Prevalence of factor V G1691A (factor V-Leiden) and prothrombin G20210A gene mutations in a recurrent miscarriage population.

Factor V G1691A (FV-Leiden) and prothrombin G20210A mutations are major inherited risk factors for venous thrombosis. Recently, it was suggested that both mutations, through stimulation of venous and placental thrombosis events, were strongly associated with recurrent idiopathic miscarriages, although other studies disputed such a link. The aim of this study was to determine the prevalence of prothrombin G20210A and factor V G1691A (R506Q, FV-Leiden) mutations in women with recurrent idiopathic abortions and to recommend management for high-risk mutation carriers. One hundred ten women with two or more consecutive unexplained first-trimester miscarriages (mean age +/- SD, 32.3 +/- 5.3) were compared to 67 parous women with uncomplicated pregnancies (mean age +/- SD, 33.9 +/-7.3) (P = 0.134) from the same ethnic background. The presence or absence of the prothrombin G20210A and FV-Leiden mutations was assessed by PCR and RFLP analysis, using HindIII and MnlI digestion, respectively. In women with primary habitual abortion, 45 (40.91%) carried the FV-Leiden mutation, of whom 7 were in the homozygote and 38 were in the heterozygote states, and 15 (13.64%) carried the prothrombin G20210A mutation all as heterozygotes, compared to 16.42% and 2.99% carrier rates among controls, respectively, all of whom were heterozygote carriers. Of the other risk factors analyzed, smoking (OR 1.76; 95% CI = 0.79-3.94) was more prevalent in habitual aborters compared to controls. Both FV-Leiden and factor II G20210A mutations are major inherited risk factor associated with primary recurrent miscarriages. Women with a family or personal history of thrombosis should be screened before or early in the pregnancy for FV-Leiden and factor II G20210A mutations.

Cervicovaginal coinfections with human papillomavirus and Chlamydia trachomatis.

Human papillomavirus (HPV) and Chlamydia trachomatis (CT) are the two most common sexually transmitted pathogens, and infection with either reportedly was associated with cervical intraepithelial neoplasia (CIN) in women. In view of their similar mode of transmission, CT infection was examined as a possible HPV cofactor in the etiology of CIN disease. In total, 129 women were included in the study, of whom 80 were negative (mean age 34.17 +/- 6.9) and 49 were positive (mean age 33.16 +/- 6.8) for HPV DNA (assessed by PCR). CT DNA was determined in endocervical and first-catch urine specimens by PCR. Whereas HPV-positive and HPV-negative women were similar with respect to age (p = 0.419) and pregnancy outcomes (p = 0.628), the number of smokers (p = 0.001), women with multiple male sex partners (p = 0.002) or with abnormal cytology (p < 0.001) was higher in the HPV-positive group. There was an increase in CT infection rate in HPV-positive (29/49) as compared to HPV-negative (10/80) women (p < 0.01). Within HPV-positive patients, there was no significant difference between CT-positive and CT-negative patients with regards to the risk factors studied. Collectively, this suggests that CT infection is a cofactor of HPV in CIN disease development, possibly by modulating the host's immunity and/or precipitation of chronic inflammation.