Rheumatoid Arthritis


Rheumatoid Arthritis


Rheumatoid arthritis is a form of arthritis or an inflammatory disease of joints. A common disorder affecting more than 1% of Americans the prevalence can increase to more than 5% in women above the age of 65. Usually manifesting in the latter decades above 40-50 years, it typically affects multiple joints including those in the hands, feet and limb girdles. Systemic inflammation also occurs resulting in fatigue, weight loss and depression. The disorder is brought on by the body’s own immune system attacking cartilage, joints, tendons and ligaments resulting in morning stiffness, throbbing pain and swelling of joints finally leading to joint deformities that are characteristic of the disease. Hand deformities result in tenting of the distal finger joints known as swan neck deformity, a z shaped thumb deformity and radial wrist deviation and ulnar deviation of the fingers. The joints affected in the hand are usually the proximal joints closest to the palm. This is different from osteoarthritis, in which the distal joints are affected in addition to evening stiffness instead of morning stiffness.


Felt to be partially related to complex gene inheritance, related to the HLA MHC Human Leukocyte Antigens of the Major Histocompatibility Complex and environmental effects, the disease is only present in less than 15% of identical twins.


A well established environmental trigger is smoking which has been noted to increase the risk of development of RA in susceptible individuals by many fold.


-Smoking is thought to trigger citrullation of arginine, causing autoimmunity to develop with the final development of Anti Citrullinated Antibodies playing a role in the disease.


Other equally strong risk factors in CCP Ab positive RA patients include


-excess coffee intake


-and possibly the use of birth control pills. The above associations are less clear in CCP Ab neg RA patients.


-Women are at least two or three times the risk as men.


-Nulliparity has been shown to add to these risks where as breast feeding has been shown to decrease the risk.


-Bacteria and viruses are also implicated, the most common ones include porphyromonas gingivalis and epstein barr virus respectively.


Diagnosis requires evaluation by a rheumatologist with a careful examination and evaluation for other similar joint disorders including osteoarthritis, psoriatic arthritis, viral polyarthritis (hepB,C and parvovirus 19, chikungunya), Lymes diseae, gout and calcium pyrophosphate deposition disease or pseudogout and systemic diseases related arthritis (SLE or lupus, Sjogrens, Mixed connective tissue diease, Sarcoid, Inflammatory Bowel Disease, etc). Usually symptoms for greater than 6 weeks with several joints involved at presentation with positive inflammatory markers (ESR, CRP) and specific antibodies ( RA, CCP) usually helps make the diagnosis.


Blood tests for inflammatory markers including erythrocyte sedimentation rate, ESR and C reactive protein CRP are usually elevated. Antibodies to rheumatoid factor, RA and cyclic citrullinated Ab CCP are helpful if elevated. Other blood tests to exclude cryoglobulinemia, Hepatitis B and C, and lupus with ANA, sjogrens Ab testing are performed too.


Synovial fluid testing can exclude crystals that may be due to gout or pseudogout.


X rays of the hands and feet and joints can show characteristic deformities.


Rarely rheumatologists may recommend testing with MRI and Ultrasound of specific joints as warranted.


Once the diagnosis is confirmed the rheumatologist can begin treatment with disease modifying anti rheumatic drugs or DMARDs.




Before treatment can be started screening for certain diseases is considered including testing for latent TB ( with quantiferon TB gold assa), Hepatitis B and C.


Non steroidal anti-inflammatory treatments include Ibuprufen, aleve, etc and steroids including prednisone.


Non biologic DMARDs include methotrexate (MTX), hydroxychloroquine, sulfasalazine and leflunomide.


Biologic DMARDs include TNF inhibitors (etanercept, infliximab, adalimumab, etc, which are monoclonal antibodies (hence the ..mab ending…) and interleukin receptor antagonists (anakinra, and tocilizumab) and others including abatacept and rituximab.


Aggressive early treatment is associated with better outcomes and disease control. Usually treatment starts with NSAIDs or steroids and hydroxychloroquine (needs ophthalmic screening for possible ocular side effects) or sulfasalazine as DMARDs are recommended early in the RA disease process to avoid rapid deterioration of joints. If poor response or more severe disease is present then MTX may be added to NSAIDs. If a poor response is obtained then switching or adding a TNF inhibitor is an option. Your rheumatologist will usually help guide you in the decision making process for what suits you best.   


Frequent regular rheumatologic appointments and necessary lab testing (CBC, Chemistry and Liver function tests LFTs) is important to avoid development of side effects.


Tips for RA:


Follow a rheumatologist and physiotherapist at regular intervals


Start DMARDs soon under the supervision of a rheumatologist


Have monthly labs or as warranted by your physician


See a neurologist if symptoms of carpal tunnel syndrome develop


See an ophthalmologist regularly if on Hydroxychloroquine


See a nephrologist or kidney specialist if abnormalities develop in kidney functions.