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Takayasu Arteritis Workup

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

Approach Considerations

Laboratory test results in individuals with Takayasu arteritis tend to be nonspecific. The erythrocyte sedimentation rate may be high, generally greater than 50 mm/h, in early disease but normal later. Leukocyte count may be normal or slightly elevated. A moderate, normochromic anemia may be present in individuals with active disease.[12, 17]

Autoantibodies observed in other connective tissue diseases, including rheumatoid factor, antinuclear antibodies, anticardiolipin antibodies, and antineutrophil cytoplasmic antibodies (ANCA), are as common as in the general population. Circulating antiendothelial antibodies may be present in high titers. This finding is considered nonspecific, because it is reported sporadically and may be present in other connective tissue diseases and in angiitis obliterans. Antiaorta antibodies may be present, but testing for them seldom is performed, if ever.

Some researchers found that the levels of soluble vascular cell adhesion molecule–1 (VCAM-1) were significantly higher in patients with Takayasu arteritis compared with normal, healthy controls and that they were also significantly higher in older patients than in younger ones, suggesting that VCAM-1 may serve as a marker of disease activity and progression with age. Tripathy et al reported that cell adhesion molecule levels remain elevated in patients with inactive Takayasu arteritis.[26]

Hypoalbuminemia and increased levels of fibrinogen, alpha2-globulin, and gamma globulin are common. Urinalysis may be consistent with nephrotic syndrome.

HLA typing has not confirmed any definite association in North American patients. Presumably, a finding of HLA-Bw52 in such patients reinforces the diagnosis; it is not a definite diagnostic tool.

Imaging studies

While computed tomography (CT) scanning and magnetic resonance imaging (MRI) show typical patterns of stenosis or aneurysms of the arteries, angiography remains the standard for diagnosis and evaluation of the extent of disease. However, studies suggest that noninvasive imaging modalities such as MRI, ultrasonography, and 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET) allow diagnosis of Takayasu arteritis earlier in the disease course than standard angiography and provide a means for monitoring disease activity. (See the images below.)[27, 28, 29]

MRI of thorax of 15-year-old girl with Takayasu ar 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 Ta 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.
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Diagnostic Criteria

Ishikawa criteria

The Ishikawa criteria (1986) have been useful in defining Takayasu arteritis. One criterion is age younger than 40 years at diagnosis or at onset of characteristic signs and symptoms of 1-month duration.

Two major criteria involve lesions in the left and right midsubclavian artery, with the most severe stenosis or occlusion present in the mid portion of the artery from a 1 cm point proximal to the left and right, respectively, of the vertebral artery orifices to a 3-cm distal point to the orifice, as determined by angiography.

The minor criteria consist of annuloaortic ectasia or aortic regurgitation on angiography or echocardiography, and lesions of any of the following vessels:

  • Pulmonary artery
  • Left mid ̶ common carotid artery
  • Distal brachiocephalic trunk
  • Descending aorta
  • Abdominal aorta

American College of Rheumatology criteria

The American College of Rheumatology (ACR; 1990) put forward the following diagnostic criteria:

  • Angiographic criteria must show narrowing or occlusion of the entire aorta, its primary branches, or large arteries in the proximal upper or lower extremities
  • These changes are not due to arteriosclerosis, fibromuscular dysplasia, or similar causes
  • Changes are usually focal or segmental

These criteria probably allow greater flexibility to account for variability in actual clinical practice. In comparison to the Ishikawa criteria, which were established based on Japanese patients only, the ACR criteria may better reflect the North American population. The lesions can include stenosis, occlusion, or aneurysms.

The sensitivity and specificity of the American College of Rheumatology criteria are 90.5% and 97.9%, respectively.

 

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Assessing Disease Activity

Assessing disease activity in patients with Takayasu arteritis is frequently challenging, since clinical, biologic, and radiologic information do not always correlate. Prospective study criteria established by Kerr et al (National Institutes of Health) are used to assess disease activity in patients with Takayasu arteritis. New onset or worsening of 2 or more of the following features indicates active disease[12] :

  • Systemic features, such as fever and arthralgias (no identified cause)
  • Elevated erythrocyte sedimentation rate
  • Features of vascular ischemia or inflammation, such as claudication, diminished or absent pulse, bruit, carotodynia, or asymmetrical blood pressure in either the upper or lower limbs (or both)
  • Typical angiographic features

Pentraxin-3 (PTX3), a member of the superfamily of acutephase proteins such as C-reactive protein (CRP) and serum amyloid P, has been suggested as a possible biomarker for identifying disease activity in patients with an established diagnosis of Takayasu arteritis. In a cross-sectional, noninterventional study, PTX3 plasma levels were shown to be more accurate than the erythrocyte sedimentation rate (ESR) and CRP level for differentiating active from inactive disease in 57 patients with previously diagnosed Takayasu arteritis. PTX3 levels greater than 1 ng/mL were more accurate than normal thresholds of CRP and ESR for defining disease activity. Patients with unknown or equivocal disease status were excluded from the study.[30]

Certainly, PTX3 plasma levels may play a future role as a possible disease marker. However as pointed out by the authors of the study, PTX3 needs to be assessed in a broader spectrum of patients whose disease activity is unknown or equivocal before recommending using it clinically.[30]

Other measures of disease activity in Takayasu arteritis include the Birmingham Vasculitis Activity Score (BVAS), Disease Extent Index for Takayasu's Arteritis (DEI.Tak), and Indian Takayasu's Arteritis Score (ITAS). The ITAS seems to have good correlation; however, none of those scores has been validated.[31, 32]

Imaging modalities for assessment of disease activity are limited by various factors, and no consensus has been reached on their sensitivity and specificity. Computed tomography angiography is limited by the amount of exposure to contrast. Magnetic resonance angiography is useful for providing information on vessel wall thickness, edema, and contrast enhancement; however, its ability to discriminate between acute versus inactive disease has been questioned.

18-Fluorodeoxyglucose positron emission tomography (FDG-PET) is a promising imaging modality, given its noninvasiveness and ability to visualize regional distribution in the vascular tree. No consensus has been reached on its sensitivity and specificity in determining acute versus inactive disease. Increased vascular uptake may be visible on an18F-FDG scan performed years after the acute phase.[33]

Novel ligands such as radioactive PK11195 that bind to peripheral benzodiazepine receptors on activated monocyte/macrophages are under investigation to improve specificity of PET for active disease.[31]

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Angiography

Angiography, the criterion standard for the diagnosis and evaluation of Takayasu arteritis, is used to evaluate only the appearance of the lumen and cannot be used to differentiate between active and inactive lesions. (See the images below.) Takayasu arteritis can be divided into the following 6 types based on angiographic involvement:[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
    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.
    Characteristic long, tapered narrowing of the dist 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 r 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 arte 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.
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Imaging Studies

Ultrasonography

Color Doppler ultrasonography provides details of the vascular wall, lumen, and flow and is a useful tool for screening and follow-up, particularly for carotid and subclavian arteries.

CT scanning

CT helical scanning angiography is a sensitive and specific diagnostic tool. CT scanning or ultrasonography may be used to assess the thickness of the aorta. One study found that multi-slice CT scanning was useful in detecting lesions.[34]

MRA

The sensitivity of magnetic resonance angiography (MRA) is the same as or greater than that of angiography for revealing lesions in the aorta and its brachycephalic branches but is less sensitive for helping to detect smaller branch involvement. MRA that uses fast spin-echo sequences designed to enhance the detection of vessel wall edema shows promise in assessing disease activity before irreversible lesions develop.

Advances in technology have substantially improved the sensitivity and specificity of MRA, and the entire arterial vasculature can be displayed in less than 90 seconds. The risks are practically nonexistent.[35]

PET scanning

The modality 18-F-FDG-PET has been shown to be useful in monitoring disease activity and response to treatment in preliminary studies. The presence or absence of FDG uptake correlates well with a patient’s clinical state and MRI findings. Its use in patients with Takayasu arteritis requires further investigation.

Several studies have shown that whole-body PET scanning demonstrates anatomic changes consistent with the diagnosis of Takayasu arteritis.[27, 28, 29]

Other imaging modalities

Single-photon emission computed tomography (SPECT) scanning has been used to assess cerebral blood flow and may be useful in patients who undergo bypass surgery.

Gallium scanning has been used to assess inflammatory involvement of the vessels.

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Tissue Biopsy

In contrast to other vasculitides, tissue biopsy plays little to no role in the diagnosis of Takayasu arteritis, as histologic examination of the great vessels is usually possible only at the time of vascular procedures or postmortem. Biopsy of medium- to large-sized vessels may be diagnostic in early stages of the disease; however, in the chronic phase, diagnosis based on biopsy alone is inadequate. Whenever possible, the feasibility of submitting arterial tissue should be discussed with the attending surgeon prior to any surgical revascularization procedure.

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Histologic Findings

Takayasu arteritis is characterized by a special pattern of histopathologic changes. The early stage consists of a continuous or patchy granulomatous inflammatory reaction involving macrophages, lymphocytes, and multinucleated giant cells. Inflammation initially occurs in the vasa vasorum, with the artery wall becoming irregularly thickened and the lumen becoming narrowed. Takayasu arteritis progresses to a sclerotic stage, with intimal and adventitial fibrosis and scarring of the media. Lesions are initially inflammatory and later become occlusive.

In the early phase of Takayasu arteritis, histologic features include granulomatous changes in the media and adventitia of the aorta and its branches, followed by intimal hyperplasia, medial degeneration, and adventitial fibrosis of the sclerotic type. The duration is variable. Inflammatory cells—predominantly CD4 and CD8 lymphocytes, macrophages, plasma cells, histiocytes, and giant cells—invade the adventitia and media but not the intima.

In the vasoocclusive stage, the lesions are characterized by occlusion and signs of ischemia. The adventitia and media are replaced by fibrous scarring, the vasa vasorum are obliterated, and the intima undergoes irregular thickening. Medial degeneration, disruption of the elastic lamellae, and thrombosis can occur. Aneurysms can form, but no aneurysms attributed to Takayasu arteritis have been identified in the intracranial circulation. The literature reports a few cases of intracranial aneurysms that are considered to be incidental.

The ground substance in the intima is increased markedly, histochemically showing a basophilic acid mucopolysaccharide in a state of gelatinous swelling.

An increase in CD4 and decrease in CD8 lymphocytes, along with reduced B lymphocytes, have suggested a defect in T-cell regulation (cell-mediated immunity). Biopsy samples exhibit infiltrates of lymphocytes and monocytes in both the vessel walls and a peripheral nerve vasculitis. Lymphocytes and monocytes are attracted to the vessel wall either by an infectious agent or an autoimmune response, modulated by intercellular adhesion molecules (ICAMs).

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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].

 
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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.
 
 
 
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