| ID | 173 |
|---|---|
| Name | RHEUMATOID ARTHRITIS |
| Cause | |
| Signs Symptoms | |
| Diagnosis | Criteria for the diagnosis of rheumatoid arthritis2* 1. Morning stiffness (> 1 hour) 2. Arthritis of 3 or more joint areas 3. Arthritis of hand j oints 4. Symmetrical arthritis 5. Rheumatoid nodules 6. Rheumatoid factor 7. Radiological changes 8. Duration of presenting features- 6 weeks or more. Diagnosis of RA made with 4 or more criteria. (* These criteria are according to American rheumatism association, 1988 revision) |
| Investigations | Investigations: 1. CBC.Blood examination- it shows hypochromic refractory anemia. 2. ESR & CRP (C-reactive protien): These two indicators usually raise as a result of acute phase response (APR). 3. RF (Rheumatiod factor): It can be detected in about 60-80% RA cases, but it’s absence dose not exclude the diagnosis. A low RF titre is found in about 10% of normal population. So, it is a non-specific test. 4. Anti-CCP (Anti-cyclic citrullinated peptide) antibody: It is detected in about 60-80% of RA patients. A positive anti-CCP antibody is highly specific (95%) for RA and can occur before clinical onset of the disease. 5. Radiograph: Plain x-rays of the hands, wrist and feet are useful. Periarticular osteoporosis, marginal joint erosions, narrow joint spaces and bone cysts are commonly found. 6. Imaging: Recently ultrasonogram & MRI are found more sensitive in detecting bony & soft tissue changes in rheumatoid arthritis. |
| Management | Management: The objectives in the management of rheumatoid arthritis are- i. relieving pain and reduction of inflammation, ii. preservation of function and iii. prevention of deformity. To achieve these objectives, the following measures are taken as the main stays of treatment, such as- physical rest, use of disease modifying anti-rheumatic drugs (DMARDs), nonsteroidal anti-inflammatory drugs (NSAIDs) and maintenance of passive excercise. A. General measures: 1. Education of the patient regarding the disease process & long-term treatment course of RA. 2. Physical & mental rest- 2-3 weeks in exacerbation. 3. Sleeping bed should be firm on the bed with a firm pillow. B. Local measures: 1. Rest splint. 2. Passive movement of the joint; Local orthopedic correction; Hydrotherapy; & Physiotherapy may be advised. C. Medical management: 1. Management of pain & inflammation: Nonsteroidal anti-inflammatorv drugs (NSAIDs): Nonsteroidal anti-inflammatory drugs (NSAIDs) are used mainly for symptomatic relief of pain and inflammation in rheumatoid arthritis but do not improve or prevent disease process. These are not appropriate for monotherapy and should be used in conjunction with DMARDs. There are a large number of NSAIDs available for use, which are all almost of equal efficacy, such as- Celecoxib (a selective COX-2 inhibitor)- 100-200mg twice daily (or 25mg/kg 3 times daily). (Celecoxib is contraindicated in sulphonamide allergy). Naproxen 500mg twice daily. Diclofenac sodium 150mg daily in divided doses. Indomethacin upto 150mg daily in divided doses. Others- Ibuprofen 600-2400mg daily in divided doses. Ketoprofen 75-200mg daily in divided doses. Niflumic acid 500-750mg daily in divided doses. Mefenamic acid upto 600mg daily in divided doses. Corticosteroid therapy: Prednisolone, a low-dose, 5-10mg (average 7.5mg) daily orally (single morning dose) for 3 months- produce a prompt anti-inflammatory effect in RA and slows the rate of bone destruction. Sometimes, higher doses may be required to manage serious extra-articular manifestations, such as pericarditis, necrotizing scleritis. Methylprednisolone 80-120mg, or triamcinolone 10-40mg (depending on the size of the joint) intra-articular injection may be given if low 2 joints are seriously affected. This helps in symptomatic relief of joint pain and inflammation, but should not be used more than 4 times a year. When corticosteroid therapy is to be discontinued, a taperring schedule should be maintained. In RA corticosteroid is also used as a ‘bridge therapy’ to reduce disease activity until the slower action of DMARDs starts. If corticosteroid treatment is continued for long time,measures should be taken to prevent osteoporosis. 2. Disease-modifying anti-rheumatic drugs (DMARDs): DMARDs are basically the main drugs used now a days to modify or prevent the disease process or activities and thus preventing bony deformity. So, these drugs should be started as soon as diagnosis of rheumatoid disease is certain. DMARDs are slow acting agents and require about 4-6 months of treatment for a full response. If one of these drugs dose not lead to objective benefit within 6 months, it should be discontinued. If the first-choice drug fails to control disease activity within 6 months, it should be discontinued, and other DMARDs can be added. If adverse effects occur, the patient should be switched to another DMARD. If disease activity persists despite an adequate trial of two DMARDs including methotrexate, anti-TNF therapy can be considered. Synthetic DMARDs: Methotrexate: It is a synthetic DMARD, the first-choice drug in the treatment of rheumatoid arthritis. The usual initial dose is 7.5mg orally once weekly; if no satisfactory response in 1 month, dose may be increased to 15mg once weekly, the maximum dose is 20-25mg weekly if the patient can tolerate. Sulphasalazine: It is a second-line drug in the treatment of RA. Initial dose is 0.5gm orally twice daily, can be increased each week by 0.5gm until the patient improves or maximum daily dose upto 3gm. (Respond usually in 3-6 months). Leflunomide: It is a pyrimidine synthesis inhibitor, given as a 20mg single dose daily. Leflunomide is a carcinogenic & teratogenic drug so it is contraindicated in child-bearing women or men who wish to have further children. Hydroxychloroquine sulphate: It is an anti-malarial drug, often used in RA mostly in combination with other DMARDs, particularly with methotrexate & sulphasalazine. The dose is 200mg orally twice daily. Minocycline: It is a drug of modest efficacy, and is reserved for early (during the first year of RA) and mild cases. The dose ia 200mg orally daily. Biologic DMARDs: Tumor necrosis factor-a (TNF-a) inhibitors: These are a pro-inflammatory cytokine drugs. There are three inhibitor in use, viz-etanercept, infliximab & adalimumab. These are mostly given incombination with methotrexate in patients who have not responded adequately with methotrexate alone, specially in those patients with poor prognosis. Etanercept- it is given at a dose of 50mg s.c once in a week. Infliximab- it is administered at a dose of 3-10mg/kg i.v; infusions are repeated after 2, 6, 10, & 14 weeks & then administered every 8 weeks. Adalimumab- it is given at a dose of 40mg s.c every other week. Each drug is well tolerated, and helps a substancial improvement in more than 60% patients with rheumatoid arthritis. Rituximab: It is a humanized mouse monoclonal antibody. It is used in combination with methotrexate for patients whose disease has been refractory to treatment with a TNF-a inhibitor. D. Surgical treatment: 1. Surgical decompression and synovectomy of the wrist and tendon sheath of the hands. Indication- carpal tunnel syndrome; flexion contractures of the fingers resulting from fibrosis. 2. When all the measures have failed- flexor and extensor tendon synovectomy. E. Rehabilitation: 1. Change of employment. 2. Provision of a suitable wheel chair. 3. Home adjustments. 4. Physical aids and social services. |
| Introduction | Rheumatoid arthritis is a chronic or persistant systemic inflammatory disease where there is usually a symmetrical, destructive and deforming polyarthritis affecting small and large synovial joints with associated systemic disturbance, a variety of extraarticular lesions and the presence of circulating antiglobulin antibodies (rheumatoid factors). The clinical courser is prolonged with intermittent exacerbations & remissions. The disease may start at any age but, most commonly between the third and fifth decades. Females are more frequently affected than male |
| History | |
| Etiology | Etiology:2 Although the etiology of rheumatoid arthritis is still unknown, autoimmunity is held responsible for this disease. There is increasing evidence that the disease is triggered by T-lymphocyte activation in genetically predisposed individuals with defined HLA class II haplo types. The increase in frequency of disease in first degree relatives indicates the importance of genetic factors in the process of the disease. |
| Clinical Features | Clinical features: A. In the majority of patients (60-70%) the onset is insidious with prodromal symptoms like fatigue, anorexia, generalised weakness, vague masculoskeletal symptoms and specific symptoms like joint pain, stiffness, symmetrical swelling of a mumber of peripheral joints. Initially pain may be experienced only on movement of joints, but rest pain and specially early morning stiffness are characteristic. The small joints of the fingers and toes are affected first and as the disease progresses there is a tendency for involving the wrists, elbows, shoulders, knees, ankles, subtalar and midtarsal joints. Neck pain and stiffness is comnon. Swelling of the proximal interphalangeal joints gives the fingers a “spindled” appearance and swelling of the metatarsophalangeal joints results in “broadening” of the fore foot. B. In 10-15% of the patients, the onset is more acute with a rapid development of polyarthritis usually accompanied by constitutional symptoms like fever, lymphadenopathy and splenomegaly. C. A more insidious systemic onset with fever, weight loss, profound fatigue and malaise without joint symptoms occurs less often, particularly in middle aged man and confused with malignancy. Recurrent acute episodes of joint pain and stiffness in individual joints lasting only a few hours or days, is the rarest mode of onset of RA. Other associated features (extra-articular features) includes- rheumatoid nodules, rheumatoid vasculitis, pleuropulmonary manifestations, osteoporosis etc.4 |
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| Treatment | |
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| Prognosis | Prognosis: The rheumatoid arthritis passes a prolonged clinical course with intermittent exacerbations and remissions. Around 40% of RA patients become disabled within 3 years; around 80% are moderate to severely disabled within 20 years; and 25% require a large joint replacement. |
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