Human papilloma virus infection of uterine cervix and spectrum of cervical pathology in human immunodeficiency virus/AIDS
Bhawna Bhutoria Jain1, Tathagata Adhikary2, Provash C Sadhukhan3, Ayandip Nandi4
1 Department of Pathology, Rampurhat Government Medical College, Birbhum, West Bengal, India
2 MTMTB Hospital, Kolkata Municipal Corporation, Kolkata, West Bengal, India
3 ICMR Virus Unit, National Institute of Cholera and Enteric Diseases, GB4, ID and BG Hospital, Beliaghata Campus, Kolkata, West Bengal, India
4 Department of Pathology, Medical College, Kolkata, West Bengal, India
48/7, Patuapara Lane, Serampore, Hooghly - 712 201, West Bengal
Source of Support: None, Conflict of Interest: None
Background: Human papilloma virus (HPV) is one of the most common causes of sexually transmitted viral diseases worldwide. High-risk HPV types such as HPV16 and 18 are known to cause cervical dysplasia and carcinoma. In human immunodeficiency virus (HIV)-positive individual, chance of HPV coinfection and risk of cervical dysplasia/carcinoma have been found to be significantly more than in HIV-negative individuals.
Aim: In this institution-based, cross-sectional, observational study, we aim to find out the relationship of HPV infection of the uterine cervix with cervical dysplasia and neoplasia in HIV-infected/AIDS patients.
Materials and Methods: Conventional Pap smears were taken from HIV-infected individuals admitted in the department of gynecology and obstetrics and reported by the Bethesda system. A second sample was sent to the virology unit of ICMR for detection and typing of HPV. Control samples were taken from HIV-negative individuals.
Results: Fifty HIV-positive patients were included in this study. On cervical Pap smear examination, 32 cases were cytologically benign and 18 cases showed atypical cytomorphology. Twenty-four cases were HPV positive, among which 16 were cytologically atypical and 8 were benign. HPV 16 was the most common subtype (50%) followed by HPV 18 (37.5%) and others (12.5%) in HIV-positive patients. Chance of cervical dysplasia increased with age independent of HIV infection and with progressive lower CD4 count. Koilocytosis was a significant predictor of HPV infection. Majority of patients were asymptomatic. Peak incidence of HPV infection occurred in reproductive age group (20–40 years). The association between HIV and HPV coinfection (P = 0.002) and between HPV infection and cytology atypia (P < 0.0001) was statistically significant.
Conclusion: Present study highlights the necessity of routine cervical Pap smear screening in HIV infected reproductive age-group women. Early detection enables dysplasia to revert or be effectively managed.