Yüksek riskli human papilloma virüs saptanan hastaların histopatolojik sonuçları

Abstract

Amaç: Çalışmamızda Çorum ili sağlık müdürlüğü tarafından 2016-2017 yılları arasında Ulusal HPV tarama programı kapsamında Çorum ili genelinde HPV DNA taraması yapılan ve pozitiflik saptanması nedeni ile hastanemizde kolposkopik biyopsi işlemi yapılan hastaların histopatolojik sonuçları ile HPV subtiplerinin karşılaştırılması amaçlanmıştır. Yöntem: Çalışmaya HPV DNA pozitifliği nedeni ile kolposkopik biyopsi işlemi yapılan 30-65 yaş arasındaki kadınların tamamı dahil edildi. HPV tipleri tip 16, 18 ve diğerleri olarak üç kategoriye ayrıldı. Kolposkopik biyopsi materyallerine ait patoloji sonuçları normal / düşük dereceli skuamöz intraepitelyal lezyon LSIL ve yüksek dereceli skuamöz intraepitel lezyon HSIL olarak kategorize edildi. Bulgular: 212 hastaya HPV DNA pozitifliği saptanması nedeni ile kolposkopi eşliğinde servikal biyopsi yapıldı. HPV tiplerine göre bu sayı dağıtıldığında HPV tip 16,18 ve diğerlerinde sırası ile 126, 13 ve 73 olarak dağılmaktaydı. Kolposkopi sonucunda 63 hastada %30 LSIL, 56 hastada %26 HSIL saptanırken 93 hastada %44 displazi saptanmadı. HPV tiplerine göre bu sayı dağıtıldığında ise HPV tip 16, 18 ve diğerlerinde LSIL sırası ile 32 %28 , 3 %24 , 20 %28 iken, HSIL sırası ile 39 %31 , 6 %46 , 11 %15 saptandı. LSIL ve HSIL ayrımı yapmaksızın displazi saptanma yüzdeleri HPV tip 16,18 ve diğerlerinde sırası ile 79 %62.6 , 9 %69.2 , 31 %42 olarak saptandı. Hastalar yaş aralığına göre dağıtıldığında displazi saptanma yüzdesinin yaş ile beraber arttığı ve 60-65 yaş aralığında % 68 e ulaştığı görüldü. Sonuç: HPV 16 ve 18 pozitif saptanan hastaların kolposkopik biyopsilerinde displazi saptanma riski diğer subtiplere oranla daha yüksek olduğundan bu hastaların mutlaka kolposkopik biyopsi ile değerlendirilmesi gereklidir. HPV DNA insidansı toplumda yaş ilerledikçe azalmaktadır ancak özellikle 5. ve 6. dekatta HPV pozitifliği saptanması durumunda bu hastalara ivedilikle kolposkopi işlemi yapılmalıdır çünkü yaş ilerledikçe displazi saptanma yüzdesi artmaktadır.

Keywords

• HPV, serviks, kolposkopik biyopsi, displazi

Histopathological results of high risk HPV DNA detected patients

Abstract

Objective: In our study, it was aimed to compare histopathologic results and HPV subtypes of the patients who were performed colposcopy because of detected HPV DNA positivity in National HPV Screening Program between 2016-2017 years in Çorum province. Methods: All women aged 30-65 years who performed colposcopic biopsy cause of HPV DNA positivity were included in the study. HPV types were divided into three categories as types 16, 18 and others. Pathology results of colposcopic biopsy materials were categorized as Normal, Low grade squamous intraepithelial lesion CIN I and high grade squamous intraepithelial lesion CIN II/III . Results: A total of 212 patients detected HPV DNA positivity, were performed cervical biopsy accompanied by colposcopy. When distributed according to HPV types; HPV types 16, 18 and others were found to be positive in 126, 13 and 73 individuals, respectively. As a result of colposcopy, HSIL were detected in 63 patients 29% , LSIL were detected in 56 patients 26% and no dysplasia was detected in 93 patients 44% . LSIL were detected in 32 28% patients with HPV 16, in 3 24% patients with HPV 18 and in 20 28% patients with other types. HSIL were detected in 39 31% patients with HPV 16, in 6 46% patients with HPV 18 and in 11 15% patients with other subtypes. The percentages of dysplasia HSIL + LSIL were found 79 62,6% in HPV 16, 9 69.2% in HPV 18 and 31 42% in other subtypes. Patients were evaluated according to age range. A positive correlation between the detection rate of dysplasia and age was observed and it was observed that this ratio reached to 68% in the age range of 60-65 years. Conclusion: The probability of detecting dysplasia in colposcopic biopsies of patients with positive HPV 16 and 18 are higher than other subtypes. Therefore, these patients have to be absolutely evaluated with colposcopic biopsy. The incidence of HPV DNA decreases with age. However, colposcopy have to be performed immediately when HPV positivity is detected especially in the 5th and 6th decades because the percentage of dysplasia detection increases with age.

Keywords

• HPV, Cervix, colposcopic biopsy, dysplasia

References

1. 1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer 2010 Dec 15;127(12):2893-917. doi: 10.1002/ijc.25516.
2. 2. Wardak S. Human Papillomavirus (HPV) and cervical cancer. Med Dosw Mikrobiol 2016;68(1):73-84.
3. 3. Zhang L, Bi Q, Deng H, Xu J, Chen J, Zhang M, et al. Human papillomavirus infections among women with cervical lesions and cervical cancer in Eastern China: genotype-specific prevalence and attribution. BMC Infect Dis 2017 Jan 31;17(1):107. doi: 10.1186/s12879-017-2223-1.
4. 4. Sasaki Y, Iwanari O, Arakawa I, Moriya T, Mikami Y, Iihara K, et al. Cervical Cancer Screening With Human Papillomavirus DNA and Cytology in Japan. Int J Gynecol Cancer 2017 Mar;27(3):523-9. doi: 10.1097/IGC.0000000000000898.
5. 5. Fernandez AF, Rosales C, Lopez-Nieva P, Graña O, Ballestar E, Ropero S, et al. The dynamic DNA methylomes of double-stranded DNA viruses associated with human cancer. Genome Res 2009 Mar;19(3):438-51. doi: 10.1101/gr.083550.108.
6. 6. Ghosh S, Seth S, Paul J, Rahman R, Chattopadhyay S, Bhadra D, et al. Evaluation of Pap smear ,high risk HPV DNA testing in detection of cervical neoplasia with colposcopy guided or conventional biopsy as gold standard.ınt J Healthcare Biomed Res 2014;2(2) :192-7.
7. 7. Burd EM. Human papillomavirus and cervical cancer. Clin Microbiol Rev 2003 Jan;16(1):1-17. Review. PubMed PMID: 12525422.
8. 8. Gultekin M, Zayifoglu Karaca M, Kucukyildiz I, Dundar S, Boztas G, Semra Turan H, ve ark. Initial results of population based cervical cancer screening program using HPV testing in one million Turkish women. Int J Cancer 2018 May 1;142(9):1952-8. doi: 10.1002/ijc.31212. Epub 2017 Dec 23.

9. 9. Kulhan M, Kulhan NG, Seven Y, Nayki UA, Nayki C, Ata N, et al. Estimation of the prevalence and distribution of HPV genotypes and identification of related risk factors among Turkish women. Contemp Oncol (Pozn) 2017;21(3):218-23. doi: 10.5114/wo.2017.69591. Epub 2017 Sep 29.
10. 10. Zhao XL, Hu SY, Zhang Q, Dong L, Feng RM, Han R, et al. High-risk human papillomavirus genotype distribution and attribution to cervical cancer and precancerous lesions in a rural Chinese population. J Gynecol Oncol 2017 Jul;28(4):e30. doi: 10.3802/ jgo.2017.28.e30.
11. 11. Dinc B, Rota S, Onan A, Bozdayi G, Taskiran C, Biri A, ve ark. Prevalence of human papillomavirus (HPV) and HPV-16 genotyping by real-time PCR in patients with several cervical pathologies. Braz J Infect Dis 2010 Jan-Feb;14(1):19-23.
12. 12. Luo HX, Du H, Liu ZH, Zhang LJ, Wang C, Wu RF. Evaluation of CIN2+ /CIN3+ risk of different HPV subtypes infection combined with abnormal cytology status. Zhonghua Zhong Liu Za Zhi 2018 Mar 23;40(3):232-8. doi: 10.3760/cma.j.is sn.0253-3766.2018.03.015. Chinese.
13. 13. Xiaolin L, Xiaojie W, Feiyun Z, Haiyan Z, Xuejie Z, Jianqin Y. Comparison of human papillomavirus genotype distributions in cervical intraepithelial neoplasia and cervical cancer. Biomedical Research 2017; 28 (5):2284-9.
14. 14. Tezcan S, Ozgur D, Ulger M, Aslan G, Gurses I, Serin MS, ve ark. Human papillomavirus genotype distribution and E6/E7 oncogene expression in Turkish women with cervical cytological findings. Asian Pac J Cancer Prev 2014;15(9):3997-4003.
15. 15. de Oliveira GR, Vieira VC, Ávila EC, FingerJardim F, Caldeira TD, Gatti FA, et al. Human papillomavirus type distribution and HPV16 intratype diversity in southern Brazil in women with and without cervical lesions. Mem Inst Oswaldo Cruz 2017 Jul;112(7):492-8. doi: 10.1590/0074-02760160530.
16. 16. Li K, Yin R, Li Q, Wang D. Analysis of HPV distribution in patients with cervical precancerous lesions in Western China. Medicine (Baltimore) 2017 Jul;96(29):e7304. doi: 10.1097/ MD.0000000000007304.
17. 17. Bedell MA, Hudson JB, Golub TR, Turyk ME, Hosken M, Wilbanks GD, et al . Amplification of human papillomavirus genomes in vitro is dependent on epithelial differentiation. J Virol 1991; 65:2254-60.
18. 18. zur Hausen, H. Human genital cancer: synergism between two virus infections and or synergism between a virus infection and initiating events? Lancet 1982 ii:1370-2.
19. 19. Adam E, Berkova Z, Daxnerova Z, Icenogle J, Reeves WC, Kaufman RH. Papillomavirus detection: demographic and behavioral characteristics influencing the identification of cervical disease. Am. J Obstet Gynecol 2000; 182:257-64.
20. 20. Burk RD, Kelly P, Feldman J, Bromberg S, Vermund H, Deltovitz JA, at al. Landesman. Declining presence of cervicovaginal human papilllomavirus infection with age is independent of other risk factors. Sex. Transm. Dis. 1996;23:333-41.
21. 21. Jeronimo J, Castle PE, Temin S, Denny L, Gupta V, Kim JJ et al. Secondary prevention of cervical cancer: ASCO Resource-Stratified Clinical Practice Guideline. J Glob Oncol 2017;3:635–57.
22. 22. Giuiliano AR, Sedjo RL, Roe DJ, Harri R, Baldwi S, Papenfuss MR, et al. Clearance of oncogenic human papillomavirus (HPV) infection: effect of smoking (United States). Cancer Causes and Control 2002; 13: 839-46.