Immunopathology of rheumatoid arthritis

The central place of immunologic aberrations in the pathology of rheumatoid arthritis is now well established. It is the nature and interactions of these aberrations that still remain to be elucidated. Among the many puzzles being studied are the uniquely self-perpetuating nature of rheumatoid arthritis immune complexes and the role of complement and the prostaglandins in joint damage and pain.     

Early arthritis

Identifying the cause of polyarthritis can be difficult because of the extensive differential diagnosis. A thorough history and a complete physical examination are essential. Clinical factors such as disease chronology, inflammation, distribution, extra-articular manifestations, disease course are helpful in narrowing the possible causes. Many classic laboratory tests are nonspecific but these, together with specific tests and radiographs, may provide more useful diagnostic clues. Early arthritis may progress into established rheumatoid arthritis or another definite arthropathy, may resolve spontaneously, or may remain undifferentiated. To achieve better diagnosis and outcome in arthritis, it is important to recognize inflammatory arthritis first, then to establish the definitive diagnosis of arthritis and finally to estimate the risk of developing persistent or/and erosive irreversible arthritis to propose an optimal therapeutic strategy (within 3 months) in order to avoid joint destructions and function-loss and to provide a good quality of life.     

Modern treatment of rheumatoid arthritis

Modern treatment of rheumatoid arthritis. Rheumatoid arthritis is a chronic inflammatory disease of unknown etiology, which is characterised by pain, loss of capability to work, in severe cases the life expectancy is also reduced. The disease cannot be cured with current therapeutic possibilities, but complaints can be reduced, the destruction can be retarded. The treatment is more efficient in the early stage of the disease, but early diagnosis is difficult because of insidious onset and limited sensitivity of diagnostic methods. The complaints can be alleviated by nonsteroidal anti-inflammatory drugs and transient glucocorticoid treatment, but risk of continuous glucocorticoid therapy is significant. To prevent structural damage disease modifying antirheumatic drugs are used. Out of these methotrexate is the most effective and it is well tolerated. Destruction of the joints is the consequence of inflammation, so intensity of drug treatment must be adjusted to inflammatory activity. For monitoring in clinical practice the composite index disease activity score is recommended. To achieve the reduction of inflammatory activity the dosage of disease modifying drugs can be increased, they can be switched or combined, and continuous glucocorticoid treatment can be started. In cases refractory to conventional treatment it is possible to inhibit the activity of proinflammatory cytokines, which play a pivotal role in pathomechanism of rheumatoid arthritis. In synovitis limited to one joint intraarticular glucocorticoid injection can be given, in refractory cases synovectomy is indicated. Destruction of the joints can be partially corrected by exercise, orthoses and after all with surgery.     

Lymphopenia in rheumatoid arthritis.

Lymphopenia is a recognized but poorly studied feature of rheumatoid arthritis (RA). We set out to establish the prevalence and significance of lymphopenia in RA. A group of 66 RA patients was studied for one year. During this time 10 (15%) had persistent lymphopenia (lymphocyte count less than 1.00 X 10(9)/l) without evidence of Felty's syndrome. A separate study of lymphocyte subsets in 13 lymphopenic RA patients showed marked reduction in T-cell numbers with normal circulating B-cell numbers. The numbers of CD4 and CD8 positive T-cells were equally depressed. Lymphopenia may indicate more severe disease. It was not influenced by changes in disease activity or therapy.     

Nonpharmacological interventions for rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterised by persistent inflammation of synovial joints, often leading to joint destruction and disability. The major goals of treatment are to relieve pain, reduce inflammation, slow down or stop joint damage, prevent disability, and preserve or improve the patient's sense of wellbeing and ability to function.     

Nutritional considerations in rheumatoid arthritis

Rheumatoid arthritis is a chronic, systemic, inflammatory disorder of unknown etiology. The severity of the disease process adversely affects nutritional status. Articular changes, such as small joint deformities and temporomandibular joint syndrome, alter the ability to self-feed. The inflammatory process may increase metabolic rate. Ingestion, digestion, absorption, and excretion may be compromised by secondary manifestations of the disease. Comprehensive nutrition assessment incorporates evaluation of disease and treatment-specific factors, along with the usual assessment parameters. Abnormal values for certain assessment parameters do not necessarily reflect nutritional status. Treatment methods, including medications, may have an impact on nutritional status, assessment tools, and self-feeding. Nutrition management goals focus on identification and implementation of feeding strategies. Evaluation of the ability to feed oneself includes consideration of functional status, secondary manifestations, and medical treatment. Multiple feeding modalities may be required. Oral supplements, tube feedings, and parenteral nutrition may be employed to meet the nutrition needs of the individual with rheumatoid arthritis.