a.	Rheumatoid Arthritis, or "RA" is a chronic, progressive, systemic auto-immune disease primarily affecting the joints. Classically, RA is a symmetric polyarthritis mostly involving the small joints of the hands and feet. Other common sites of involvement include the temporo-mandibular (jaw) joint, cervical spine, shoulders, elbows, wrists, hips and ankles. Surprisingly, the lumbar spine is not involved.
b.	Symptoms include painful swelling of joints (see Figure 1) with prominent joint stiffness in the morning (usually > 1 hour). The swelling is caused by inflammation and invasive growth of the joint lining tissue (synovium). Inflamed synovium is referred to as "synovitis." RA is a destructive form of arthritis, with patients progressing to irreversible joint deformities if they are not correctly managed (see Figure 2).
c.	However, RA is not just a joint disease. It is a SYSTEMIC disease, meaning that patients may have signs and symptoms beyond their joints (weight loss, fatigue, fever, anemia, pleurisy, vascular inflammation, nodule formation, etc).

No, but the prevalence is relatively consistent throughout the world: ~ 1% of the general population. Accurate prevalence data from the Philippines is not available.

a.	The cause of RA is unknown. Currently, RA is believed to result from a persistently abnormal immune response directed against synovial tissue. RA probably develops when a genetically susceptible host is exposed to an environmental agent, probably an infection, which triggers the immune response to turn against joint tissue. Many microorganisms have been implicated, but none have been definitively linked. These include streptococci, mycoplasma, mycobacteria, yersinia, rubella, parvovirus B19.
b.	Family studies suggest a concordance rate of 25% in identical twin siblings of patients with RA. The fact that concordance is not 100%, suggests that the inter-play of genes and an environmental trigger(s) is necessary before RA can develop. First degree relatives of patients with RA develop the disease at a rate of ~4X that of the general population.
c.	Additionally, 3 out of every 4 patients are female, and the peak age at onset is 35 to 50 years, suggesting that female sex hormones may play a role. This is substantiated by the observation that women with active RA become quiescent during pregnancy, and their disease flares up after delivery.

a.	No laboratory test is diagnostic of RA. The "Rheumatoid Factor" or RF is frequently positive in patients with RA, but can be negative in up to 30% of patients. ~5% of the healthy general population, and up to 20% of healthy older patients may be positive for RF. RF is also seen in other medical conditions, including cancer and tuberculosis.
b.	Common, nonspecific laboratory abnormalities in RA include anemia, elevated platelet counts, and the elevation of surrogate markers of inflammation [e.g. erythrocyte sedimentation rate (ESR), and c-reactive protein (CRP)].
c.	RA is best diagnosed using a combination of history, physical exam findings, and surrogate laboratory markers of inflammation.

a.

OA is a degenerative joint disease with periods of inflammation during flares. RA is primarily an inflammatory joint disease. The pathology of OA involves wearing out of joint cartilage, while RA involves overgrowth of synovial lining tissue resulting in joint invasion and destruction. RA is more painful, and more frequently associated with swelling and disability. Uncontrolled, RA is deforming, resulting in loss of function. OA is less debilitating, until the joint cartilage is well worn out. OA can be mildly deforming, but joint function may remain. Symptoms in RA are more prominent during the morning, while those of OA are worse at the end of the day (when the joints have been used). Joint involvement is also different. As seen in Figure 3, OA spares the knuckles (top), while RA spares the most distant joints of the fingers (the joints adjacent to the fingernails, see lower photo).

a.	All patients with RA should be started on disease modifying anti-rheumatic drugs (DMARDs). These medicines are not useful in OA, but are useful in slowing the progression of RA. These medicines need monitoring because of the potential for long-term organ toxicities, and should be administered under the guidance of a rheumatologist.
b.	Examples of DMARDs include prednisone, methotrexate, sulfasalazine, hydroxychloroquine, azathioprine, cyclosporine, etanercept, remicade, and leflunomide.
c.	Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are useful for providing symptomatic relief, since DMARDs are generally slow in onset of action. However, gastrointestinal complications, particularly gastric and duodenal ulcers, are seen with long-term use. The availability of newer generation NSAIDs, called "COX-2 Specific Inhibitors," has given patients a safer option for long-term symptomatic relief of RA pain and inflammation.

RA is a chronic disease. With early diagnosis and initiation of appropriate treatment, RA is controllable, with many patients achieving near-normal functionality. Tina Wesson, winner of "Survivor Africa" and the US$1 million dollars that went with it, has RA and was receiving Methotrexate and Celebrex for her disease.

All patients with RA should be followed by a rheumatologist.