Post infection arthritis reactive

by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

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From the American College of Rheumatology

Reactive arthritis (ReA)develops roughly 2-4 weeks after a genitourinary or gastrointestinal infection.

About 10% of patients do not have a preceding symptomatic infection.

Inflammation of joints, entheses (where tendons insert onto bones), axial skeleton (spine), skin, mucous membranes, gastrointestinal tract, and eyes may occur.

A genetic marker, HLA-B27, is positive in 65-96% of patients. Patients who are HLA-B27 positive have about a 50-fold increased chance of developing ReA, but the syndrome can occur in patients who are HLA-B27 negative.

A tendency exists for more severe and long-term disease in patients with HLA-B27, along with a strong family history of the disease. The frequency of ReA after bowel infection averages 1-4% but varies greatly.

The mechanism of the interaction of the inciting organism with the host (often HLA-B27 positive) leading to the development of ReA is not known.

ReA typically follows a self-limited course, with improvement of symptoms by 3-12 months. However, the condition has a high tendency to recur, particularly with eye and genitourinary tract inflammation. Individuals who are HLA-B27 positive have a higher frequency of recurrence. A new infection or other stress factor can cause a reactivation of the disease.

About 15% of patients develop a long-term destructive arthritis or enthesitis or spondylitis. The presence of hip joint involvement, an erythrocyte sedimentation rate (ESR) higher than 30, and unresponsiveness to non-steroidal anti-inflammatory drugs (NSAIDs) indicate a poorer prognosis in ReA.

Prevalence of HLA-B27 and ReA is higher in white people than in black people.

ReA following food-borne bowel infections affects males and females with the same frequency. Disease associated with venereally acquired infections occurs in a male-to-female ratio of 9:1.

Most patients are aged 20-40 years.

Nongonococcal urethritis, if present, can be one of the presenting symptoms for both postvenereal and post-bowel forms. Mild painful urination, purulent discharge, prostatitis and epididymitis in men, and vaginal discharge and/or cervicitis in women can be seen.

The onset is most often acute, with malaise, fatigue, and fever. An asymmetrical lower extremity arthritis is the major presenting symptom. Low back pain occurs in 50% of patients. Heel pain is common because of enthesopathies at the Achilles or plantar fascial insertion on the calcaneus.

Peripheral joint involvement is typically asymmetric and most frequently affects the weight-bearing joints (ie, knees, ankles, hips), but the shoulders, wrists, and elbows are also affected.

In more chronic and severe cases, the small joints of the hands and feet can also be involved. Dactylitis (ie, sausage digits) can be observed, as in other spondyloarthropathies.

While low back pain may be present in 50% of patients, most patients with acute disease have minimal findings on physical examination except for decreased ability to flex the spine.

Patients with more chronic and severe axial disease may develop physical findings similar to ankylosing spondylitis.

As with other spondyloarthropathies, the enthesopathy of ReA may be associated with findings of inflammation (ie, pain, tenderness, swelling) at the Achilles insertion. Other sites include the plantar fascial insertion on the calcaneus, ischial tuberosities, iliac crests, tibial tuberosities, and ribs.

Keratoderma blennorrhagica on the palms and soles is indistinguishable from pustular psoriasis and is suggestive of chronic ReA.

Erythema nodosum can be observed but is uncommon.

Nails can become thickened and look like fungal infection or psoriatic nail disease, but nail pitting is not observed.

Circinate balanitis can also be observed.

Other mucosal signs and symptoms include painless white patches in the mouth.

Conjunctivitis is part of the classic triad of Reiter syndrome, and it can occur before or at the onset of arthritis.

Other ocular lesions include acute uveitis (20% of patients), episcleritis, keratitis, and corneal ulcerations. The lesions have a tendency to recur.

Bowel infections are a common triggering event for ReA. Culprits include Salmonella, Shigella, Yersinia, and Campylobacter species. The frequency of ReA after these enteric infections is about 1-4%.

Some patients continue with intermittent bouts of diarrhea and abdominal pain.

Other manifestations of the disease include mild kidney disease with protein and blood found in the urine.

Cardiac conduction abnormalities can be observed, and aortitis with aortic regurgitation occurs in 1-2% of patients.

Acute phase reactants, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are usually greatly elevated.

Other laboratory findings include a normocytic normochromic anemia along with mild leukocytosis and thrombocytosis during the acute phase. Urinalysis can show aseptic pyuria.

Synovial fluid analysis reveals a high white blood cell count, most often with elevated polymorphonuclear leukocytes acutely. Gram stain and culture results are negative and are necessary to exclude septic arthritis. Throat, stool, or urogenital tract cultures can be performed in an attempt to isolate the causative organism. Test results for rheumatoid factor and antinuclear antibodies are negative.

Early in the disease, no abnormalities are found on x-ray. In more advanced or long-term disease, periosteal reaction at sites of tendon insertion can be observed. Heel spurs are a common sign in long-term cases. Spinal x-ray findings include sacroiliitis and bone spurs. Sacroiliitis occurs in less than 10% of acute cases but may be observed in 50% of those patients with chronic severe disease. Bone spurs are usually asymmetrical and are found most commonly in the thoracolumbar region.

An EKG should be performed in patients having a prolonged course of the disease to evaluate for cardiac conduction disturbances.

Needle aspiration of a joint may be necessary to rule out septic or crystalline arthritis.

The treatment of ReA is modified according to the severity of symptoms.

NSAIDs are the foundation of therapy. These agents should be used on a regular basis to achieve a good anti-inflammatory effect.

The choice of a specific agent depends on the individual response to treatment. Physical therapy should be started to help reduce pain and to avoid muscle wasting in severe cases.

Steroids can be used as either intra-articular injection or systemic therapy.

Joint injections can produce long-lasting improvement and help avoid the use of other systemic therapy. Sacroiliac joints can be injected, usually under ultrasound guidance.

Systemic corticosteroids can be used, particularly in patients with poor response to NSAIDs or in those who develop adverse effects related to their use.

Since the current concepts on the pathogenesis of ReA indicate that an infectious agent is the trigger of the disease, antibiotics might help. Studies have suggested that appropriate treatment of the acute urogenital infection can prevent ReA and that treatment of acute ReA with a 3-month course of tetracycline reduces the duration of illness. No evidence indicates that antibiotic therapy benefits enteric-related ReA.

In patients with chronic symptoms or in patients with persistent inflammation despite the use of the agents mentioned above, other second-line drugs may be used. Experience with disease-modifying antirheumatic drugs (DMARDs) has been mostly in RA and in psoriatic arthritis, but makes sense for severe ReA.

Sulfasalazine can be beneficial in some patients. In a recent 36-week trial of sulfasalazine versus a placebo in the spondyloarthropathies, patients with ReA who were taking sulfasalazine had a 62.3% response rate compared to 47.7% for the placebo group in peripheral arthritis (P = 0.09).

In patients who present with rheumatoid-like disease, methotrexate can be used. Several reports have shown good response, but controlled studies are lacking. Patients with ReA and HIV/AIDS should not be placed on methotrexate or other immunosuppressive agents.

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