon gamma.]]
*Giant cell are one of many inflammatory cells that are recruited and produce growth factor which narrows and obstructs the vessels.<ref name="SamsonCorbera-Bellalta2017">{{cite journal|last1=Samson|first1=Maxime|last2=Corbera-Bellalta|first2=Marc|last3=Audia|first3=Sylvain|last4=Planas-Rigol|first4=Ester|last5=Martin|first5=Laurent|last6=Cid|first6=Maria Cinta|last7=Bonnotte|first7=Bernard|title=Recent advances in our understanding of giant cell arteritis pathogenesis|journal=Autoimmunity Reviews|volume=16|issue=8|year=2017|pages=833–844|issn=15689972|doi=10.1016/j.autrev.2017.05.014}}</ref><ref name="pmid17303991">{{cite journal| author=Eberhardt RT, Dhadly M| title=Giant cell arteritis: diagnosis, management, and cardiovascular implications. | journal=Cardiol Rev | year= 2007 | volume= 15 | issue= 2 | pages= 55-61 | pmid=17303991 | doi=10.1097/01.crd.0000218853.05856.b6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17303991  }} </ref>
*[[Large cell|Giant cell]] are one of many [[Inflammation|inflammatory]] cells that are recruited and produce [[growth factor]] which narrows and obstructs the [[Blood vessel|vessels]].<ref name="SamsonCorbera-Bellalta2017">{{cite journal|last1=Samson|first1=Maxime|last2=Corbera-Bellalta|first2=Marc|last3=Audia|first3=Sylvain|last4=Planas-Rigol|first4=Ester|last5=Martin|first5=Laurent|last6=Cid|first6=Maria Cinta|last7=Bonnotte|first7=Bernard|title=Recent advances in our understanding of giant cell arteritis pathogenesis|journal=Autoimmunity Reviews|volume=16|issue=8|year=2017|pages=833–844|issn=15689972|doi=10.1016/j.autrev.2017.05.014}}</ref><ref name="pmid17303991">{{cite journal| author=Eberhardt RT, Dhadly M| title=Giant cell arteritis: diagnosis, management, and cardiovascular implications. | journal=Cardiol Rev | year= 2007 | volume= 15 | issue= 2 | pages= 55-61 | pmid=17303991 | doi=10.1097/01.crd.0000218853.05856.b6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17303991  }} </ref>
*The concentric inflammation occurs in segments.<ref name="DiazDeBroff2005">{{cite journal|last1=Diaz|first1=Vicente A.|last2=DeBroff|first2=Brian M.|last3=Sinard|first3=John|title=Comparison of Histopathologic Features, Clinical Symptoms, and Erythrocyte Sedimentation Rates in Biopsy-Positive Temporal Arteritis|journal=Ophthalmology|volume=112|issue=7|year=2005|pages=1293–1298|issn=01616420|doi=10.1016/j.ophtha.2005.02.016}}</ref>
*The concentric [[inflammation]] occurs in segments.<ref name="DiazDeBroff2005">{{cite journal|last1=Diaz|first1=Vicente A.|last2=DeBroff|first2=Brian M.|last3=Sinard|first3=John|title=Comparison of Histopathologic Features, Clinical Symptoms, and Erythrocyte Sedimentation Rates in Biopsy-Positive Temporal Arteritis|journal=Ophthalmology|volume=112|issue=7|year=2005|pages=1293–1298|issn=01616420|doi=10.1016/j.ophtha.2005.02.016}}</ref>
*Macrophages in the adventia 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.<ref name="pmid17303991">{{cite journal| author=Eberhardt RT, Dhadly M| title=Giant cell arteritis: diagnosis, management, and cardiovascular implications. | journal=Cardiol Rev | year= 2007 | volume= 15 | issue= 2 | pages= 55-61 | pmid=17303991 | doi=10.1097/01.crd.0000218853.05856.b6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17303991  }} </ref>
*[[Macrophage|Macrophages]] in the [[adventitia]] produce [[interleukin 6]]. While in the [[Tunica intima|intima]] and media of the [[Blood vessel|vessel]], [[Macrophage|macrophages]] produce [[Vascular endothelial growth factor|vascular endothelial growth factor (VEGF)]] and [[Metalloproteinase|metalloproteinases]] which destroy the [[internal elastic lamina]].<ref name="pmid17303991">{{cite journal| author=Eberhardt RT, Dhadly M| title=Giant cell arteritis: diagnosis, management, and cardiovascular implications. | journal=Cardiol Rev | year= 2007 | volume= 15 | issue= 2 | pages= 55-61 | pmid=17303991 | doi=10.1097/01.crd.0000218853.05856.b6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17303991  }} </ref>
*An increased activated platelets express P-selectin which may cause vessel inflammation and thromboembolic events.<ref name="pmid1634709">{{cite journal| author=Goodwin JS| title=Progress in gerontology: polymyalgia rheumatica and temporal arteritis. | journal=J Am Geriatr Soc | year= 1992 | volume= 40 | issue= 5 | pages= 515-25 | pmid=1634709 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1634709  }} </ref>
*An increased activated platelets express P-selectin which may cause vessel inflammation and thromboembolic events.<ref name="pmid1634709">{{cite journal| author=Goodwin JS| title=Progress in gerontology: polymyalgia rheumatica and temporal arteritis. | journal=J Am Geriatr Soc | year= 1992 | volume= 40 | issue= 5 | pages= 515-25 | pmid=1634709 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1634709  }} </ref>
*Temporal arteritis arises from giant cells, which are fused monocytes cells that are normally involved in the body immune response.
*Temporal arteritis arises from giant cells, which are fused monocytes cells that are normally involved in the body immune response.

Revision as of 22:35, 10 April 2018

Temporal Arteritis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Temporal Arteritis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography or Ultrasound

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Temporal arteritis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Temporal arteritis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Temporal arteritis pathophysiology

CDC on Temporal arteritis pathophysiology

Temporal arteritis pathophysiology in the news

Blogs on Temporal arteritis pathophysiology

Directions to Hospitals Treating Temporal arteritis

Risk calculators and risk factors for Temporal arteritis pathophysiology

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

  • 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. The distribution of involved arteries are as follows:

Commonly involved sites:[8][9][10][11]

  • 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:[10]

Genetics

  • Temporal artertis has an association with the HLA-DR4 haplotype.[12]
  • An association between Toll-like receptor 4 gene polymorphism and biopsy-proven GCA has been found.[13]

Associated Conditions

Gross Pathology

  • On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

  • On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

References

  1. Salvarani, C.; Pipitone, N.; Boiardi, L.; Hunder, G. G (2007). "Do we need treatment with tumour necrosis factor blockers for giant cell arteritis?". Annals of the Rheumatic Diseases. 67 (5): 577–579. doi:10.1136/ard.2007.086330. ISSN 0003-4967.
  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. 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.
  5. 5.0 5.1 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.
  6. 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.
  7. Goodwin JS (1992). "Progress in gerontology: polymyalgia rheumatica and temporal arteritis". J Am Geriatr Soc. 40 (5): 515–25. PMID 1634709.
  8. 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.
  9. 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.
  10. 10.0 10.1 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.
  11. 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.
  12. 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.
  13. 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.
  14. Caylor TL, Perkins A (2013). "Recognition and management of polymyalgia rheumatica and giant cell arteritis". Am Fam Physician. 88 (10): 676–84. PMID 24364483.
  15. Salvarani, Carlo; Cantini, Fabrizio; Hunder, Gene G (2008). "Polymyalgia rheumatica and giant-cell arteritis". The Lancet. 372 (9634): 234–245. doi:10.1016/S0140-6736(08)61077-6. ISSN 0140-6736.
  16. Alvarez-Lafuente, R (2005). "Human parvovirus B19, varicella zoster virus, and human herpes virus 6 in temporal artery biopsy specimens of patients with giant cell arteritis: analysis with quantitative real time polymerase chain reaction". Annals of the Rheumatic Diseases. 64 (5): 780–782. doi:10.1136/ard.2004.025320. ISSN 0003-4967.
  17. Russo MG, Waxman J, Abdoh AA, Serebro LH (1995). "Correlation between infection and the onset of the giant cell (temporal) arteritis syndrome. A trigger mechanism?". Arthritis Rheum. 38 (3): 374–80. PMID 7880192.
  18. 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.

Template:WikiDoc Sources