Reactive arthritis (formerly Reiter syndrome)

Patient information: Reactive arthritis (formerly Reiter syndrome)

Author
David T Yu, MD
Section Editor
Joachim Sieper, MD
Deputy Editor
Paul L Romain, MD

Disclosures

REACTIVE ARTHRITIS OVERVIEW — Reactive arthritis is a type of arthritis in which the joints become painful and swollen after an infection. The infection might have been in the intestines, genitals, or the urinary tract.

Reactive arthritis belongs to a family of arthritis conditions called spondyloarthritis (spondyloarthropathies or spondyloarthritides). This family of arthritis disorders includes ankylosing spondylitis, undifferentiated spondyloarthropathy, and arthritis associated with psoriasis (psoriatic arthritis), Crohn’s disease, and ulcerative colitis. (See “Patient information: Ankylosing spondylitis and spondyloarthritis” and “Patient information: Psoriatic arthritis” and “Patient information: Crohn’s disease” and “Patient information: Ulcerative colitis”.)

Some clinicians use the term “Reiter syndrome” instead of “reactive arthritis”.

REACTIVE ARTHRITIS CAUSES — Two types of bacteria are responsible for most cases of reactive arthritis:

Bacteria that cause bowel infections — These include the bacterial species Salmonella, Shigella, Campylobacter, and Yersinia. These bacteria often cause diarrhea, which can last up to one month. (See “Patient information: Food poisoning (food-borne illness)”.)
Bacteria that cause genital infections — These include Chlamydia trachomatis, a sexually transmitted infection. Chlamydia can cause pelvic pain, burning with urination, and a pus-like or watery vaginal or penile discharge. Some people have no symptoms with their infection. (See “Patient information: Chlamydia”.)
REACTIVE ARTHRITIS RISK FACTORS — Your genetic makeup may play a role in your risk of developing reactive arthritis. Especially important are genes involved in immune defense. The HLA-B gene, for example, produces a protein that helps the body respond to certain infections, and it may play a role in reactive arthritis.

There are many variants of the HLA-B gene. One of these, HLA-B27, is strongly linked to ankylosing spondylitis, a disease with features similar to reactive arthritis but which lacks an identifiable infectious trigger. People who carry the HLA-B27 gene type may have an increased risk of developing reactive arthritis. However, many people with reactive arthritis do not carry HLA-B27. A blood test for HLA-B27 is available, but often isn’t needed to help diagnose reactive arthritis. (See “Patient information: Ankylosing spondylitis and spondyloarthritis”.)

REACTIVE ARTHRITIS SYMPTOMS — Typical symptoms of reactive arthritis include joint pain and swelling that develops suddenly, usually one to four weeks after an episode of infection. Frequently, the pain and swelling involve a small number of joints (three or less), typically including the knee, ankle, or joints of the feet. Some patients have tendonitis affecting the Achilles tendon, behind the ankle, or the plantar fascia, on the sole of the foot where it attaches to the heel.

Conjunctivitis (inflammation of the covering of the eyes) can also occur in people with reactive arthritis.

Pain with urination or in the pelvis can also occur in some people.

REACTIVE ARTHRITIS DIAGNOSIS — The most reliable way to diagnose reactive arthritis is to identify the bacterial trigger in the stool or urine. Blood tests may be helpful but are not as specific as identifying the bacteria in the stool or urine. However, reactive arthritis can be diagnosed in a person with symptoms, even if a culture has not been done.

REACTIVE ARTHRITIS TREATMENT

Antibiotics — Antibiotics may be used to treat an active genital infection. However, there is no convincing evidence that antibiotics will improve joint pain or shorten the course of reactive arthritis after the joint pain has developed.

Nonsteroidal antiinflammatory drugs — Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen, naproxen, or indomethacin are usually recommended to reduce joint pain and swelling. Relatively large doses of an NSAID may be needed on a regular basis for up to two weeks to determine if the NSAID is effective. (See “Patient information: Nonsteroidal antiinflammatory drugs (NSAIDs)”.)

Other treatments — If you do not improve with NSAIDs, your clinician may recommend a glucocorticoid (also called a steroid) injection into the joint. Additional treatment with glucocorticoids (taken by mouth or as an injection) might be necessary for a short period if you have severe pain or joint swelling.

Another medication, such as one of the disease modifying antirheumatic drugs (DMARDs, eg, sulfasalazine or methotrexate), or a medication that interferes with the action of tumor necrosis factor (TNF) (a TNF inhibitor or blocker such as etanercept, infliximab or adalimumab) may be recommended if your symptoms do not improve with NSAIDs or with glucocorticoid treatment. In this case, you should see a specialist in inflammatory joint diseases (a rheumatologist) to confirm that your symptoms are caused by reactive arthritis. (See “Patient information: Disease modifying antirheumatic drugs (DMARDs)” and “Patient information: Sulfasalazine and the 5-aminosalicylates”.)

Eye treatment — Eye inflammation can occur in people with reactive arthritis, and is sometimes treated with glucocorticoid eye drops. If you develop eye pain or blurry vision, you should see an ophthalmologist to determine if your symptoms are due to conjunctivitis or a more serious eye problem such as inflammation of the iris (called iritis or anterior uveitis). (See “Uveitis: Etiology; clinical manifestations; and diagnosis”.)

WHEN WILL I GET BETTER? — Most people with reactive arthritis have a mild course of joint pain that resolves spontaneously and never comes back. In some people, the disease will intermittently cause symptoms. In others, the disease is persistent.

If your back becomes painful and stiff and does not improve with time, reactive arthritis may have developed into a spondyloarthropathy. (See “Clinical manifestations, diagnosis, and management of undifferentiated spondyloarthritis and related spondyloarthritides” and “Patient information: Ankylosing spondylitis and spondyloarthritis”.)

WHERE TO GET MORE INFORMATION — Your healthcare provider is the best source of information for questions and concerns related to your medical problem.

Related topics for patients, as well as selected articles written for healthcare professionals, are also available. Some of the most relevant are listed below.

Patient Level Information:

Patient information: Ankylosing spondylitis and spondyloarthritis
Patient information: Psoriatic arthritis
Patient information: Crohn’s disease
Patient information: Ulcerative colitis
Patient information: Food poisoning (food-borne illness)
Patient information: Chlamydia
Patient information: Nonsteroidal antiinflammatory drugs (NSAIDs)
Patient information: Disease modifying antirheumatic drugs (DMARDs)
Patient information: Sulfasalazine and the 5-aminosalicylates

Professional Level Information:

Neutrophilic dermatoses
Pathogenesis of spondyloarthritis
Reactive arthritis (formerly Reiter syndrome)
Uveitis: Etiology; clinical manifestations; and diagnosis

The following organizations also provide reliable health information.

National Library of Medicine
(www.nlm.nih.gov/medlineplus/healthtopics.html)
Spondylitis Association of America
(www.spondylitis.org)
National Institute of Arthritis and Musculoskeletal and Skin Diseases
(301) 496-8188 (www.nih.gov/niams/)
American College of Rheumatology
(404) 633-3777
(www.rheumatology.org)
The Arthritis Foundation
(800) 283-7800
(www.arthritis.org)

REFERENCES
Healy PJ, Helliwell PS. Classification of the spondyloarthropathies. Curr Opin Rheumatol 2005; 17:395.
D’Agostino MA, Olivieri I. Enthesitis. Best Pract Res Clin Rheumatol 2006; 20:473.
Leirisalo-Repo M. Reactive arthritis. Scand J Rheumatol 2005; 34:251.
Sieper J, Rudwaleit M, Braun J, van der Heijde D. Diagnosing reactive arthritis: role of clinical setting in the value of serologic and microbiologic assays. Arthritis Rheum 2002; 46:319.