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Arteritis [ edit ]

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Takayasu 
Takayasu's arteritis
Takayasu Arteritis.jpg
Classification and external resources
Medical specialtiesImmunology , rheumatology
ICD - 10M31.4
ICD - 9-CM446.7
OMIM207600
DiseasesDB12879
MedlinePlus001250
eMedicineMed/2232 ped/1956 neuro/361radio/51
MeSHD013625
[ Edit this entry's Wikidata ]
Takayasu arteritis ( Takayasu arterifis, the TA ) is an involving the aorta and its major branches, and the pulmonary artery of the non-specific chronic progressive inflammatory disease [1] : 841 [2] . Disease caused by Japanese doctors Mikito Takayasu (Mikito Takayasu) was first reported in 1908, is also known as Takayasu's disease , Takayasu's disease [3] .
Atherosclerosis is more common in Asia than in young women. The incidence of males and females is about 1:8-9 [2] [4] . The peak incidence of female is about 20 years old, and the incidence is about 90% before 30 years old. After 40 years of age, the incidence is less, and men do not have accurate peak age of onset [5] . The cause of Takayasu arteritis is not yet clear, and may be related to factors such as immune damage caused by infection or genetic factors.

table of Contents

  [ hide ] 
  • 1Pathophysiology
  • 2clinical manifestations
  • 3Diagnosis
    • 3.1diagnostic criteria
    • 3.2Auxiliary inspection
  • 4treatment
    • 4.1Drug Treatment
    • 4.2Interventional treatment
    • 4.3Surgical treatment
  • 5prognosis
  • 6References

Pathophysiology [ edit ]

Patients with arterial wall full-thickness inflammation occur in the aorta and its major branches or in the pulmonary artery due to autoimmune or genetic factors . A large number of inflammatory cells infiltrate in the early blood vessel wall, mainly lymphocytes , plasma cells , occasionally polymorphonuclear neutrophils and multinucleated giant cells , extensive arterial wall in the late involvement of the fibrosis and scar formation [6] . Involvement intimal thickening, leading to vascular stenosis, occlusion or thrombus formation [4] , some patients arterial wall damage due to inflammation middle, elastic fibers and smooth muscle fiber necrosis, resulting in arteries, false aneurysm or aortic dissection .

Clinical manifestations [ edit ]

  • Systemic Symptoms: A few patients may have systemic discomfort, fatigue, fever, loss of appetite, nausea, and other non-specific systemic symptoms before local symptoms or signs appear.
  • Local symptoms: diversity, according to the different blood vessels involved, there are symptoms and signs of organ ischemia. According to the vascular lesions, Lupi-Herrea classification can be divided into four types: brachiocephalic type (aortic arch syndrome), thoracic-abdominal aortic type, extensive type and pulmonary artery type [7] .
  1. Brachiocephalic type: mainly involving the aortic arch and its branches, causing varying degrees of ischemia in the brain and upper limbs. Dizziness, headache, memory loss, black spots on unilateral or bilateral vision, decreased visual acuity, reduced vision, and even blindness in patients with cerebral ischemia. Masticatory muscle weakness and chewing pain. Severe cerebral ischemia may have repeated syncope, convulsions, aphasia, hemiplegia, or coma. Patients with upper limb ischemia may have unilateral or bilateral upper limb weakness, coldness, soreness, numbness, or even muscle atrophy.
  2. Thoracic-abdominal aortic type: mainly involving the descending aorta or celiac artery. The lower extremity arterial ischemia causes lower limb weakness, soreness, coldness of the skin, and intermittent claudication , such as renal vascular hypertension caused by renal artery stenosis . The diastolic blood pressure increased significantly, and patients may have headaches, dizziness, and heart palpitations. When the descending aorta is severely constricted, most of the blood discharged from the heart flows to the upper extremities, causing elevation of blood pressure in the upper limbs . Insufficiency of the aortic valve leads to systolic hypertension .
  3. Extensive: Involving multiple blood vessels, belonging to multiple lesions, characterized by brachiocephalic type and thoracic-abdominal aortic type.
  4. Pulmonary Artery Type: About half of the patients may have pulmonary arterial involvement, and pulmonary arterial involvement alone is rare. Mild or moderate pulmonary hypertension can occur in the late stages, with palpitations, shortness of breath, or heart failure .

Diagnosis [ edit ]

Diagnostic criteria [ edit ]

Women under the age of 40 are subject to unilateral or bilateral limb, cerebral artery ischemic symptoms appear, the recent sudden emergence of resistant hypertension or high blood pressure, no pulse or signs appear ( carotid artery , radial artery and brachial artery pulse weakened or disappeared) When there are symptoms of retinopathy, the disease should be suspected. At present, the diagnostic criteria of aortoarteritis adopt the classification criteria proposed by the American College of Rheumatology in 1990 [8] :
  1. The onset age is below 40 years old;
  2. Intermittent dyskinesia of the limb: When one or more limbs are active, fatigue and muscle discomfort increase gradually, and the upper limbs are obvious;
  3. One side or both sides of the radial artery weakened;
  4. Bilateral upper limb systolic blood pressure difference is greater than 10mmHg;
  5. One or both sides of the subclavian artery or abdominal aorta smell and noise;
  6. Angiographic abnormalities: Aortic primary branch or proximal or distal aorta stenosis or occlusion, lesions often focal or segmental, and not caused by atherosclerosis , fibromuscular dysplasia or similar causes.
Satisfaction of the above 3 or more can be diagnosed as Takayasu arteritis. The diagnostic standard has a sensitivity of 90.5% and a specificity of 97.8%.

Auxiliary check [ edit ]

  • Blood tests: There are currently no specific serologic markers [9] and they are generally reactions to inflammatory activity. Erythrocyte sedimentation rate (ESR) can be detected , and ESR is an important indicator reflecting the disease activity of this disease. The ESR can be increased when the atherosclerotic disease is active, and the ESR is normal after the disease is stable. C-reactive protein is positive, its clinical significance is the same as ESR, and it is one of the indicators of disease activity of this disease. A small number of patients have elevated white blood cells, increased platelets, or chronic mild anemia during active disease.
  • Film degree exam
    • Color Doppler ultrasonography: The degree of stenosis or occlusion of the aorta and its main branches (carotid artery, subclavian artery, renal artery, etc.) can be probed, and the arterial pressure of the limb can also be measured. This is the preferred examination for screening for arteritis, but Exploration of distal branch vessels is difficult.
    • CT angiography (CTA): It is the first choice for the diagnosis and follow-up of patients with arterial vasculature, which can directly show changes in the lumen of the involved vessel, the diameter of the vessel, the smoothness of the vessel wall, and the extent and length of the affected vessels . [10] However, CTA examination can not observe the change of blood vessel wall thickness.
    • Magnetic resonance imaging (MRI): It can show the shape and structure of the affected blood vessels and the edema around the blood vessel wall, which helps to judge whether the disease is active or not.
    • Digital Subtraction Angiography (DSA): It is the gold standard for the diagnosis of Takayasu arteritis, which can be used to understand the location, extent, and extent of vascular lesions in detail. However, the disadvantage of DSA is that it does not appear clearly in the visceral arterioles such as the intrarenal arterioles.

Treatment [ edit ]

Medication [ edit ]

About 20% of arteritis is self-limited, and these patients can be followed up without complications. There are early upper respiratory tract, lung or other organ infections. The effective control of infection may have a certain significance in preventing the development of the disease. Commonly used drugs are glucocorticoids and immunosuppressants . Glucocorticoids are currently the main therapeutic drugs for TAMA, and timely medication can effectively improve symptoms and relieve the disease. Generally oral prednisone daily 1mg/kg, and gradually reduce after one month of maintenance, usually with a decline in ESR and C-reactive protein. In the normal reduction of the indicator, the dose was reduced to 5-10 mg daily for a long period of time. Active severe cases can try high-dose methylprednisolone intravenous therapy. Long-term use should prevent the occurrence of osteoporosis . The use of immunosuppressants in combination with glucocorticoids can enhance the efficacy Commonly used immunosuppressants include cyclophosphamide , methotrexate and azathioprine . In the use of immunosuppressive agents, blood routines, urine routines, and liver and kidney function should be monitored to prevent adverse reactions.
Symptomatic support treatment includes lowering blood pressure, dilating blood vessels, and improving microcirculation. Dilation of blood vessels and improvement of microcirculation drugs such as aspirin and dipyridamole reduce blood viscosity, reduce red blood cell aggregation, prolong blood clotting time, protect blood vessels, improve arterial function, and facilitate restoration of aortic arteritis. People with high levels of suspicion of tuberculosis should also be treated for tuberculosis.

Interventional treatment [ edit ]

Interventional treatment provides a minimally invasive, curative and reliable treatment for arteritis. Percutaneous transluminal angioplasty is currently used to treat renal artery stenosis and abdominal aorta, subclavian artery stenosis, etc., to obtain better results.

Surgical treatment [ edit ]

The purpose of surgical treatment is mainly to resolve renal vascular hypertension and cerebral ischemia. Methods include: endarterectomy and autologous venous patch repair, revascularization, bypass grafting, autologous renal transplantation, and renal revascularization.

Prognosis [ edit ]

TKA is a chronic progressive vascular disease. If the condition is stable, the prognosis is good. The prognosis depends on the degree of hypertension and the condition of blood supply to the brain. Prompt and timely use of glucocorticoid combined with immunosuppressive agents can improve prognosis. The main cause of death for arteritis is cerebral hemorrhage and renal failure .

References [ edit ]

  1. Moved to^ James, William D.; Berger, Timothy G.; et al. Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. 2006. ISBN 0-7216-2921-0 .
  2. ^ 移至：2.0 2.1 American College of Physicians (ACP). Medical Knowledge Self-Assessment Program (MKSAP-15): Rheumatology. "Systemic Vasculitis." Pg. 65-67. 2009, ACP. 存檔副本. [2010-11-28]. （原始內容存檔於2010-10-30）.
  3. 移至^ M. Takayasu. A case with peculiar changes of the central retinal vessels. Acta Societatis ophthalmologicae Japonicae, Tokyo 1908, 12:554-555
  4. ^ 移至：4.0 4.1 Takayasu Arteritis - Pediatrics (eMedicine)
  5. 移至^ Watts R,Al-Taiar A,Mooney J,et a1．The epidemiology of Takayasu arteritis in the UK. Rheumatology,2009,48:1008-101
  6. 移至^ John Barone, M.D. USMLE Step 1 Lecture Notes. "Vascular Pathology." 2008, Kaplan Inc. pg 101
  7. 移至^ RonMd AA，Ricard C．Vascular manifestations of systemic autoimmune diseases．Florida: CRC,200l:25l-273
  8. 移至^ Arend WP, Michel BA, Bloch DA, Hunder GG, Calabrese LH, Edworthy SM, Fauci AS, Leavitt RY, Lie JT, Lightfoot RW Jr, et al.The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis.Arthritis Rheum.1990 Aug;33(8):1129-1134
  9. 移至^ Kasuya N, Kishi Y, Isobe M, Yoshida M, Numano F. P-selectin expression,but not GPIIb/IIIa Activation,is enhanced in the inflammatory stage of Takayasu's arteritis:Circ J 2006,70:600-604
  10. Moved to^ Yadav MK.Takayasu arteritis:clinical and CT-arIgiography profile of 25 patients and a brief review of literature.Indian Heart J,2007,59:468-474
Authoritative control
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