There is no single test to determine whether or not a person has reactive arthritis. Instead, doctors must gather information to rule out or hone in on the cause of a patient’s symptoms. Information may be gathered from a patient interview, physical exam, lab tests, and medical imaging. A definitive diagnosis may take several days or even months.
Patient Interview and Physical Exam
During the office visit, patients should:
- Let their doctors know about recent prior or ongoing infections
- Describe their joint pain and other symptoms, as well as when symptoms started
A doctor will examine the patient, listening to the patient’s heart and checking for things such as swollen joints, swollen fingers and toes, tender spots, and skin and eye abnormalities.
If a sexually transmitted disease (STD) or infection of the urethra is suspected, the doctor may also look at the patient’s genitals to note any rashes, sores, or abnormal discharge. The doctor may swab the area to run lab tests that check for infection.
If a doctor suspects a patient has reactive arthritis, he or she will typically order lab tests.
Confirm infection. After an infection, the blood will contain certain antibodies. A doctor who suspects reactive arthritis may order a blood test to determine the presence of these antibodies; however, these tests may take several days and are not always accurate or easy interpret.
Inflammatory markers. When a person has an inflammatory condition like reactive arthritis, signs of inflammation are present in the blood. A blood sample may be taken to test for inflammatory markers such as:
- CRP. When there is inflammation in the body, the liver produces a protein called C-Reactive Protein (CRP).
- Erythrocyte sedimentation rate (ESR). The faster red blood cells (erythrocytes) fall to the bottom of a tube filled with the patient’s blood, the greater the degree of inflammation.
An abnormally high CRP level and ESR support the notion that symptoms are caused by reactive arthritis or another inflammatory condition. (One exception: people who have reactive arthritis due to chlamydia may not have notably high inflammatory markers.)
HLA-B27. People with a gene called HLA-B27 are more likely to develop reactive arthritis. Experts estimate only about 8% of people around the world have this gene1, but they account for 50% to 96% of reactive arthritis cases.2,8,9 Testing for this gene can be done with a blood sample.
Joint fluid. Most joints contain a small amount of fluid, called joint fluid or synovial fluid. This fluid can be extracted using a needle and syringe and then tested for signs of an infection or a crystal arthritis, such as gout. This procedure is called joint aspiration.
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A doctor may order none, some, or all of these lab tests depending on the patient’s symptoms, costs, and other circumstances.
Doctors may recommend an x-ray or MRI of the painful joint. An x-ray may suggest joint swelling or other irregularities. An MRI can provide much more detailed images, but it takes longer and is more expensive.
Doctors use the above diagnostic tools to rule out other conditions that can produce the same or similar symptoms. For example, a gonorrhea infection that has spread to the bloodstream, septic arthritis, and Lyme disease can also cause joints to feel painful and swollen. When patients with chronic diarrhea develop joint pain, doctors may consider inflammatory bowel disease as a possible diagnosis.
- Leirisalo M, Skylv G, Kousa M, et al. Follow-up study on patients with Reiter’s dis- ease and reactive arthritis, with special reference to HLA-B27. Arthritis Rheum 1982;25(3):249–59. As cited in Sieper J. Pathogenesis of reactive arthritis. Curr Rheumatol Rep 2001;3(5):412–8.
- Reveille JD, “HLA-B27 and the seronegative spondyloarthropathies,” American Journal of the Medical Sciences, vol. 316, no. 4, pp. 239–249, 1998. As cited in M. H. Abdelrahman MH, Mahdy S, Khanjar IA, et al., “Prevalence of HLA-B27 in Patients with Ankylosing Spondylitis in Qatar,” International Journal of Rheumatology, vol. 2012, Article ID 860213, 2012. doi:10.1155/2012/860213.
- Sieper J. Pathogenesis of reactive arthritis. Curr Rheumatol Rep 2001;3(5):412–8.