Pelvik inflamatuar hastalık ve kontrasepsiyon : Üçüncü basamak merkezde kesitsel bir çalişma

Abstract

Amaç: Bu bilgiler ışığında çalışmamızın amacı; üçüncü basamak bir merkezde pelvik inflamatuar hastalık (PID) için tedavi edilen hasta popülasyonunda kullanılan kontraseptif yöntemler ile PID' nin klinik ve laboratuvar özellikleri ve klinik sonuçları arasındaki ilişkiyi araştırmak. Gereç ve Yöntem: 2017-2019 yılları arasında üçüncü basamak bir merkezde PID tanısı ile tedavi edilen 974 hastanın hastane veri tabanına kaydedilen anamnez, muayene bulguları, vajinal ve sitolojik örneklerin mikrobiyolojik ve patolojik değerlendirme sonuçlarının kullanıldığı kesitsel bir çalışmadır. . Bulgular: Bakır-Rahim İçi Araç (Cu-RİA), PID öyküsü olan kadınlarda en sık kullanılan kontraseptif yöntemdi. Servikovajinal kültür sonuçları değerlendirildiğinde; E.coli pozitifliği CU-RİA ve Levonorgesteron RİA (LNG-RİA) kullanan hastalarda daha sıktı (<0.001). Prezervatif kullananlarda Grup B streptococcus (<0.001) ve diğer streptococcus türlerinde (= 0.006) üreme sıklığı daha yüksekti. Staphylococcus (= 0.041) ve clamydia trochomatis pozitifliği kombine oral kontraseptif (COC) kullananlarda daha yüksek iken, C. Trochomatis büyümesi depo medroksiprogeteron asetat (DMPA) kullanıcılarında sık görülmüştür (<0.001). diğer gruplarla karşılaştırıldığında (p = 0.008). Sonuç: Kontraseptif yöntemler genital florayı etkileyebilir ve PID gelişimi için predispozan bir faktör olabilir veya PID gelişimini önleyebilir.

Keywords

• Kontraseptif Ajanlar
• Pelvik inflamatuar hastalık
• Rahim içi araçlar
• Uzun Etkili Geri Dönüşümlü Kontrasepsiyon

Pelvic inflammatory disease and contraception: a cross-sectional study in teritary center

Abstract

Aim: The purpose of our study in the light of this information; to investigate the relationship between the contraceptive methods used in the patient population treated for pelvic inflammatory disease (PID) in a tertiary center with clinical and laboratory features and clinical outcome of PID. Material and Method: This is a cross-sectional study using the anamnesis, examination findings, microbiological and pathological evaluation results of vaginal and cytological samples recorded in the hospital database of 974 patients treated with a diagnosis of PID in a tertiary center between 2017 and 2019. Results: Copper-Intrauterine Device (Cu-IUD) was the most commonly used contraceptive method in women with a history of PID. When the cervicovaginal culture results are evaluated; E.coli positivity was more frequent in patients using CU-IUD and Levonorgesterone IUD (LNG-IUD) (<0.001). The frequency of reproduction was higher in Group B streptococcus (<0.001) and other streptococcus species (= 0.006) in those using condoms. While staphylococcus (= 0.041) and clamydia trochomatis positivity was higher in combined oral contraceptives (COC) users, C. Trochomatis growth was frequent in depot medroxyprogeterone acetate (DMPA) users (<0.001).Re-hospitalization was more common in the DMPA group compared to the other groups (p = 0.008). Conclusion: Contraceptive methods may affect the genital flora and may be a predisposing factor for the development of PID or prevent the development of PID.

Keywords

• Contraceptive Agents
• Intrauterine Devices
• Long-Acting Reversible Contraception
• Pelvic inflammatory disease

References

1. Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, 2015. MMWR. Recommendations and reports: Morbidity and mortality weekly report. Recommendations and Reports 2015; 64: 1-137.
2. Ford GW, Decker CF. Pelvic inflammatory disease. Disease-a-month: DM 2016; 62: 301.
3. Campbell S, Monga A. (Eds.). Gynaecology by ten teachers. London: Arnold. 2000, (pp. 41-54).
4. Kansagara D, Englander H, Salanitro A, et al. Risk prediction models for hospital readmission: a systematic review. JAMA 2011; 306: 1688-98.
5. Lee NC, Rubin GL, Grimes DA. Measures of sexual behavior and the risk of pelvic inflammatory disease. Obstet Gynecol 1991; 77: 425-30.
6. Kreisel K, Torrone E, Bernstein K, Hong J, Gorwitz R. Prevalence of pelvic inflammatory disease in sexually experienced women of reproductive age—United States, 2013–2014. MMWR Morb Mortal Wkly Rep 2017; 66: 80–3.
7. Trent M, Haggerty CL, Jennings JM, Lee S, Bass DC, Ness R. Adverse adolescent reproductive health outcomes after pelvic inflammatory disease. Arch Pediatr Adolesc Med 2011; 165: 49-54.
8. Goyal M, Hersh A, Luan X, Localio R, Trent M, Zaoutis T. National trends in pelvic inflammatory disease among adolescents in the emergency department. J Adolesc Health 2013; 53: 249-52.

9. Matters JS, Catchpole M, Smith C. Chlamydia trachomatis: summary and conclusions of CMO’s Expert Advisory Group. 1998. London: Department of Health.
10. Centers for Disease Control and Prevention 1998 Guidelines for the Treatment of Sexually Rransmitted Diseases, MMWR Morb Mortal Wkly Rep 1997; 47: 1- 111.
11. Jatlaoui TC, Riley HEM, Curtis KM. The safety of intrauterine devices among young women: a systematic review. Contraception 2017; 95: 17–39.
12. Stanwood NL, Garrett JM, Konrad TR. Obstetriciangynecologists and the intrauterine device: A survey of attitudes and practice. Obstet Gynecol 2002; 99: 275–80.
13. Madden T, Allsworth JE, Hladky KJ, Secura GM, Peipert JF. Intrauterine contraception in Saint Louis: A survey of obstetrician and gynecologists’knowledge and attitudes. Contraception 2010; 81: 112–6.
14. Fraser IS. Non-contraceptive health benefits of intrauterine hormonal systems. Contraception, 2010; 82: 396–403.
15. Schindler AE. Non-contraceptive benefits of oral hormonal contraceptives. Int J Endocrinol Metab 2013; 11: 41-7.
16. Havens JM, Olufajo OA, Cooper ZR, Haider AH, Shah AA, Salim A. Defining rates and risk factors for readmissions following emergency general surgery. JAMA Surg 2016; 151: 330–6.
17. Brunham RC, Gottlieb SL, Paavonen J. Pelvic inflammatory disease. N Engl J Med 2015; 372: 2039-48.
18. McGregor JA, French JI, Jones W, et al. Bacterial vaginosis is associated with prematurity and vaginal fluid mucinase and sialidase: results of a controlled trial of topical clindamycin cream. Am J Obstet Gynecol 1994; 170: 1048-59.
19. Draper DL, Landers DV, Krohn MA, Hillier SL, Wiesenfeld HC, Heine RP. Levels of vaginal secretory leukocyte protease inhibitor are decreased in women with lower reproductive tract infections. Am J Obstet Gynecol 2000; 183: 1243-8.
20. Hubacher D. Intrauterine devices and infection: review of the literature. Indian J Med Res 2014; 140: S53–7.
21. Liabsuetrakul T, Peeyananjarassri K. Mechanical dilatation of the cervix during elective caeserean section before the onset of labour for reducing postoperative morbidity. Cochrane Database Syst Rev 2018; 8: CD008019.
22. Sel G, Harma MI. Bacterial colonization of intrauterine device samples from patients without a history of pelvic inflammatory disease. Ann Med Res 2020; 27: 1036-9.
23. Witkin SS, Minis E, Athanasiou A, Leizer J, Linhares IM. Chlamydia trachomatis: the persistent pathogen. Clin Vaccine Immunol 2017; 24: e00203-17.
24. Birgisson NE, Zhao Q, Secura GM, Madden T, Peipert JF. Positive Testing for Neisseria gonorrhoeae and Chlamydia trachomatis and the risk of pelvic inflammatory disease in IUD users. J Womens Health (Larchmt) 2015; 24: 354-9.
25. Lurie S, Asaala H, Harari OS, Golan A, Sadan O. Uterine cervical non-gonococcal and non-chlamydial bacterial flora and its antibiotic sensitivity in women with pelvic inflammatory disease: did it vary over 20 years? Isr Med Assoc J 2010; 12: 747–50.
26. Audu BM, Kudi AA. Microbial isolates and antibiogram from endocervical swabs of patients with pelvic inflammatory disease. J Obstet Gynaecol 2014; 24: 161–4.
27. Judlin P, Liao Q, Liu Z, Reimnitz P, Hampel B, Arvis P. Efficacy and safety of moxifloxacin in uncomplicated pelvic inflammatory disease: the MONALISA study. BJOG 2010; 117: 1475–84.
28. Schindler AE. Non-contraceptive benefits of hormonal contraceptives. Minerva Ginecol 2010; 62: 319-29.
29. Huber JC, Bentz EK, Ott J, Tempfer CB. Non-contraceptive benefits of oral contraceptives. Expert Opin Pharmacother 2008; 9: 2317-25.
30. Brooks PJ, Edwards DJ, Blithe DL, et al. Effects of combined oral contraceptives, depot medroxyprogesterone acetate, and the levonorgestrel releasing Intrauterine system on the vaginal microbiome. Contraception 2017; 95: 405-13.
31. Rifkin SB, Smith MR, Brotman RM, Gindi RM, Erbelding EJ. Hormonal contraception and risk of bacterial vaginosis diagnosis in an observational study of women attending STD clinics in Baltimore, MD. Contracept 2009; 80: 63–7.
32. O’Hanlon DE, Lanier BR, Moench TR, Cone RA. Cervicovaginal fluid and semen block the microbicidal activity of hydrogen peroxide produced by vaginal lactobacilli. BMC Infect Dis 2010; 10: 120.
33. O’Hanlon DE, Moench TR, Cone RA. In vaginal fluid, bacteria associated with bacterial vaginosis can be suppressed with lactic acid but not hydrogen peroxide. BMC Infect Dis 2011; 11: 200.
34. Donders G, Bellen G, Janssens D, Van Bulck B, Hinoul P, Verguts J. Influence of contraceptive choice on vaginal bacterial and fungal microflora. Eur J Clin Microbiol Infect Dis 2017; 36: 43-8.
35. Jacobson JC, Turok DK, Dermish AI, Nygaard IE, Settles ML. Vaginal microbiome changes with levonorgestrel intrauterine system placement. Contraception 2014; 90: 130–5.
36. Hashway SA, Bergin IL, Bassis CM, et al. Impact of a hormone-releasing intrauterine system on the vaginal microbiome: a prospective baboon model. J Med Primatol 2014; 43: 89–99.
37. Borgdorff H, Verwijs MC, Wit FWNM et al. The impact of hormonal contraception and pregnancy on sexually transmitted infections and on cervicovaginal microbiota in african sex workers. Sex Transm Dis 2015; 42: 143–52.
38. Mitchell CM, McLemore L, Westerberg K, et al. Long-term effect of depot medroxyprogesterone acetate on vaginal microbiota, epithelial thickness and HIV target cells. J Infect Dis 2014; 210: 651–5.