Takayasu's arteritis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2] Shaghayegh Habibi, M.D.[3]

In Takayasu’s arteritis, the most commonly involved vessels include the left subclavian artery (50%), left common carotid artery (20%), brachiocephalic trunk, renal arteries, celiac trunk, superior mesenteric artery, and pulmonary arteries (50%). Infrequently, the axillary, brachial, vertebral, coronary, and iliac arteries are involved. The pathogenesis of Takayasu’s arteritis is poorly understood. Takayasu’s arteritis characterized by segmental and patchy granulomatous inflammation of the aorta and its major derivative branches.This inflammation leads to arterial stenosis, thrombosis, and aneurysms. Three factors that have been suggested to have association with susceptibility, development and progression of Takayasu’s arteritis are genetic influences, immunologic mechanisms and relationship to tuberculosis. The cause of Takayasu’s arteritis is idiopathic but genetic, immunologic and infectious factors play important role in the development of Takayasu’s arteritis. Takayasu arteritis has a worldwide distribution, it is observed more frequently in Asian countries such as Japan, Korea, China, India, Thailand, and Singapore. Female are more commonly affected. Common risk factors in the development of Takayasu’s arteritis include genetic predisposition, female sex, age <40, asian ethnicity. Common complications of Takayasu’s arteritis include hardening and narrowing of blood vessels, High blood pressure, Heart failure, Stroke, Transient ischemic attack. Common symptoms of Takayasu’s arteritis include headache, malaise, arthralgias, bruit, claudication, hypertension, visual disturbance. The most common finding is a systolic blood pressure difference (>10 mm Hg) between arms. Hypertension due to renal artery involvement is found in approximately 50% of patients. Absent or diminished pulses are the clinical hallmark of Takayasu arteritis. Chest radiographs may reveal widening of the ascending aorta, irregular descending aorta, aortic calcifications, and rib notching (late findings). Most people with Takayasu’s arteritis respond to steroids such as prednisone. The usual starting dose is approximately 1 milligram per kilogram of body weight per day (for most people, this is approximately 60 milligrams a day). The two most important aspects of treatment: are controlling the inflammatory process and controlling hypertension.

In 1830, Rokushu Yamamoto, who practised Japanese oriental medicine described the first case of Takayasu’s arteritis. In 1905, Mikito Takayasu repoted a case of a 21 year old woman with characteristic fundal arteriovenous anastamoses as “a case of peculiar changes in the central retinal vessels.” In 1905, Onishi and Kagosha reported cases associated with absent radial pulses.

Takayasu arteritis may be classified according to angiographic findings into 6 subtypes. These systems are useful in that they allow a comparison of patient characteristics according to the vessels involved and are helpful in planning surgery, but they offer little by way of prognosis. The most commonly involved vessels include the left subclavian artery (50%), left common carotid artery (20%), brachiocephalic trunk, renal arteries, celiac trunk, superior mesenteric artery, and pulmonary arteries (50%). Infrequently, the axillary, brachial, vertebral, coronary, and iliac arteries are involved.

The pathogenesis of Takayasu’s arteritis is poorly understood. Takayasu’s arteritis characterized by segmental and patchy granulomatous inflammation of the aorta and its major derivative branches.This inflammation leads to arterial stenosis, thrombosis, and aneurysms. Three factors that have been suggested to have association with susceptibility, development and progression of Takayasu’s arteritis are genetic influences, immunologic mechanisms and relationship to tuberculosis.

The cause of Takayasu’s arteritis is idiopathic but genetic, immunologic and infectious factors play important role in the development of Takayasu’s arteritis.

Takayasu’s arteritis should be distinguished from other conditions that cause arthritis and rash.

Takayasu arteritis has a worldwide distribution, it is observed more frequently in Asian countries such as Japan, Korea, China, India, Thailand, and Singapore. The incidence of Takayasu arteritis is approximately 0.26 per 100,000 individuals worldwide. Female are more commonly affected by Takayasu arteritis than male. Mean age of onset of Takayasu arteritis is approximately 30 years.

Common risk factors in the development of Takayasu’s arteritis include genetic predisposition, female sex, age <40, asian ethnicity.

According to the United States Preventive Services Task Force (UPSTF), screening for Takayasu’s arteritis is not recommended.

The symptoms of Takayasu’s arteritis typically develop between 15 and 30 years of age. Common complications of Takayasu’s arteritis include hardening and narrowing of blood vessels, High blood pressure, Heart failure, Stroke, Transient ischemic attack. The five year survival rate in Takayasu arteritis is over 90%.

Common symptoms of Takayasu’s arteritis include headache, malaise, arthralgias, bruit, claudication, hypertension, visual disturbance. Less common symptoms of Takayasu’s arteritis include fever, weight loss, carotodynia or vessel tenderness, Raynaud’s syndrome, stroke, transient ischemic attacks, seizures, erythema nodosum.

A thorough physical examination is essential, with particular attention to peripheral pulses, blood pressure in all 4 extremities, ophthalmologic examination. The most common finding is a systolic blood pressure difference (>10 mm Hg) between arms. Hypertension due to renal artery involvement is found in approximately 50% of patients. Absent or diminished pulses are the clinical hallmark of Takayasu arteritis, but pulses are normal in many patients and upper limbs are affected more often Than lower limbs. Ophthalmologic examination may show retinal ischemia, Retinal hemorrhages, cotton-wool exudates, venous dilatation and beading, microaneurysms of peripheral retina, optic atrophy, vitreous hemorrhage, wreathlike peripapillary arteriovenous anastomoses.

There are no diagnostic laboratory tests for Takayasu’s arteritis. Testing for acute phase reactants such as the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may provide additional support for the presence of a systemic inflammatory process; Normochromic normocytic anemia suggestive of the anemia of chronic disease.

There are no ECG findings associated with Takayasu’s arteritis.

Chest radiographs may reveal widening of the ascending aorta, irregular descending aorta, aortic calcifications, and rib notching (late findings).

Echocardiography may be helpful in the diagnosis of Takayasu’s arteritis and its complications. Findings on an echocardiography suggestive of Takayasu’s arteritis include aortic regurgitation. Doppler ultrasound is a useful non-invasive procedure for the assessment of vessel wall inflammation in patients with Takayasu’s arteritis. Ultrasonography is limited by operator-dependent artefacts from overlying structures and bowel gas. In Takayasu’s arteritis, ultrasound can be helpful in detecting sub-millimeter changes in wall thickness of the carotid arteries.

CT scan manifestations in Takayasu arteritis include mural thickening (typical manifestation), calcification in the thickened wall and double ring enhancement pattern.

MRI can demonstrate mural thickening with luminal stenosis of the aorta and branching vessels of the aortic arch. It can directly visualize the vessel wall independent of luminal diameter and can be helpful in diagnosis of inflammation in early vasculitis.

PET scan is useful in diagnosis of Takayasu’s arteritis by providing valuable information about cellular activity within an inflamed arterial wall even before morphologic changes on other imaging studies. In patients with TA, MRA shares the similar features of TA with CTA images, and can be used in the diagnosis and follow-up of patients undergoing treatment, especially those who are young.

There are no other diagnostic studies associated with Takayasu’s arteritis.

Most people with Takayasu’s arteritis respond to steroids such as prednisone. The usual starting dose is approximately 1 milligram per kilogram of body weight per day (for most people, this is approximately 60 milligrams a day). The two most important aspects of treatment: are controlling the inflammatory process and controlling hypertension.

Surgical options may need to be explored for those who do not respond to steroids. Re-perfusion of tissue can be achieved by large vessel reconstructive surgery such as bypass grafting.

There are no established measures for the primary prevention of Takayasu’s arteritis.

Diet modification is necessary to manage hypertension or renal failure in Takayasu’s arteritis. Any activity limitations depend on the severity of the disease and complications.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

In 1830, Rokushu Yamamoto, who practised Japanese oriental medicine described the first case of Takayasu’s arteritis. In 1905, Mikito Takayasu reported a case of a 21 year old woman with characteristic fundal arteriovenous anastomoses as “a case of peculiar changes in the central retinal vessels.” In 1905, Onishi and Kagosha reported cases associated with absent radial pulses.

• In 1830, Rokushu Yamamoto, who practised Japanese oriental medicine described the first case of Takayasu’s arteritis.^[1] 

• In 1905, Mikito Takayasu reported a case of a 21 year old woman with characteristic fundal arteriovenous anastomoses as “a case of peculiar changes in the central retinal vessels.”^[2]
• In 1905, Onishi and Kagosha reported cases associated with absent radial pulses.^[3]
• In 1920, the first postmortem case of panarteritis was described. She was a 25 year old woman who suffered from retinal ischemia.^[1]
• In 1951, Shimizu and Sano named this pathological condition “pulseless disease.”^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Takayasu arteritis may be classified according to angiographic findings into 6 types which is useful in planning for surgery. The most commonly involved vessels include the left subclavian artery (50%), left common carotid artery (20%), brachiocephalic trunk, renal arteries, celiac trunk, superior mesenteric artery, and pulmonary arteries (50%). Takayasu arteritis may be classified according to clinical finding into 4 groups of group I, IIA, IIB, and III.

• Takayasu arteritis may be classified according to angiographic findings into 6 types:^[1]

Type	Vessel involvement
Type I	Branches from the aortic arch
Type IIa	Ascending aorta, aortic arch and its branches
Type IIb	Ascending aorta, aortic arch and its branches, thoracic descending aorta
Type III	Thoracic descending aorta, abdominal aorta, and/or renal arteries
Type IV	Abdominal aorta and/or renal arteries
Type V	Combined features of types IIb and IV

• Takayasu arteritis may be classified according to clinical finding into 4 groups:^[2]

Group	Clinical features
Group I	Uncomplicated disease, with or without pulmonary artery involvement
Group IIA	Mild/moderate single complication together with uncomplicated disease
Group IIB	Severe single complication together with uncomplicated disease
Group III	Two or more complications together with uncomplicated disease

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

The pathogenesis of Takayasu’s arteritis is poorly understood. Takayasu’s arteritis characterized by segmental and patchy granulomatous inflammation of the aorta and its major derivative branches.This inflammation leads to arterial stenosis, thrombosis, and aneurysms. Three factors that have been suggested to have association with susceptibility, development and progression of Takayasu’s arteritis are genetic influences, immunologic mechanisms, and relationship to tuberculosis. The most important conditions associated with Takayasu’s arteritis include ankylosing spondylitis, inflammatory bowel disease, and Behçet’s syndrome. On gross pathology, stiff and rigid aorta on palpation, gelatinous appearance of thickened adventitia, and sharp line of demarcation between normal and diseased segments might be seen. On microscopic histopathological analysis characteristic findings of Takayasu’s arteritis include inflammation around the vasa vasorum and at the medio-adventitial junction, edema of the media and adventitia, giant cell granulomatous reaction, laminar necrosis, and fragmentation of elastic fibers.

• The pathogenesis of Takayasu’s arteritis is poorly understood.^[1]
• Granulomatous inflammation of the aorta and its major branches might lead to Takayasu’s arteritis.
• Cell-mediated mechanisms are considered as a main pathogenesis mechanism of Takayasu’s arteritis and it is similar to giant cell arteritis.
• This inflammation leads to arterial stenosis, thrombosis, and aneurysms.
• Irregular fibrosis of the blood vessels due to chronic vasculitis may lead to intimal fibrosis.
• There are three factors that have associated with disease susceptibility, development and progression:
  • Relationship to tuberculosis (TB)
  • Genetic influences
  • Immunologic mechanisms

Relationship to tuberculosis (TB)

• It has been suggested that Takayasu arteritis is associated with TB. Following evidences support this hypothesis:^[2]

• • Granulomatous inflammation with the Langhans-type of giant cells in many cases of Takayasu arteritis
  • Intermittent coexistence of Takayasu arteritis with pulmonary and extrapulmonary tuberculosis
  • Hypersensitivity to the tuberculosis organism

Genetic influences

• Geographic distribution of Takayasu arteritis, with high prevalence in Japan and Korea, suggests that genetic factors are probably play a role in the pathogenesis of Takayasu arteritis.

• Takayasu arteritis has been associated with different human leukocyte antigen (HLA) alleles in different populations. In Japan and Korea, there is a clear association with the extended haplotype:^[3]
  • HLA-B*52
  • HLA-DRB1*1502
  • HLA-DRB5*0102
  • HLA-DQA1*0103
  • HLA-DQB1*0601
  • HLA-DPA1*02
  • HLA-DPB1*0901

Immunologic mechanisms

Because of rheumatic-type complaints in many Takayasu arteritis patients, the relationship between Takayasu arteritis and autoimmune and collagen vascular disorders has been suggested.

• Immunohistopathologic examination has shown that the infiltrating cells in aortic tissue mainly consist of killer cells, especially gamma delta T lymphocytes. 
• These cells may cause vascular injury by releasing large amounts of the cytolytic compound perforin.
• It has been reported that γδT cells, αβT cells (CD4 and CD8), and natural killer cells play an important role in the vascular injury.^[4]
• No specific autoantigens have yet been identified.

• The most important conditions associated with Takayasu’s arteritis include:
  • Ankylosing spondylitis
  • Inflammatory bowel disease (IBD)
  • Behçet’s syndrome

On gross pathology characteristic findings of Takayasu’s arteritis are as follows:^[5]

• Stiff and rigid aorta on palpation
• Gelatinous appearance of thickened adventitia
• Enlarged para-aortic lymph nodes in the area of renal and subclavian arteries
• Sharp line of demarcation between normal and diseased segments

On microscopic histopathological analysis characteristic findings of Takayasu’s arteritis are as follows:^[5]

• Inflammation around the vasa vasorum and at the medio-adventitial junction
• Edema of the media and adventitia
• Giant cell granulomatous reaction
• Laminar necrosis
• Fragmentation of elastic fibers
• Rapid or more severe inflammation leads to:
  • Loss of smooth muscle cells
  • Medial weakening
  • Vascular dilatation
  • Aneurysm formation

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

The cause of Takayasu’s arteritis has not been identified. To review risk factors for the development of Takayasu’s arteritis, click here.

The cause of Takayasu’s arteritis has not been identified. To review risk factors for the development of Takayasu’s arteritis, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Takayasu’s arteritis should be distinguished from other conditions that cause arthritis and rash. The differentials include other large and medium-vessel vasculitides such as giant cell arteritis, polyarteritis nodosa, other systemic ilnesses such as as systemic lupus erythematosus, rheumatoid arthritis, rhupus, mixed connective tissue disease, systemic sclerosis, Sjogren’s syndrome, Bechet’s disease, Kikuchi’s disease, serum sickness, psoriatic arthritis and human papilloma B19 virus infection.

Takayasu’s arteritis should be distinguished from other conditions that cause arthritis and rash. The differentials include other large and medium-vessel vasculitides such as giant cell arteritis, polyarteritis nodosa, other systemic ilnesses such as as systemic lupus erythematosus, rheumatoid arthritis, rhupus, mixed connective tissue disease, systemic sclerosis, Sjogren’s syndrome, Bechet’s disease, Kikuchi’s disease, serum sickness, psoriatic arthritis and human papilloma B19 virus infection. The following table differentiates between them:

Abbreviations: ANA: Antinuclear antibody, RF: Rheumatoid factor, Anti-CCp: Anti-cyclic citrullinated protein antibody, Anti U1RNP: Anti-U1 ribonucleoprotein antibodies , Anti Sm : Anti-Sm antibodies, Anti Ro: Anti Ro antibody also called anti-Sjögren’s-syndrome-related antigen A antibody, Anti-dsDNA: Anti-double stranded DNA.

Disease		Arthritis					Auto-antibodies							Raynaud phenomenon	Rash pattern	Distinguishing/specific features
		Polyarthritis	Tenderness	Edema	Deformity /Erosion	Pattern	ANA	RF	Anti-CCp	Anti U1RNP	Anti Sm	Anti Ro	Anti-dsDNA
Vasculitis	Takayasu[1]	–	+/-	+/-	–	Transient extremity	–	–	–	–	–	–	–		Erythema nodosum, pyoderma gangrenosum	Absent or weak peripheral pulse
	Giant cell[2]	–	+	+	–	Distal extremity	–	–	–	–	–	–	–	–	Rare	Involvement of cranial branches of arteries, visual loss
	Poly-arteritis nodosa[3]	–	+/-	–	–	General and mild	–	–	–	–	–	–	–		Tender erythematous nodules, purpura, livedo reticularis, bullous or vesicular eruption	Testicular pain or tenderness and neuropathies
Systemic lupus erythematosus[4]		+	+	+	–	Small joints	↑	–	–	–	↑	↑	–	+	Malar rash and photosensitivity
Rheumatoid arthritis (RA)[5]		+	+	+	+	Small and large joints	–	↑↑	↑↑	–	–	–	–	+	Subcutaneous nodules	Erosive arthropathy
Rhupus[6]		+	+	+	+	Small and large joints	↑	↑	↑	↑	↑	–	↑	+	Malar rash and photosensitivity	Erosive arthropathy
Mixed connective tissue disease (MCTD)[7]		–	–	–	+	Small and large joints	–	↑↑	↑	–	–	–	–	+	Cutaneous eruptions, gottron’s papules, photodistributed erythema, poikiloderma, and calcinosis cutis	Overlapping features of SLE, systemic sclerosis (SSc), and polymyositis (PM) that lead to more than one diagnosis
Undifferentiated connective tissue disease (UCTD)[8]		+	–	–	–	Lower extremity	↑	↑	–	–	↑	–	–	+	Erythematous macules, patches, or papules with delicate scale	Multiple connective tissue diseases with no enough criteria for a single diagnosis
Systemic sclerosis (SSc)[9]		+/-	+	+	+/-	Lower extremity	↑↑	–	–	–	↑	–	↑	+	Hyperkeratosis, edema, and erythema	Sclerodactyly, Telangiectasias, Calcinosis, Malignant hypertension, acute renal failure
Sjögren’s syndrome[10]		+/-	+/-	–	–	Lower extremity, axiallary creases	↑	–	–	–	↑	↑	–	–	Xerosis, scaly skin, annular erythema	Keratoconjunctivitis sicca
Behçet’s syndrome[11]		+/-	+/-	+/-	–	medium and large joints	–	–	–	–	–	–	–	–	Recurrent and usually painful mucocutaneous ulcers, acneiform lesions, papulo-vesiculo-pustular eruptions, superficial thrombophlebitis	Male dominancy
Kikuchi’s disease[12]		–	+/-	–	–	medium and large joints	↑/↓	–	–	–	–	–	–	–	Transient skin rashes, malar rash, erythematous macules, patches, papules, or plaques	May be associated with SLE
Serum sickness[13]		+	+	+/-	–	General	–	–	–	–	–	–	–	–	Pruritic rash, urticaria and/or serpiginous macular rash	Self-limited
Psoriatic arthritis[14]		–	–	–	–	Small and large joints	–	–	–	–	–	–	–	–	Psoriasis and onychodystrophy	Dactylitis (sausage digits)
Human parvovirus B19 infection[15]		+	+	–	–	Small joints	–	–	–	–	–	–	–	–	Erythematous rashes	Rare in adults, fifth’s disease in children

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Takayasu arteritis has a worldwide distribution, it is observed more frequently in Asian countries such as Japan, Korea, China, India, Thailand, and Singapore. The incidence of Takayasu arteritis is approximately 0.26 per 100,000 individuals worldwide. Females are more commonly affected by Takayasu arteritis than males. Mean age of onset of Takayasu arteritis is approximately 30 years.

• The incidence of Takayasu arteritis is approximately 0.26 per 100,000 individuals worldwide.^[1]
• The incidence of Takayasu arteritis is approximately 0.15 per 100,000 individuals among European people.^[2]

• The prevalence of Takayasu arteritis is estimated to be 0.26 to 0.64 per 100,000 individuals.^[3]
• The prevalence of Takayasu arteritis is estimated to be 0.47 to 3.3 per 100,000 individuals among European people.^[2]

• The mortality rate of Takayasu arteritis over five years is less than 5%.^[4]

• Takayasu arteritis commonly affects individuals between 4 and 63 years of age.^[2]
• Mean age of onset of Takayasu arteritis is approximately 30 years.
• More than 85% of patients with Takayasu arteritis are younger than 40 years old.

• Takayasu arteritis usually affects individuals of Asian or Indian race.^[5]
• Patients with Takayasu arteritis have a higher incidence of aortic arch involvement in Japan.
• Patients with Takayasu arteritis have a higher incidence of abdominal involvement in India.

• Females are more commonly affected by Takayasu arteritis than males. The female to male ratio is approximately 9 to 1.^[5]

• Takayasu arteritis is a rare disease.^[6]
• The majority of Takayasu arteritis cases are reported in Japan, South East Asia, India, and Mexico.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Common risk factors in the development of Takayasu’s arteritis include genetic predisposition, infections, female gender, age <40 and Asian ethnicity.

Common risk factors in the development of Takayasu’s arteritis include:^[1][2]

• Female gender
• Age <40
• Asian ethnicity
• Genetic predisposition
  • HLA-B*52
  • HLA-DRB1*1502
  • HLA-DRB5*0102
  • HLA-DQA1*0103
  • HLA-DQB1*0601
  • HLA-DPA1*02
  • HLA-DPB1*0901
• Infectious agents such as:
  • Spirochetes
  • Mycobacterium tuberculosis
  • Streptococcal organisms

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

According to the United States Preventive Services Task Force, screening for Takayasu’s arteritis is not recommended.

According to the United States Preventive Services Task Force, screening for Takayasu’s arteritis is not recommended.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

The symptoms of Takayasu’s arteritis typically develop between 15 and 30 years of age. Common complications of Takayasu’s arteritis include hardening and narrowing of blood vessels, High blood pressure, Heart failure, Stroke, Transient ischemic attack. The five year survival rate in Takayasu arteritis is over 90%.

• The symptoms of Takayasu’s arteritis typically develop between 15 and 30 years of age.^[1]
• If left untreated, patients with Takayasu’s arteritis may progress to develop high blood pressure, stroke, or heart failure.
• Takayasu’s arteritis can be divided into two phases:^[2][3]
  • Pre-pulseless phase
    • Present with non-specific constitutional symptoms of vasculitis such as:
      • Fatigue
      • Fever of unknown origin
      • Weight loss
      • Myalgia
      • Arthralgia

• • Subsequent pulseless phase
    • Present with involvement of the branches of aorta and specific symptoms secondary to occlusion of the branches of aorta such as:
      • Subclavian artery:
        • Claudication in the upper extremities
        • Subclavian steal syndrome
      • Carotid and vertebral arteries:
        • Headache
        • Vertigo
        • Syncope
        • Convulsions
        • Forgetfulness
      • Coronary arteries:
        • Chest pain
      • Ascending aorta:
        • Aortic regurgitation

Common complications of Takayasu’s arteritis include:^[1]

• Hardening and narrowing of blood vessels
• High blood pressure
• Carditis
• Heart failure
• Stroke
• Transient ischemic attack (TIA)
• Aneurysm in the aorta
• Heart attack

• Takayasu arteritis is a chronic relapsing and remitting disease.^[4]
• Takayasu arteritis is associated with significant morbidity.

• The five year survival rate in patients suffering from Takayasu arteritis is over 90%.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Sumanth Khadke, MD[2], Ogechukwu Hannah Nnabude, MD

Compliance with avoidance is important. The key to avoidance is proper evaluation and detection of causative allergen. Wear appropriate clothing to protect against irritants at home and in a work environment. ^{[1] [2]}

High-potency topical corticosteroids, e.g. clobetasol propionate 0.05% cream, may be used to reduce the inflammation. ^[3] As a general rule, high-potency corticosteroids should not be used on thin skin, e.g. face, genitals, intertriginous areas, to avoid the risk of skin atrophy. Antihistamines such as hydroxyzine and cetirizine are recommended to control pruritus. Systemic steroids are advised in severe cases but should be tapered gradually to prevent recurrences. Friction should be avoided as well as the use of soaps, perfumes, and dyes. Emollients are used for hydrating the skin. Tacrolimus ointment and pimecrolimus cream are immunomodulating drugs that inhibit calcineurin and are helpful in allergic contact dermatitis.