Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Takayasu Arteritis

  • Author: Jefferson R Roberts, MD; Chief Editor: Herbert S Diamond, MD  more...
 
Updated: Apr 13, 2016
 

Background

Takayasu arteritis is a rare, systemic, inflammatory large-vessel vasculitis of unknown etiology that most commonly affects women of childbearing age. It is defined as "granulomatous inflammation of the aorta and its major branches" by the Chapel Hill Consensus Conference on the Nomenclature of Systemic Vasculitis.[1] See the image below. (See Etiology and Epidemiology.)

Complete occlusion of the left common carotid arte Complete occlusion of the left common carotid artery in a 48-year-old woman with Takayasu disease. Also note narrowing of the origin of the right subclavian artery and a narrowed small vessel with subsequent aneurysmal dilatation on the right side. Image courtesy of Robert Cirillo, MD.

Takayasu arteritis commonly occurs in woman younger than age 50 years; however, it has been reported in patients as young as age 6 months (see Pediatric Takayasu Arteritis). Takayasu arteritis can manifest as isolated, atypical, and/or catastrophic disease. It can involve any or all of the major organ systems. The disease has been reported in all parts of the world, although it appears to be more prevalent in Asians. (See Epidemiology.)

Angiography-based categories

Takayasu arteritis can be divided into the following six types based on angiographic involvement (see Workup)[2] :

  • Type I - Branches of the aortic arch
  • Type IIa - Ascending aorta, aortic arch, and its branches
  • Type IIb - Type IIa region plus thoracic descending aorta
  • Type III - Thoracic descending aorta, abdominal aorta, renal arteries, or a combination
  • Type IV - Abdominal aorta, renal arteries, or both
  • Type V - Entire aorta and its branches

Patient education

Patients need to understand the nature of the disease and the need to take medications to prevent complications. When in remission or when experiencing mild forms of Takayasu arteritis, patients are tempted to stop antihypertensive drugs, thus increasing their risk of serious neurologic and other systemic complications. (See Treatment and Medication.)

Next

Pathophysiology

Takayasu arteritis is an inflammatory disease of large- and medium-sized arteries, with a predilection for the aorta and its branches. Advanced lesions demonstrate a panarteritis with intimal proliferation.

Lesions produced by the inflammatory process can be stenotic, occlusive, or aneurysmal. All aneurysmal lesions may have areas of arterial narrowing. Vascular changes lead to the main complications, including hypertension, most often due to renal artery stenosis or, more rarely, stenosis of the suprarenal aorta; aortic insufficiency due to aortic valve involvement; pulmonary hypertension; and aortic or arterial aneurysm.

Congestive heart failure is a common finding, much more so than dilated cardiomyopathy, myocarditis, and pericarditis, which also have been reported. In patients in whom the pulmonary artery is involved, the right artery appears to be affected more than the left, with patients developing pneumonia, interstitial pulmonary fibrosis, and alveolar damage.

Other pathophysiologic consequences include hypotensive ischemic retinopathy, vertebrobasilar ischemia, microaneurysms, carotid stenosis, hypertensive encephalopathy, and inflammatory bowel disease. Rarely, Takayasu arteritis has also been associated with glomerulonephritis, systemic lupus, polymyositis, polymyalgia rheumatica, rheumatoid arthritis, Still disease, and ankylosing spondylitis.

Previous
Next

Etiology

The etiology of Takayasu arteritis is unknown. The underlying pathologic process is inflammatory, with several etiologic factors having been proposed, including infection with spirochetes, Mycobacterium tuberculosis, and streptococcal organisms, and circulating antibodies due to an autoimmune process. Genetic factors may play a role in the pathogenesis.

An antigen may stimulate aortic tissue, leading to the expression of heat shock protein–65, which, in turn, induces major histocompatibility (MHC) class I–related chain A (MICA). Natural killer cells and gamma-delta T cells expressing NKG2D receptors may infiltrate and recognize MICA on vascular smooth muscle cells, leading to acute inflammation. Proinflammatory cytokines are also released from the natural killer and T-cells, inducing the production of matrix metalloproteinases (MMPs) and amplifying the inflammatory response. This, in turn, would induce more MHC antigen and stimulate molecule expression on vascular cells, recruiting more mononuclear cells.

Histocompatibility complexes are activated through Toll-like receptors. Th1 lymphocytes, through interferon-gamma, activate macrophages, which, in turn, release vascular endothelial growth factor (VEGF). This ultimately results in smooth muscle migration and intimal proliferation. Th17 cells induced by the interleukin (IL)–23 microenvironment also contribute to vascular lesions through activation of infiltrating neutrophils.

Previous studies have shown that the cellular infiltrate in Takayasu arteritis contains about 15% each of CD4+ and CD8+ T cells. IL-6 is a proinflammatory cytokine mainly synthesized by activated monocytes, macrophages, and T cells. IL-6 activates B cells and enhances T-cell cytotoxicity, natural killer cell activity, fibroblast proliferation, and acute-phase protein synthesis. Amplification of proinflammatory cytokine genes from aortic tissue reveals strong expression of IL-6 transcripts.[3]

In a case report, M tuberculosis and its 65-kd heat shock protein was implicated in the etiology. Patients with Takayasu arteritis were found to have higher immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) titers against the M tuberculosis extract than did patients without the condition.[4]

One article reported the presence of CD3+ T cells and IgG antibodies reactive to circulating antimycobacterial heat shock protein 65 (mHSP65) antibodies and to its human homologue, hHSP60.[5] This suggests a possible cross-reactivity of immune response between mHSP65 and hHSP60. Case reports suggesting the role of antiendothelial cell, anticardiolipin, and antiaorta antibodies also exist.

In Japanese patients, human leukocyte antigen Bw52 (HLA-Bw52), which is in linkage disequilibrium with human leukocyte antigen DR4 (HLA-DR4), has been observed with increased frequency. Patients with the Bw52 genotype had a higher rate of aortic regurgitation. However, studies of HLA antigens in North American populations have not confirmed this.

A study comparing HLA-B alleles in Mexican patients with Takayasu arteritis and tuberculosis showed distinct, specific alleles. Takayasu arteritis was characterized by HLA-B39, -B44 and -B52; pulmonary tuberculosis, by HLA-B35; and extrapulmonary tuberculosis, by HLS-B39 and -B40.[6] Takayasu arteritis is associated with HLA-B22 in the United States.

One study demonstrated an association between several cases of Takayasu arteritis and CD36 deficiency (CD36d).[7] The human CD36 antigen is a multifunctional membrane glycoprotein that belongs to the class B scavenger receptor family. It is expressed on monocytes, platelets, and endothelial cells, and contributes to myocardial fatty acid transport. In patients with CD36d, myocardial I-15-(p-iodophenyl)-3-(R,S)-methyl pentadecanoic acid (BMIPP) uptake was absent.

Previous
Next

Epidemiology

Occurrence in the United States

Takayasu arteritis is estimated to affect 2.6 persons per million annually. The prevalence is 2.6-6.4 persons per million population. Any discrepancy in terms of pinpointing the prevalence is attributed to genetic factors and difficulty in diagnosis.

Between 1971 and 1983 in Olmsted County, Minnesota, three cases were recorded, thus establishing an annual incidence of 2.6 cases per million population.[8]

International occurrence

Worldwide incidence of Takayasu arteritis is estimated at 2.6 cases per million per year. Although the disease has a worldwide distribution, it is observed more frequently in Asian countries such as Japan, Korea, China, India, Thailand, and Singapore, as well as in Turkey, Israel, and Central and South America. About 100-200 new cases of Takayasu arteritis are registered each year in Japan.[9]

The prevalence of the disease in Sweden is similar to that in the United States (ie, 2.6-6.4 persons per million population). In the United Kingdom, the annual incidence is 0.15 case per million.

Race-, sex-, and age-related demographics

Takayasu arteritis is observed more frequently in patients of Asian or Indian descent. Japanese patients with Takayasu arteritis have a higher incidence of aortic arch involvement. In contrast, series from India report higher incidences of abdominal involvement.[9, 10]

Approximately 80% of patients with Takayasu arteritis are women; however, the high female-to-male ratio seems to decrease west of Japan. In India, the female-to-male ratio is as low as 1.6:1.[9]

Most patients with Takayasu arteritis are aged 4-63 years, with the mean age of onset being approximately 30 years. Fewer than 15% of cases present in individuals older than 40 years.

Previous
Next

Prognosis

Takayasu arteritis is associated with substantial morbidity and may be life-threatening. Its course usually extends for many years, with varying degrees of activity. Approximately 20% of patients have a monophasic and self-limited disease. In others, Takayasu arteritis is progressive or relapsing/remitting and requires immunosuppressive treatment.[11, 12, 13]

A National Institutes of Health study of 60 patients with Takayasu arteritis showed that 20% of patients had a monophasic illness, self-limiting illness and therefore did not require immunosuppressive treatment. In the remaining 80% of patients, who did not have a monophasic illness and who experienced a single exacerbation, immunosuppressive therapy resulted in remission in 60%. Of these, one half experienced relapse after immunosuppressive therapy was stopped.

Complications

The overall morbidity in Takayasu arteritis depends on the severity of the lesions and their consequences. Complications of the disease include the following:

  • Stroke
  • Intracranial hemorrhage
  • Seizures
  • Graft stenosis and/or occlusion
  • Ischemia
  • Organ failure
  • Complications of hypertension
  • Fetal injury
  • Valvular heart disease
  • Retinopathy
  • Renovascular hypertension

Long-term use of corticosteroids can lead to infection, adrenal suppression, cataracts, hyperglycemia, hypertension (which complicates blood pressure control), osteoporosis, and aseptic necrosis.

Morbidity and mortality

Takayasu arteritis is a chronic relapsing and remitting disorder. The overall 10-year survival rate is approximately 90%; however, this rate is reduced in the presence of major complications.[11]

The 5- and 10-year survival rates are approximately 69% and 36%, respectively, in patients with 2 or more complications. The 5- and 10-year survival rates associated with 1 or fewer complications are 100% and 96%, respectively.[14]

Strict management of traditional cardiovascular risk factors such as dyslipidemia, hypertension, and lifestyle factors that increase the risk of cardiovascular disease is mandatory to minimize secondary cardiovascular complications. These complications are the major cause of death in Takayasu arteritis.

A 2008 study assessing quality of life with Takayasu arteritis showed worse scores for physical and mental health compared with many other chronic diseases associated with peripheral vascular disease. Disease remission is the only factor that positively influences physical and mental quality of life.[15] Patients with rheumatoid arthritis or ankylosing spondylitis rated their quality of life as similar to those with Takayasu arteritis.[16]

Previous
 
 
Contributor Information and Disclosures
Author

Jefferson R Roberts, MD Chief of Rheumatology Service, Tripler Army Medical Center; Assistant Clinical Professor of Medicine, Uniformed Services University of the Health Sciences

Jefferson R Roberts, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, Society for Simulation in Healthcare

Disclosure: Nothing to disclose.

Coauthor(s)

Rodger Stitt, MD Department of Internal Medicine, Tripler Army Medical Center, Honolulu

Rodger Stitt, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

 

Disclosure: Nothing to disclose.

Phalgoon A Shah, MD Resident Physician, Department of Medicine, Tripler Army Medical Center

Phalgoon A Shah, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Gabriel Bucurescu, MD, MS Staff Neurologist, Neurology Service, Philadelphia Veterans Affairs Medical Center

Gabriel Bucurescu, MD, MS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Nothing to disclose.

Robert E Wolf, MD, PhD Professor Emeritus, Department of Medicine, Louisiana State University School of Medicine in Shreveport; Chief, Rheumatology Section, Medical Service, Overton Brooks Veterans Affairs Medical Center

Robert E Wolf, MD, PhD is a member of the following medical societies: American College of Rheumatology, Arthritis Foundation, Society for Leukocyte Biology

Disclosure: Nothing to disclose.

Mohammed Mubashir Ahmed, MD Associate Professor, Department of Medicine, Division of Rheumatology, University of Toledo College of Medicine

Mohammed Mubashir Ahmed, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, American Federation for Medical Research

Disclosure: Nothing to disclose.

Acknowledgements

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

B Mark Keegan, MD, FRCPC Assistant Professor of Neurology, College of Medicine, Mayo Clinic; Master's Faculty, Mayo Graduate School; Consultant, Department of Neurology, Mayo Clinic, Rochester

B Mark Keegan, MD, FRCPC is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Minnesota Medical Association

Disclosure: Novartis Consulting fee Consulting

Sydney Louis, MBBCh, MD Emeritus Professor, Department of Neurology, The Warren Alpert Medical School of Brown University

Sydney Louis, MBBCh, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Michael G Rossman, MD, LTC, MC, FS Fellow, Department of Rheumatology, Walter Reed Army Medical Center

Michael G Rossman, MD, LTC, MC, FS is a member of the following medical societies: American College of Physicians, American College of Rheumatology, American Medical Association, and Society of US Army Flight Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society

Disclosure: Nothing to disclose.

References
  1. Jennette JC, Falk RJ, Andrassy K, Bacon PA, Churg J, Gross WL. Nomenclature of systemic vasculitides. Proposal of an international consensus conference. Arthritis Rheum. 1994 Feb. 37(2):187-92. [Medline].

  2. Hata A, Noda M, Moriwaki R, Numano F. Angiographic findings of Takayasu arteritis: new classification. Int J Cardiol. 1996 Aug. 54 Suppl:S155-63. [Medline].

  3. Arnaud L, Haroche J, Mathian A, Gorochov G, Amoura Z. Pathogenesis of Takayasu's arteritis: a 2011 update. Autoimmun Rev. 2011 Nov. 11(1):61-7. [Medline].

  4. Aggarwal A, Chag M, Sinha N, Naik S. Takayasu's arteritis: role of Mycobacterium tuberculosis and its 65 kDa heat shock protein. Int J Cardiol. 1996 Jul 5. 55(1):49-55. [Medline].

  5. Kumar Chauhan S, Kumar Tripathy N, Sinha N, Singh M, Nityanand S. Cellular and humoral immune responses to mycobacterial heat shock protein-65 and its human homologue in Takayasu's arteritis. Clin Exp Immunol. 2004 Dec. 138(3):547-53. [Medline]. [Full Text].

  6. Soto ME, Vargas-Alarcón G, Cicero-Sabido R, Ramírez E, Alvarez-León E, Reyes PA. Comparison distribution of HLA-B alleles in mexican patients with takayasu arteritis and tuberculosis. Hum Immunol. 2007 May. 68(5):449-53. [Medline].

  7. Yagi K, Kobayashi J, Yasue S, Yamaguchi M, Shiobara S, Mabuchi H. Four unrelated cases with Takayasu arteritis and CD36 deficiency: possible link between these disorders. J Intern Med. 2004 Jun. 255(6):688-9. [Medline].

  8. Hall S, Barr W, Lie JT, Stanson AW, Kazmier FJ, Hunder GG. Takayasu arteritis. A study of 32 North American patients. Medicine (Baltimore). 1985 Mar. 64(2):89-99. [Medline].

  9. Numano F, Kobayashi Y. Takayasu arteritis--beyond pulselessness. Intern Med. 1999 Mar. 38(3):226-32. [Medline].

  10. Jain S, Kumari S, Ganguly NK, Sharma BK. Current status of Takayasu arteritis in India. Int J Cardiol. 1996 Aug. 54 Suppl:S111-6. [Medline].

  11. Phillip R, Luqmani R. Mortality in systemic vasculitis: a systematic review. Clin Exp Rheumatol. 2008 Sep-Oct. 26(5 Suppl 51):S94-104. [Medline].

  12. Kerr GS, Hallahan CW, Giordano J, Leavitt RY, Fauci AS, Rottem M, et al. Takayasu arteritis. Ann Intern Med. 1994 Jun 1. 120(11):919-29. [Medline].

  13. Maksimowicz-McKinnon K, Clark TM, Hoffman GS. Limitations of therapy and a guarded prognosis in an American cohort of Takayasu arteritis patients. Arthritis Rheum. 2007 Mar. 56(3):1000-9. [Medline].

  14. Park MC, Lee SW, Park YB, Chung NS, Lee SK. Clinical characteristics and outcomes of Takayasu's arteritis: analysis of 108 patients using standardized criteria for diagnosis, activity assessment, and angiographic classification. Scand J Rheumatol. 2005 Jul-Aug. 34(4):284-92. [Medline].

  15. Abularrage CJ, Slidell MB, Sidawy AN, Kreishman P, Amdur RL, Arora S. Quality of life of patients with Takayasu's arteritis. J Vasc Surg. 2008 Jan. 47(1):131-6; discussion 136-7. [Medline].

  16. Akar S, Can G, Binicier O, Aksu K, Akinci B, Solmaz D, et al. Quality of life in patients with Takayasu's arteritis is impaired and comparable with rheumatoid arthritis and ankylosing spondylitis patients. Clin Rheumatol. 2008 Jul. 27(7):859-65. [Medline].

  17. Maksimowicz-McKinnon K, Clark TM, Hoffman GS. Limitations of therapy and a guarded prognosis in an American cohort of Takayasu arteritis patients. Arthritis Rheum. 2007 Mar. 56(3):1000-9. [Medline].

  18. Soto ME, Espinola N, Flores-Suarez LF, Reyes PA. Takayasu arteritis: clinical features in 110 Mexican Mestizo patients and cardiovascular impact on survival and prognosis. Clin Exp Rheumatol. 2008 May-Jun. 26(3 Suppl 49):S9-15. [Medline].

  19. Francès C, Boisnic S, Blétry O, Dallot A, Thomas D, Kieffer E. Cutaneous manifestations of Takayasu arteritis. A retrospective study of 80 cases. Dermatologica. 1990. 181(4):266-72. [Medline].

  20. Arend WP, Michel BA, Bloch DA, Hunder GG, Calabrese LH, Edworthy SM, et al. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum. 1990 Aug. 33(8):1129-34. [Medline].

  21. Siglock TJ, Brookler KH. Sensorineural hearing loss associated with Takayasu's disease. Laryngoscope. 1987 Jul. 97(7 Pt 1):797-800. [Medline].

  22. Raza K, Karokis D, Kitas GD. Cogan's syndrome with Takayasu's arteritis. Br J Rheumatol. 1998 Apr. 37(4):369-72. [Medline].

  23. Miller DV, Maleszewski JJ. The pathology of large-vessel vasculitides. Clin Exp Rheumatol. 2011 Jan-Feb. 29(1 Suppl 64):S92-8. [Medline].

  24. Gilden D, White TM, Nagae L, Gurdin WH, Boyer PJ, Nagel MA. Successful Antiviral Treatment of Giant Cell Arteritis and Takayasu Arteritis. JAMA Neurol. 2015 Aug. 72 (8):943-6. [Medline].

  25. Katz-Agranov N, Tanay A, Bachar DJ, Zandman-Goddard G. What to do when the Diagnosis of Giant Cell Arteritis and Takayasu's Arteritis Overlap. Isr Med Assoc J. 2015 Feb. 17 (2):123-5. [Medline]. [Full Text].

  26. Tripathy NK, Chandran V, Garg NK, Sinha N, Nityanand S. Soluble endothelial cell adhesion molecules and their relationship to disease activity in Takayasu's arteritis. J Rheumatol. 2008 Sep. 35 (9):1842-5. [Medline].

  27. Schmidt WA, Blockmans D. Use of ultrasonography and positron emission tomography in the diagnosis and assessment of large-vessel vasculitis. Curr Opin Rheumatol. 2005 Jan. 17(1):9-15. [Medline].

  28. Andrews J, Mason JC. Takayasu's arteritis--recent advances in imaging offer promise. Rheumatology (Oxford). 2007 Jan. 46(1):6-15. [Medline].

  29. Andrews J, Al-Nahhas A, Pennell DJ, Hossain MS, Davies KA, Haskard DO, et al. Non-invasive imaging in the diagnosis and management of Takayasu's arteritis. Ann Rheum Dis. 2004 Aug. 63(8):995-1000. [Medline]. [Full Text].

  30. Dagna L, Salvo F, Tiraboschi M, et al. Pentraxin-3 as a marker of disease activity in takayasu arteritis. Ann Intern Med. 2011 Oct 4. 155(7):425-33. [Medline].

  31. Direskeneli H, Aydin SZ, Merkel PA. Assessment of disease activity and progression in Takayasu's arteritis. Clin Exp Rheumatol. 2011 Jan-Feb. 29(1 Suppl 64):S86-91. [Medline].

  32. Magnani L, Versari A, Salvo D, et al. [Disease activity assessment in large vessel vasculitis]. Reumatismo. 2011. 63(2):86-90. [Medline].

  33. Blockmans D. PET in vasculitis. Ann N Y Acad Sci. 2011 Jun. 1228:64-70. [Medline].

  34. Fujita T, Ohtsuka M, Uchida E, Yamaguchi H, Nakajima T, Akazawa H, et al. Takayasu arteritis evaluated by multi-slice computed tomography in an old man. Int J Cardiol. 2008 Apr 10. 125(2):286-7. [Medline].

  35. Ragab Y, Emad Y, El-Marakbi A, Gheita T. Clinical utility of magnetic resonance angiography (MRA) in the diagnosis and treatment of Takayasu's arteritis. Clin Rheumatol. 2007 Aug. 26(8):1393-5. [Medline].

  36. Salvarani C, Magnani L, Catanoso M, et al. Tocilizumab: a novel therapy for patients with large-vessel vasculitis. Rheumatology (Oxford). 2012 Jan. 51(1):151-6. [Medline].

  37. Unizony S, Stone JH, Stone JR. New treatment strategies in large-vessel vasculitis. Curr Opin Rheumatol. 2013 Jan. 25(1):3-9. [Medline].

  38. Yokoe I, Haraoka H, Harashima H. A patient with Takayasu's arteritis and rheumatoid arthritis who responded to tacrolimus hydrate. Intern Med. 2007. 46(22):1873-7. [Medline].

  39. Maksimowicz-McKinnon K, Hoffman GS. Takayasu arteritis: what is the long-term prognosis?. Rheum Dis Clin North Am. 2007 Nov. 33(4):777-86, vi. [Medline].

  40. Hoffman GS, Merkel PA, Brasington RD, et al. Anti-tumor necrosis factor therapy in patients with difficult to treat Takayasu arteritis. Arthritis Rheum. 2004 Jul. 50(7):2296-304. [Medline].

  41. Youngstein T, Peters JE, Hamdulay SS, Mewar D, Price-Forbes A, Lloyd M, et al. Serial analysis of clinical and imaging indices reveals prolonged efficacy of TNF-a and IL-6 receptor targeted therapies in refractory Takayasu arteritis. Clin Exp Rheumatol. 2014 May-Jun. 32(3 Suppl 82):S11-8. [Medline].

  42. Tanaka F, Kawakami A, Iwanaga N, Tamai M, Izumi Y, Aratake K, et al. Infliximab is effective for Takayasu arteritis refractory to glucocorticoid and methotrexate. Intern Med. 2006. 45(5):313-6. [Medline].

 
Previous
Next
 
Complete occlusion of the left common carotid artery in a 48-year-old woman with Takayasu disease. Also note narrowing of the origin of the right subclavian artery and a narrowed small vessel with subsequent aneurysmal dilatation on the right side. Image courtesy of Robert Cirillo, MD.
Characteristic long, tapered narrowing of the distal aorta and iliac vessels. Image courtesy of Robert Cirillo, MD.
Image obtained in the same patient as in Image 2 reveals narrowing of the proximal descending aorta and right brachiocephalic artery. Image courtesy of Robert Cirillo, MD.
Aortogram of a 15-year-old girl with Takayasu arteritis. Note large aneurysms of descending aorta and dilatation of innominate artery. Image courtesy of Christine Hom, MD.
MRI of thorax of 15-year-old girl with Takayasu arteritis. Note aneurysms of descending aorta. Image courtesy of Christine Hom, MD.
Coronal MRI of abdomen of 15-year-old girl with Takayasu arteritis. Note thickening and tortuosity of abdominal aorta proximal to kidneys. Image courtesy of Christine Hom, MD.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.