Longitudinal outcomes of high-risk human papillomavirus (HPV) infections as competing-risks events following cervical HPV test at baseline visit in the *NIS-LAMS** cohort

Imagem de Miniatura
Citações na Scopus
1
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
I R O G CANADA, INC
Autores
SYRJANEN, K.
SHABALOVA, I.
SARIAN, L.
NAUD, P.
DERCHAIN, S.
KOZACHENKO, V.
ZAKHARCHENKO, S.
ROTELI-MARTINS, C.
NEROVJNA, R.
Citação
EUROPEAN JOURNAL OF GYNAECOLOGICAL ONCOLOGY, v.33, n.4, p.341-352, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: The complex natural history of human papillomavirus (HPV) infections following a single HPV test can be modeled as competing-risks events (i.e., no-, transient- or persistent infection) in a longitudinal setting. The covariates associated with these compet ng events have not been previously assessed using competing-risks regression models. Objectives: To gain further insights in the outcomes of cervical HPV infections, we used univariate- and multivariate competing-risks regression models to assess the covariaies associated with these competing events. Study Design and Methods: Covariates associated with three competing outcomes (no-, transient- or persistent HR-HPV infection) were analysed in a sub-cohort of 1,865 women prospectively followed-up in the NIS (n = 3,187) and LAMS Study (n = 12,114). Results: In multivariate competing-risks models (with two other outcomes as competing events), permanently HR-HPV negative outcome was significantly predicted only by the clearance of ASCUS+Pap during FU, while three independent covariates predicted transient HR-HPV infections: i) number of recent (< 12 months) sexual partners (risk increased), ii) previous Pap screening history (protective), and history of previous CIN (increased risk). The two most powerful predictors of persistent HR-HPV infections were persistent ASCUS+Pap (risk increased), and previous Pap screening history (protective). In pair-wise comparisons, number of recent sexual partners and previous CIN history increase the probability of transient HR-HPV infection against the HR-HPV negative competing event, while previous Pap screening history is protective. Persistent ASCUS+Pap during FU and no previous Pap screening history are significantly associated with the persistent HR-HPV outcome (compared both with i) always negative, and ii) transient events), whereas multiparity is protective. Conclusions: Different covariates are associated with the three main outcomes of cervical HPV infections. The most significant covariates of each competing events are probably distinct enough to enable constructing of a risk-profile for each main outcome.
Palavras-chave
HPV, Outcomes, Competing events, Competing-risks regression model, Transient infection, Persistent infection, Prospective follow-up, NIS Cohort, LAMS Study
Referências
  1. Belinson S, 2008, CANCER EPIDEM BIOMAR, V17, P2350, DOI 10.1158/1055-9965.EPI-08-0004
  2. Brummer O., 2006, GYNECOL ONCOL, V102, P517
  3. Dalstein V., 2003, INT J CANCER, V106, P396
  4. Fine JP, 1999, J AM STAT ASSOC, V94, P496, DOI 10.2307/2670170
  5. Herrero R, 2000, J NATL CANCER I, V92, P464, DOI 10.1093/jnci/92.6.464
  6. Hildesheim A., 1994, J INFECT DIS, V169, P235
  7. KATAJA V, 1990, EUR J EPIDEMIOL, V6, P9, DOI 10.1007/BF00155542
  8. KATAJA V, 1993, AM J EPIDEMIOL, V138, P735
  9. Kjaer SK, 1997, CANCER EPIDEM BIOMAR, V6, P799
  10. Koshiol J, 2008, AM J EPIDEMIOL, V168, P123, DOI 10.1093/aje/kwn036
  11. Kulmala SMA, 2007, CANCER EPIDEM BIOMAR, V16, P17, DOI 10.1158/1055-9965.EPI-06-0649
  12. Kulmala Satu-Maria A, 2007, J Med Virol, V79, P771, DOI 10.1002/jmv.20839
  13. Longatto-Filho A, 2005, ACTA CYTOL, V49, P500, DOI 10.1159/000326195
  14. Longatto A, 2006, INT J GYNECOL CANCER, V16, P955, DOI 10.1111/j.1525-1438.2006.00582.x
  15. Louvanto K, 2011, BMC INFECT DIS, V11, DOI 10.1186/1471-2334-11-179
  16. Louvanto K, 2010, J INFECT DIS, V202, P436, DOI 10.1086/653826
  17. Louvanto K, 2010, J CLIN MICROBIOL, V48, P2665, DOI 10.1128/JCM.00783-10
  18. Melkert P.W., 1993, INT J CANCER, V53, P919
  19. OSTOR AG, 1993, INT J GYNECOL PATHOL, V12, P186
  20. Putter H, 2007, STAT MED, V26, P2389, DOI 10.1002/sim.2712
  21. Sarian L., 2005, J MED SCREEN, V12, P142
  22. Schiffman M., 2007, LANCET, V370, P890
  23. Schiffman M., 2005, VIROLOGY, V337, P76
  24. SYRJANEN K, 1988, BRIT J OBSTET GYNAEC, V95, P1096, DOI 10.1111/j.1471-0528.1988.tb06785.x
  25. SYRJANEN K, 1985, BRIT J OBSTET GYNAEC, V92, P1086, DOI 10.1111/j.1471-0528.1985.tb03017.x
  26. Syrjanen K, 2011, INT J STD AIDS, V22, P315, DOI 10.1258/ijsa.2009.009365
  27. Syrjanen K, 2011, EUR J GYNAECOL ONCOL, V32, P17
  28. Syrjanen K., 2000, PAPILLOMAVIRUS INFEC, P142
  29. SYRJANEN K, 1992, OBSTET GYNECOL, V79, P675
  30. Syrjanen K., 2005, ANTICANCER RES, V25, P3469
  31. Syrjanen KJ, 1996, EUR J OBSTET GYN R B, V65, P45, DOI 10.1016/0028-2243(95)02303-A
  32. Syrjanen K.J., 2003, 5 INT MULT C EUROGIN, P1
  33. Syrjanen KJ, 1997, NEW DEVELOPMENTS IN CERVICAL CANCER SCREENING AND PREVENTION, P93
  34. Syrjanen K.J., 2008, J GYNECOL ONCOL, V29, P205
  35. Syrjanen S., 2005, INT J STD AIDS, V16, P217
  36. Syrjanen S., 2005, REPROD BIOL, V119, P219
  37. Syrjanen S, 2003, SEX TRANSM DIS, V30, P680, DOI 10.1097/01.OLQ.0000079519.04451.D4
  38. Syrjanen S, 2005, EUR J GYNAECOL ONCOL, V26, P491
  39. Syrjanen S, 2004, J CLIN MICROBIOL, V42, P505, DOI 10.1128/JCM.42.2.505-511.2004
  40. Syrjanen Stina, 2002, J Low Genit Tract Dis, V6, P97, DOI 10.1097/00128360-200204000-00006
  41. Wang S.S., 2009, BIOMARKERS, V18, P113
  42. Winer RL, 2003, AM J EPIDEMIOL, V157, P218, DOI 10.1093/aje/kwf180
  43. Wright Thomas C Jr, 2009, J Fam Pract, V58, pS3
  44. Xue X., 2010, BIOMARKERS, V19, P159