Presentation
The active disease presents itself as fatigue, loss of appetite, muscle and joint pain and stiffness. The muscle pain is more prominent in the mornings after a period of inactivity. Following the active disease, it goes into a period of remission. The active disease is usually called the flare up marked by red, warm, painful, tender and swollen joints as a result of inflammation of the synovium.
Complications
Rheumatoid arthritis may not limit itself only to the joints but can also affect various other parts of the body such as eyes, lungs, skin, blood vessels, heart and other major organs. Moreover most of the patients affect by rheumatoid arthritis suffer from emotional distress.
Effect of rheumatoid arthritis on the skin
Rheumatoid arthritis can produce small lumps on the skin called the rheumatoid nodules in 1/5 th of the people. They develop on the skin over the elbows, heels, fingers or forearm. Ulcers due to vasculitis can cause changes on the skin and may indicate a serious disease activity [4].
Effect of rheumatoid arthritis on the eye
Rheumatoid arthritis can cause inflammation of the episclera, a condition called scleritis. It is usually mild but in some extreme cases can become red, painful and inflamed and may even lead to vision loss.
Effect of rheumatoid arthritis on the heart and blood vessels
Rheumatoid arthritis can result in the accumulation of fluid around the heart resulting in pericarditis. Inflammation of the heart muscle itself, myocarditis can develop in some rare conditions. Vasculitis, the inflammation of the blood vessels can also occur, which can affect many organs [5].
Effects of rheumatoid arthritis on the lungs
Rheumatoid nodules can develop in the lungs resulting in collapsed lung, coughing up blood or pleural effusion [6]. Interstitial lung diseases and pulmonary hypertension may also develop as a result of rheumatoid arthritis.
Effect of Rheumatoid arthritis on blood cells
Rheumatoid arthritis can cause anemia and can result in Felty's syndrome. In this condition, the spleen is enlarged, the white blood cell count decreases and may even lead to lymphoma in rare conditions.
Workup
Diagnosis is usually made by several tests such as blood tests involving the Erythrocyte Sedimentation Rate and C-reactive protein (CRP). X-rays are made to evaluate joints. Various imaging techniques such as MRI and CT scans are useful to evaluate and diagnose rheumatoid arthritis.
The laboratory studies used in the diagnosis of rheumatoid arthritis fall under three categories such as the hematological parameters, immunological parameters and markers of inflammation [7].
Hence some of such tests include, Erythrocyte Sedimentation Rate, C-reactive protein, complete blood count, Rheumatoid factor assay, anti–nuclear antibody assay, anti-cyclic citrullinated peptide and anti-mutated citrullinated vimentin assay [8].
These biomarkers can not only help in early diagnosis of the disease, but also can help in assessing the prognosis of the disease.
Treatment
Treatment of rheumatoid arthritis aims at reducing the inflammation of the joints, relieving pain, preventing joint damage and minimizing disability. Treatment is mostly symptomatic as there is no cure for the disease.
The treatment involves exercise and lifestyle modifications, medications and surgery in some extreme cases. The medications for treating rheumatoid arthritis include, NSAIDs, corticosteroids, DMARDs (Disease Modifying Anti–Rheumatic Drugs) and immunesuppressants [9].
Prognosis
Rheumatoid arthritis is a debilitating disease. Though treatment can delay and reduce the severity of the disability, there is no cure for this condition.
If the disease pattern is not altered by any medication, there is an ultimate destruction of the joints. The bone and the cartilages get eroded and the surface on which the joint moves is destroyed, resulting in rigidity and immobility of the joint, leading to a loss in the range of motion.
It may take years for the disease to progress to this stage, though the process may be hastened in some individuals. In very rare cases, when the organs such as the blood vessels are affected, life-threatening vasculitis may develop [3].
Usually, the symptoms appear within the first two years of occurrence of the disease and manifests as pain, stiffness and immobility. As the disease progresses it results in 'burnt out' disease where there is severe immobility, deformity but very little inflammation.
Etiology
Etiology of occurrence of rheumatoid arthritis has not yet been identified and various researches are being carried out to identify the cause. It has been suggested that rheumatoid arthritis can be caused by both genetic and environmental factors. The Human Leukocyte Antigen (HLA) type is identified to be the gene linked with rheumatoid arthritis [1]. Of this, the HLA-DRB1 contains a sequence for the shared epitope and is found to be linked with the occurrence of rheumatoid arthritis.
Antibodies like RF and anti-CCP are associated with the occurrence of rheumatoid arthritis [2]. Apart from the genetic cause, it has been documented that various other causes such as smoking, bacteria, endocrinology and reproductive and psychological factors can predispose to the occurrence of rheumatoid arthritis.
Epidemiology
Woman are found to be more prone to be affected by this condition than men. It has been estimated that this disease is prevalent in 1% of women and 0.4% of men and 3.6% of women and 1.7% of men have a lifetime risk of acquiring this disease. The highest incidence is among the individuals between 40 to 75 years of age and the ratio of occurrence of this disease between women and men is 2:1. Rheumatoid arthritis is more common in the northern Europe and Northern America, but less common in Asia and Africa.
Pathophysiology
The pathophysiology of rheumatoid arthritis is complex and is not completely understood.
Initially, the external factors such as smoking, triggers an autoimmune response in susceptible individuals. This results in the hyperplasia of the cells in the synovial joint and activation of the endothelial cells. These are early events that later progresses into bone and cartilage destruction due to uncontrolled inflammation. The mononuclear phagocytes, CD4 T-cells, osteoclasts, fibroblasts and neutrophils play a major role in the development of symptoms while, the B-cells produce autoantibodies.
Moreover there is an abnormal production of inflammatory mediators, cytokines, chemokines and growth factors that result in the further deterioration of bones and cartilages. The inflammation and the abnormal proliferation of the synovia, otherwise known as the pannus, ultimately results in the destruction of cartilage, bones, blood vessels, tendons and ligaments.
Though only the articular structures are the primary sites involved, other structures are also affected as a result of this inflammation.
Prevention
Summary
Rheumatoid arthritis is an autoimmune disorder that presents itself as a chronic inflammatory condition. An external trigger such as smoking, drinking, trauma or infection can trigger the immune system resulting in this condition. Rheumatoid arthritis is characterized by synovial hypertrophy and chronic inflammation of the joints. There may be extraarticular manifestations of this condition.
Genetic predisposition for the occurrence of this disease is still a topic of debate. Small joints of the hands and feet are the most affected in this condition and symmetric polyarthritis is its classical presentation. Early intervention of the condition is mandatory to avoid further complications.
Patient Information
Rheumatoid arthritis is a chronic inflammatory condition that affects mainly the joints, though it can also affect other organs. Though the specific cause of the disease is not known, it can triggered by various factors such as smoking.
Treatment of rheumatoid arthritis must be tailored according to individual needs and is usually a combination of drug and non-drug therapies. Early intervention can prevent progression of the disease and can prevent further deterioration of the joints and other associated complications.
References
- Lipsky PE. Harrison's Principles of Internal Medicine. In: Isselbacher KJ, Braunwald E, Fauci AS, et al.Rheumatoid arthritis. 17th ed. New York, NY: McGraw-Hill; 1994:1648-55.
- Barton A, Worthington J. Genetic susceptibility to rheumatoid arthritis: an emerging picture. Arthritis Rheum. Oct 15 2009;61(10):1441-6.
- van Venrooij WJ, van Beers JJ, Pruijn GJ. Anti-CCP antibodies: the past, the present and the future. Nat Rev Rheumatol. Jun 7 2011;7(7):391-8
- van der Heijde DM. Radiographic imaging: the ‘gold standard' for assessment of disease progression in rheumatoid arthritis. Rheumatology (Oxford). Jun 2000;39 suppl 1:9-16
- Lindhardsen J, Ahlehoff O, Gislason GH, et al. Risk of atrial fibrillation and stroke in rheumatoid arthritis: Danish nationwide cohort study. BMJ. 2012;344:e1257.
- Komano Y, Harigai M, Koike R, Sugiyama H, Ogawa J, Saito K. Pneumocystis jiroveci pneumonia in patients with rheumatoid arthritis treated with infliximab: a retrospective review and case-control study of 21 patients. Arthritis Rheum. Mar 15 2009;61(3):305-12
- Ahlmén M, Svensson B, Albertsson K, Forslind K, Hafström I. Influence of gender on assessments of disease activity and function in early rheumatoid arthritis in relation to radiographic joint damage. Ann Rheum Dis. Jan 2010;69(1):230-3.
- Bang H, Egerer K, Gauliard A, et al. Mutation and citrullination modifies vimentin to a novel autoantigen for rheumatoid arthritis. Arthritis Rheum. 2007;56(8):2503–11
- Luqmani R, Hennell S, Estrach C, Basher D, Birrell F, Bosworth A, et al. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of rheumatoid arthritis (after the first 2 years). Rheumatology (Oxford). Apr 2009;48(4):436-9.
- Macedo AM, Oakley SP, Panayi GS, Kirkham BW. Functional and work outcomes improve in patients with rheumatoid arthritis who receive targeted, comprehensive occupational therapy. Arthritis Rheum. Nov 15 2009;61(11):1522-30.