How is Reiter syndrome caused, the diagnosis of Reiter syndrome

The cause of the disease is still unknown. It is thought to be related to infection, immune abnormalities, and genetics. Because the disease can be seen in people living in a group living environment, and the onset is very urgent, there is a history of intestinal or urinary tract infection, antibiotics seem to be effective, 33% of 47% of patients have positive urine culture for Chlamydia trachomatis, so it has long been believed that chlamydia, spirochetes, dysentery bacilli, 4th bacteria, mycoplasma, hepatitis B virus, herpes virus, etc. are infectious**, but none have been confirmed.

In contrast, it is hypothesized that the inflammatory mechanism associated with the immune response in vivo plays a decisive role in hyperglobulinemia, such as increased erythrocyte sedimentation rate and increased C-reactive protein. In addition, the frequency of anti-prostate antibodies in the blood of patients was significantly higher than that of the normal population, suggesting that the inflammation in the body was the result of an autoimmune response. It has been reported to occur more often after sexual intercourse in the United Kingdom and the United States, and after bacillary dysentery in Europe, Africa, the Middle East, and the Far East.

Hello, there are three clinical features of Reiter's syndrome: urethritis, conjunctivitis, and arthritis, so it is also called urethral, eye, and joint syndrome. Infection and genetic factors are associated with the onset of the disease. Pediatric Wright syndrome is less common clinically.

The triad of typical arthritis, nongonococcal urethritis, and conjunctivitis is not difficult to confirm the diagnosis, and suspicion should be high in patients with asymmetric oligoarthritis with negative serology, especially in young adults; Although the presence of a prodromal infection is important for diagnosis, it is often insidious and easily overlooked by doctors and patients. Heel pain and other symptoms of tendon disease, dactylitis, and various forms of mucosal lesions increase the likelihood of the disease.

1.Pathogen culture.

Urethral swab culture can be performed, and cervical scrub cells can be used for direct fluorescent antibody and enzyme-linked immunoassay if available. When intestinal symptoms are subtle or mild, stool cultures can be helpful in identifying the precipitating organism and can provide a diagnostic basis for suspected reactive arthritis. However, it should be noted that most patients present with an infection that occurred several weeks ago, and cultures of the organism are often negative.

2.Markers of inflammation.

In the acute phase, there may be an elevated white blood cell count, a rapid erythrocyte sedimentation rate, and an elevated CRP. Mild normocytic anemia may occur in chronic patients. Complement levels may be elevated.

3.Synovial fluid and synovial examination.

Synovial fluid has mild to severe inflammatory changes, decreased synovial fluid viscosity, mildly to moderately elevated white blood cell count, predominantly neutrophils, and the presence of macrophages containing vacuoles of nuclear dust and entire white blood cell counts, sometimes called Wright cells, but it is not specific for Wright syndrome. Synovial biopsy shows nonspecific inflammatory changes, but usually has more neutrophil infiltrates than rheumatoid arthritis. Infectious agent antigens can be identified in synovial membrane and synovial fluid using immunohistochemistry, PCR, or molecular hybridization.

Detect. HLA-B27 antigen is associated with axial arthropathy, carditis, and ocular meningitis osmosis, so a positive antigen is helpful in the diagnosis. As with other spondyloarthropathies, rheumatoid factor and antinuclear antibodies are usually negative.

5.Radiological tests.

X-rays of the sacroiliac joints and affected joints and spine should be taken at the beginning of diagnosis. A small number of patients develop sacroiliitis early in the disease. The majority of patients with chronic Reiter syndrome end up with unilateral (early) or bilateral (late) sacral plexus nucleus iliac joint abnormalities; Asymmetric paravertebral "comma" ossification is a unique imaging finding in Reiter's syndrome and psoriatic arthritis.