Rheumatoid Arthritis

Introduction

Introduction Rheumatoid arthritis, also known as rheumatoid arthritis (RA), is a chronic systemic inflammatory disease whose etiology is not yet known. Rheumatoid arthritis is currently recognized as an autoimmune disease. May be related to differences in endocrine, metabolism, nutrition, geography, occupation, psychology and social environment, bacterial and viral infections and genetic factors, with chronic, symmetrical, multiple synovial arthritis and extra-articular lesions as the main clinical Performance, belonging to autoimmune inflammatory diseases.

Cause

Cause

Causes

The cause of rheumatoid arthritis is not clear, and it is generally considered to be closely related to factors such as heredity, environment and infection.

genetic factors:

The risk of illness in grade 1 relatives of patients with rheumatoid arthritis is 1.5 times higher than that of the general population. The results of the twin study show that among the various factors associated with rheumatoid arthritis, genetic factors account for 50% to 60%. Susceptible genes associated with the onset of rheumatoid arthritis include HLA-DR, PADI4, and PTPN22.

Infection factors:

Certain viral and bacterial infections may act as a triggering factor to initiate an immune response in an individual carrying a susceptible gene, which in turn leads to the onset of rheumatoid arthritis. Pathogens associated with the onset of rheumatoid arthritis include Epstein-Barr virus, parvovirus B19, influenza virus, and M. tuberculosis.

Sex hormones:

The incidence of rheumatoid arthritis is between 1:2 and 4, suggesting that sex hormones may be involved in the disease. In addition, women with rheumatoid arthritis can be relieved during pregnancy, and relapse easily 1 to 3 months after delivery, suggesting that progesterone levels or estrogen-progesterone disorders may be associated with the onset of rheumatoid arthritis.

other factors:

Factors such as smoking, cold, trauma and mental stimulation may be associated with the development of rheumatoid arthritis.

Pathogenesis

It is not clear how the above-mentioned pathogenic factors break the immune tolerance and initiate the autoimmune process. At present, the pathogenesis of rheumatoid arthritis mainly has the following hypotheses.

Molecular simulation:

The molecular simulation hypothesis suggests that certain components of the pathogen have similar epitopes to the autoantigen, and the resulting immune response against the pathogen may respond to its own components, resulting in damage to its own tissue.

Epitope expansion:

Epitope expansion refers to the expansion of response of T cells or B cells to individual epitopes in the early stages of an immune response to responses to other epitopes. In the very early stages of rheumatoid arthritis, only a small number of antibodies may be detected in the body, and as autoimmune responses progress, a variety of autoantibodies appear.

Fuzzy recognition:

Studies have found that the binding of HLA and antigen is not strictly structurally specific. The same antigen can be recognized by multiple HLA phenotypes, and the same HLA molecule can bind different antigens separately, which becomes a fuzzy recognition. The occurrence of rheumatoid arthritis may cause the onset of HLA-DR4/1 or other class II HLA gene carriers through fuzzy recognition between T cell receptors and HLA-DRB1.

pathology

The main pathological change of rheumatoid arthritis is synovitis, which is characterized by synovial hyperplasia and inflammatory cell infiltration. Synovial changes in rheumatoid arthritis can be divided into inflammatory phase, vasospasm formation and fibrosis phase. Angiogenesis is an important pathological feature of the synovial membrane of rheumatoid arthritis and plays an important role in the process of cartilage and bone destruction in rheumatoid arthritis. The main pathological basis of extra-articular manifestations is vasculitis. Rheumatoid nodules are characteristic manifestations. The center of the nodules is cellulose-like necrotic tissue, surrounded by "grid-like" tissue cells, fibroblasts and macrophages.

Examine

an examination

Related inspection

Synovial fluid routine examination of eosinophilic number lupus anticoagulant factor PPD test anti-cyclic citrullinated peptide antibody (anti-CCP)

Auxiliary inspection

1. Regular inspection:

(1) Blood routine: About 30% of patients with rheumatoid arthritis have anemia, mostly positive cell anemia. Platelet elevation during the active period of the disease. In a few cases, there is a decrease in white blood cells, such as Felty syndrome.

(2) Acute phase reactants: Most patients with rheumatoid arthritis have an increased erythrocyte sedimentation rate and elevated C-reactive protein during the active phase, and return to normal when the condition is relieved.

2. Autoantibodies:

(1) Rheumatoid factor (RF): 75% to 85% of patients are positive for serum rheumatoid factor and are associated with disease and extra-articular manifestations.

(2) Anti-citrullinated protein antibody (ACPA): Anti-citrullinated protein antibody is a generic term for autoantibodies containing citrullinated epitopes, and is highly sensitive and specific for the diagnosis of rheumatoid arthritis. Sexuality and is closely related to the condition and prognosis of rheumatoid arthritis.

3. Synovial fluid examination:

The joint fluid of patients with rheumatoid arthritis is generally inflammatory. The total number of white blood cells can reach (10~10000)×10/L, and the cell classification is mainly neutrophils.

4. Imaging examination:

(1) X-ray examination: early X-ray showed swelling of soft tissue around the joint and osteoporosis near the joint; joint surface damage, joint space stenosis, joint fusion or dislocation may occur as the disease progresses.

(2) Magnetic resonance imaging (MRI): Magnetic resonance imaging is superior to X-ray films in displaying joint lesions, and has been increasingly used in the diagnosis of rheumatoid arthritis in recent years. Magnetic resonance imaging can show synovial thickening, bone marrow edema and mild articular surface erosion at the beginning of arthritic reactions, which is beneficial for the early diagnosis of rheumatoid arthritis.

(3) Ultrasound: High-frequency ultrasound can clearly show the joint cavity, joint synovium, bursae, joint cavity effusion, articular cartilage thickness and morphology, color Doppler flow imaging (CDFI) and color Doppler energy The map (CDE) can visually detect the distribution of blood flow in the joint tissue, reflect the synovial hyperplasia, and has high sensitivity. Ultrasound can also dynamically determine the amount of joint fluid and the distance from the body surface to guide joint puncture and treatment.

Diagnosis

Differential diagnosis

In the diagnosis of rheumatoid arthritis, attention should be paid to osteoarthritis, gouty arthritis, reactive arthritis, psoriatic arthritis and other connective tissue diseases (systemic lupus erythematosus, Sjogren's syndrome, scleroderma) Identification of arthritis caused by et al.

(1) Osteoarthritis: The disease is degenerative osteoarthrosis. The age of onset is more than 40 years old, mainly involving the weight-bearing joints such as knee and spine. Joint pain is aggravated during exercise, and joint swelling and effusion may occur. Finger osteoarthritis is often misdiagnosed as rheumatoid arthritis, especially when there is a Heberden nodule in the distal interphalangeal joint and a Bouchard nodule in the proximal knuckle. inflammation. Osteoarthritis usually has no migratory pain, and most patients have normal erythrocyte sedimentation rate, negative for rheumatoid factor or positive for low titer. X-ray showed narrow joint space, lip-like hyperplasia or osteophyte formation at the edge of the joint.

(2) Gout: Chronic gouty arthritis is sometimes similar to rheumatoid arthritis. Gouty arthritis is more common in middle-aged and elderly men. It is often recurrent. The predilection site is the unilateral first metatarsophalangeal joint or ankle joint. Invasion of knees, ankles, elbows, wrists and hand joints, blood uric acid levels are usually increased in acute attacks, and chronic gouty arthritis can occur in joints and auricles.

(3) psoriatic arthritis: psoriatic arthritis is mainly affected by the distal joints of the fingers or toes, and joint deformities may occur, but rheumatoid factor is negative, and skin or nail lesions with psoriasis are associated.

(4) Ankylosing spondylitis: This disease mainly invades the spine, but the surrounding joints can also be affected, especially those with knee, ankle and hip joints as the first symptom, which needs to be differentiated from rheumatoid arthritis. The disease has the following characteristics:

1 more common in young men;

2 mainly invades the ankle joint and the spine, and the peripheral joints are mainly affected by the asymmetrical joints of the lower limbs, often with tendonitis;

390-95% of patients were positive for HLA-B27;

4 types of rheumatoid factor negative;

5 X-ray changes in the ankle and spine are extremely helpful for diagnosis.

(5) Arthritis caused by connective tissue disease: Sjogren's syndrome, systemic lupus erythematosus can have joint symptoms, and some patients are positive for rheumatoid factor, but they all have corresponding characteristic clinical manifestations and autoantibodies.

(6) Others: Identification of atypical rheumatoid arthritis with a single or minor joint onset is associated with infectious arthritis (including tuberculosis infection), reactive arthritis, and rheumatic fever.

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