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Not to be confused with arthritis.
Classification and external resources
ICD-10 I77.6, M31
ICD-9 447.6
DiseasesDB 13750
MeSH D001167

Arteritis is the inflammation of the walls of arteries,[1] usually as a result of infection or auto-immune response. Arteritis is a complex disorder that is still not completely understood in entirety.[2] Arteritis may be distinguished by its different types, based on the organ systems that are affected by the disease.[2] A complication of arteritis is thrombosis which can be fatal.


Arteritis may be primary, or secondary some other disease process. The primary types are given in the table below:.

Comparison of major types of arteritis
Arteritis Affected organs Histopathology
Takayasu's arteritis Large vessels,[3] including Aorta and arch branches[4] Histiocytes, giant cells[4]
Giant cell arteritis, also often called temporal arteritis (although these differ slightly) superficial temporal artery, other medium- and large-sized vessels,[5] e.g. the ones supplying the head, eyes and optic nerves Lymphocytes, macrophages, and multinucleated giant cells[5]
Polyarteritis nodosa CNS, PNS damage, kidneys, GI tract, skeletal muscle, heart[4] Neutrophils, fibrinoid necrosis[4]

An example of a secondary arteritis is arteritis caused by the fungal pathogen Candida albicans.[6]

Giant Cell Arteritis

Giant cell arteritis contain two different types of artertides that are almost scientifically indistinguishable from one another.[2] Giant cell arteritis includes two types, these are Temporal arteritis and Takayasu’s arteritis. Both of these types contain an occupancy of medium and larger size arteries which are categorized based on the infiltration of the giant cells.[2]

Takayasu Arteritis

This type of arteritis is found to be most common in females with a median age of 25 years.[7] Takayasu arteritis is also most common in women of Asian descent that are in their reproductive years.[7] However, over the past decades, Takayasu arteritis patients are increasing in Africa, Europe, and North America.[7] Takayasu’s arteritis is an inflammatory disease that mainly affects the larger vessels such as the aorta and its surrounding branches.[7] Research of Takayasu arteritis in the Western parts of the world still remain limited. An estimation suggests that each year, the rate of cases in a million people is 2.6.[8]

Temporal Arteritis

Temporal Arteritis, the second type of giant cell arteritis, is also a chronic, inflammatory disease that involves the middle to larger sized arteries.[9] Most commonly, Temporal Arteritis incidents were found in Scandinavian descents, this includes Scandinavian Americans as well.[9] However, the incidence rate differs based on population, region and races.[9] Temporal Arteritis is not uncommon in North America either.[9] The incidence rate is around 0.017% for individuals over 50 years of age.[9]

Symptoms of temporal arteritis are classified as specific and nonspecific .[9]

Non specific symptoms:[9]

  • Headache
  • Low grade fever
  • Sweating
  • Anorexia
  • Weight loss
  • General malaise

Specific symptoms:[9]

  • Claudication of the jaw
  • Engorged tender vessels

Specific symptoms are usually are developed in the advanced stages of Temporal artieritis.[9]


Symptoms of general arteritis may include:[3]

  • inflammation
  • fever
  • increased production of red blood cells (erythrocyte)
  • limping
  • reduced pulse


Diagnosis of Arteritis is based on unusual medical symptoms.[10] At this time, conditions should be distinguished between similar symptoms such as, Ehlers-Danlos and Marfan syndrome, tuberculosis, syphilis, spondyloarthopathies, Cogans’s syndrome, Buerger’s, Behcet’s, and Kawasaki disease.[10] There are several diagnoses approaches that can be used. For example, imaging techniques such as angiography, computer tomography angiography (CTA), magnetic resonance angiography (MRA), and ultrasonography, are being used not only for the diagnosis of arteritis, but additionally to help monitor the disease.[10]


Angiography is commonly used for the diagnosis of Takayasu’s arteritis.[10] Especially in the advanced stages when artery stenosis, occlusion, aneurysm formation occurs, and so forth.[10] However, angiography is an aggressive examination, where patients receive large doses of radition.[10] Therefore, it is not recommended for long term patients of Takayasu arteritis.[10]


CTA can determine the lumen of aorta and the surrounding branches, and identify vessel wall lesions in middle to advanced stages of arteritis.[10] CTA diagnosis can also display the intravascular blood flow.[10] Similar to angiography, CTA also requires patients to take high dosages of radiation.[10]


MRA is used to diagnose early stages of Takayasu’s arteritis, such as the thickening of the vessel wall.[10] MRA also includes clear pictures of how thick the vessel wall is becoming.[10] Disadvantages of MRA are that it is a very expensive procedure, and may produce poor images for distal branches and aortic calcification.[10]


Ultrasonography is an ideal method of diagnosing patients in early stages of arteritis when there is inflammation in the vessel walls.[10] This method also shows the blood flow that occurs in the vessel.[10] Ultrasonography has become an ideal method for diagnosis because it is non- invasive.[10] It is also commonly used for long term monitoring in Takayasu’s arteritis. Disadvantages of this method are its difficulties to identify some vascular lesions, and also, the operative’s skill affects the reliability of the results.[10]

Treatment Methods[edit]


Those suffering from arteritis are first treated with an oral glucocorticoid, such as prednisone, daily for a period of three months.[3] After three months, treatment will be administered every other day, if possible.[3] If the disease worsens with the new treatment schedule, a cytotoxic agent will be given, in addition to glucorticoids.[3] The cytotoxic agents used most commonly are azathioprine, methotrexate, or cyclophosphamide.[3] If the patient begins to recover, the dosage of glucorticoids is decreased.[3] When disease becomes inactive in the patient, the dosage of drugs will be further reduced, tapered to cessation.[3] Conversely, if the disease is still active, the dosage of drugs will be increased.[3] After six months, if the drugs cannot be reduced to a consumption of every other day, or, in twelve months, the drugs cannot be stopped completely, then the treatment is deemed to be a failure.[3]


Pulse therapy is done with a high dose of corticosteroid, often methylprednisolone, and this method has proven to be successful for some patients.[11] Immunosuppressive pulse therapy, such as with cyclophosphamide, has also demonstrated relief of symptoms associated with arteritis.[12]


  1. ^ "Arteritis" at Dorland's Medical Dictionary
  2. ^ a b c d Hollier, L. H. (1 January 1989). "Arteritis". Perspectives in Vascular Surgery and Endovascular Therapy 2 (1): 1–8. doi:10.1177/153100358900200101. 
  3. ^ a b c d e f g h i j Gail S. Kerr, Claire W. Hallahan, Joseph Giordano, Randi Y. Leavitt, Anthony S. Fauci, Menachem Rottem, Gary S. Hoffman; Takayasu Arteritis. Annals of Internal Medicine. 1994 Jun;120(11):919-929.
  4. ^ a b c d Stevens & Lowe: Pathology. At
  5. ^ a b eMedicine Specialties > Temporal Arteritis Author: Christopher H Lee, MD. Coauthor(s): Jean Marie Hammel, MD. Updated: Sep 8, 2009
  6. ^ Nagi-Miura N, Harada T, Shinohara H et al. (Jun 2006). "Lethal and severe coronary arteritis in DBA/2 mice induced by fungal pathogen, CAWS, Candida albicans water-soluble fraction". Atherosclerosis 186 (2): 310–20. doi:10.1016/j.atherosclerosis.2005.08.014. PMID 16157343.  |first10= missing |last10= in Authors list (help); |first11= missing |last11= in Authors list (help)
  7. ^ a b c d Kerr, Gail S.; Claire W. Hallahan; Joseph Giordano; Randi Y. Leavitt; Anthony S. Fauci; Menachem Rottem; Gary S. Hoffman (June 1994). "Takayasu Arteritis. Annals of Internal Medicine" 120 (11). pp. 919–929. 
  8. ^ Kerr, Gail S; Claire W. Hallahan; Joseph Giordano; Randi Y. Leavitt; Anthony S. Fauci; Menachem Rottem; Gary S. Hoffman (June 1994). "Takayasu Arteritis. Annals of Internal Medicine" 120 (11). pp. 919–929. 
  9. ^ a b c d e f g h i Chen, Chun-Hsiung; Kung, Shih-Ya; Tsai, Ying-Yang; Liao, Hsien-Tzung; Chou, Chung-Tei; Huang, De-Feng (2005). "Temporal Arteritis". Journal of the Chinese Medical Association 68 (7): 333–335. doi:10.1016/S1726-4901(09)70170-4. PMID 16038374. 
  10. ^ a b c d e f g h i j k l m n o p q Wen, Dan; Du, Xin; Ma, Chang-Sheng (1 December 2012). "Takayasu Arteritis: Diagnosis, Treatment and Prognosis". International Reviews of Immunology 31 (6): 462–473. doi:10.3109/08830185.2012.740105. PMID 23215768. 
  11. ^ Chevalet, P; Barrier, J. H.; Pottier, P; Magadur-Joly, G; Pottier, M. A.; Hamidou, M; Planchon, B; El Kouri, D; Connan, L; Dupond, J. L.; De Wazieres, B; Dien, G; Duhamel, E; Grosbois, B; Jego, P; Le Strat, A; Capdeville, J; Letellier, P; Agron, L (2000). "A randomized, multicenter, controlled trial using intravenous pulses of methylprednisolone in the initial treatment of simple forms of giant cell arteritis: A one year followup study of 164 patients". The Journal of rheumatology 27 (6): 1484–91. PMID 10852275.  edit
  12. ^ Bose, P. (29 November 2012). "TAKAYASU'S ARTERITIS". Journal of Neurology, Neurosurgery & Psychiatry 83 (Suppl 2): A1–A1. doi:10.1136/jnnp-2012-304200a.2.