Health  Vol.7 No.2 , February 2015
Influence of Contraception on Basic Vaginal States: A Prospective Study
Abstract: To evaluate the influence of contraceptive methods on the basic vaginal states (BVSs) in women in fertile age, 108 women consulting for birth control (14 - 45 years) were included in a prospective study. The vaginal content was sampled both before they began using the chosen contraceptive method (see below) and three months later, and then analyzed using the Balance of Vaginal Content (BAVACO) methodology. Five BVSs were defined: 1) normal microbiota; 2) normal microbiota with vaginal inflammatory reaction (VIR); 3) intermediate microbiota; 4) bacterial vaginosis and 5) non-specific microbial vaginitis. The following contraceptive methods were considered: combined oral contraceptive pill (COCP), intrauterine device (IUD), condom (CON), the rhythm method (RHYT) and simultaneous double protection (COCP + CON). The McNemar statistical test was used. COCP (n = 71): 20 samples retained normal BVSs and two were altered; nine out of the 49 altered samples returned to normal; IUD (n = 4): two samples modified their normal BVS to III and IV; CON (n = 25): the VIR increased in 20% of the samples; RHYT (n = 6): four samples retained the normal BVS; and COCP + CON (n = 2): samples preserved their initial BVS (II). The increased frequency of BVS I in the COCP group was significant (x2 = 3.3; p = 0.04). The relative frequency of each BVS was significantly modified, attributed to the type of contraceptive method used. The intake of hormones corrects alterations and retains a normal BVS. The contraceptive methods that use an external factor of local contact either maintain or alter the microbiota and VIR.
Cite this paper: Fosch, S. , Yones, C. , Trossero, M. , Grosso, O. and Perazzi, B. (2015) Influence of Contraception on Basic Vaginal States: A Prospective Study. Health, 7, 238-244. doi: 10.4236/health.2015.72028.

[1]   Reid, G., McGroarty, J.A., Tomeczek, L. and Bruce, A.W. (1996) Identification and Plasmid Profiles of Lactobacillus Species from the Vagina of 100 Healthy Women. FEMS Immunology and Medical Microbiology, 15, 23-26.

[2]   Fosch, S., Yones, C., Trossero, M. and Grosso, O. (2013) The Influence of Different Contraceptive Methods on Vaginal Microbiota: Clinical Study. Health, 5, 19-24.

[3]   Andrews, W., Hauth, J., Cliver, S., Conner, M., Goldenberg, R. and Goepfert, A. (2006) Association of Asymptomatic Bacterial Vaginosis with Endometrial Microbial Colonization and Plasma Cell Endometritis in Non Pregnant Women. American Journal of Obstetrics and Gynecology, 195, 1611-1616.

[4]   MGregor, J.A. (2000) French J. L. Bacterial Vaginosis in Pregnancy. Obstetrical & Gynecological Survey, 55, 1-19.

[5]   Vodstrcil, L.A., Hocking, J.S., Law, M., Walker, S., Tabrizi, S.N., et al. (2013) Hormonal Contraception Is Associated with a Reduced Risk of Bacterial Vaginosis: A Systematic Review and Meta-Analysis. PloS ONE, 8, e73055.

[6]   Gupta, K., Hillier, S.L., Hooton, T.M., Roberts, P.L. and Stamm, W.E. (2000) Effects of Contraceptive Method on the Vaginal Microbialflora: A Prospective Evaluation. The Journal of Infectious Diseases, 181, 595-601.

[7]   Tibaldi, C., Capello, N., Latino, M., Masuelli, G., Marini, S. and Benedetto, C. (2009) Vaginal and Endocervical Microorganisms in Symptomatic and Asymptomatic Non-Pregnant Females: Risk Factors and Rates of Occurrence. Clinical Microbiology and Infection, 15, 670-679.

[8]   Riggs, M., Klebanoff, M., Nansel, T., Zhang, J., Schwebke, J. and Andrews, W. (2007) Longitudinal Association between Hormonal Contraceptives and Bacterial Vaginosis in Women of Reproductive Age. Sexually Transmitted Diseases, 34, 954-959.

[9]   (2010) Guía Práctica Integral (Clínica-Laboratorio) de diagnóstico de vaginosis y vaginitis en la atención primaria de la (MEF). Actualización 2010. Acta Bioquímica Clínica Latinoamericana, 44, 359-369.

[10]   Hans, F.N. (2004) Citodiagnóstico Ginecológico. 1o Edición, Buenos Aires Médica Paramericana 2004.

[11]   Levin, R.J. (2004) Measuring Female Genital Functions—A Research Essential but still a Clinical Luxury? Sexual and Relationship Therapy, 19, 191-200.

[12]   Huggyns, G.R. and Preti, G. (1981) Vaginal Odors and Secretions. Clinical Obstetrics and Gynecology, 24, 355-377.

[13]   Boskey, E.R., Cone, R.A., Whaley, K.J. and Moench, T.R. (2001) Origins of Vaginal Acidity: High D/L Lactate Ratio Is Consistent with Bacteria Being the Primary Source. Human Reproduction, 16, 1809-1813.

[14]   Gorodeski, G.I., Hopfer, U., Liu, C.C. and Margles, E. (2005) Estrogen Acidifies Vaginal pH by Up-Regulation of Proton Secretion via the Apical Membrane of Vaginal-Ectocervical Epithelial Cells. Endocrinology, 146, 816-824.

[15]   Madden, T., Grentzer, J.M., Secura, G.M., Allsworth, J.E. and Peipert, J.F. (2012) Risk of Bacterial Vaginosis in Users of the Intrauterine Device: A Longitudinal Study. Sexually Transmitted Diseases, 39, 217-222.

[16]   Schreiber, C.A., Meyn, L.A., Creinin, M.D., Barnhart, K.T. and Hillier, S.L. (2006) Effects of Long-Term Use of Nonoxynol-9 on Vaginal Flora. Obstetrics & Gynecology, 107, 136-143.

[17]   Moraes, P.S. and Taketomi, E.A. (2000) Allergic Vulvovaginitis. Annals of Allergy, Asthma Immunology, 85, 253-265.

[18]   Ramirez de Knott, H.M., McCormick, T.S., Oshtory Do, S., Goodman, W., Ghannoum, M.A., Cooper, K.D. and Nedorost, S.T. (2005) Cutaneous Hypersensitivity to Candida albicans in Idiopathic Vulvodynia. Contact Dermatitis, 53, 214-218.