Introduction:
Rheumatoid ArthritisThe cause is still not very clear, and most of them are currently considered to be autoimmune diseases of the human body. They can also be regarded as a chronic syndrome, which is characterized by non-specific inflammation of the peripheral joints. At this time, the diseased joint and its surrounding tissues are progressively destroyed, and the synovitis is persistent and recurrent, which may lead to destruction of cartilage and bone in the joint, joint dysfunction, and even disability. Vasculitis lesions involve various organs of the body, so this disease is also known as rheumatoid disease. The incidence of rheumatoid arthritis is higher in women than in men, and women are 2 to 3 times more likely than men; the incidence rate in European and American countries is significantly higher than that in Chinese.
Cause:
I. Causes of the disease
The cause is not completely clear. Rheumatoid arthritis is a disease that is closely related to factors such as the environment, cells, viruses, genetics, sex hormones, and neuropsychiatric states.
(1) Bacterial factors Experimental studies have shown that group A streptococci and peptidoglycan may be a persistent stimulator of RA, and group A streptococci have long-lasting antigens in the body, stimulating the body to produce antibodies. , caused by immunopathological damage. The arthritis animal model produced by Mycoplasma is similar to human RA, but does not produce rheumatoid factor (RF) specific to human RA. Bacterial or bacterial antigenic material has never been found in the synovial fluid and synovial tissue of RA patients, suggesting that bacteria may be involved in the onset of RA, but lacks direct evidence.
(2) Viral factors The relationship between RA and viruses, especially EB virus, is one of the issues that scholars at home and abroad pay attention to. Studies have shown that arthritis caused by EB virus infection is different from RA, and RA patients have strong reactivity with EB virus than normal people. There is a persistently high level of anti-EBV-membrane antigen antibody in serum and synovial fluid of RA patients, but so far no Epstein-Barr virus nuclear antigen or capsid antigen antibody has been found in the serum of RA patients.
(3) Genetic factors The incidence of this disease is high in some families. In the population survey, human leukocyte antigen (HLA)-DR4 was found to be associated with RF-positive patients. HLA studies have found that DW4 is associated with the pathogenesis of RA. 70% of patients are HLA-DW4 positive, and patients have susceptibility genes at this point, so inheritance may play an important role in the pathogenesis.
(4) Sex hormone studies have shown that the incidence of RA is between 1:2 and 4, the condition of pregnancy is reduced, and the incidence of contraceptives is reduced. Animal models show that LEW/n females have high sensitivity to arthritis and low male incidence. After male rats are treated with castration or treated with β-estradiol, arthritis occurs in the same way as female mice, indicating that sex hormones are in RA. It plays a role in the onset.
Cold, damp, fatigue, malnutrition, trauma, mental factors, etc., are often the predisposing factors of this disease, but most patients often have no obvious incentives before.
(two) pathogenesis
The pathogenesis is not fully understood, and it is considered that RA is an autoimmune disease that has been widely recognized. Those with HLA-DR4 and DW4 antigens have high sensitivity to external environmental conditions, viruses, bacteria, neuropsychiatric and endocrine factors. When invading the body, they change the HLA antigenic determinant to make HLA Nuclear cells become targets of immunosuppression. Since the HLA gene produces a property that can carry a T cell antigen receptor and an immune-related antigen, when an external stimulating factor is recognized by a macrophage, T cell activation and release of a series of immune media are generated, thereby generating an immune response.
Intercellular interactions result in excessive activation of B cells and plasma cells to produce a large number of immunoglobulins and rheumatoid factors (RF), resulting in the formation of immune complexes and deposition on synovial tissue, simultaneously activating complement and producing multiple allergies. Toxins (C3a and C5a chemokines). Local factors such as IL-1, tumor necrosis factor a, and leukotriene B4 produced by monocytes and macrophages can stimulate my nucleated leukocytes to migrate into the synovium. Local angiogenesis of prostaglandin E2 can also promote the entry of inflammatory cells into the inflammatory site, phagocytose immune complexes and release lysosomes, including neutral proteases and collagenases, destroy collagen elastic fibers, and make the synovial surface and articular cartilage damage. RF can also be seen in the flash cells of the lubricated membrane, the proliferating lymphoid follicles and the synovial cells, and the IgG-RF complex can also be seen. Therefore, even if the infection factor does not exist, RF can be continuously generated, causing the onset of the lesion. Become a chronic inflammation.
The RF synovium is characterized by the presence of several products secreted by active lymphocytes, macrophages, and other cells. These cellular active substances include a variety of factors: T lymphocytes secrete such as interleukin II (IL-2), IL-6. , granulocyte-macrophage stimulating factor (GM-CSF), tumor necrosis factor a, variant growth factor β: factors derived from activated macrophages include IL-1, tumor necrosis factor a, IL-6, GM-CSF Macrophage CSF, platelet-derived growth factor: Active substances secreted by other cells in the synovium (fibroblasts and endogenous cells) include IL-1, IL-6, GM-CSF and macrophage CSF. These cellular active substances can account for many of the characteristics of rheumatoid synovitis, including inflammation of the synovial tissue, proliferation of the synovium, damage to cartilage and bone, and the whole body of RA. The cellular active substances IL-1 and tumor necrosis factor activate activated chondrocytes and produce collagenase and proteolytic enzymes to destroy local cartilage.
RF includes IgG, IgA, and IgM, and plays an important role in the occurrence of systemic diseases. IgG-RF itself has both antigen and antibody binding sites, and can form diploids or multimers by itself. The immune complex containing IgG is deposited in the synovial tissue, which stimulates the synovial membrane to produce IgM0 and IgA type RA. IgG-RF, in turn, binds to an immune complex containing IgG, which has a greater ability to activate complement than a simple IgG-containing immune complex.
Joint lesion
(1) Changes in synovial membrane: joint lesions begin with synovial membrane, synovial congestion, edema. The synovial membrane near the edge of the cartilage is most pronounced. There is fibrin exudate covering on the surface of the synovial membrane. The synovial membrane has lymphocytes, plasma cells and a small amount of multinucleated granulocyte infiltration. Cells infiltrated in the lower layer of the synovial membrane form a "lymphoid nodule", some of which accumulate around small blood vessels. The surface cells of the synovial membrane proliferate in a fence-like shape, and the surface villi proliferate. In the late stage, most of the infiltrating cells are plasma cells, and there is exudate in the joint cavity.
(2) Granuloma formation: After the acute inflammation subsides, the oozing waves are gradually absorbed. Fibroblasts proliferate around the capillaries at the site of cell infiltration. The synovial cells are columnar and arranged in a fence, and the synovial membrane is thickened and fluffy. The blood vessels in the synovial membrane proliferate, and the blood vessels in the synovium increase, which is a granuloma, which adheres to the cartilage and invades the cartilage. There are lysosomal vacuoles in the endothelium cells; there are plasma cells around the blood vessels, and "rheumatoid cells" are found in the synovium.
(3) Changes in articular cartilage and subchondral bone: As the granulation tissue of the granulation tissue, which is caused by the synovial membrane, intrudes into the cartilage, it gradually spreads to the central part of the cartilage, blocking the cartilage from absorbing nutrients from the synovial fluid, and the cartilage is gradually absorbed. At the same time, due to the release of protein degrading enzymes and collagenase in the lysosome, the cartilage matrix is destroyed and dissolved, resulting in extensive destruction of the articular cartilage, narrowing of the joint space, rough joint surface, adhesion formation after vasospasm, and fibrous tissue proliferation. Extensive adhesions are formed in the joint cavity, which significantly restricts joint function and forms fibrous rigidity. After most of the articular cartilage surface is absorbed, the large area of the subchondral bone breaks and grows at the same time, forming new bone between the bone ends, and causing the joint bone tough.
Due to long-term repeated fluid accumulation in the joint, the joint capsule and its surrounding ligaments are pulled and prolonged and relaxed. In addition, the destruction of the articular surface and the bone end narrows the joint space and makes the joint ligament more relaxed. Due to joint inflammation and cartilage surface damage, patients are often in a forced position due to pain. Protective muscles occur in the muscles around the joints. Muscles, tendons, ligaments, and fascia around the joints are also invaded by the lesions, and even rupture, eventually leading to dislocation of the joint or deformity of the bone.
2. Extra-articular performance
(1) Rheumatoid subcutaneous nodules: Rheumatoid subcutaneous nodules are reliable evidence for the diagnosis of rheumatoid arthritis. The nodules are granulomatous changes, and the central necrotic area contains IgG and RF immune complexes. Surrounded by fibroblasts, lymphocytes and monocytes, it eventually becomes dense connective tissue.
(2) tendon and tendon sheath, bursitis inflammation: tendon and tenosynovitis are common in the hands and feet, tendon and sheath have lymphocytes, monocytes, plasma cells infiltration. In severe cases, the nodules on the palate can be touched, and the tendons can be broken and adhered, which is the cause of the deformity of the surrounding joints. The bursitis is more common with Achilles bursitis, and localized synovitis often forms at the tendon attachment, which may even cause local bone hyperplasia or defect. Bursitis may also occur in the axilla, forming a popliteal cyst.
symptom:
The onset is slow, and there are several prodromal symptoms such as fatigue, weight loss, poor appetite, low fever, and tingling in the hands and feet.
First, joint symptoms:
(1) Morning stiffness: The first symptom of the joint, often before the joint pain. The joint stiffness is painful when it starts to move, and the morning stiffness is reduced or disappeared when the joint activity increases. The joint morning stiffness is obvious in the morning and relieves in the afternoon.
(B) joint swelling and pain: more symmetry, often invaded and metacarpophalangeal joints, wrist joints, shoulder joints, interphalangeal joints, ankle joints and knee joints. Joint redness, swelling, heat, pain, and movement disorders.
(3) Malformation: In the later cases, the metacarpophalangeal joint flexion and ulnar deviation are generally present; if it occurs on the toes, the appearance of the claw-toe deformity appears.
Second, extra-articular manifestations: is part of the systemic manifestations of rheumatoid arthritis or its complications. The joint disease of this disease can be disabling, but it will not kill. Extra-articular manifestations are often the cause of death from this disease.
(A) rheumatoid nodules: seen in 15 to 20% of patients, more common in the forearm often under pressure on the extension side, such as the ulnar side and the olecranon. A soft amorphous knot is attached under the skin or a rubber-like knot fixed to the periosteum. Subcutaneous rheumatoid nodules are more common in patients with strong serum rheumatoid factor.
(B) rheumatoid vasculitis: rheumatoid vasculitis is the basic disease of this disease, in addition to the joints and tissues around the joints, vasculitis can occur elsewhere in the body. It is characterized by distal vasculitis, skin ulcers, peripheral neuropathy, pericarditis, visceral arteritis such as heart, lung, intestine, spleen, pancreas, kidney, lymph nodes and testicles.
(C) rheumatic heart disease: cardiac involvement, myocardial, valvular or aortic root rheumatoid granuloma formation, or myocardial, endocardial and annulus lymphocytes infiltration or fibrosis.
(D) rheumatoid lung disease: chronic fibrosis pneumonia is more common, pulmonary fibroin-like necrosis and mononuclear cell infiltration, fever, dyspnea, cough and chest pain.
(5) Kidney damage.
(6) Ocular manifestations: Uveitis is a common disease of juvenile rheumatoid arthritis, which often causes keratitis in human rheumatoid arthritis.
(7) Felty syndrome: It is a serious rheumatoid arthritis, which often causes splenomegaly, neutropenia, high positive rate of serum rheumatoid factor, and positive antinuclear antibody.
(8) Sjogren's syndrome: It is a chronic inflammatory autoimmune disease. It mainly invades the lacrimal gland and the size of the salivary gland, resulting in the reduction or lack of gland destruction and secretion. The clinical manifestations are dryness syndrome mainly composed of the eye and oral mucosa.
(9) Digestive tract damage.
diagnosis:
The diagnosis of typical cases is generally not difficult, but in the early stage, especially when the beginning of single arthritis and X-ray changes are not obvious, follow-up observation can be confirmed.
Internationally, the American College of Rheumatology 1985 diagnostic criteria were adopted. The standard was revised in 1987 to remove the damage examination and the poor specificity of joint pain and tenderness. The requirements for morning stiffness and joint swelling are more stringent.
1. Typical rheumatoid arthritis This type of diagnosis requires 7 of the following criteria, of which standard 1 to 5 joint symptoms or signs must last at least 6 weeks.
(1) There is joint stiffness when getting up in the morning.
(2) At least one joint has pain or tenderness when it is active.
(3) At least 1 joint has swelling (not only hyperplasia, soft tissue thickening or effusion).
(4) At least one other joint is swollen (the interval between symptoms of 2 joints is not more than 3 months).
(5) Symmetrical swelling of the same joint on both sides (the proximal interphalangeal joint, metacarpophalangeal joint, and metatarsophalangeal joint may have symptoms, but not absolute symmetry).
(6) Subcutaneous nodules.
(7) The typical X-ray changes in rheumatoid arthritis not only have degenerative changes, but also include at least decalcification of the bone around the affected joint.
(8) The agglutination test was positive, and the rheumatoid factor test results were positive in any two different laboratories, and the positive rate of the normal control group was not more than 5%.
(9) There is a very small amount of mucin precipitation in the synovial fluid (liquid turbidity, containing debris; synovial inflammatory exudate contains more than 2 × 109 / L white blood cells, no crystallization).
(10) Histological changes characteristic of the following three or more types of synovial membranes: significant villus hypertrophy; synovial surface cell proliferation; chronic inflammatory cell infiltration, tendency to form lymphoid nodules; surface and cavity Medium fibrin deposition and cell necrosis.
(11) Specific histological changes of nodules: granuloma with necrosis of central cells, "fence" of proliferating monocytes outside the periphery, fibrous wrap around the periphery and chronic inflammatory cell infiltration.
2. Cases with which the diagnosis of rheumatoid arthritis can be diagnosed must meet 5 of the above criteria, and the joint symptoms and signs of the standard 1 to 5 items must last for at least 6 weeks.
3. The diagnosis of rheumatoid arthritis requires three of the above criteria, including at least one of the standard 1 to 5 joint symptoms, and at least one of the signs lasts for more than 6 weeks.
4. Suspected rheumatoid arthritis may have two of the following criteria, and joint symptoms last for at least 3 weeks.
(1) Morning stiffness.
(2) Pain during tenderness or activity.
(3) History of joint swelling or what you see.
(4) Subcutaneous nodules.
(5) Increased blood cell sedimentation rate or C-reactive protein.
(6) iritis (except for rheumatoid arthritis in children, the value of this standard is not large).
The above are the four types of diagnostic criteria developed by the American College of Rheumatology based on the symptoms of the patient. The clinician can observe and observe according to the situation and take appropriate action.
Identification
The disease must be differentiated from the following diseases:
(1) The age of onset of proliferative osteoarthritis is more than 40 years old, and there is no systemic disease. There is no redness and swelling in the joints. The injured joints are more common with weight-bearing knees and spine. There is no migration. Muscle atrophy and joint deformity are lip-like hyperplasia or osteophyte formation. The erythrocyte sedimentation rate is normal and RF is negative.
(B) rheumatoid arthritis This disease is particularly confused with the onset of rheumatoid arthritis, the following points can be identified: 1 onset usually rapid, with sore throat, fever and increased white blood cells; 2 with large limb joints Frequently affected, for migratory joint swelling and pain, no permanent damage after the disappearance of joint symptoms; 3 often accompanied by carditis; 4 serum anti-streptolysin "O", anti-streptokinase and anti-hyaluronidase Positive, but RF negative; 5 salicylic acid preparations often quickly and significantly.
(C) tuberculous arthritis rheumatoid arthritis is limited to a single joint or a few joints should be identified with the disease. The disease may be associated with other areas of tuberculosis, such as spinal tuberculosis often with paraspinal abscess, more common in more than two joints. X-ray examination is not easy to distinguish in the early stage. If there is local bone destruction or paravertebral abscess shadow, it can help diagnosis. Joint cavity fluid is often positive for tuberculosis culture. Anti-tuberculosis treatment is effective.
(four)Psoriatic arthritis Joint reactions are similar to rheumatoid arthritis, and often involve small joints and large joints, but psoriasis lesions are observed on the patient's body (as confirmed by dermatologists).
(5) Other connective tissue diseases (both with multiple arthritis)
1. Systemic lupus erythematosus is indistinguishable from early rheumatoid arthritis. The former occurs mostly in young women. It can also occur in the proximal interphalangeal joint and metacarpophalangeal joint synovitis, but the joint symptoms are not heavy, generally no cartilage and bone. Quality damage, systemic symptoms are obvious, and there are many organ damage. Typically, the face has a butterfly or disc-shaped erythema. Lupus cells, anti-ds-DNA antibodies, Sm antibodies, and lupus test positives all contribute to diagnosis.
2.sclerodermaIt occurs in women aged 20 to 50 years. Symmetrical hand stiffness, finger and knee pain in the early stage of edema and swelling of surrounding soft tissue caused by joint synovitis are easily confused with RA. The early stage of the disease is self-limiting, and often suddenly disappears after a few weeks, and Raynaud's phenomenon appears, which is beneficial to the diagnosis of this disease. Hardening and atrophy period shows skin hardening, and it is easy to identify when it is "chat-like".
3. The clinical symptoms of mixed connective tissue disease are similar to RA, but with high titer granular fluorescent antinuclear antibody, high titer anti-soluble ribonucleoprotein (RNP) antibody positive, and Sm antibody negative.
4. Muscle pain and edema of dermatomyositis are not limited to the vicinity of the joints, heart and kidney lesions are more common, and joint lesions are rare. ANA(+), anti-PM-1 antibody, anti-Jo-1 antibody positive.
(six)gout Early symptoms are similar to rheumatoid arthritis, especially the inflammatory response of the facet joints. However, the disease is more common in men, and the blood uric acid content is significantly increased, and its onset is closely related to dietary composition.
complication:
(1) Pneumonia: Due to decreased immunity and bacterial infection, patients often have pneumonia.
(B) urinary tract infection: patients with rheumatoid arthritis, if not pay attention to daily life, or suffering from a cold, often prone to urinary tract infection.
(C) Cushing's syndrome: patients with hormones for too long, often due to inhibition of adrenal function in the body and Cushing's syndrome. Common symptoms include the full moon face, buffalo back, and weight gain.
(4) Oral ulcers: Patients with rheumatoid arthritis often develop oral ulcers after taking immunosuppressive agents, and may also have adverse reactions such as nausea and vomiting, anorexia, rash, and loss of taste.
(5) Infectious diseases: Patients have been suffering from this disease for too long, and their autoimmune function has declined. When certain infectious diseases are prevalent in society, they are more susceptible to infection than normal people.
(6) In severe cases, abnormal bones may be present, and even joint dislocation may occur.
treatment:
Western medicine treatment
Rheumatoid arthritis has no specific treatment so far, and still stays in the treatment of inflammation and sequelae. Comprehensive treatment, most patients can get a certain effect. The current treatment aims to: 1 control inflammation of joints and other tissues, relieve symptoms; 2 maintain joint function and prevent deformity; 3 repair damaged joints to relieve pain and restore function.
(a) general therapy
Those with fever, joint swelling and pain, systemic symptoms should stay in bed until the symptoms basically disappear. After two weeks of improvement, the activity should be gradually increased to avoid excessive use of the bed, resulting in joint disuse and even promotion of joint rigidity. The protein and various vitamins in the diet should be sufficient. If the anemia is significant, a small amount of blood transfusion can be given. If a chronic lesion such as tonsillitis is allowed, the patient's health may be removed as soon as possible.
(two) drug treatment
1. Non-steroidal anti-inflammatory drugs (NSAIDS) are used in primary or mild cases, and their mechanism of action mainly inhibits the effect of cyclooxygenase on the inhibition of prostaglandin production to achieve anti-inflammatory and pain-relieving effects. But it does not prevent the natural process of rheumatoid arthritis. This class of drugs has different metabolic pathways in the body, and interactions between them do not advocate joint application, and attention should be paid to individualization.
(1)Salicylic acidPreparation: It can resist rheumatism, anti-inflammatory, antipyretic and pain relief. Dosage daily 2 ~ 4g, if the effect is not ideal, you can increase the dose, sometimes 4 ~ 6 grams per day to be effective. Usually taken after meals or with antacids, enteric-coated tablets can also be used to reduce gastrointestinal irritation.
(2)Indomethacin: A hydrazine acetate derivative with anti-inflammatory, antipyretic and analgesic effects. Patients who can not tolerate aspirin can be switched to this drug, the usual dose of 25mg 2 to 3 times a day, more than 100mg per day is prone to side effects. Side effects include nausea, vomiting, diarrhea, stomach ulcers, headache, dizziness, and depression.
(3) Propionic acid derivatives: It is a kind of medicine that can replace aspirin, including ibuprofen. The effects of ibuprofen napoproxen and fenbufne are similar to those of aspirin. Side effects of the digestive tract are small. Common dose: ibuprofen 1.2 ~ 2.4g per day, divided into 3 ~ 4 times service, naproxen 250mg each time, 2 times a day. Side effects include nausea, vomiting, diarrhea, peptic ulcer, gastrointestinal bleeding, headache, and central nervous system disorders such as irritability.
(4) Acid-killing drugs: It is an anthranilic acid derivative, and its effect is similar to that of aspirin. Anti-acidic 250mg each time, 3 to 4 times a day. Chloroacid is 200 to 400 mg each time, 3 times a day. Side effects include gastrointestinal reactions such as nausea, vomiting, diarrhea, and loss of appetite. Occasionally rash, kidney damage, headache, etc.
2. Gold preparations are currently recognized for their positive effects on rheumatoid arthritis. Commonly used gold sodium thiomalate myochrysin. Usage 10mg intramuscular injection in the first week, 25mg in the second week. If there is no adverse reaction, 50mg per week thereafter. When the total amount reaches 300-700mg, most patients will start to work. When the total amount reaches 600-1000mg, the condition can be improved steadily. The maintenance amount is 50 mg per month. Due to the possibility of recurrence after stopping the drug, the foreign useful maintenance for many years, straight for life. The earlier the gold preparation is used, the more effective it is. The effect of gold preparations is slow, effective from 3 to 6 months, and should not be combined with immunosuppressants or cytotoxic drugs. If the total amount of the treatment has reached 1000mg, and the condition has not improved, the drug should be discontinued. The effect of oral gold preparations is similar to that of gold injections. Side effects have increased stool frequency, rash, stomatitis, tight damage, etc., can be restored after stopping the drug.
The oral gold preparation Auranofin is a hydroxy compound of gold phosphide. The dose is 6mg once a day, and it will take effect after 2~3 months. It is better for patients with short duration of disease. The side effects are lighter than the injection, which is usually diarrhea, but it is transient, and the effective rate of remission is 62.8%.
3.Penicillamine It is a thiol-containing amino acid drug that has a certain effect in the treatment of chronic rheumatoid arthritis. It selectively inhibits certain immune cells to reduce IgG and IgM. Side effects include thrombocytopenia, leukopenia, proteinuria, allergic rash, loss of appetite, optic neuritis, muscle weakness, increased transaminase, etc. The oral administration of 250mg per day for the first month, 250mg for the second month, 2 times a day. No significant effect in the third month of 250mg each time, three times a day. The total dose is 750mg per dose for the maximum dose. Most of the clinical symptoms improved within 3 months, and the symptoms were improved and maintained in small doses for about one year.
4.Chloroquine It has a certain anti-rheumatic effect, but it is very slow, and it usually takes 6 weeks to 6 months to reach the maximum effect. It can be used as a salicylic acid preparation or as an auxiliary drug in the dose of corticosteroids. Each time oral 250 ~ 500mg, 2 times a day. There are often more gastrointestinal reactions such as nausea, vomiting and loss of appetite during the course of treatment. Long-term application should pay attention to the degeneration of the retina and optic atrophy.
5.Levamisole It can reduce pain and shorten the time of joint stiffness. The dose is 50 mg for the first shot, 1 time per day, 50 mg for the second week, 2 times a day, 50 mg for the third week, 3 times a day. Side effects include dizziness, nausea, allergic rash, loss of vision, lethargy, neutropenia, thrombocytopenia, liver damage, and proteinuria.
6. Immunosuppressive agents are suitable for patients with severe rheumatoid arthritis who are ineffective in other drugs. Azathioprine is commonly used in patients who have discontinued drug or hormone reduction, 50 mg each time, 2 to 3 times a day. Cyclophosphamide 50 mg each time, 2 times a day. After the symptoms or laboratory tests have improved, gradually reduce the amount. The maintenance amount is 1/2 to 2/3 of the original therapeutic amount. Continuous use for 3 to 6 months. Side effects include myelosuppression, leukopenia and thrombocytopenia, hepatotoxic damage and digestive tract reaction, alopecia, amenorrhea, hemorrhagic granule inflammation.
Methotrexate(MTX) has immunosuppressive and anti-inflammatory effects, can reduce erythrocyte sedimentation rate, improve bone erosion, 5 to 15 mg intramuscular or oral per week, 3 months for a course of treatment. Side effects include anorexia, nausea, vomiting, stomatitis, hair loss, white blood cell or thrombocytopenia, drug-induced interstitial pneumonia and rash. It may become another palliative drug selected after gold and penicillamine.
7.Adrenocorticotropic hormone Adrenal cortical hormones have joint swelling and pain, control inflammation, anti-inflammatory and analgesic effects, but the effect is not lasting, and has no effect on the etiology and pathogenesis. Once the drug is stopped, it will recur. There was no improvement in RF, erythrocyte sedimentation rate and anemia. Long-term application can lead to serious side effects, so it is not used as a routine treatment. It is limited to those who cause extra-articular damage caused by severe vasculitis and affect the function of the organs. For example, those with ocular complications have the risk of blindness, those with central nervous system disease, and cardiac conduction resistance. Stagnation, joints with active active synovitis can be used for a short period of time, or NSAIDS, penicillamine and other treatments are not good, the symptoms are heavy, affecting daily life, small doses of corticosteroids can be added to the original drugs. The effect can be increased as appropriate. After the symptoms are controlled, the amount should be gradually reduced to the minimum maintenance amount.
Hydrogen prednisolone suspension can be used for local intra-articular injection, suitable for some single large joint refractory lesions, each injection of 25 ~ 50mg intra-articular cavity, to prevent joint infection and bone destruction. Desulxed terbutin acetate is a long-acting corticosteroid suitable for intra-articular administration, with a single dose of 10 mg and a knee joint of 30 mg.
8.Tripterygium It has good curative effect after many years of clinical application and experimental research in China. There are non-steroidal anti-inflammatory effects, but also immunosuppressive or cytotoxic effects, can improve symptoms, reduce ESR and RF titer, tripterygium wilfordii 60mg / d, 1 to 4 weeks can have clinical effects. Side effects include irregular menstruation and menopause in women, decreased sperm count, rash, white blood cell and thrombocytopenia, abdominal pain and diarrhea. Can be eliminated after stopping the drug.
Kunming Mountain Sea Bream, similar to Tripterygium wilfordii, 2 to 3 tablets each time, 3 times a day. The course of treatment is from 3 to 6 months. Side effects: dizziness, dry mouth, sore throat, loss of appetite, abdominal pain, amenorrhea.
9. Other treatments ThymosinPlasmapheresis therapy has yet to be explored.
(3) The purpose of physiotherapy is to use hyperthermia to increase local blood circulation, relax muscles, achieve anti-inflammatory, anti-inflammatory and analgesic effects, and exercise to maintain and enhance joint function. There are several types of physiotherapy methods: hot water bottle, hot bath, wax bath, infrared light, and the like. After the physiotherapy, it is accompanied by massage to improve local circulation and relax muscle spasm.
The purpose of exercise is to preserve the joint's active function and strengthen muscle strength and endurance. After the symptom relief in the acute phase subsides, as long as the patient can tolerate, active or passive joint exercise activities should be performed regularly and regularly.
(4) Surgical treatment In the past, surgery has always been considered to be suitable only for cases of advanced deformity. At present, early synovectomy can be tried for patients with only 1 or 2 joints who are seriously damaged and who are not treated with salicylate. In the later stage, the lesion is still, and the joint has obvious deformity. The osteotomy can be performed. The joint rigidity or destruction can be used for arthroplasty and artificial joint replacement. Weight-bearing joints can be used for arthrodesis and the like.
The details are as follows:
(1) synovectomy: mainly used for metacarpophalangeal joints, wrist joints and knee joints, etc., can be used to remove the synovial membrane of the lesion. After synovectomy, the joint function should be gradually restored with the help of the brace.
(2) joint irrigation + mirror glioma resection: in the large joints, especially the knee joint, can be removed under the arthroscopy synovial, and repeated washing, in order to replace the components of joint fluid to relieve arthritis symptoms and improve The purpose of joint function.
(3) Arthroplasty: For the weight-bearing joints, especially the metatarsophalangeal joints of the feet, when the claw-toed deformity affects the weight bearing, the humeral head resection can be performed to form new joints to improve the weight-bearing function and relieve pain. purpose.
(4) Artificial joint replacement: For patients with severe rheumatoid arthritis, when the hip or knee joint is seriously damaged, so that it cannot be repaired, artificial joint replacement can be used as appropriate. Such conditions are more common in older patients.
The above content is for reference only, please consult the relevant physician or relevant medical institution if necessary.
prevention:
Because rheumatoid arthritis is good or bad, there is no cure method that can only control temporary conditions. Therefore, special attention should be paid to health care in diet and life. The following points are suggestions for diet and exercise:
(1) Diet should choose foods that are easy to digest. The cooking method should be light and refreshing, and eat less spicy, greasy and cold food.
(B) Eat more appetizing foods such as jujube, coix seed, etc., especially coix seed has the effect of dehumidifying hurricane, boiled into coix porridge or cooked with mung bean is a good choice.
(C) to reduce the intake of fat as much as possible, the source of calories should be based on sugar and protein, if the weight exceeds the standard, gradually reduce weight.
(4) If the body is hot, eat more mung beans, watermelon and other foods; if it is cold, you should eat sheep or beef, but the intake should not be too much.
(5) If you take itaspirinYou must take the medicine after a meal because it is easy to cause damage to the stomach and is prone to iron deficiency anemia.
(6) Appropriately supplement vitamin A, C, D, E or mineral foods containing calcium, iron, copper, zinc and selenium to enhance the immunity of the group and prevent tissue oxidation or anemia.
(7) If taking steroids is likely to cause an increase in appetite, sodium retention and osteoporosis, it is necessary to control the intake of food to avoid an increase in body weight, while seasonings and processed foods with high salt content are minimized and eaten. Calcium-containing foods such as skim milk, traditional tofu, etc.
(8) Reduce the bedtime for a long time, and should not be intense during exercise, you can choose to sit or stay in bed for exercise. If you are sitting, you can straighten your right leg, raise your calf and foot, and leave it 30 centimeters above the ground. After five seconds, let go, and your left foot repeats with the same movement. You can make several more times a day. The ability to load is the principle.
(9) Pay attention to heat preservation when getting up in the morning in winter, you can do some warm-up exercises. The action is as follows: straighten your hands forward, palm down, down, backwards, or stretch your hands, or raise your hands to the face, palms toward the face, inhale, hands stretch upwards and outwards And then slowly put it down.
(10) In the cold winter, you should pay attention to keep warm. When you have joint pain, you can try hot water bath to relieve pain.
(11) Do not arbitrarily treat traditional joint pains such as massage, massage, cupping, etc., so as not to cause the disease to worsen, causing irreparable harm or delaying the golden timing of treatment.
(12) Patiently cooperate with the doctor for long-term treatment, regular medication, regular visits, and a designated professional rehabilitation practitioner to perform correct rehabilitation treatment. If any uncomfortable situation occurs, you should immediately inform Doctors.
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