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  • Title: The association between pregnancy and human papilloma virus prevalence.
    Author: Smith EM, Johnson SR, Jiang D, Zaleski S, Lynch CF, Brundage S, Anderson RD, Turek LP.
    Journal: Cancer Detect Prev; 1991; 15(5):397-402. PubMed ID: 1661203.
    Abstract:
    This study examined the effects of pregnancy on the prevalence of HPV infection, comparing 69 pregnant and 54 nonpregnant age-frequency matched female patients. HPV prevalence was detected by DNA hybridization using the ViraPap/ViraType dot blot procedure. The prevalence of HPV among pregnant women increased with gestational age from 8.0% in the first trimester, to 16.7% in the second, and 23.1% in the third trimester. This finding suggests that HPV infection may be activated by hormonal or other effects of pregnancy and may explain why number of pregnancies is known to be associated with increased risk of cervical dysplasia and cancer. Oncogenic HPV types 16/18 and 31/33/35 were identified with almost equal frequency in the study population whereas HPV 6/11 was seen rarely. The logistic regression models indicate that there were no significant differences between HPV positive and HPV negative groups by age, income, number of sex partners, age of first intercourse, average frequency of intercourse per month, number of pregnancies, oral contraceptive duration, or pregnancy status. There were no interaction effects. A current Pap result of cervical dysplasia (OR = 8.9; 95% confidence interval: 2.1, 38.8), oral contraceptive use (OR = 0.1; 0.03, 0.6), and education (OR = 1.4; 1.1, 1.8) were significant predictors of HPV status. Between October 1987-May 1988, researchers compared 69 pregnant patients with 54 age matched nonpregnant patients at the University of Iowa Medical School Hospital in Iowa City to examine the effects of pregnancy on the prevalence of human papilloma virus (HPV) infection. Almost all cases and controls were White. Pregnant women had more risks for cervical dysplasia and cancer than nonpregnant women: a simultaneous diagnosis of dysplasia/squamous intraepithelial lesions [odds ration(OR) 7.4], current and past smoking (p.001 and p.05), greater number of partners (p.05) and pregnancies (p(.001), an earlier age at 1st intercourse (p.001), a higher frequency of intercourse/month, less education (OR 1.4), and poorer. In addition, pregnant women tended not to use condoms (p.01) which can prevent transmission of sexually transmitted diseases. Oral contraceptive (OC) use had a protective effect (OR 0.1), but duration of OC use did not significantly change the ORs. The 2 groups had basically the same overall frequency of HPV (15.9% pregnant and 14.8% nonpregnant), but HPV frequency increased as did gestational age. For example, it was 8% for the 1st trimester, 16.7% for the 2nd trimester, and 23.1% for the 3rd trimester. This increase in frequency suggested that it occurs with activation of latent HPV infection or increased HPV plasmid replication during pregnancy. The researchers hypothesized that high progesterone levels may activate transcriptional HPV replication or change an immune response. Other studies demonstrated that increasing parity is linked with cervical cancer. Thus the researchers proposed that other researchers to set up longitudinal studies to follow pregnant and postpartum women to see if condylomas, cervical dysplasia, and cancer subsequently develop. These studies will allow researchers to determine if HPV status during the 2nd and 3rd trimesters predicts disease.
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