Approach

There is no specific test for diagnosing ReA. Rather, a group of tests is used to confirm the suspicion in a patient who has clinical symptoms suggestive of an inflammatory arthritis in the postvenereal or postdysentery period.

Tests for rheumatoid factor, seen with rheumatoid arthritis, and antinuclear antibody, found in many autoimmune conditions, are usually negative.

Acute-phase reactants

The acute-phase reactants, such as erythrocyte sedimentation rate or C-reactive protein (CRP), are often elevated in the acute stage but tend to normalize if the disease becomes chronic.

HLA-B27

Only a small percentage of HLA-B27 positive individuals will develop ReA. The predictive value of testing for HLA-B27 is dependent upon a clinical estimate of the likelihood of ReA; the majority of patients presenting with musculoskeletal complaints will not have ReA.[54]

While HLA-B27 is not specific to, or required for the diagnosis of ReA, its presence in the proper clinical context improves the accuracy of the diagnosis.[55][56][57][58]

Laboratory tests

Identifying the usual causative organisms that trigger infection is helpful in establishing a diagnosis. Urogenital and stool cultures are very helpful at the time of the inciting infection; however, these cultures are usually negative after the onset of arthritis. Nonetheless, they are easy to perform and should be carried out at the onset of arthritis.

Routine cultures and cultures to rule out gonorrhea and other infectious processes should be performed on synovial fluid. Crystal analysis should also be performed on synovial fluid to rule out gout or any other crystal-induced arthritis.

Polymerase chain reaction (PCR) analysis of bacterial components in the synovial tissue or fluid is useful in confirming a diagnosis but not practical. PCR analysis should also be performed on urine at the onset of arthritis; however, it is often negative at this stage.

Nucleic acid amplification tests are indicated in asymptomatic men or women with suspected sexually acquired reactive arthritis.[59][60]

It is possible to check for serologies of the known causative bacterial agents, but it remains difficult to prove causality so ordering these tests is not generally recommended.[61]

Radiography

Radiographs should be performed on the axial skeleton of any patient with suspected chronic ReA. While radiographs of peripheral joints can show some ReA features, these are less specific for ReA.

There are no specific radiographic findings early in the disease except for soft tissue swelling. In the chronic form of the disease, joint space narrowing and erosions can be found in the small joints of the hands and feet. Plain radiographs of the axial skeleton display asymmetric sacroiliitis in one third of patients with chronic ReA.[62][63]

Enthesitis can be seen in chronic ReA in the form of fluffy periosteal new bone formation at sites of tendon and ligamentous insertions. Calcifications at the area of the Achilles' tendon and exuberant spurs on the calcaneus are commonly seen. Nonmarginal syndesmophytes can be found on the lumbar and thoracic spine as a result of chronic enthesitis of the paraspinal ligaments.

MRI

MRI may be more sensitive in detecting early sacroiliitis, but no controlled studies have been performed. MRI analysis of the sacroiliac joints can be particularly useful in any patient with suspected ReA with low back or buttock pain. MRI may reveal erosive changes or ankylosis of the sacroiliac joints, and bone marrow changes around the sacroiliac joints indicative of active sacroiliitis.

Ultrasound

Ultrasound of extremities may complement x-ray.[64] It can identify synovial hypertrophy; increased vascularity is apparent on Doppler imaging.[64]

European guidelines suggest that ultrasound might provide additional information to conventional radiography when monitoring structural changes in peripheral spondyloarthritis.[65]

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