Giant cell arteritis and polymyalgia rheumatica

Introduction to giant cell arteritis and rheumatic polymyalgia Giant cell arteritis (GCA) is a systemic vasculitis syndrome characterized by invasion of the cranial artery. In the 19th century, Jonathon Hutchinson first described a male patient who had difficulty wearing a cap due to tenderness of the radial artery. Since then, the clinical features of GCA have been gradually identified. It is a chronic granulomatous vasculitis, a giant cell artery discovered in the early years. Inflammatory cases are almost all involved in the radial artery, accompanied by ankle headache, tenderness of the scalp and radial artery, so it is also known as temporal arteritis (TA), granulomatous vasculitis or cranial arteritis. It is now known that TA mainly involves the branches of arteries emanating from the aortic arch, and may also involve other medium-sized arteries. The vascular inflammation site can form granuloma, which contains a large number of giant cells, so it is now called giant cell arteritis. Giant cells are any large cells that can have one or more nuclei, such as multinuclear giant cells (MGCs). It includes two diseases with similar pathology and different clinical manifestations, namely, temporal arteritis (TA) and multiple arteritis (Takayasusdisease). GCA is characterized by axillary headache, intermittent mandibular movement disorder and blindness. All ages are over 50 years old. basic knowledge The proportion of illness: 0.001% Susceptible population: long-term smokers Mode of infection: non-infectious Complications: arteritis

Causes of giant cell arteritis and rheumatic polymyalgia

(1) Causes of the disease

The specific etiology of GCA and PMR is still unclear. Although the incidence of the two is related to age, geographical distribution and ethnicity, the specific roles of age, environmental and genetic factors in the pathogenesis are not clear. PMR and GCA have Family aggregation, the incidence of whites in Europe and America is significantly higher than that of blacks, and there is the same ethnic background between whites in northern Europe and the United States. HLA-DR4 is twice as frequent in GCA as normal controls, so HLA-DR4 may be The main genetic factors, further experiments found that HLA-DR4 allele HLA-DRB1 is most closely related to GCA, and its genetic polymorphism is mainly located in the second hypervariable region.

Some scholars believe that parvovirus B19 and Chlamydia pneumoniae are related to the pathogenesis of GCA, but the exact results need further research.

(two) pathogenesis

Humoral immunity and cellular immunity are involved in the pathogenesis of GCA. The pathological features are mainly affecting the aorta, accompanied by chronic inflammatory processes of various cytokines. The specific cytokines present in GCA and PMR-affected tissues affect the clinical manifestations of the disease. The cytokine composition is different. In GCA, the affected iliac arteries have IFN- and adiponectin produced by T lymphocytes, IL-1, IL-6 and metastatic growth factor (TGF-) produced by macrophages. IL-6 levels are elevated in both GCA and PMR, and their levels are related to disease activity. IFN- is a key cytokine in GCA, forming with giant cells, thickening of intima, and tissue deficiency. Blood and neovascularization are associated with elevated levels of TNF- in GCA and PMR. In PMR, TGF-, IL-1 and adiploid transcripts are detected in the radial artery, but no IFN-. Transcripts, Table 1 shows the distribution of cytokines in different lesions of the radial artery in GCA, suggesting that the arterial wall, especially the adventitia, is a local cell-mediated immune response site.

GCA patients with high IFN- expression in the brachial artery often have typical multinucleated giant cells (MGCs). Unlike macrophages, MGCs have important secretory functions in addition to phagocytosis, and MGCs secrete platelet transforming growth factor (PDGF). The latter can stimulate the intimal hyperplasia, and MGCs also secrete vascular endothelial growth factor (VEGF), which is the key mediator of the formation of neovascularization in the arterial wall. Concentric hypervascular intimal hyperplasia is an important potential pathological damage mechanism of GCA. The researchers believe that intimal hyperplasia is the result of the response of the vessel wall to injury, and it is also a repair mechanism, in which PDGF is an important stimulating factor for intimal hyperplasia, PDGF is derived from giant cells and macrophages. It distinguishes GCA from other vascular lesions. For example, PDGF in atherosclerotic diseases is mainly derived from resident smooth muscle cells, not monocytes.

Early reports of PMR peripheral blood CD8 cells are inconsistent. There are reports that CD8 cells are elevated and decreased. It is even thought that the decline of CD8 cells is related to the disease activity of PMR. Recent studies have revealed that PMR is active regardless of disease activity or not. There was no significant change in the percentage and absolute count of blood CD8 cells. In GCA, almost all lesions were associated with effector macrophages. Macrophages differentiated from IFN--secreting T lymphocytes. Route and acquire a range of potential damage capabilities. In GCA, macrophages secrete pro-inflammatory cytokines to aggravate inflammation. In addition, macrophages located in the vascular membrane play a role in oxidative destruction by lipid peroxidase. Vascular smooth muscle cells and their matrix components; these macrophages also provide reactive oxygen intermediates, which together with nitrogen intermediates cause endothelial cell protein digestion; membrane macrophages also produce oxygen free radicals and metalloproteinases, Lead to the lysis of the elastic layer of the media, the macrophages in the middle layer of the artery, in addition to releasing the tissue-destroying enzyme, Cytokines (such as platelet growth factor PDGF, vascular endothelial growth factor VEGF) mediate tissue repair, leading to intimal hyperplasia, resulting in vascular occlusion, blocked blood flow, inflammation is also an important factor affecting endothelial cells, causing neovascularization, which An inflammatory process mainly occurs at the junction of the inner and middle membranes and the outer layer of the blood vessels, so the intima and media of the arteries are the major lesions of GCA.

Cell adhesion molecules also affect the pathogenesis of GCA, and endothelial cells also play an important role. The level of soluble endothelial leukocyte adhesion molecule (ELAM-1) in the serum of GCA patients is elevated, and it is also detected on biopsy specimens of the radial artery. Other adhesion molecules suggest that adhesion molecules are involved in the migration of leukocytes to damaged blood vessels and the interaction between cells, and these processes are involved in the formation of granuloma. The expression of adhesion molecules in neovascularization is much larger than other parts of blood vessels. Recently, Cid Immunohistochemical analysis showed that different adhesion molecules may regulate the interaction between leukocytes and endothelial cells at different levels of the radial artery, while serum E-selectin levels were elevated in PMR patients.

In GCA and PMR, the deposition of immunoglobulins and complements was found in the cells or junctions of the partially involved radial arterial elastic membrane. This finding suggests the presence of antibodies or immune complexes in the blood against the arterial wall, GCA. The levels of circulating immune complexes in the serum of patients with PMR increased during the active phase of the disease, and their concentrations were positively correlated with ESR and -globulin levels, and decreased after treatment of the disease. The pathological features of GCA granuloma formation were more suggestive. The role of cellular immunity in the pathogenesis of GCA.

In GCA, vasculitis is most common in the branches of the aortic arch, but occasionally it can involve any arteries and some veins in the body. The affected vessels are often distributed in segments or flaky, and may also involve longer vessels, taken from the active phase of GCA. Vascular specimens showed that severely involved blood vessels were more common in the superficial temporal artery, vertebral artery and ophthalmic artery and posterior ciliary artery, followed by intracranial artery, extracranial artery and central retinal artery, and autopsy data showed that the aorta was proximal and far End, internal and external carotid arteries, subclavian artery, radial artery and abdominal artery involvement are also common, but intracranial arterial involvement is rare. In some cases, even if the symptoms have been relieved, arterial biopsy is persistent, weak chronic Inflammation exists. In general pathology, GCA is easy to form an aortic aneurysm, dissection and stenosis. The main branches of the aorta are also prone to stenosis. It is not uncommon for cases of various lesions secondary to GCA coronary and aortic arch. As with the thoracic aorta, the abdominal aorta can also be affected, aneurysms and related symptoms can occur, and intestinal infarction can occur, GCA Upper and lower limbs can affect blood vessels supplying the primary, intermittent claudication, when GCA involving large vessels, the damage is difficult to distinguish with arteritis.

In the early stage of disease or mildly damaged cases, lymphocyte aggregation can be seen, limited to the inner and outer elastic layer or outer membrane. Usually, the intimal thickening is accompanied by obvious cell infiltration. When the lesion is severe, the whole blood vessel can be involved, necrosis. The arterial wall (including the elastic layer) and the granuloma can be seen in multinucleated giant cells containing phagocytic debris and foreign bodies, tissue cells, T lymphocyte-assisted lymphocytes and some plasma cells and fibroblasts, eosinophils It can occur, but neutrophils are rare, and there may be thrombosis in the inflammatory activity site. Later, these sites can be recanalized. The inflammation is most obvious at the junction of the mesial elastic layer and the intima, and the elastic fiber is broken and cleaved. Aggregated giant cells are closely related. Cellulose necrosis is rare in necrotic vessels. Giant cells are not found in the whole blood vessels. By increasing the pathological examination range of vasculitis, the detection rate of giant cells can be increased, and the cell infiltration in the chronic phase of vasculitis disappears. Intimal fibrosis, thickening of the intima.

In addition to the above-mentioned manifestations of vasculitis, the systemic manifestations of GCA are related to the inflammatory process and the role of cytokines, and the involvement of terminal organs is associated with corresponding vascular occlusion.

However, in addition to the possible vasculitis of PMR, there are few pathological findings, occasional reports of granulomatous myocarditis and hepatitis. There are no abnormal findings in PMR muscle biopsy or only non-specific type II muscle fiber atrophy. Some patients with PMR may have There are lymphocyte-based synovitis in the knee joint, sterno-lock joint, shoulder joint and ankle joint. Most synovitis is subclinical. There is no abnormality in X-ray examination, but synovitis can be seen by magnetic resonance imaging (MRI). The radionuclide examination suggests that the bone intake of the PMR patient is increased in some patients.

Giant cell arteritis and rheumatoid polymyalgia prevention

Smoking cessation is an important measure of prevention. Comprehensive data from home and abroad, 80% to 95% of patients smokers. Clinical observations show that smoking cessation can relieve pain, stable condition, and re-smoking symptoms, so patient advice should be given. The patient is strictly prohibited from smoking.

Giant cell arteritis and rheumatoid polymyalgia complications Complications

The pathological features and clinical manifestations of this disease are multi-system damage, and the comorbidities are also diverse.

Giant cell arteritis and rheumatic polymyalgia symptoms Common symptoms Sore throat, low fever, morning stiffness, poor scalp necrosis, dull pain, ptosis, unexplained, fever, scalp tenderness

GCA is a significant heterogeneity, systemic inflammatory disease, diverse clinical manifestations, from unexplained fever, intermittent claudication to blindness, and early description of GCA emphasizes clinical manifestations of involvement of the branches of the ophthalmic artery and external carotid artery. However, GCA itself can almost involve the whole body arteries, so it can analyze various clinical manifestations according to the blood supply range of the affected arteries. GCA and PMR can be two parts of a single disease spectrum, which can cause onset of PMR. When it develops seriously, it becomes GCA, GCA. Some of the same basic symptoms as PMR, such as fatigue, weight loss, fever, etc., about 50% of patients with GCA have clinical features of PMR, such as morning stiffness, soreness and pain in the proximal joint muscles.

1. Patients with systemic symptoms often complain of discomfort, fatigue, fever, anorexia, weight loss, fever is generally low fever, even up to 40 ° C, some patients may have night sweats, GCA unexplained fever is more common than PMR, for older patients appear significant The anorexia and weight loss should also be noted for the exclusion of tumors.

2. Symptoms associated with vasculitis of the external carotid artery. Headache and scalp tenderness are the most common symptoms of GCA. About half of the patients have this as the first symptom. GCA headache is characteristic and is located on one or both sides of the ankle. , described as extracranial, dull pain, acupuncture-like pain or burning pain, mostly persistent, can also be intermittent, patients with occipital artery involvement may have occipital pain, and difficult to comb, and sleep pillow The contact with the pillow is prone to pain, and there is also a report of scalp necrosis. The ear canal, the auricle and the parotid gland can be painful when the arteries of the ear are involved.

Intermittent dyskinesia and pain, especially in masseter muscle chewing, are highly specific. This symptom is highly specific to GCA. It occurs in about 50% of patients with GCA, the maxillary artery and the lingual artery are involved, and can be chewed and spoken. There are reports of pain in the jaw joint and tongue, and there are reports of tongue gangrene.

When the radial artery is involved, it is prominent, bead-like change, tenderness, and can be beaten, but it can also be pulse-free. However, the normalization of the radial artery does not exclude GCA.

3. Symptoms associated with ocular vascular vasculitis In patients with GCA, visual impairment is the most common symptom secondary to ocular arteritis, and it is also a more serious result. Patients with GCA ocular involvement may account for eyesight due to vision. 20% of the patients who suffer from the disease, 60% of them can develop blindness. Recently, due to the increased awareness of the disease, the treatment has been timely, and the blindness rate has dropped significantly, about 6% to 10%.

Most patients complained of sudden visual impairment. A detailed history can be found. About 40% of patients may have headache, fever, discomfort and signs and symptoms of PMR before, blindness may be the first symptom or other symptoms. Suddenly occurring after weeks or months, it is painless. It is common after the headache disappears. The initial manifestation is blurred vision or visual field defect. It can progress to complete blindness within a few days. Blindness can be bilateral or unilateral. If untreated, the contralateral eye can be affected within 1 to 2 weeks, and the ocular lesion usually changes greatly, which is related to the location of the affected blood vessel and the blood supply range.

The posterior ciliary artery supplies the optic nerve, which is one of the most commonly involved vessels of GCA. Therefore, optic nerve ischemia often occurs. Optic nerve atrophy is often seen in ophthalmoscopy. The muscles from the ophthalmic artery supply extraocular muscles, about 5%. The patient's blood vessels can be affected, double vision and ptosis, and can be preceded by blindness. The central retinal artery supplies blood to the retina. It is the terminal branch of the ophthalmic artery. It is less affected, so it is exuded, hemorrhagic and vasculitis. Retinopathy is uncommon. Less than 10% of patients with ocular involvement are associated with central retinal artery occlusion. About 10% of patients with GCA may have transient darkness, and about 80% of untreated patients can develop permanent. blindness.

The visual impairment of GCA is generally irreversible. Male patients have more chances of visual impairment than female patients. It should be noted that visual abnormalities can be a combination of many ischemic diseases, such as optic nerve, extraocular muscles, and optic chiasm. And the ischemia of the brain itself.

4. About 10% to 15% of the symptoms associated with aortic involvement may occur in the aortic arch, thoracic aorta, etc. The vascular murmur and blood vessels may be heard in the neck, subclavian, infraorbital or arterial branches. Tensile, about 88% of large blood vessels are involved in women. The typical age of onset is relatively small, and there are no general symptoms such as fatigue. It is often difficult to diagnose. From the onset to the diagnosis, even if the treatment is effective, some patients can still Thoracic aortic aneurysm appeared 15 years after diagnosis of GCA. Pathologically, giant cell infiltration was observed. These patients had more negative radial artery biopsy, less headache, intermittent dyskinesia and visual acuity. However, there were often intermittent dyskinesias in the upper limbs. The above clinical manifestations can distinguish the involvement of the large blood vessels from the cerebral arteries, and the neck, armpits and radial artery can be murmured when the body is examined.

The main symptoms of aortic involvement are intermittent dyskinesia of the upper and lower limbs, occasionally due to subclavian steal syndrome, intermittent or persistent cerebral ischemia in the aortic arch vascular stenosis, and very few Due to intracerebral artery disease, the abdominal aorta can also be affected. GCA can have symptoms of abdominal aortic aneurysm and intestinal necrosis, but the kidney is rarely affected, the specific cause is unknown.

5. About 30% of patients with neurological manifestations may have neurological lesions. The lesions may be diverse, but the most common are neuropathy, transient cerebral ischemia and stroke. The former includes mononeuropathy, peripheral polyneuropathy and Influence on the lower limbs, it is speculated that the above lesions are caused by the trophic artery involvement of the brain, but the specific reasons remain to be determined. Carotid artery and vertebral basilar artery stenosis, occlusion may cause hemiplegia and brain stem lesions, rare epilepsy, cerebrovascular events or mental disorders In the case of central nervous system diseases, in fact, although most of the GCA lesions occur in the elastic blood vessels, no lesions are found in the epidural vessels. However, the involvement of the aortic arch, including the subclavian artery, can lead to the subclavian artery stealing. Signs and cerebral ischemia, intracranial arteries are rarely involved, because the intracranial arteries are not easy to check, and elderly patients often suffer from atherosclerotic disease, the frequency of GCA leading to significant ischemia of the central nervous system is not clear, peripheral nerves System involvement is also less common.

6. Respiratory system Although GCA rarely invades pulmonary blood vessels, 10% of patients have significant respiratory involvement, especially when GCA is associated with PMR symptoms. Respiratory symptoms include cough, sputum or innocence, sore throat or sound. Hey, imaging examinations and pathogen examinations are mostly abnormal, antibiotic treatment is ineffective, and the causes of respiratory symptoms are not clear, and may be related to local tissue ischemia and the high irritability of affected tissues.

7. Proximal osteoarticular muscle pain and morning stiffness PMR is characterized by symmetrical proximal joint and muscle pain, soreness and morning stiffness. The shoulder, neck and pelvic muscles are most prominent, often symmetrically distributed. Sometimes the distal muscles and joints can also be affected. More than 70% of patients with scapular pain first occur, and then develop to the proximal extremities, neck, chest, buttocks, etc., directly affecting the patient's life, the above symptoms can suddenly start It can also conceal the onset of illness for several weeks to several months. The pain and morning stiffness are aggravated in the morning and during activities. These symptoms may be heavier and the patient's daily activities are limited, so that they cannot turn over and take a deep breath. The muscles may have tenderness and affect. Activity and loss of atrophy, and muscle contracture may occur, muscle strength is usually normal, but often affected by pain assessment, in the PMR, although the patient complained a lot, the symptoms are very heavy, but the body is rarely related to this The positive signs showed typical symptoms that did not match.

PMR can coexist with GCA. 10% to 15% of simple PMR is associated with GCA during radial artery biopsy. On the other hand, 50% to 70% of patients with GCA are associated with PMR and are diagnosed as simple PMR patients. Headaches and changes in vision should be alert to the possibility of developing a GCA.

8. Joint symptoms Most patients have no obvious tenderness in the joint muscles, especially the shoulder and hip joints. This is different from the obvious characteristics of myositis tenderness. GCA itself has no synovitis lesions, but in the knee joint, occasionally the shoulder joint, A moderate amount of joint effusion can occur in the wrist joint. Spanish scholars report that the incidence of distal PMR in the distal PMR is 20%, and the incidence of arthritis in PMR with GCA is 56%, while the incidence of GCA alone. For 11%, carpal tunnel syndrome and acral edema can occur in patients with PMR, sometimes making diagnosis difficult, while GCA patients are absent.

Recent studies have shown that PMR joint pain is not uncommon. It is common for large joints such as shoulders, knees and wrist joints, and sterno-lock joint involvement. PMR joint lesions mainly manifest as tendinitis and synovitis, and primary PMR can also cause In the destruction of the joints, Paice performed a tomographic examination of the sterno-lock joints of 25 patients with PMR. It was found that 11 of them had joint erosion damage, most of them were symmetrical, and the duration of PMR was more than 6 months. Multicenter studies have shown that PMR mild to moderate synovitis mainly affects the proximal joints, the spine and limbs, such as the shoulder joints are most often involved; another 15% to 50% of peripheral joint synovitis, with knee joints The most common and wrist joints, radionuclide bone scan showed 96% of PMR patients with abnormalities, 80% of the shoulder joints and 16% of the hand, wrist, knee radionuclide uptake, magnetic resonance (MRI) examination also showed PMR subacromial / deltoid yinitis is the most common injury in the shoulder. MRI examination showed that the incidence of external joint and soft tissue swelling in the knee joint of PMR patients (50%) was significantly higher than that of rheumatoid arthritis (10%, P =0.02), and joint effusion, synovitis, tendon sheath The incidence of inflammation was not significantly different between the two.

9. Clinical manifestations of rheumatic polymyalgia Patients have almost all systemic symptoms, with fever being the most common, weight loss and fatigue are also common, sometimes the disease is more insidious, sometimes the onset is acute, there can be clear time boundaries, myalgia is The typical manifestations of this disease can be misdiagnosed as frozen shoulder or cervical myopathy in the early stage when only the neck and shoulder muscles are involved. As the disease progresses, the range of muscle involvement gradually expands, which can affect the entire proximal muscle group, including the upper arm and shoulder. , hip, thigh and other parts, morning stiffness can last 1 ~ 2h, patient activity is limited, but unlike rheumatoid arthritis, the latter is mainly characterized by limited joint activity, such as button buttons, the disease is due to the proximal end Muscles are involved, get up, get on the bus, stand up from the chair, comb the hair and other movements, about 1/3 of the patients can not take care of themselves, about 25% of patients with mild synovitis at the shoulder, wrist, knee joints For arthritis, such patients tend to be more women, and the course of disease is long, the number of recurrences is high, and the clinical process is relatively serious. About 10% of patients may have edema of the distal limbs, which is more common in elderly patients with onset disease. Pain and multiple Yan different, often no obvious weakness and muscle atrophy, and not with muscle enzyme elevation, biopsy nor myositis-like changes.

Examination of giant cell arteritis and rheumatic polymyalgia

1. Hematology: The most significant laboratory changes in PMR and GCA are acute phase reactants - a significant increase in erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels, with erythrocyte sedimentation rates typically >50 mm/h or even over 100 mm/h. CRP is elevated within a few hours of the onset of PMR, and CRP is also elevated in patients with normal erythrocyte sedimentation rate. After effective treatment, CRP generally falls to normal within 1 week, while ESR declines slowly, requiring 1 to 2 months or longer. ESR and elevated CRP often indicate recurrent disease. If other clinical features of PMR and GCA, pathological features are typical, even if ESR is normal, the diagnosis cannot be excluded.

About 50% of patients with PMR can have positive cells, anemia of positive pigments, and thrombocytopenia, which is related to the degree of inflammation, and the above indicators of GCA can be normal, in PMR and GCA, rheumatoid factor, antinuclear antibody and others. Autoantibodies have higher titers than normal peers, normal complement levels, and no increase in cryoglobulin and monoclonal globulin.

About one-third of patients with liver function, especially alkaline phosphatase can be elevated, more common in GCA than PMR alone, muscle enzyme (creatine kinase, aldolase) is normal in both PMR and GCA, serum amyloid Elevated A level is an indicator of the activity of PMR. If the level is high or decreases, it will indicate the activity or repetition. Therefore, the serum amyloid A assay has certain effects on the clinical glucocorticoid. value.

2. Imaging examination

Color two-dimensional ultrasound is gradually used for the diagnosis of GCA, color Doppler shows about 22% to 30% of the halo artery hypoechoic halo sign, confirmed by biopsy as GCA, hypoechoic halo sign represents blood vessels Wall edema, the diagnosis in GCA is more significant, sensitivity can reach 73% ~ 86%, specificity is 78% ~ 100%, hypoechoic can disappear after hormone therapy, ultrasound examination of thoracic aorta and abdominal aorta It is helpful for diagnosis and can be found with or without aneurysm formation.

In GCA, angiography of the radial artery is of little value for diagnosis, and the biopsy site of the radial artery cannot be determined. Although PMR has no characteristic imaging changes, X-ray examination, radionuclide scanning, MRI, and ultrasonography are used to determine PMR. The joint involvement still has some value.

3. Other inspections

(1) Electromyography and muscle biopsy: no abnormal findings were found in electromyography, no diagnostic significance for PMR, no characteristic changes in histology of PMR muscle biopsy specimens, non-specific type II muscle fiber atrophy, slippery when muscle was used Liquid and synovial examination showed that the white blood cell count of synovial fluid was located at 1×1098×109/L, mainly monocytes, and synovial biopsy showed mild synovial cell proliferation accompanied by slight lymphocytic infiltration. The examination is of little significance and clinical practice is rare.

(2) Radial artery biopsy: If the PMR patient has symptoms and signs suggesting GCA, or no response to 15 mg of prednisone per day, a radial artery biopsy should be considered. In addition, if an elderly patient has unexplained fever, With the increase of ESR, the infection and tumor detection can not explain the radial artery biopsy, the radial artery biopsy positive can be diagnosed, the specificity of GCA is 100%.

Clinical studies have shown that patients with PMR with impaired or disappeared brachial artery pulsation have a higher positive rate of radial artery biopsy even in the absence of other local symptoms, and a higher positive rate of biopsy when non-specific headache occurs. Radial artery biopsy The positive rate and the degree of ESR increase, the presence or absence of visual symptoms, gender, age, length of onset, and whether there is no correlation between GPR in patients with PMR, and 10% of patients with PMR with local radial artery signs have radial artery biopsy Can be negative.

In order to improve the positive rate of radial artery biopsy in suspected GCA patients, the radial artery with headache side can be selected for biopsy, and the blood vessels at the site with tenderness and bead-like changes are selected. There is no significant difference in the positive rate of arterial trunk and distal branches. Because GCA vascular lesions are sometimes distributed in segments, 2 to 3 cm blood vessels should be taken and multi-segmented to increase the positive rate.

In addition, the bilateral iliac artery is higher than the unilateral positive rate, which can improve the sensitivity of the diagnosis by 11% to 60%. If the clinical high degree of suspected GCA, one side of the radial artery biopsy is negative, the contralateral radial artery biopsy should be performed.

Diagnosis and differentiation of giant cell arteritis and rheumatic polymyalgia

The clinical manifestations of GCA are diverse, easily misdiagnosed or missed, and the unexplained fever and erythrocyte sedimentation rate in the elderly should be considered in GCA, the 1990 American College of Rheumatology (ACR) GCA classification criteria, which emphasize age.

The diagnosis of PMR mainly depends on clinical manifestations. There are 6 diagnostic criteria: 1 the age of onset is >50 years old. At least 2 muscle pains and morning stiffness in the 2 neck, scapula and pelvic belt, time 1 week. 3ESR and/or CRP are elevated. 4 low-dose hormone (prednisone 15mg / d) is effective. 5 no muscle loss or muscle atrophy and muscle redness and heat. 6 Exclude other lesions similar to PMR, such as RA, myositis, tumors and infections, etc., if the above 6 can be diagnosed as PMR.

The susceptible population of GCA and PMR, history characteristics, clinical manifestations and pathological features are easily differentiated from other vasculitis, and the following diseases should be excluded: atherosclerosis (especially carotid atherosclerosis), myositis, unexplained Fever, infective endocarditis, non-Hodgkin's lymphoma, multiple myeloma, rheumatoid arthritis, systemic lupus erythematosus, arteritis, tuberculosis, etc., in addition to thyroid myopathy.

PMR with peripheral arthritis and RA with PMR-like symptoms were easily misdiagnosed. Caporali et al followed 116 patients with PMR and RA with PMR-like symptoms. 94 patients were diagnosed with PMR and 22 with RA. After 1 year of follow-up, 19 patients with newly diagnosed PMR developed RA. Only 65 patients were diagnosed with PMR at the end of follow-up. Although synovitis of the peripheral joints helps to distinguish the two, early diagnosis of the disease remains. It must be difficult.

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