Utilidad del genotipado del virus del papiloma humano con el método COBAS 4800 en las lesiones intraepiteliales escamosas de bajo grado (LSIL).

Abstract

Low-grade squamous intraepithelial cervical lesion (LSIL) is a preinvasive neoplasia. Human papilloma virus (HPV) is involved in its origin. In our work we analyzed the newly diagnosed LSIL in our area (IMAS, Barcelona) with the aim of studying the utility of HPV genotyping by the technique COBAS 4800. That technique allow us to classify lesions as HPV16 positive, HPV18 positive or high-risk HPV others than 16 or 18 (HPVno16no18) The mean age of the patients was 33.8 ± 11.1 years. Of all lesions, 19.6 % were positive for HPV16, 4.9% for HPV18 and 63.6 % for HPVno16no18. The different age distribution was significant only for HPV18, being more frequent in patients over 39 years. At two years of follow up, the cure rate of LSIL was 74.1%, persistence rate of 16.3%, 9.8% of progression to CIN2 + and 2.1% to CIN3. HPV16 positivity was more frequent in lesions that progressed to CIN2+, while non-detection of high-risk HPV (hrHPV) for regression ones. The absolute risk of HPV16 for progression to CIN2+ was 32.1%, 14.3% for HPV18 and 5.8% for HPVno16no18. None of the HPVneg cases evolved to CIN2+. None of the LSIL caused by HPV16 in patients more than 39 years progressed to CIN2+. The presence of HPV16 conferred a 7.4 times greater risk of developing CIN2+ that its absence. This relative risk was the only one statistically significant. In older patients (either over 29 or 39 years) the relative risk was lower than for younger. The absolute risks for HPV16 for healing was 53.6%, for HPV18 57.1%, 75.4% for HPVno16no18, and 87.5 % for HPVneg. In older patients (either over 29 or 39 years) the absolute risk of cure was higher than for younger. The relative risks for healing for HPV16 and HPVneg (0.7 and 1.3 respectively) were the only ones statistically significant, which were higher for patients over 39 years. Of the 8 patients who were treated with conization after prior diagnosis of CIN2+, none of the infected by HPVno16no18 exclusively showed CIN2 + in the surgical piece, as opposed to 100% of those infected with HPV16. The median time to progression to CIN2+ was 16.2±15.8 months from diagnosis, and the median time to regression of 13.5±9.2 months. Age does not influenced either the median time to progression to CIN2+ or the healing of LSIL. LSIL lesions caused by HPV16 more quickly progressed to CIN2+ than those produced by HPV18, and those ones than those produced by HPVno16no18. This difference was statistically significant. LSIL lesions caused by HPV16 cured more slowly than those produced by other viral genotypes. Those produced by HPVno16no18 and HPVneg evolved similarly to cure, at a greater speed than the rest. LSIL lesions caused by HPV16 are more likely to progress to CIN2+ and faster, so tight control and immediate colposcopy are crucial. LSIL lesions in which we can’t detect a high-risk HPV do not progress to CIN2+, so its control should be different from the others LSIL, conservative management sine die could be acceptable from a clinical point of view according to our data.

Date of Award	3 Dec 2013
Original language	Spanish
Supervisor	Francesc Alameda Quitllet (Director), Ramon Carreras Collado (Director) & Gemma Mancebo Moreno (Director)