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Case Reports
. 1980 Dec 1;138(7 Pt 2):1034-8.
doi: 10.1016/0002-9378(80)91103-5.

Chlamydia trachomatis infection in Fitz-Hugh-Curtis syndrome

Case Reports

Chlamydia trachomatis infection in Fitz-Hugh-Curtis syndrome

S P Wang et al. Am J Obstet Gynecol. .

Abstract

We studied 23 patients with pelvic inflammatory disease associated with symptoms of pleuritic up'per abdominal pain, characteristic of Fitz-Hugh-Curtis syndrome (FHC). A fourfold or greater change in antibody titer to Chlamydia trachomatis was demonstrated by microimmunofluorescence in 14; an IgG antibody titer greater than or equal to 1:1,024 was seen in 13; and IgM antibody was demonstrated in 11. Twenty (87%) of the 23 FHC patients, including all of the 12 with paired sera obtained at least 6 weeks apart, had serologic evidence of acute C. trachomatis infection. Neisseria gonorrhoeae was isolated from seven (30%) of the 23 FHC cases, and C. trachomatis was isolated from three of 10. Two groups of matched controls were studied; one group with PID but without FHC, and the other without PID. A larger proportion of patients with FHC had serologic evidence of acute C. trachomatis infection than either of the two control groups (p less than 0.05 for each comparison). Among those with antibody to C. trachomatis, the geometric mean antibody titer for the FHC group (1:724) was significantly higher than that for the PID group (1:138) or for the non-PID group (1:103). Thus, FHC is not solely attributable to infection with N. gonorrhoeae; most cases are associated with acute C. trachomatis infection.

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