Endometritis: the clinical-pathologic syndrome.

OBJECTIVE The purpose of this study was to evaluate histologically proved endometritis as a clinical syndrome that is distinct from laparoscopically confirmed salpingitis. STUDY DESIGN This was a cross-sectional study of 152 women in an urban hospital with a suspected pelvic inflammatory disease. All women provided a standardized medical history and underwent physical examination, endometrial biopsy, and laparoscopy. We defined endometritis by the presence of plasma cells in endometrial stroma and neutrophils in the endometrial epithelium. RESULTS Of 152 women who were enrolled, 43 women had neither endometritis nor salpingitis; 26 women had endometritis alone without salpingitis, and 83 women had salpingitis. Those women with endometritis alone more often had douched recently, had a current intrauterine device, and were in menstrual cycle day 1 to 7, compared with women with no endometritis or salpingitis (P =.007,.04,.005, respectively) or women with acute salpingitis (P =.03,.01,.02, respectively). Infection with Neisseria gonorrhoeae and/or Chlamydia trachomatis was found more frequently in women with endometritis alone than in women with no endometritis or salpingitis (P <.001) and less frequently than in women with salpingitis (P =.05). Lower quadrant, adnexal, cervical motion, rebound tenderness, peritonitis, tenderness score, fever, and laboratory abnormalities that indicated inflammation and detection of gonorrheal or chlamydial infection were significantly less common in women with endometritis alone than in women with salpingitis but were somewhat more common in women with endometritis alone than among women with no salpingitis or endometritis. CONCLUSION Among women with suspected pelvic inflammatory disease, the histopathologic manifestations of endometritis were associated with clinical manifestations, infection, and specific risk factors that were intermediate in frequency between women with salpingitis and women with neither endometritis nor salpingitis.

[1]  D. Woolley,et al.  Menstruation: induction by matrix metalloproteinases and inflammatory cells. , 1999, Journal of reproductive immunology.

[2]  N. Hessol,et al.  Risk factors for plasma cell endometritis among women with cervical Neisseria gonorrhoeae, cervical Chlamydia trachomatis, or bacterial vaginosis. , 1998, American journal of obstetrics and gynecology.

[3]  R. Peeling,et al.  Prevalence and correlates of antibody to chlamydial heat shock protein in women attending sexually transmitted disease clinics and women with confirmed pelvic inflammatory disease. , 1997, The Journal of infectious diseases.

[4]  K. Holmes,et al.  Acute pelvic inflammatory disease : Associations of clinical and laboratory findings with laparoscopic findings , 1997 .

[5]  K. Holmes,et al.  Role of bacterial vaginosis-associated microorganisms in endometritis. , 1996, American journal of obstetrics and gynecology.

[6]  N. Hessol,et al.  Commonly Used Diagnostic Criteria for Pelvic Inflammatory Disease Have Poor Sensitivity for Plasma Cell Endometritis , 1995, Sexually transmitted diseases.

[7]  N. Weiss,et al.  The intrauterine device and primary tubal infertility. , 1992, The New England journal of medicine.

[8]  W. Stamm,et al.  Simplified microtiter cell culture method for rapid immunotyping of Chlamydia trachomatis , 1991, Journal of clinical microbiology.

[9]  M A Krohn,et al.  Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation , 1991, Journal of clinical microbiology.

[10]  K. Holmes,et al.  Histopathology of endocervical infection caused by Chlamydia trachomatis, herpes simplex virus, Trichomonas vaginalis, and Neisseria gonorrhoeae. , 1990, Human pathology.

[11]  K. Holmes,et al.  Association Between Vaginal Douching and Acute Pelvic Inflammatory Disease , 1990 .

[12]  K. Holmes,et al.  Endometrial Histopathology in Patients with Culture‐proved Upper Genital Tract Infection and Laparoscopically Diagnosed Acute Salpingitis , 1990, The American journal of surgical pathology.

[13]  E. Kessel,et al.  Pelvic inflammatory disease with intrauterine device use: a reassessment. , 1989, Fertility and sterility.

[14]  K. Holmes,et al.  Diagnosis and clinical manifestations of bacterial vaginosis. , 1988, American journal of obstetrics and gynecology.

[15]  M. Lehtinen,et al.  Microbiological and histopathological findings in acute pelvic inflammatory disease , 1987, British journal of obstetrics and gynaecology.

[16]  J. Schacter,et al.  The occurrence of chlamydial and gonococcal salpingitis during the menstrual cycle. , 1986, JAMA.

[17]  K. Holmes,et al.  Microbial causes of proven pelvic inflammatory disease and efficacy of clindamycin and tobramycin. , 1986, Annals of internal medicine.

[18]  R. Sweet,et al.  Etiology of Acute Salpingitis: Influence of Episode Number and Duration of Symptoms , 1981, Obstetrics and gynecology.

[19]  H. Rotterdam Chronic endometritis. A clinicopathologic study. , 1978, Pathology annual.

[20]  K. Holmes,et al.  Disseminated gonococcal infections caused by Neisseria gonorrhoeae with unique nutritional requirements. , 1975, The Journal of infectious diseases.

[21]  L. Jacobson,et al.  Objectivized diagnosis of acute pelvic inflammatory disease. , 1969 .