Infectious Diseases in Obstetrics and Gynecology Table 4: Frequencies and adjusted odds ratios (ORs) and 95% conﬁdence intervals (CIs) for chlamydial elementary bodies optical-density (OD) units, in case and control subjects stratiﬁed by age. OD units <0.10 0.10–0.199 0.20–0.399 ≥0.40 <0.10 0.10–0.199 0.20–0.399 ≥0.40 <0.10 0.10–0.199 0.20–0.399 ≥0.40 <0.10 0.10–0.199 0.20–0.399 ≥0.40 Case subjects 69 32 18 16 55 22 15 19 58 41 19 11 66 43 21 16 Control subjects 82 42 37 43 103 47 20 38 88 38 31 30 69 46 25 27 OR (95% CI) 1.0 0.9 (0.5–1.6) 0.6 (0.3–1.1) 0.4 (0.2–0.9) Trend = .007 1.0 0.9 (0.5–1.6) 1.4 (0.7–3.0) 0.9 (0.5–1.8) Trend = .908 1.0 1.6 (0.9–2.8) 0.9 (0.5–1.8) 0.6 (0.3–1.2) Trend = .227 1.0 1.0 (0.6–1.7) 0.9 (0.4–1.7) 0.6 (0.3–1.3) Trend = .217 4 Age 24–49 Age 50–56 Age 57–66 Age ≥67 highest antibody titers rarely moved to the lowest tertile over time [12]. Another explanation is the lack of sensitivity of antich- lamydial antibody serologic testing. Only about 60% of women with PID develop detectable serology, and the test does not detect gonorrhea, another cause of PID. This lack of sensitivity would have resulted in erroneously missing some women with prior PID and would have resulted in an odds ratio biased toward the null. Moreover, it is possible that ovarian cancer itself or its treatment might acutely reduce chlamydia titers, and therefore mask an association. Strengths of this study include the population-based ascertainment of cases and controls, the standardized collec- tion and storage of bloods, the measurement of chlamydia EB antibodies at a reference, research laboratory, with laboratory personnel masked to case-control status, and evidence of an independent eﬀect after adjustment for potentially confounding factors. In summary, our ﬁndings do not support previous evidence of a link between chronic persistent chlamydia infection, the most common cause of PID, and risk for ovarian cancer. ACKNOWLEDGMENTS The authors thank the women with ovarian cancer and those without cancer who participated in this study as well as their dedicated physicians, in particular Drs. Michael Hopkins and Eric Jennison. They also thank a dedicated team of staﬀ including Katie Farrow, Ya Du, Jenny Lo, Sheri Hutchison, Tammy DeBruce, Tamara Cursio, Briana Mayle, and Elizabeth Hallman. REFERENCES [1] R. B. Ness and C. Cottreau, “Possible role of ovarian epithelial inﬂammation in ovarian cancer,” Journal of the National Cancer Institute, vol. 91, no. 17, pp. 1459–1467, 1999. [2] X. O. Shu, Y. T. Gao, J. M. Yuan, R. G. Ziegler, and L. A. Brinton, “Dietary factors and epithelial ovarian cancer,” British Journal of Cancer, vol. 59, no. 1, pp. 92–96, 1989. [3] H. A. Risch and G. R. Howe, “Pelvic inﬂammatory disease and the risk of epithelial ovarian cancer,” Cancer Epidemiology Biomarkers and Prevention, vol. 4, no. 5, pp. 447–451, 1995. [4] R. B. Ness, J. A. Grisso, C. Cottreau, et al., “Factors related to inﬂammation of the ovarian epithelium and risk of ovarian cancer,” Epidemiology, vol. 11, no. 2, pp. 111–117, 2000. [5] L. Westrom and D. Eschenbach, “Pelvic inﬂammatory dis- ease,” in Sexually Transmitted Diseases, K. K. Holmes, P. G. Sparling, P.-A. Mardh, et al., Eds., pp. 783–810, McGraw-Hill, New York, NY, USA, 3rd edition, 1999. [6] C. R. Cohen and R. C. Brunham, “Pathogenesis of chlamydia induced pelvic inﬂammatory disease,” Sexually Transmitted Infections, vol. 75, no. 1, pp. 21–24, 1999. [7] P.-A. Ma˚rdh, “Tubal factor infertility, with special regard to chlamydial salpingitis,” Current Opinion in Infectious Diseases, vol. 17, no. 1, pp. 49–52, 2004. [8] I. Simms, K. Eastick, H. Mallinson, et al., “Associations between Mycoplasma genitalium, Chlamydia trachomatis and pelvic inﬂammatory disease,” Journal of Clinical Pathology, vol. 56, no. 8, pp. 616–618, 2003.