Rheumatoid arthritis is a systemic connective tissue disease, a progressive polyarthritis that involves not only joints but also extra-articular tissues. It is a common disease, often involving both knee joints, and can be combined with other joints. It is more common in women, with a male to female ratio of 1:25. The age of prevalence is 16 to 55, and the joints involved are in the order of prevalence: hand, knee, wrist, ankle, elbow, foot, and hip, often symmetrically. Although the disability rate is high, if the disease is diagnosed early and treated actively, the joint function may return to normal.
Etiology.
The etiology is still unknown and may be related to the following factors.
1, infection: microbial infections such as EBV or branched in the body may be the cause of RA, but it has not been confirmed.
2, autoimmunity: immunoglobulin-producing lymphocytes and plasma cells infiltrate the synovial membrane; high levels of antibody (immunoglobulin)-rheumatoid factor (RF) in the blood, and rheumatoid factor is also found in the lymph nodes and synovial membrane; immune complexes in the synovial fluid leukocytes.
3, genetic: seropositive rheumatoid arthritis is more prevalent in families. In the etiology of rheumatoid arthritis , environmental factors are at least as important as genetics.4. Endocrine factors.
Pathology.
Rheumatoid arthritis is a systemic connective tissue disease that involves both joints and extra-articular tissues.
1, joint pathology
(1) Synovium: In the early stages of acute arthritis, the synovium is thickened, congested and edematous, the villi are proliferated, the vascular opacities cover the articular cartilage from the edge of the articular cartilage and erode the bone, and the synovial fluid is increased, thin and cloudy. Late stage vascular opacities mechanize and form thick fibrous tissue, leading to fibrous ankylosis of the joint.
(2) Articular cartilage: erosion by multiple enzymes (collagenase, protease, elastase) becomes roughened, thinning and limited necrosis, in contrast to osteoarthritis, which first invades the non-weight-bearing portion and can be followed by proliferative changes.
(3) Joint capsule: thickened in advanced stages due to edema and fibrosis.
(4) Proximal joint bone: early osteoporosis.
2.Extra-articular lesions
(1) Subcutaneous nodules
(2) Muscle lesions: muscle atrophy is common and more pronounced in the muscles associated with inflamed joints.
(3) tendon lesions: may have thickening, fibrosis-like and fibrosis
(4) Bursa: Occasionally occurs at the bony convexity, with thick walls, similar to synovial changes
(5) Pulmonary lesions: there may be pleural effusion, isolated rheumatoid nodules in the lungs, diffuse interstitial fibrosis of the lungs
Clinical manifestations.
1, Onset.
There is acute or chronic, single joint or multiple joints. Typical onset is a progressive development of symmetrical polyarthritis of the small joints of the hands and feet.
2. Typical musculoskeletal symptoms and signs.
(1) Joint pain, swelling, and stiffness: Early on, there is often pike swelling of the proximal interphalangeal joints of the hand and painful swelling of the metacarpophalangeal joints, with fluid accumulation in the large joints, especially the knee joints.
(2) Morning stiffness: joint stiffness in the morning, gradually reduced after activity
(3) Muscle atrophy
(4) Deformity: Mild deformity may occur in the early stage due to muscle spasm, but becomes obvious in the late stage, such as “goose neck deformity” of the fingers, ulnar deviation deformity of the metacarpophalangeal joint, knee flexion deformity, hip flexion deformity, etc.
(5) Subcutaneous nodules
3.Extra-articular manifestations
(1) Systemic symptoms: fever, weight loss and fatigue are the manifestations of disease activity.
(2) Skin and vascular changes: hairy extremities, Raynaud’s phenomenon
(3) Anemia: The typical anemia of rheumatoid arthritis is chronic infectious anemia with normal or slightly low hemoglobin.
Laboratory tests: normal hemoglobin or low hemoglobin anemia. Blood sedimentation is elevated in the acute phase, and C-reactive protein test is positive in the early phase. The positive rate of rheumatoid factor is 60-80%, but a negative test does not negate the diagnosis. Immunoglobulin electrophoresis is elevated in 70% of seropositive cases for IgM and 25% for IgG. Synovial fluid: cloudy, low viscosity, poor quality mucin clots, and increased cell and protein content. Synovial biopsy: The picture of rheumatoid arthritis is a synovial membrane showing fibrin deposition and proliferation of synovial cells.
X-Ray: Early changes: soft tissue swelling; periarticular osteoporosis; joint surface erosion and subchondral cyst formation; narrowing of the joint space due to destruction of articular cartilage. Late changes: marked unevenness and severe erosion of the joint surface; joint subluxation; extensive osteoporosis; secondary degenerative changes; bony ankylosis.
Treatment: Treatment should be based on the stage and severity of the disease
1.General treatment.
Bed rest: effective for early cases, acute exacerbation or complications; brace braking: can relieve pain, muscle spasm and prevent deformity in the acute stage; but intermittent braking should be taken to move the joint properly; painkillers: no anti-inflammatory effect.
2.Drug treatment
(1) Non-hormonal anti-inflammatory drugs: ibuprofen; anti-inflammatory pain; naproxen; botaxone; salicylate
(2) Corticosteroids: systemic application of corticosteroids is limited to difficult cases because of the ease of drug resistance and complications after high dose use. Systemic corticosteroids must be applied in small doses. Prednisolone should not exceed 7.5 mg per day and should be reduced by 1 mg or less per week to prevent symptoms from worsening again after sudden discontinuation of the drug. Systemic application of corticosteroids should be discontinued when there is no clinical effect within 2 weeks. Long-term systemic application of large doses of corticosteroids and sudden discontinuation can cause severe sensorimotor neuropathy, resulting in wrist or foot ptosis. Intra-articular injection of corticosteroids: Intra-articular injection of corticosteroids is recommended with prednisolone acetate, 25 mg each time, added to 4-10 ml of 1~2% procaine, once a week, limited to 3~4 times. Frequent intra-articular injection of corticosteroids, coupled with prolonged weight-bearing, can cause serious osteoporosis and joint destruction, which is more likely to occur in the knee joint, so frequent intra-articular injection should be contraindicated.
(3) Other drugs: Immunosuppressive drugs: azathioprine, cyclophosphamide 50 mg, tretinoin, penicillamine.
3.Surgical treatment.
At present, surgical treatment can be considered at all stages of the disease, regardless of whether the disease activity is fully controlled or not. In the early stage, preventive surgery, such as synovectomy of the knee, can be performed to remove the lesion and relieve pain. In the late stages, surgery to correct deformity or improve joint function, such as osteotomy, fusion, or artificial knee replacement, is performed. At present, artificial joint replacement has become a routine treatment for advanced rheumatoid arthritis and has achieved excellent clinical results.