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      Syndemic synergy of HPV and other sexually transmitted pathogens in the development of high-grade anal squamous intraepithelial lesions

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          Abstract

          Background

          Anal intraepithelial neoplasia is associated with high-risk human papillomavirus (hrHPV) as a precursor to anal cancer. However, factors other than hrHPV are likely to be involved and further study of cofactors is required because of the possibility of syndemic interactions.

          Methods

          Three hundred and fourteen patients underwent 457 operations. Histopathology and hrHPV testing using the Digene Hybrid Capture 2 (HC 2) method were performed. Demographic factors and sexually transmissible infections (STIs) were recorded.

          Results

          Results showed that hrHPV alone was associated with HSIL (OR = 4.65, p < 0.001). None of the other STIs were alone associated with HSIL but amplification of risk was found when hrHPV infection occurred with HIV (OR = 11.1); syphilis (OR = 5.58); HSV 2 (OR = 7.85); gonorrhoea (OR = 6.45) and some other infections.

          Conclusions

          These results suggest that hrHPV is a sufficient cause of anal HSIL. Seropositivity for HIV, HSV 2, T. pallidum, HBV and HCV and a history of gonorrhoea or chlamydia exert a powerful amplifying factor increasing the risk of HSIL above the risk with hrHPV alone. Other co-factors which are associated with an increased risk of HSIL are increased age, male gender, MSM behaviour and self-reported history of more than 50 sexual partners. This pattern of disease in patients with warts is characteristic of a syndemic with potential serious increased risk of anal carcinoma.

          Highlights

          • High-risk HPV is a necessary and sufficient cause of progression from LSIL to HSIL.

          • HIV, HSV 2, HBV and HCV are associated with an amplified risk of hrHPV induced HSIL.

          • Gonorrhoea, chlamydia, and syphilis are associated with increased odds HSIL.

          • HSIL shows syndemic interaction patterns with STIs and behavioural/social factors.

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          Most cited references72

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          Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer.

          The incidence of anal cancer has increased among both men (160%) and women (78%) from 1973 to 2000 in the U.S. The authors conducted a population-based case-control study of anal cancer to examine factors that may account for this increase. Men (n = 119 patients) and women (n = 187 patients) who were diagnosed with anal cancer between 1986 and 1998 in the Seattle area were ascertained through the local Surveillance, Epidemiology, and End Results registry. Control participants (n = 1700) were ascertained through random-digit telephone dialing. Participants were interviewed in person and provided blood samples. Archival tumor tissue was tested for human papilloma virus (HPV) DNA, and serum samples were tested for HPV type 16 (HPV-16). Overall, 88% of tumors (all histologies) in the study were found to be positive for HPV. HPV-16 was the most frequent HPV type detected (73% of all tumors), followed by HPV-18 (6.9%), regardless of gender. However, 97.7% of tumors from men who were not exclusively heterosexual contained HPV DNA. The risk of anal cancer increased among men (odds ratio [OR], 5.3; 95% confidence interval [95% CI], 2.4-12.0) and women (OR, 11.0; 95% CI, 5.5-22.1) who had > or = 15 sexual partners during their lifetime. Among men who were not exclusively heterosexual and women, receptive anal intercourse was related strongly to the risk of anal cancer (OR, 6.8 [95% CI, 1.4-33.8] and OR, 2.2 [95% CI, 1.4-3.3], respectively). Current smokers among men and women were at particularly high risk for anal cancer, independent of age and other risk factors (OR, 3.9 [95% CI, 1.9-8.0] and OR, 3.8 [95% CI, 2.4-6.2], respectively). The high proportion of tumors with detectable HPV suggests that infection with HPV is a necessary cause of anal cancer, similar to that of cervical cancer. Increases in the prevalence of exposures, such as cigarette smoking, anal intercourse, HPV infection, and the number of lifetime sexual partners, may account for the increasing incidence of anal cancer in men and women. Copyright 2004 American Cancer Society.
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            Cancer risk in people infected with human immunodeficiency virus in the United States.

            Data are limited regarding cancer risk in human immunodeficiency virus (HIV)-infected persons with modest immunosuppression, before the onset of acquired immunodeficiency syndrome (AIDS). For some cancers, risk may be affected by highly active antiretroviral therapy (HAART) widely available since 1996. We linked HIV/AIDS and cancer registries in Colorado, Florida and New Jersey. Standardized incidence ratios (SIRs) compared cancer risk in HIV-infected persons (initially AIDS-free) during the 5-year period after registration with the general population. Poisson regression was used to compare incidence across subgroups, adjusting for demographic factors. Among 57,350 HIV-infected persons registered during 1991-2002 (median CD4 count 491 cells/mm(3)), 871 cancers occurred during follow-up. Risk was elevated for Kaposi sarcoma (KS, SIR 1,300 [n = 173 cases]), non-Hodgkin lymphoma (NHL, 7.3 [n = 203]), cervical cancer (2.9 [n = 28]) and several non-AIDS-defining malignancies, including Hodgkin lymphoma (5.6 [n = 36]) and cancers of the lung (2.6 [n = 109]) and liver (2.7 [n = 14]). KS and NHL incidence declined over time but nonetheless remained elevated in 1996-2002. Incidence increased in 1996-2002 compared to 1991-1995 for Hodgkin lymphoma (relative risk 2.7, 95%CI 1.0-7.1) and liver cancer (relative risk infinite, one-sided 95%CI 1.1-infinity). Non-AIDS-defining cancers comprised 31.4% of cancers in 1991-1995, versus 58.0% in 1996-2002. For KS and NHL, risk was inversely related to CD4 count, but these associations attenuated after 1996. We conclude that KS and NHL incidence declined markedly in recent years, likely reflecting HAART-related improvements in immunity, while incidence of some non-AIDS-defining cancers increased. These trends have led to a shift in the spectrum of cancer among HIV-infected persons. (c) 2008 Wiley-Liss, Inc.
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              The Lower Anogenital Squamous Terminology Standardization project for HPV-associated lesions: background and consensus recommendations from the College of American Pathologists and the American Society for Colposcopy and Cervical Pathology.

              The terminology for human papillomavirus (HPV)-associated squamous lesions of the lower anogenital tract has a long history marked by disparate diagnostic terms derived from multiple specialties. It often does not reflect current knowledge of HPV biology and pathogenesis. A consensus process was convened to recommend terminology unified across lower anogenital sites. The goal was to create a histopathologic nomenclature system that reflects current knowledge of HPV biology, optimally uses available biomarkers, and facilitates clear communication across different medical specialties. The Lower Anogenital Squamous Terminology (LAST) project was co-sponsored by the College of American Pathologists (CAP) and the American Society for Colposcopy and Cervical Pathology (ASCCP) and included 5 working groups; three work groups performed comprehensive literature reviews and developed draft recommendations. Another work group provided the historical background and the fifth will continue to foster implementation of the LAST recommendations. After an open comment period, the draft recommendations were presented at a consensus conference attended by LAST work group members, advisors and representatives from 35 stakeholder organizations including professional societies and government agencies. Recommendations were finalized and voted upon at the consensus meeting. The final approved recommendations standardize biologically-relevant histopathologic terminology for HPV-associated squamous intraepithelial lesions and superficially invasive squamous carcinomas across all lower anogenital tract sites and detail appropriate use of specific biomarkers to clarify histologic interpretations and enhance diagnostic accuracy. A plan for disseminating and monitoring recommendation implementation in the practicing community was also developed. The implemented recommendations will facilitate communication between pathologists and their clinical colleagues and improve accuracy of histologic diagnosis with the ultimate goal of providing optimal patient care.
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                Author and article information

                Contributors
                Journal
                Papillomavirus Res
                Papillomavirus Res
                Papillomavirus Research
                Elsevier
                2405-8521
                07 November 2017
                December 2017
                07 November 2017
                : 4
                : 90-98
                Affiliations
                [a ]Sexual Health Services, Royal Perth Hospital; School of Medicine and Pharmacology, University of Western Australia, Perth, WA 6000, Australia
                [b ]Departments of Molecular Microbiology & Immunology and Obstetrics & Gynaecology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90033, USA
                [c ]Department of Microbiology and Infectious Diseases, Royal Perth Hospital; PathWest Laboratory Medicine, WA, Australia
                [d ]Departments of Microbiology and Immunology and Pathology and Laboratory Medicine, University of Western Australia, Crawley, Western Australia 6009, Australia
                [e ]Department of Anatomical Pathology, PathWest Laboratory Medicine (WA), Barry Marshall Drive, Murdoch, WA 6150, Australia
                [f ]Medical School and School of Biomedical Sciences, University of Western Australia, Perth, Australia
                [g ]Department of Clinical Immunology, Royal Perth Hospital and PathWest Laboratory Medicine, Perth, Australia
                [h ]Harry Perkins Institute of Medical Research, QEII Medical Centre, Nedlands, Australia
                [i ]Centre for Medical Research, The University of Western Australia, Crawley, Western Australia 6009, Australia
                Author notes
                [* ]Correspondence to: 6th Floor, MRF Building, rear 50 Murray Street, Perth, WA 6000, Australia.6th Floor, MRF Building, rear 50 Murray StreetPerthWA6000Australia michael.phillips@ 123456perkins.uwa.edu.au
                Article
                S2405-8521(17)30041-1
                10.1016/j.pvr.2017.10.004
                5883243
                29179876
                0aed4754-2c54-47c1-a1e1-26ad18fd1204
                © 2017 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 6 June 2017
                : 30 October 2017
                : 31 October 2017
                Categories
                Article

                hsil,anal warts,sexually transmissible infections,high-risk hpv,hiv,syndemic

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