Giant cell arteritis

Introduction to giant cell arteritis Giant cell arteritis (giant cellarteritis) is a wide range of vascular diseases. It used to be called cranial arteritis, temporal arteritis, granulomatous arteritis, and later recognized that any large artery in the body can be involved. Its pathological features are named giant cell arteritis, which is a special type of granulomatous arteritis. Clinical manifestations are mostly caused by changes in vascular occlusion. basic knowledge The proportion of the disease: the incidence rate is about 0.001% -0.002% Susceptible population: more common in the elderly, the average age of onset is 70 years old (50 to 90 years old) Mode of infection: non-infectious Complications: dizziness, insomnia

Cause of giant cell arteritis

GCA is extensive arteritis, which can be affected by the middle and aorta. It is common in carotid artery branches, such as superficial temporal artery, vertebral artery, ophthalmic artery and posterior ciliary artery, followed by internal carotid and external carotid artery; about 10% to 15% Large arteries such as the aortic arch, proximal and distal aorta are involved; while the lung, kidney, and splenic arteries are less involved, and the affected arterial lesions are segmentally hopped, which is the involvement of the distal aorta of patchy hyperplasia; and the lungs, kidneys, The splenic artery is less involved, and the affected arterial lesions are segmental jump distribution, which is patchy proliferative granuloma. The tissue sections of the inflammation area show lymphocytes, macrophages, tissue cells and multinucleated giant cells infiltrating, and the elastic basement membrane Centralized full-thickness arteritis can lead to rupture of the vessel wall, thickening of the intima, stenosis of the membrane, and occlusion [5,6]. The most characteristic of multinucleated giant cells in infiltrating cells, occasionally eosinophils, Granulocyte-like fibrin deposition is rare.

(1) Causes of the disease

The etiology of GCA and PMR is unknown. The family morbidity investigation found that the first-degree relatives of GCA and PMR patients had more morbidity, and most of them had HLA-DR4 and CW3 suggesting genetic susceptibility. The GCA inflammatory response was concentrated in the intra-arterial elastic membrane. It may be related to some of the autoantigens. Immunohistochemical studies have also found that there are immunoglobulin deposits in the wall of the iliac artery of inflammation. The infiltrating inflammatory cells are mainly TH cells, and the lymphocytes of the peripheral blood of the patient are in the test tube. Human arteries and muscle resistance are sensitive.

(two) pathogenesis

The GCA inflammatory response is concentrated in the intra-arterial elastic membrane, which may be related to some of the autoantigens. The lymphocytes around the patient's blood are sensitive to human arteries and muscle antigens in vitro. Studies have found that there are immunoglobulins in the wall of the iliac artery of inflammation. Protein deposition, infiltrating inflammatory cells are mainly T cells. In addition, elevated levels of IL-2 and IFN- mRNA in the specimens suggest that there are T cell-dependent immunopathological responses in the pathogenesis.

Giant cell arteritis prevention

As the cause of this disease is still unclear, there is currently no effective prevention method, but attention should be paid to prevent complications.

Giant cell arteritis complications Complications, dizziness, insomnia

Common complications of GCA:

1, chew pause (jaw claudication) and swallowing or language pause.

2, depending on eyelid drooping or visual impairment, blindness is one of the serious complications of GCA.

3, some patients may have earache, dizziness and hearing loss.

4, depression, memory loss, insomnia and so on.

Giant cell arteritis symptoms Common symptoms Pulseless depression, dizziness, insomnia, inflammation, calf ulcer, tinnitus, inflated superficial temporal artery, drooping, drooping, weight loss

GCA is generalized arteritis, moderate and large arteries are often involved, common in carotid artery branches, such as superficial cervical artery, vertebral artery, ophthalmic artery and posterior ciliary artery, followed by internal carotid and external carotid artery; about 10% to 15% Large arteries such as the aortic arch, proximal and distal aorta are involved; and the lungs, kidneys, and splenic arteries are less involved.

More common in the elderly, the average age of onset is 70 years old (50 to 90 years old), more women than men (2:1), often sudden onset, typical manifestations of symptoms associated with arteritis.

1. Headache: It is the most common symptom, which is tension pain or superficial burning of the side or both sides of the ankle, forehead or occiput. Painful nodules or knots of the surface may sometimes touch the surface. The swelling of the superficial temporal artery and so on.

2. Skin damage : The affected scalp may be inflamed and swollen due to ischemia. Buccal, ulcer, necrosis, common senile purpura, senile arterial calf ulcer and necrosis may occur as the disease progresses.

3. Other symptoms of insufficiency of cranial artery : typical intermittent exercise pause, double vision, drooping eyelid or visual impairment, about 10% to 20% of patients have one or both sides of blindness or transient visual impairment, black Blindness is one of the serious complications.

4. Other arterial involvement: intermittent dyskinesia of the upper extremity or intermittent claudication of the lower extremities; when the carotid artery, subclavian artery or radial artery is involved, vascular murmurs may be heard, pulsation weakened or pulsation disappeared (no pulse), etc.; aortic arch or When the aorta is involved, it can lead to the separation of the aortic arch wall layer, resulting in an aneurysm or dissection aneurysm, requiring an angiographic diagnosis.

5. Central nervous system performance : GCA may have depression, memory loss and other symptoms such as insomnia.

Anyone over the age of 50, there is no obvious cause of fever, burnout, weight loss, anemia, erythrocyte sedimentation> 50mm / h, accompanied by recent headaches, visual impairment or other signs of insufficient blood supply to the cranial artery, such as masticatory muscle intermittent dyskinesia , tinnitus, dizziness, etc., you can consider the diagnosis.

Inspection of giant cell arteritis

GCA and PMR have no specific experimental indicators, only mild to moderate positive pigmented cell anemia, serum albumin is slightly reduced, blood sputum protein electrophoresis shows increased 2 globulin, serum transaminase and alkaline phosphatase activity is light Increased degree, etc., the more prominent experimental abnormalities are increased erythrocyte sedimentation rate (GCA activity period is often as high as 100mm / h), and C-reactive protein quantitative increase.

Arterial biopsy

Superficial temporal artery or occipital artery biopsy is the most reliable method for the diagnosis of GCA. The positive rate of superficial temporal artery biopsy is between 40% and 80%, and the specificity is 100%. Because of the segmental jump distribution of GCA lesions, biopsy should be performed. Take a few cm length, it is appropriate to have a tender or nodular part, and continuous pathological section to improve the detection rate, radial artery biopsy is safer, one side of the biopsy negative can be used for the other side or choose the pillow Arterial biopsy.

Brachial angiography

It has certain value for the diagnosis of GCA. It can be found that the radial artery is irregular and narrow, and it can also be used as an indication for the biopsy site of the radial artery.

3. Selective aortic angiography

Selective angiography, such as aortic arch and its branch arteries, can be performed when suspected aortic involvement.

Diagnosis and diagnosis of giant cell arteritis

Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

Differential diagnosis

1. Nodular polyarteritis: mainly invading small and medium arteries, such as renal artery (70% to 80%), celiac artery or mesenteric artery (30% to 50%), rarely involving the radial artery.

2. Allergic vasculitis: mainly involving small blood vessels, small veins or capillaries, obvious skin lesions such as maculopapular rash, papules, cyanosis, ecchymoses, nodules, ulcers, etc.

3. Wegener granuloma: above, lower respiratory tract granuloma, generalized small and medium arteritis and focal necrotic glomerulonephritis (80%) as the main features.

4. Aortic arch arteritis: Aortic arch arteritis has a wide range of lesions, often causing segmental stenosis of the arteries, arterial dilatation before and after occlusion or constriction, and GCA invading the aorta is rare.

5. Others: Identification should be based on malignant tumors, systemic or systemic infections or other causes of fever, headache, anemia, blindness, etc.

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