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      Evaluación, mediante RCP, de la infección por el virus de papiloma humano en muestras de pacientes con diagnóstico clínico o citológico

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          Abstract

          Objetivo: Detección y tipificación del VPH mediante Reacción en Cadena de la polimerasa con iniciadores genéricos MY09 y MY11 y RCP-Múltiple, en muestras de pacientes con diagnóstico citológico de coilocitosis y lesión intraepitelial escamosa de bajo grado, o diagnóstico clínico de condilomatosis y papilomatosis. Métodos: Se procesaron 70 muestras citológicas del área genital a las que se realizó extracción de ADN y detección y tipificación viral mediante técnicas moleculares (RCP y RCP múltiple). Ambiente; Laboratorio de Genética Molecular del Instituto de Oncología y Hematología, Resultados: De las muestras evaluadas, 31 resultaron positivas en la detección molecular del VPH. De éstas, 29 correspondieron a VPH de bajo riesgo (tipos 11 y/o 6), una a infección mixta con bajo y alto riesgo (tipos 6 y 33) y otra a coinfección con virus de alto riesgo (tipos 18 y 33). Conclusiones: Los resultados obtenidos resaltan la utilidad de la RCP en el diagnóstico y tipificación del VPH y ponen en evidencia una relación, ya establecida, entre VPH de bajo riesgo y displasias leves, así como la posible sobrestimación de infección por VPH en los diagnósticos de referencia.

          Translated abstract

          Objectives: The aim of this study was the HPV detection and typification by PCR with MY09 and MY11 primers and a Multiplex-PCR assay, in patients samples with cytological diagnostic of koilocytosis and low grade squamous intrapithelial lesion, or clinical diagnostic of condylomatosis and papillomatosis. Methods: Seventy cytological samples of the genital area were assessed for DNA extraction and viral detection and typification by molecular techniques (PCR and Multiplex PCR). Setting: Laboratorio de Genética Molecular-Instituto de Oncología y Hematología, Results: From 70 evaluated samples, 31 were positive for HPV detection, with 29 samples corresponding to low risk HPV (types 6 and/or 11), one corresponding to high and low risk HPV mixture infection (types 6 and 33) and one corresponding to high risk HPV coinfection (types 18 and 33). Conclusions: These results reflect the PCR utility to the HPV detection and typification, and evidence a well known relation between low risk HPV and moderated displasias, as well as the possible overstimate of HPV infection in the reference diagnostic.

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          Most cited references63

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          Overview of the European and North American studies on HPV testing in primary cervical cancer screening.

          Several studies suggest that HPV testing is more sensitive than cytology in primary cervical screening. These studies had different designs and were reported in different ways. Individual patient data were collected for all European and North American studies in which cytology was routinely performed and HPV testing was included as an additional parallel test. More than 60,000 women were included. The sensitivity and specificity of HPV testing were compared with routine cytology, both overall and for ages <35, 35-49 and 50+. The age-specific prevalence of high risk HPV (hr-HPV) was also analysed. HPV testing was substantially more sensitive in detecting CIN2+ than cytology (96.1% vs. 53.0%) but less specific (90.7% vs. 96.3%). The sensitivity of HPV testing was similar in all studies carried out in different areas of Europe and North America, whereas the sensitivity of cytology was highly variable. HPV sensitivity was uniformly high at all ages, whereas the sensitivity of cytology was substantially better in women over the age of 50 than in younger women (79.3% vs. 59.6%). The specificity of both tests increased with age. Positivity rates for HPV testing in women without high-grade CIN were region dependent. These results support the use of HPV testing as the sole primary screening test, with cytology reserved for women who test HPV positive. Large demonstration projects are needed to fully evaluate this strategy. Copyright 2006 Wiley-Liss, Inc.
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            Epidemiologic profile of type-specific human papillomavirus infection and cervical neoplasia in Guanacaste, Costa Rica.

            Detailed epidemiologic studies of cervical type-specific human papillomavirus (HPV) infection in large populations are scarce. We recruited a population-based cohort in Guanacaste, Costa Rica. Participants were interviewed, screened for cervical neoplasia, and tested for >40 HPV types by use of MY09/11 L1 consensus primer polymerase chain reaction. We estimated the risk factors for infection and the associations between type-specific HPV infections and cervical intraepithelial neoplasia (CIN) and cancer in 8514 sexually active women who had not undergone a hysterectomy. The overall HPV prevalence was 26.5%. The most common type was HPV-16 (3.6% of the population). HPV prevalence showed a U-shaped age-specific curve. Sexual behaviors were the main determinants of oncogenic and nononcogenic infections; age at first sexual intercourse was not independently associated with infection. Barrier contraceptive use was somewhat protective against infection. Oncogenic infections were strongly associated with risk of all grades of CIN and of cancer. Types 16, 18, and 58 were the most common in women diagnosed with CIN3 and cancer. Except for those that included HPV-16, multiple-type infections were associated with an increased risk (compared with that for single-type infections) of all grades of CIN and of cancer. We confirmed the bimodal age pattern of HPV infection in Guanacaste and the sexually transmitted nature of both oncogenic and nononcogenic HPV types.
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              Risks for incident human papillomavirus infection and low-grade squamous intraepithelial lesion development in young females.

              Low-grade squamous intraepithelial lesions (LSILs) have been described as a benign cytological consequence of active human papillomavirus (HPV) replication. Several studies have reported that certain behavioral and biological risks exist for LSIL, suggesting that HPV alone is not sufficient for the development of LSIL. However, because most of these studies have been cross-sectional, it is not known whether behavioral and biological risks are simply risks for HPV infection itself. To prospectively examine risks of incident HPV infection in HPV-negative females and of incident LSIL development in females with HPV infection. Prospective cohort study conducted between 1990-2000, with a median follow-up of 50 months. Females aged 13 to 21 years who attended 2 family planning clinics in the San Francisco bay area; 496 had prevalent HPV infection and 105 were HPV-negative. Incident development of HPV infection and LSIL, analyzed by various demographic, behavioral, and clinical risk factors. Fifty-four incident HPV infections occurred in the 105 females who were HPV-negative at study entry (median duration of follow-up for those who remained HPV-negative was 26 months). Multivariable analysis showed that risks of HPV included sexual behavior (relative hazard [RH], 10.10; 95% confidence interval [CI], 3.24-31.50 per new partner per month), history of herpes simplex virus (RH, 3.54; 95% CI, 1.37-9.10), and history of vulvar warts (RH, 2.73; 95% CI, 1.27-5.87). Current use of oral contraceptives had a significantly protective effect (RH, 0.49; 95% CI, 0.28-0.86). Among the 496 individuals who were HPV-positive at baseline or in follow-up, there were 109 incident cases of LSIL during the follow-up interval, with a median follow-up time of 60 months for those who never developed LSIL. Human papillomavirus infection was the most significant risk factor for development of LSIL. The multivariable model showed the following risks for LSIL: HPV infection for less than 1 year (RH, 7.40; 95% CI, 4.74-11.57); HPV infection for 1 to 2 years (RH, 10.27; 95% CI, 5.64-18.69); HPV infection for 2 to 3 years (RH, 6.11; 95% CI, 1.86-20.06); and daily cigarette smoking (RH, 1.67; 95% CI, 1.12-2.48). Our results indicate distinct risks for HPV and LSIL. In addition, most women with HPV infection in our study did not develop LSIL within a median follow-up period of 60 months. These findings underscore the hypothesis that certain biological risks thought to be associated with LSIL are, in fact, risks for acquisition of HPV. Cigarette smoking was a risk specific to LSIL, supporting the role of tobacco in neoplastic development.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                og
                Revista de Obstetricia y Ginecología de Venezuela
                Rev Obstet Ginecol Venez
                Sociedad de Obstetricia y Ginecología de Venezuela (Caracas )
                0048-7732
                December 2008
                : 68
                : 4
                : 240-247
                Affiliations
                [1 ] Instituto de Oncología y Hematología, MPPS Venezuela
                [2 ] Universidad Central de Venezuela Venezuela
                Article
                S0048-77322008000400006
                9cee7248-10fc-437e-8f0e-56290dafebbc

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Venezuela

                Self URI (journal page): http://www.scielo.org.ve/scielo.php?script=sci_serial&pid=0048-7732&lng=en
                Categories
                OBSTETRICS & GYNECOLOGY

                Obstetrics & Gynecology
                HPV,SIL,PCR,Cytology,VPH,LIE,RCP,Citología
                Obstetrics & Gynecology
                HPV, SIL, PCR, Cytology, VPH, LIE, RCP, Citología

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