Kam Shojania, MD FRCPC (biography and disclosures) and Neda Amiri, BSc MD (biography and disclosures) Show What I did before As the most common autoimmune disease, Rheumatoid Arthritis (RA) affects about 300,000 Canadians.1,2 The disease is often diagnosed in adults between the third to fifth decades of life. Furthermore, women are 2-3 times are as likely to have the disease.2 The chronic synovial inflammation can lead to articular damage, causing physical disability and lower quality of life in this population. Twenty-five years ago, RA was diagnosed on average 2 years after onset and the limited available treatment was escalated depending on symptoms. This resulted in significant physical disability, chronic pain and an overall disease mortality of 20% over 10 years.3 During my training in the 1990s, according to national and international guidelines at the time, the “treatment pyramid” of RA started with rest and exercise, education, physical therapy and NSAIDs. The next tier consisted of disease modifying drugs including Methotrexate. Meanwhile, glucocorticoids (GCs) and surgical treatment were “backbones” of the treatment throughout the course of the disease.4 What changed my practice The past two decades, however, have seen a major paradigm shift in treatment of patients with RA. The Canadian Rheumatology Association (CRA)5, American College of Rheumatology (ACR)6, and European League against Rheumatism (EULAR)7 have put forward revised guidelines in the recent years in their treatment approaches for rheumatoid arthritis. More than ever there is an emphasis on early diagnosis and appropriate treatment with disease-modifying anti-rheumatic drugs (DMARDs). Furthermore, newer treatments have provided options for those patients that were once deemed to have refractory disease. What I do now 1. Diagnosing RA early makes it easier to treat In order to optimize long term prognosis, we need to confirm the presence of RA early. While the complete criteria for diagnosis of RA is covered elsewhere8, the most common features include inflammatory arthritis (AM pain/stiffness lasting >30 minutes) affecting >3 joints, elevated markers of inflammation (CRP/ESR), and Rheumatoid Factor or Anti-CCP positivity. Additional points are awarded for duration of symptoms. Early in the course of the disease, radiological evidence of inflammation/erosion may not be present, and are certainly not necessary for diagnosis. In MRI studies, there is evidence of joint erosions as early as 4 months from the onset of symptoms in absence of any X-ray findings.9 However, if joint erosions are visible at diagnosis, no other findings are needed for diagnosis. Once diagnosis of RA is suspected, RF, anti-CCP and CRP levels should be obtained. 2. All patients with RA should be on a DMARD (Methotrexate is the preferred first choice) It has been repeatedly demonstrated that early diagnosis and treatment, can prevent joint damage and make remission easier to achieve. Initiation of DMARDS in the first 6 months of diagnosis can reverse loss of function in 80% of patients, and induce remission in 42-48% of patients.10 Furthermore, early diagnosis and treatment can prevent loss of function that can often mark the natural history of the disease. This has led to coining of the term, “therapeutic window” in diagnosis and treatment of RA, in which opportunity exists for DMARDs to decisively influence the long-term prognosis including remission of the disease.11,12 Numerous studies over the past decade have set to determine the optimal steps in treatment of RA with DMARDS. While the patient’s preference and risk profile has to be taken into consideration, in absence of any contraindication, Methotrexate has been consistently recommended to be the initial agent of choice for treatment of RA as well as the component of any multidrug treatment plan.13 Overall, Methotrexate offers an excellent risk-benefit ratio and long-term adherence compared with other DMARDS. Major side effects include GI upset, increased liver enzymes, myelosuppresion and stomatitis. Rarely, patients may develop liver toxicity or pneumonitis. Methotrexate monotherapy can achieve remission in 25-30% of patients with RA.10 However, if remission is not achieved, options for additional agents include traditional DMARDs including hydroxychloroquinolone, sulfasalazine, leflunomide or the new biologics (anti-TNF (Tumor necrosis factor) agents, abatacept, tocilizumab, rituximab). The website, www.rheuminfo.com, includes patient information sheet as well as an educational video. Prior to starting patients on Methotrexate, we recommend that physicians ensure patients are not pregnant or breastfeeding, obtain screening labs including CBC, Creatinine, liver enzymes, HepB, HepC, HIV, CRP. Methotrexate can be started at 15 mg weekly PO. Follow up CBC, Creatinine, AST, ALT and CRP should be done on monthly basis. 3. NSAIDS do not change the outcomes in RA NSAIDS decrease inflammation in RA by inhibiting the COX enzyme, which converts arachidonic acid to inflammatory prostaglandins. Therefore, NSAID use in patients with RA is almost universal. However, NSAIDS are associated with major morbidities including increased risk of GI ulceration (2% per year).14 They also play a role in development of hypertension and impairing the anti-platelet function of Aspirin, which may further contribute to the cardiovascular risk of patients with RA.15 Therefore, given their adverse event profile along with lack of disease modifying property, the aim should be to minimize the use of NSAIDS in patients with RA. They can be used as ‘bridging’ therapy while waiting for DMARDs to take effect. 4. Steroids increase morbidity in RA GCs have been used in treatment of RA for more than 60 years. While they exert potent anti-inflammatory effects, their adverse reaction profile is extensive.16 Today, the use of GC is often limited to “bridge therapy” (as above), treatment of RA flares or intra-articular injection. A recent study, using the RA cohort in BC, showed that use of GCs was associated with a 68% increased risk of myocardial infarction (MI). They also showed that the current dose and cumulative use were also independently associated with an increased risk of MI (10% per additional year on GCs and 13% per 5 mg/day increase).17 Similar studies have demonstrated that RA patients on GCs have higher incidence of carotid plaque, congestive heart failure and hypertension.18-20 Given this, I aim to minimize the use of GCs for the smallest dose and the shortest period in my patients with RA. 5. Smoking increases incidence and severity of RA I recommend smoking cessation to all my patients with RA. Smoking is the best-studied environmental factor in RA. In addition to causing more severe disease, it also increases the risk of seropositive RA (RF or anti-CCP positivity).21 Disease onset in smokers occurs earlier and they have greater radiologic progression compared to the non-smokers.22 Furthermore, smokers have been shown to have poorer response to DMARDs including anti-TNF agents even when adjusted for RF or anti-CCP status.23 While the exact reason for this remains unknown, it is hypothesized that interaction between smoking and DMARDs may contribute. All Rheumatologists in BC have committed to see a new inflammatory polyarthritis within 3 months and most will see the patients with suspected diagnosis of inflammatory arthritis within 2-4 weeks. We recommend the family physicians who suspect their patients have early RA, contact their local rheumatologist to expedite the referral. References:
Further Reading: BC Guidelines for RA http://www.bcguidelines.ca/pdf/rheumatoid_arthritis.pdf Please indicate how this article will change your practice:  What is the criteria to diagnose rheumatoid arthritis?A patient was classified as having RA if at least four of these seven criteria were satisfied; four of the criteria must have been present for at least six weeks: morning stiffness, arthritis of three or more joint areas, arthritis of the hands, and symmetric arthritis.
What number indicates you have rheumatoid arthritis?The normal level of anti-CCP is less than 20 Units. (At Hospital for Special Surgery, anti-CCP is reported in Units. Some labs report this same result using a different measurement notation, that is, as less than 20 EU/ml.) A level above 20 suggests the possibility of RA.
What is the normal range for rheumatoid factor?Value, normal less than 15 IU/mL. Titer, normal less than 1:80 (1 to 80)
What 4 lab tests are considered for diagnosing a patient with RA?Blood Tests to Help Diagnose Rheumatoid Arthritis (RA). Rheumatoid factor. Rheumatoid factor is an antibody (protein) found in the blood. ... . Anti-CCP antibody test. ... . C-reactive protein (CRP). ... . Erythrocyte sedimentation rate test (ESR). ... . Anti-nuclear antibody (ANA). ... . The 14-3-3η (eta) protein.. |
What is the minimum number of points that would suggest a diagnosis of rheumatoid arthritis (ra)?
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