Co-infection of sexually transmitted pathogens and Human Papillomavirus in cervical samples of women of Brazil

Carregando...
Imagem de Miniatura
Citações na Scopus
25
Tipo de produção
article
Data de publicação
2017
Editora
BIOMED CENTRAL LTD
Indexadores
Título da Revista
ISSN da Revista
Título do Volume
Autores
AMORIM, Aline Teixeira
MARQUES, Lucas Miranda
CAMPOS, Guilherme Barreto
LOBAO, Tassia Neves
LINO, Vanesca de Souza
CINTRA, Ricardo Cesar
ANDREOLI, Maria Antonieta
BOCCARDO, Enrique
BRAGA JUNIOR, Antonio Carlos Ricardo
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
BMC INFECTIOUS DISEASES, v.17, article ID 769, 12p, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Some sexually transmitted infectious agents, such as Chlamydia trachomatis and Herpes simplex, cause local inflammation, and could contribute to Human Papillomavirus (HPV) and cervical lesion progression. Thus, the aim of this study was to determine any association between the presence of microorganisms of gynecological importance, sexual behavior, clinical and demographical variables to the development and progress of cervical lesions. Methods: One hundred and thirty-two women between 14 and 78 years and living at Vitoria da Conquista, Bahia, Brazil, were included (62 individuals with cervical lesions and 70 without lesions). They answered a questionnaire to provide data for a socioeconomic and sexual activity profile. Samples of cervical swabs were collected and analyzed by PCR to detect genital microorganisms and HPV. Quantitative PCR was used to detect and quantify Ureaplasma urealyticum and Ureaplasma parvum. Univariate and multiple logistic regression were performed to measure the association with the cervical lesions, and an odds ratio (OR) with 95% confidence intervals (95% CI) were calculated. The Mann-Whitney U test was also used to compare the microorganism load in the case and control groups. The significance level was 5% in all hypotheses tested. Results: Cervical lesions were associated with: women in a stable sexual relationship (OR = 14.21, 95% CI = 3.67-55.018), positive PCR for HPV (OR = 16.81, 95% CI = 4.19-67.42), Trichomonas vaginalis (OR = 8.566, 95% CI = 2.04-35.94) and Gardnerella vaginalis (OR = 6.13, 95% CI = 1.53-24.61), adjusted by age and qPCR for U. parvum. U. parvum load showed a statistical difference between the case and control groups (p-value = 0.002). Conclusion: Variables such as stable relationship, HPV, T. vaginalis, G. vaginalis were associated with cervical lesions in epidemiological studies. U. parvum load was higher in woman with cervical lesions compared with women without lesions. Additional studies are needed to better understand the role of these factors in cervical lesion development.
Palavras-chave
Cervical cancer, HPV, U. Parvum, Sexually transmitted infections
Referências
  1. Baseman JG, 2005, J CLIN VIROL, V32, pS16, DOI 10.1016/j.jcv.2004.12.008
  2. Bosch FX, 2006, INT J GYNECOL OBSTET, V94, pS8, DOI 10.1016/S0020-7292(07)60004-6
  3. Bosch FX, 2002, J CLIN PATHOL, V55, P244, DOI 10.1136/jcp.55.4.244
  4. BUSOLO F, 1981, B I SIEROTER MILAN, V60, P31
  5. Carestiato Fernanda N., 2006, Braz J Infect Dis, V10, P331, DOI 10.1590/S1413-86702006000500006
  6. Castellsague X, 2002, VIRUS RES, V89, P191, DOI 10.1016/S0168-1702(02)00188-0
  7. Castle PE, 2001, CANCER EPIDEM BIOMAR, V10, P1021
  8. Castle Philip E, 2003, J Natl Cancer Inst Monogr, P29
  9. de Mendonca VG, 2010, REV BRAS GINECOL OBS, V32, P476
  10. Deguchi T, 2004, SEX TRANSM DIS, V31, P192, DOI 10.1097/01.OLQ.0000114653.26951.71
  11. Deguchi T, 2014, INT J STD AIDS
  12. Ekiel AM, 2009, J KOREAN MED SCI, V24, P1177, DOI 10.3346/jkms.2009.24.6.1177
  13. Franco E, 1999, Rev Panam Salud Publica, V6, P223, DOI 10.1590/S1020-49891999000900001
  14. GLOBOCAN, 2012, EST CANC IND MORT PR
  15. GUIJON F, 1992, INT J GYNECOL OBSTET, V37, P185, DOI 10.1016/0020-7292(92)90379-W
  16. IARC, 2007, HUM PAP IARC MON EV, V90
  17. IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2012, IARC MONOGRAPHS EVAL, V100B
  18. Instituto Nacional de Cancer (BR), 2014, EST 2014 INC CANC BR
  19. Klingelhutz AJ, 2012, VIROLOGY, V424, P77, DOI 10.1016/j.virol.2011.12.018
  20. Klomp JM, 2008, AM J OBSTET GYNECOL, V199, DOI 10.1016/j.ajog.2008.04.036
  21. Kong FR, 2000, J CLIN MICROBIOL, V38, P1175
  22. Liu L, 2014, SCAND J INFECT DIS, V46, P637, DOI 10.3109/00365548.2014.922696
  23. Lukic A, 2006, ANTICANCER RES, V26, P4843
  24. McGowin CL, 2009, BMC MICROBIOL, V9, DOI 10.1186/1471-2180-9-139
  25. Razin S, 1998, MICROBIOL MOL BIOL R, V62, P1094
  26. Shaw E, 2016, BMC INFECT DIS, V16, DOI 10.1186/s12879-016-1446-x
  27. Shimada Y, 2014, INT J STD AIDS, V25, P294, DOI 10.1177/0956462413504556
  28. [Anonymous], BACTERIAL LOADS UREA
  29. Verteramo R, 2009, BMC INFECT DIS, V9, DOI 10.1186/1471-2334-9-16
  30. Xiaolei C, 2014, EUR J GYNAECOL ONCOL, V35, P571
  31. Yoshida T, 2007, SEX TRANSM DIS, V34, P416, DOI 10.1097/01.olq.0000243621.89212.40
  32. Zhang Zuo-Feng, 1995, Annals of Epidemiology, V5, P325, DOI 10.1016/1047-2797(94)00101-X
  33. zur Hausen H, 2009, VIROLOGY, V384, P260, DOI 10.1016/j.virol.2008.11.046
  34. [Anonymous], 2013, PNUD IPEA FJP ATLAS