covid
Buscar en
Revista Colombiana de Cancerología
Toda la web
Inicio Revista Colombiana de Cancerología Determinants of LSIL Regression in Women from a Colombian Cohort
Información de la revista
Vol. 14. Núm. 4.
Páginas 199-209 (enero 2009)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 14. Núm. 4.
Páginas 199-209 (enero 2009)
Acceso a texto completo
Determinants of LSIL Regression in Women from a Colombian Cohort
Determinantes de la regresión de lesiones cervicales de bajo grado en una cohorte de mujeres colombianas
Visitas
3446
Mónica Molano1,
Autor para correspondencia
mmolano@cancer.gov.co

Corresponding Grupo de Investigación en Biología del Cáncer. Instituto Nacional de Cancerología. Av. 1a N° 9-85. Tel.: 571 3341111, ext. 4205.
, Mauricio González2, Óscar Gamboa3, Natasha Ortiz2, Joaquín Luna4, Gustavo Hernandez5, Héctor Posso6, Raúl Murillo3, Nubia Muñoz7, for the INC HPV Study Group
1 Grupo de Investigación en Biología del Cáncer – Instituto Nacional de Cancerología de Colombia
2 Grupo de Investigación Clínica - Instituto Nacional de Cancerología de Colombia
3 Subdirección de Investigaciones - Instituto Nacional de Cancerología de Colombia
4 Grupo de Ginecología Oncológica - Instituto Nacional de Cancerología de Colombia
5 Grupo de Investigación Epidemiológica - Instituto Nacional de Cancerología de Colombia
6 Liga Colombiana de Lucha Contra el Cáncer Seccional Bogotá, Bogotá, Colombia
7 Profesora Emérita - Instituto Nacional de Cancerología, Bogotá, Colombia
Este artículo ha recibido
Información del artículo
Resumen
Bibliografía
Descargar PDF
Estadísticas
Abstract
Objective

To analyze the role of Human Papillomavirus (HPV) and other risk factors in the regression of cervical lesions in women from the Bogotá Cohort.

Methods

200 HPV positive women with abnormal cytology were included for regression analysis. The time of lesion regression was modeled using methods for interval censored survival time data. Median duration of total follow-up was 9 years.

Results

80 (40%) women were diagnosed with Atypical Squamous Cells of Undetermined Significance (ASCUS) or Atypical Glandular Cells of Undetermined Significance (AGUS) while 120 (60%) were diagnosed with Low Grade Squamous Intra-epithelial Lesions (LSIL). Globally, 40% of the lesions were still present at first year of follow up, while 1.5% was still present at 5 year check-up. The multivariate model showed similar regression rates for lesions in women with ASCUS/AGUS and women with LSIL (HR=0.82, 95% CI 0.59–1.12). Women infected with HR HPV types and those with mixed infections had lower regression rates for lesions than did women infected with LR types (HR=0.526, 95% CI 0.33–0.84, for HR types and HR=0.378, 95% CI 0.20–0.69, for mixed infections). Furthermore, women over 30 years had a higher lesion regression rate than did women under 30 years (HR=1.53, 95% CI 1.03–2.27). The study showed that the median time for lesion regression was 9 months while the median time for HPV clearance was 12 months.

Conclusions

In the studied population, the type of infection and the age of the women are critical factors for the regression of cervical lesions.

Key words:
Human papillomavirus
cervical intraepithelial neoplasm
risk factors
follow-up studies
Resumen
Objetivo

Analizar el papel del virus del papiloma humano (VPH) y otros factores en la regresión de lesiones del cuello del útero en mujeres de la cohorte de Bogotá, Colombia.

Métodos

El tiempo medio de seguimiento fue nueve años. Se incluyeron 200 mujeres VPH positivas con citología anormal. El tiempo de regresión de lesión fue modelado mediante análisis de supervivencia censurando por intervalos.

Resultados

80 mujeres (40%) tuvieron células escamosas atípicas de significado indeterminado (ASCUS) o células glandulares atípicas de significado indeterminado (AGUS) y 120 (60%) tuvieron lesiones escamosas intraepiteliales de bajo grado (LEI-BG). El 40% de las lesiones estaban presentes en el primer año de seguimiento, mientras que el 1,5% aún estaba a los cinco años. Se observaron tasas similares de regresión para ASCUS/AGUS y LEI-BG (HR=0,82, IC 95% 0,59–1,12). Mujeres infectadas con VPH de alto riesgo y aquéllas con infecciones mixtas tuvieron tasas inferiores de regresión de las lesiones que las mujeres con VPH de bajo riesgo (HR=0,526, IC 95% 0,33–0,84, para los VPH de alto riesgo, y HR=0,378, IC 95% 0,20–0,69, para las infecciones mixtas). Las mujeres mayores de 30 años tuvieron una mayor tasa de regresión de lesiones que las menores de 30 (HR= 1,53, IC 95% 1,03–2,27). El tiempo medio de regresión de las lesiones fue 9 meses, y el tiempo medio para la eliminación del VPH fue 12 meses.

Conclusiones

En la población estudiada, el tipo de infección y la edad de las mujeres son factores críticos para la regresión de lesiones cervicales.

Palabras Clave:
virus del papiloma humano
regresión de lesiones cervicales
factores de riesgo
estudios de seguimiento
El Texto completo está disponible en PDF
References
[1.]
P. Holowaty, A.B. Miller, T. Rohan, T. To.
Natural history of dysplasia of the uterine cervix.
J Natl Cancer Inst, 91 (1999), pp. 252-258
[2.]
A.B. Bos, M. van Ballegooijen, G.J. van Oortmarssen, M.E. van Marle, J.D. Habbema, E. Lynge.
Non-progression of cervical intraepithelial neoplasia estimated from population-screening data.
Br J Cancer, 75 (1997), pp. 124-130
[3.]
N.S. Murthy, S. Sardana, N. Narang, S.S. Agarwal, S. Sharma, D.K. Das.
Biological behaviour of moderate dysplasia—a prospective study.
Indian J Cancer, 33 (1996), pp. 24-30
[4.]
A.G. Ostör.
The natural history of cervical intraepithelial neoplasia: a critical review.
Int J Gynecol Pathol, 12 (1993), pp. 186-192
[5.]
K. Nasiell, V. Roger, M. Nasiell.
Behavior of mild cervical dysplasia during long-term follow-up.
Obstet Gynecol, 67 (1986), pp. 665-669
[6.]
M. Plummer, M. Schiffman, P.E. Castle, D. Maucort-Boulch, C.M. Wheeler, ALTS Group.
A 2-year prospective study of human papillomavirus persistence among women with a cytological diagnosis of atypical squamous cells of undetermined significance or low-grade squamous intraepithelial lesion.
J Infect Dis, 195 (2007), pp. 1582-1589
[7.]
N.F. Schlecht, R.W. Platt, E. Duarte-Franco, M.C. Costa, J.P. Sobrinho, J.C. Prado, et al.
Human papillomavirus infection and time to progression and regression of cervical intraepithelial neoplasia.
J Natl Cancer Inst, 95 (2003), pp. 1336-1343
[8.]
M.A. Nobbenhuis, T.J. Helmerhorst, A.J. van den Brule, L. Rozendaal, F.J. Voorhorst, P.D. Bezemer, et al.
Cytological regression and clearance of high-risk human papillomavirus in women with an abnormal cervical smear.
Lancet, 358 (2001), pp. 1782-1783
[9.]
M. Molano, H. Posso, E. Weiderpass, A.J. van den Brule, M. Ronderos, S. Franceschi, et al.
Prevalence and determinants of HPV infection among Colombian women with normal cytology.
Br J Cancer, 87 (2002), pp. 324-333
[10.]
M. Molano, A.J. van den Brule, H. Posso, E. Weiderpass, M. Ronderos, S. Franceschi, et al.
Low grade squamous intra-epithelial lesions and human papillomavirus infection in Colombian women.
Br J Cancer, 87 (2002), pp. 1417-1421
[11.]
A.M. de Roda Husman, J.M. Walboomers, A.J. van der Brule, C.J. Meijer, P.J. Snijders.
The use general primers GP5 and GP6 elongated at their 3’ ends with adjacent highly conserved sequences improves human papillomavirus detection by PCR.
J Gen Virol, 76 (1995), pp. 1057-1062
[12.]
M.V. Jacobs, P.J. Snijders, A.J. van den Brule, T.J. Helmerhorst, C.J. Meijer, J.M. Walboomers.
A general primer GP5+/GP6(+)-mediated PCR-enzyme immunoassay method for rapid detection of 14 high-risk and 6 low-risk human papillomavirus genotypes in cervical scrapings.
J Clin Microbiol, 35 (1997), pp. 791-795
[13.]
A.J. van den Brule, R. Pol, N. Fransen-Daalmeijer, L.M. Schouls, C.J. Meijer, P.J. Snijders.
GP5+/6+ PCR followed by reverse line blot analysis enables rapid and high-throughput identification of human papillomavirus genotypes.
J Clin Microbiol, 40 (2002), pp. 779-787
[14.]
H. Trottier, S. Mahmud, M.C. Costa, J.P. Sobrinho, E. Duarte-Franco, T.E. Rohan, et al.
Human papillomavirus infections with multiple types and risk of cervical neoplasia.
Cancer Epidemiol Biomarkers Prev, 15 (2006), pp. 1274-1280
[15.]
A. Hildesheim, M.H. Schiffman, P. Gravitt, A.G. Glass, C.E. Greer, T. Zhang, et al.
Persistence of type-specific human papillomavirus infection among cytologically normal women.
J Infect Dis, 169 (1994), pp. 235-240
[16.]
G.Y.F. Ho, R. Bierman, L. Beardsley, C.J. Chang, R.D. Burk.
Natural history of cervicovaginal papillomavirus infection in young women.
N Engl J Med, 338 (1998), pp. 423-428
[17.]
P.E. Castle, M. Schiffman, R. Herrero, A. Hildesheim, A.C. Rodriguez, M.C. Bratti, et al.
A prospective study of age trends in cervical human papillomavirus acquisition and persistence in Guanacaste Costa Rica.
J Infect Dis, 191 (2005), pp. 1808-1816
[18.]
N. Muñoz, G. Hernandez-Suarez, F. Méndez, M. Molano, H. Posso, V. Moreno, et al.
Persistence of HPV infection and risk of high-grade cervical intraepithelial neoplasia in a cohort of Colombian women.
Br J Cancer, 100 (2009), pp. 1184-1190
[19.]
M. Edelman, A.S. Fox, E.M. Alderman, W. Neal, A. Shapiro, E.J. Silver, et al.
Cervical Papanicolaou smear abnormalities in inner city Bronx adolescents: prevalence, progression, and immune modifiers.
Cancer, 87 (1999), pp. 184-189
[20.]
A.J. Kirby, D.J. Spiegelhalter, N.E. Day, L. Fenton, K. Swanson, E.M. Mann, et al.
Conservative treatment of mild/moderate cervical dyskaryosis: long-term outcome.
Lancet, 339 (1992), pp. 828-831
[21.]
F.J. Montz, B.J. Monk, J.M. Fowler, L. Nguyen.
Natural history of the minimally abnormal Papanicolaou smear.
Obstet Gynecol, 80 (1992), pp. 385-388
[22.]
K. Nasiell, M. Nasiell, V. Va lavinková.
Behavior of moderate cervical dysplasia during long-term follow-up.
Obstet Gynecol, 61 (1983), pp. 609-614
[23.]
L. Kjellberg, G. Hallmans, A.M. Ahren, R. Johansson, F. Bergman, G. Wadell, et al.
Smoking, diet, pregnancy and oral contraceptive use as risk factors for cervical intra-epithelial neoplasia in relation to human papillomavirus infection.
Br J Cancer, 82 (2000), pp. 1332-1338
[24.]
N. Muñoz, S. Franceschi, C. Bosetti, V. Moreno, R. Herrero, J.S. Smith, et al.
Role of parity and human papillomavirus in cervical cancer: the IARC multicentric case-control study.
Lancet, 359 (2002), pp. 1093-1101
[25.]
M. Molano, A. Van den Brule, M. Plummer, E. Weiderpass, H. Posso, A. Arslan, et al.
Determinants of clearance of human papillomavirus infections in Colombian women with normal cytology: a population-based, 5-year follow-up study.
Am J Epidemiol, 158 (2003), pp. 486-494
[26.]
A.B. Moscicki, N. Hills, S. Shiboski, K. Powell, N. Jay, E. Hanson, et al.
Risks for incident human papillomavirus infection low-grade squamous intraepithelial lesion development in young females.
JAMA, 285 (2001), pp. 2995-3002
[27.]
H. Richardson, M. Abrahamowicz, P.P. Tellier, G. Kelsall, R. du Berger, A. Ferenczy, et al.
Modifiable risk factors associated with clearance of type-specific cervical human papillomavirus infections in a cohort of university students.
Cancer Epidemiol Biomarkers Prev, 14 (2005), pp. 1149-1156
[28.]
H. Grisales, A.P. Vanegas, A.M. Gaviria, J. Castaño, M.A. Mora, M. Borrero, et al.
Prevalence of epithelial squamous cell abnormalities and associated factors in women of a rural town of Colombia.
Biomedica, 28 (2008), pp. 271-283
[29.]
S. Vaccarella, R. Herrero, P.J. Snijders, M. Dai, J.O. Thomas, N.T. Hieu, et al.
Smoking and human papillomavirus infection: pooled analysis of the International Agency for Research on Cancer HPV Prevalence Surveys.
Int J Epidemiol, 37 (2008), pp. 536-546
Copyright © 2010. Instituto Nacional de Cancerología
Descargar PDF
Opciones de artículo