Giant cell arteritis scleritis

Introduction to giant cell arteritis scleitis Giant cell arteritis (GCA), also known as temporal arteritis, cranial arteritis or granulomatous arteritis, is an unexplained systemic vasculitis. It mainly involves the carotid artery of the vascular system and the moderately extracranial arteries (the superficial temporal artery, the spinal artery and the ophthalmic artery, etc.). basic knowledge The proportion of illness: 0.0021% Susceptible people: no special people Mode of infection: non-infectious Complications: neck and shoulder pain

Cause of giant cell arteritis inflammatory scleritis

(1) Causes of the disease

HLA-B8 and HLA-DR4 have a certain correlation with GCA, but it is not very certain.

(two) pathogenesis

The characteristics of autoimmune diseases, the specific mechanism is still unclear.

Giant cell arterial inflammatory scleritis prevention

There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease.

Giant cell arterial scleritis complications Complications neck and shoulder pain

40% to 60% of patients with GCA have PMR, which is painful or stiff in the neck, shoulders, buttocks. In most cases, shoulder pain is the first symptom, and the rest is the onset of hip and neck pain. In the morning or at rest Muscle stiffness is more common after a period of time, 20% to 40% of patients with GCA, PMR is the first symptom, and 15% of patients with PMR have GCA. When PMR signs of vasculitis, ESR should be performed immediately. If the ESR increases, a large dose of oral glucocorticoids should be given as soon as possible.

Giant cell arterial inflammatory sclera symptoms common symptoms visual impairment single eye blindness paralysis insomnia angina edema muscle pain hyperemia response dull diplopia

Eye performance

The clinical manifestations of the eye often appear several weeks after the onset of systemic disease. Blindness is the most common ocular symptom. The incidence of blindness in early reports is as high as 35% to 50%. With the improvement of diagnosis and treatment, the incidence is decreasing. To 7% to 8%, the occurrence of blindness is due to anterior ischemic optic neuropathy (AION) or central retinal artery or its branch obstruction, when the two main ciliary states of the optic nerve and choroid are supplied. Arterial occlusion can lead to arterial AION in patients with GCA, which is characterized by single-eye blindness or transient blackness, sometimes alternating between eyes, lasting 2 to 3 minutes, rarely lasting 5 to 30 minutes, and transient blackmont is going to be The most important aura symptoms of blindness, such as not being treated in time, 40% to 50% of patients may have sudden changes in sudden vision, often bilateral, can occur at the same time or successively, other eye performance Color vision disorder, afferent pupillary disorder (Marcus Gunn pupil) and severe optic disc edema, fundus examination of arterial AION manifested as pale optic disc edema, ciliary artery occlusion and cotton-like exudation, To identify the non-arterial of AION.

Diplopia is also a common clinical manifestation of GCA persistence. Diplopia can be caused by cerebral nerve palsy in VI, or by cerebrospinal neuropathy in III. In some cases, ocular dyskinesia is caused by ocular muscle ischemia, not Caused by neuropathy.

Because GCA is involved, the middle artery and a small amount of ocular tissue, no typical conjunctiva, cornea, sclera, superficial sclera, uveal or retinal vasculitis, sometimes small blood vessels of the ciliary anterior and ciliary long arteries can be affected, Scleritis can also occur.

GCA patients have rare scleritis, but when older patients with scleritis have significant ESR, double vision, decreased vision, AION, central retinal artery and its branches, it is possible to consider GCA. It is reported that the incidence of polymyalgia rheumatica (PMR) in patients with scleritis is 0.68%. Scleritis is associated with systemic disease activity. One of 172 cases of scleritis by Foster et al. GCA of PMR.

2. Non-eye performance

The most common clinical manifestation of GCA is that about 2/3 of the patients have one or both headaches, which are also the initial or first symptoms of the disease. The headache is characterized by beating or tingling, usually on the temporal or occipital side. Causes insomnia, most patients can also have other cranial symptoms such as scalp tenderness or intermittent pain during chewing, about half of patients may be accompanied by systemic symptoms such as fatigue, fever, loss of appetite and weight loss, etc. These symptoms can be GCA The first performance, because of its non-specificity, can not cause the patient to pay attention, until the specific scalp tenderness or intermittent pain or serious vision loss during chewing, go to the hospital.

Although the carotid and extracranial arteries are the most commonly affected arteries of GCA, the aorta and its branches in the upper limbs and neck can also be involved, resulting in cardiovascular and cerebrovascular diseases, upper extremity pain, carotid artery, subclavian artery or Brachial murmurs, sometimes pulsation of the carotid and upper extremity arteries weakened or disappeared, occasional coronary arteritis caused by angina pectoris, congestive heart failure and myocardial infarction, can also cause neurological diseases, such as peripheral neuropathy, hemiplegia, suddenness Hearing loss, unresponsiveness, depression, mental symptoms and brain dryness.

Giant cell arterial scleritis

In most patients, ESR is increased, but 10% to 15% of GCA patients can have normal ESR, and other acute reactants such as C-reactive protein (CRP), fibrinogen, and elevated globulin can be seen in patients with GCA. Increased white blood cells, anemia, and serum alkaline phosphatase (AKP), glutamic-oxaloacetic transaminase (GOT), and gamma-glutamyltransferase (GT) may also occur. Prolonged prothrombin time and peripheral blood CD8+ lymphocyte reduction may occur.

Ultrasound examination

Concealed scleritis can be confirmed, especially in the posterior sclera.

2. Superficial temporal artery biopsy

This method can confirm the disease. In a few cases, the facial artery and occipital artery biopsy can be localized due to arterial involvement. Therefore, when it is suspected that there is inflammation in a segmental artery, the artery should be taken within a few centimeters of the artery (usually 1 More than 5 cm), a careful histological examination was performed. The pathological diagnosis was based on the presence of non-granulomatous inflammation of the arterial wall or granulomatous inflammation associated with epithelial cells, and multinucleated giant cells. Infiltration, some cases have Langerhans cells, of which multinucleated giant cells are the most characteristic, but pathology does not necessarily require the discovery of giant cells to diagnose the disease, because the affected arteries are mostly segmental, hopping, GCA and Patients with elevated ESR may also have negative results of radial artery biopsy. If the clinically highly suspected GCA is negative for the first radial artery biopsy, a contralateral arterial biopsy may be performed to further confirm the diagnosis. The biopsy should be performed within 1 week of glucocorticoid therapy. Because the positive rate of patients who did not receive glucocorticoid treatment was 82%, and glucocorticoid treatment decreased to 60% at 1 week.

Diagnosis and differentiation of giant cell arterial scleritis

All patients over the age of 60, have headaches, transient visual impairment or even blindness, PMR, unexplained persistent fever, anemia or ESR increase should consider the diagnosis of GCA, when the patient has symptoms of the eye or GCA and When ESR is increased, high-dose oral glucocorticoid therapy should be administered immediately, even if biopsy is not performed.

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