Definition: Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology with symmetric, chronic, progressive polyarthritis as the main manifestation. Clinical manifestations: There is individual variation in the disease and its course, ranging from transient, mild oligoarthritis to acute progressive polyarthritis. The most commonly affected joints are the proximal interphalangeal, metacarpophalangeal, wrist, elbow, shoulder, knee and toe joints; the cervical spine, temporomandibular joints, sternoclavicular and acromioclavicular joints may also be involved with limited motion; hip joint involvement is rare. Arthritis often presents with symmetric, persistent swelling and pressure pain, and morning stiffness often lasts for more than an hour. The most common joint deformities are ankylosis of the wrist and elbow joints, subluxation of the metacarpophalangeal joints, ulnar deviation of the fingers, and “swan neck” and “buttonhole flower”-like manifestations. In severe cases, the joints become fibrous or bony ankylosis, and the muscles around the joints atrophy and spasm, resulting in loss of joint function, making life unmanageable. In addition to joint symptoms, extra-articular or visceral damage, such as rheumatoid nodules, heart, lung, kidney, peripheral nerve and eye lesions, may also occur. How to diagnose: To exclude synovitis caused by other diseases, confirmed by clinical or imaging examinations, if there are radiological typical RA bone destruction changes can be clearly diagnosed, otherwise, the number of joints involved, the disease duration, the level of inflammatory indicators and rheumatoid factor, anti-cyclic citrullinated peptide antibody test to clarify the diagnosis. How to treat: including drug treatment, surgical treatment and psychological rehabilitation treatment. Commonly used drugs are divided into four major categories, namely non-steroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), glucocorticoids and botanicals. (1) NSAIDs: they have anti-inflammatory, analgesic, antipyretic and anti-swelling effects by inhibiting cyclooxygenase activity and reducing prostaglandin synthesis. Such as ibuprofen, naproxen, loxoprofen, diclofenac, aclofenac, indomethacin, meloxicam, nimesulide, celecoxib, etc. (2) DMARDs: These drugs are slower to work than NSAIDs, and it takes about 1-6 months for clinical symptoms to improve significantly, so they are also called slow-acting drugs. Commonly used non-biological DMARDs: methotrexate oral 7.5~15mg/week, salazosulfapyridine oral 1000mg 2~3 times/day, leflunomide oral 10~20mg 1 time/day, hydroxychloroquine oral 200mg 1~2 times/day. . Commonly used biological DMARDs: etanercept, infliximab, adalimumab, etc. (3) Glucocorticoids: can rapidly reduce joint pain and swelling. In patients with acute attack of arthritis, or severe disease with involvement of organs such as heart, lung, eye and nervous system, short-acting hormones can be given, and their doses are adjusted according to the severity of the disease. During the course of treatment, adverse reactions should be prevented and treated, especially proton pump inhibitors to prevent gastrointestinal reactions and calcium and vitamin D supplements to prevent osteoporosis. (4) Botanical preparations: e.g. Radix Rehmanniae, total peony glycosides, etc. Treatment strategy: In today’s world, where RA cannot be cured, preventing joint destruction, protecting joint function, and maximizing the patient’s quality of life are our highest goals; therefore, early, combined, and intensive treatment is the key to reducing disability. The principles of treatment for RA are rapid administration of glucocorticoids and or NSAIDs to relieve pain and inflammation and early use of DMARDs to reduce or delay bone destruction. Prognosis: Males have a better prognosis than females; those with late onset of disease have a better prognosis than those with early onset of disease; those with a high number of joints involved at the onset of disease or with metatarsophalangeal joints involved, or those with more than 20 joints involved in the course of disease have a poor prognosis; those with persistent high titers of rheumatoid factor and anti-cyclic citrullinated peptide antibodies, persistent increased sedimentation, increased C-reactive protein, and increased eosinophils in the blood indicate a poor prognosis; those with severe peripheral symptoms (fever, anemia, malaise) and those with severe peripheral symptoms (fever, anemia, malaise) have a poor prognosis. The prognosis is poor if there are severe peripheral symptoms (fever, anemia, weakness) and extra-articular manifestations (rheumatoid nodules, sclerositis, interstitial lung disease, pericardial disease, systemic vasculitis and other visceral injuries); the prognosis is poor if the symptoms are difficult to control with short-term hormone therapy or the maintenance dose of hormone cannot be reduced to less than 10 mg/day.