Rheumatoid Arthritis (Disease Modifying Anti-Rheumatic Drugs (DMARDs)…
Autoantibodies (rheumatoid factor and anti-CCP.
Inflamed and thickened synovial lining.
Involvement of tissues and other organs may also occur
Can contribute to accelerated atherosclerosis with MI.
Systemic disease = increase in mortality.
First degree relatives have an increased risk by 4-fold. Also first degree relatives with another autoimmunity (T1DM, SLE etc).
Possession of tissue type HLA-DR4.
Patients with diseases such as RA have genes that predispose to autoimmunity in general by making the immune system hyperactive and then, in addition, particular HLA genes that determine the ability to respond to specific antigens.
Smoking greatly increases risk, via alteration of proteins in the inflamed lungs through citrullination.
Antibodies to citrullinated proteins.
Prodromal period as abnormal immune responses build up before clinical disease develops.
Swelling and stiffness of small joints in the hands and feet (wrists, mcps, pips, mtps).
Usually insidious and progressive but onset can also be sudden.
Treatment and Management
To relieve pain, improve function, and to prevent the joint damage that causes deformity and disability.
To prevent premature death as a complication of RA.
Remission is defined as a composite disease activity score (DAS) of 2.6 or less.
Treat to target approach, encourages measurement of DAS at each visit and progressive treatment escalation every 3 months to reach the target range.
To manage increased mortality, particularly in those with extra-articular features of the disease.
Physiotherapy to maintain muscle mass and preservation of strength.
Occupational therapy to protect joints and optimise function.
Orthotics and joint supports.
Due to side effects used at a low dose daily.
Potent immunosuppressive agents and their use increases the risk of infections such as pneumonia.
Often used early in the course of the disease for rapid suppression of RA in more severe cases.
Aims to give max. anti-inflammatory effect in the joint with minimal systemic effects.
Useful for when large joints are affected.
Withdrawing steroid therapy can be difficult.
If treatment is prolonged - concurrent use of medication is needed to ameliorate side effects (e.g. bisphosphonates).
-Worldwide prevalence of about 1%.
-More common in females
-Peak age of onset = 30-60
-Although can occur in childhood
-anti-CCP antibodies (a positive result is highly specific to RA), so can be useful in distinguishing from other conditions.
Main means of imaging joints and looking for erosive changes.
Important for the differentiation from SLE.
Can visualize the build-up of the inflamed joint lining tissue that causes joint erosions, as well as the early stages of erosions.
MRI is useful to determine which patients require early use of potent agents to prevent progressive joint damage.
Able to show early joint inflammation and detect the presence of early erosive joint damage.
Symptomatic relief of pain and stiffness
Limited by side-effects
Decreased renal blood flow may occur with impairment of kidney function.
COX-2 selective inhibitors can be expected to be pro-thrombotic.
Step-wise treatment strategy
Earliest possible intervention with DMARDs
Use MTX (unless contra-indications such as abnormal liver function or pregnancy).
If control is not achieved, try combination therapy with MTX, salazopyrin, and hydroxychloroquine.
MTX + Leflunomide
Steroids used early in severe cases then tapered as control is achieved with DMARDs.
If combination therapy with standard DMARDs is ineffective, then an anti-TNF agent is used in combination with MTX.
MTX, Leflunomide and sulphasalazine: Fortnightly blood count, LFTs, CRPs for 2 months, and thereafter monthly.
Monitor for liver fibrosis.
Baseline respiratory function tests and chest X-ray.
Monitor for infection, re-awakening TB/HEP.
Worsening heart failure
Development of anti-nuclear antibodies and Lupus.