Evaluating the link between Ovarian Cancer and Chlamydia
Date: June 22nd, 2018
Link between Chlamydia and Ovarian Cancer
As revealed by two diverse cohorts and control groups, a woman's risk of developing ovarian cancer is doubled by a history of Chlamydia infection. Based on the level approved for serum levels of Chlamydia plasmid-encoded Pgp3 (a serologic marker of Chlamydia infection), the odds ratio for ovarian cancer ranked as high as 2.53 versus the control groups. While assessing two cohorts of women with other cut points, the ovarian cancers odds ratio varied from 1.43 to 2.25.
Experts that mark sexually transmitted infections (STIs) didn't have links with ovarian cancer as claimed by Britton Trabert (the M.D of the National Cancer Institute in Rockville, Maryland). Mr. Trabert also asserted that; 'Our findings support an association between Chlamydia-associated pelvic inflammatory disease [PID] and ovarian cancer. Null associations with other infections further support the specificity of the findings.
Cancer risk reduction
If replicated, this study supports future studies to evaluate potential cancer risk reduction through treatment of Chlamydia infections and PID.' This remark brings an earlier treatment and diagnosis of ovarian cancer under a new spotlight to see the disease's potential implications. As asserted by Dr. Elaine Mardis of Nationwide Children's Hospital in Columbus, this discovery will give rise to better long-term outcomes for ovarian cancer.
Dr. Mardis also said; 'Ovarian cancer is typically diagnosed at quite a late stage and has a poor prognosis. This study focused on the evaluation of a common sexually transmitted disease, and the most important take-home point is that we might go a long way in preventing ovarian cancer through routine screening for agents, such as Chlamydia trachomatis.' More so, the medical evaluation was necessitated by evidence linking PID to ovarian cancer.
Link between Chlamydia and ovarian cancer
Let's consider a case study published last year in the American Journal of Epidemiology that involved 13 studies. There was a strong link between Chlamydia-associated pelvic inflammatory disease and borderline tumors, but not a complete case of ovarian cancer. In first-world countries, C. trachomatis remains the prominent factor of PID, but it's difficult to substantiate Chlamydia infection or pelvic inflammatory disease in epidemiologic studies.
The women's cohorts and control groups had 278 Polish women; in one group, they all had ovarian cancer while the other didn't. More so, 160 women represented the NCI-sponsored Prostate, Lung, Colorectal, and Ovarian (PLCO) screening trial (and a control group of 159 women).
The assay setup could unravel the presence of Pgp3, markers of Chlamydia and serologic markers for other common sexually transmitted infections. Mr. Trabert's team conducted analytical surveys with standard laboratory benchmark figures for Pgp3.
Also, the team set up two extra benchmarks that were significant to the Polish women evaluation and the PLCO cohort. At the end of the survey, markers for other infections (hepatitis B or C, human papillomavirus, and herpes simplex virus-1 or 2,) did not show any significant link with ovarian cancer in either of the cohorts. But Mr. Trabert said the Polish women cohort showed serum Pgp3 at the standard benchmark level. Also, they had links with ovarian cancers odds ratio of 1.63 (95% CI 1.20-2.22) compared with the control group. The odds ratio rises to 2.00 at the second antibody benchmark (95% CI 1.38-2.89) and still rises to 2.19 when the highest antibody titer cutoff was applied (95% CI 1.29-3.73).
Some infection markers lacked well-known links with ovarian cancer. As seen in the cohorts; hepatitis B or C, Mycoplasma genitalium, HPV, Epstein Barr virus, herpes simplex virus-1 or 2, and cytomegalovirus.