Ankylosing spondylitis and infections of the female urogenital tract

Abstract

Thirty-two female patients with confirmed ankylosing spondylitis (AS) and 33 women of similar age with pure ileitis terminalis Crohn were examined for genitourinary infection. Urethral syndrome was found in 15 out of 32 patients with AS: 11 of them had urethritis and 4 urethritis associated with vaginitis. Five women of the control group suffered from urethritis. In all cases with genitourinary infection, Chlamydia trachomatis was isolated. By comparing the AS-patients (urogenital infection group and the non-infected group) with regard to other present clinical parameters, it was found, as expected, that the erythrocyte sedimentation rate in the 1st hour was significantly higher in the infected group. In addition, the infected patients had a significantly higher incidence of enthesopathy, involvement of the spinal column, and higher C-reactive protein values (CRP > or = 5 mg/l). A family history of AS was equally present. Other clinical parameters, such as inflammatory involvement of the joints and HLA-B27 correlation, did not differ significantly between infected and non-infected patients.

Spondyloarthritis, Acute Anterior Uveitis, and Fungi: Updating the Catterall–King Hypothesis

“…The selective reporting of C. trachomatis in only a subset of AS patients in the first study and the lack of comparison to a control group in both studies means these results are difficult to interpret. A study of genital infections in women with AS reported a similarly high C. trachomatis rate detected by cell culture (15/32), which was significantly higher than the rate measured in controls (5/33) ( 99 ). However, a similar study performed in men with AS using sensitive molecular methods found much lower rates of C. trachomatis (1/32), which were indistinguishable from controls (3/120) ( 98 ); note that this study found high rates of C. trachomatis antibodies in these AS patients (20/32) ( 98 ), as reported earlier in this paragraph.…”

Pathogenese der ankylosierenden Spondylitis?Mechanismen der Krankheitsentstehung und Chronifizierung

“…Andererseits ist auch denkbar, dass synoviale T-Zell-Klone mit autoreaktiven u. o. kreuzreaktiven Eigenschaften proliferieren, eine chronische Arthritis unterhalten und körpereigenes Gewebe attackieren [13]. Auch bei Patienten mit länger bestehender, aktiver AS fanden sich gehäuft Hinweise auf persistierende Infektionen mit C. trachomatis [21] und Klebsiella pneumoniae [14,25,35].…”