FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1505068903> ?p ?o ?g. }

• W1505068903 endingPage "200" @default.
• W1505068903 startingPage "189" @default.
• W1505068903 abstract "Human papillomavirus (HPV) infection is one of the most common sexually transmitted infections worldwide and causes cervical and anal cancer, as well as its associated precancer lesions of cervical intraepithelial neoplasia (CIN) and anal intraepithelial neoplasia (AIN). HPV also causes a proportion of vulvar, vaginal and penile squamous cell cancers (1Monk BJ Tewari KS The spectrum and clinical sequelae of human papillomavirus infection.Gynecol Oncol. 2007; 107: S6-S13Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar). There is increasing evidence that HPV plays an important role in head and neck cancer. HPV also causes cutaneous and anogenital warts, which are of low malignant potential. Cell-mediated immunity is important for the control of HPV infection. Immunosuppression for solid organ transplantation decreases the capacity to eradicate new HPV infection, and enables increased HPV replication in latently infected cells. As a result, transplant recipients have a substantially increased risk of HPV-associated malignancies compared with the general population. Transplant patients also experience an increased occurrence of extensive and treatment-refractory cutaneous and anogenital warts. HPV is a double-stranded DNA virus that infects the basal epithelial cells of keratinized skin, mucous membranes and the transformation zone of the cervix. Different HPV types have tissue tropism for cutaneous versus mucosal membranes in different body sites, with varying level of malignant potential (2de Sanjose S Quint WG Alemany L et al.Human papillomavirus genotype attribution in invasive cervical cancer: A retrospective cross-sectional worldwide study.Lancet Oncol. 2010; 11: 1048-1056Abstract Full Text Full Text PDF PubMed Scopus (1881) Google Scholar,3Tilston P Anal human papillomavirus and anal cancer.J Clin Pathol. 1997; 50: 625-634Crossref PubMed Scopus (65) Google Scholar). HPV types can be broadly classified into “high risk” and “low risk” types based on their propensity to cause cancer. In a large, global epidemiological study, Munoz and others found that at least 40 HPV types were associated with neoplasms. Of these, 18 were classified as “low risk” and associated with anogenital warts, mild cervical dysplasia and recurrent respiratory papillomatosis, and 12 were considered “high risk” including types 16 and 18 (4Munoz N Bosch FX de Sanjose S et al.Epidemiologic classification of human papillomavirus types associated with cervical cancer.N Engl J Med. 2003; 348: 518-527Crossref PubMed Scopus (4990) Google Scholar). More frequent HPV types associated with various clinical manifestations are listed in Table 1 (5Palefsky JM Epidemiology of human papillomavirus infections.UpToDate. 2012; Google Scholar).Table 1:HPV and tissue tropismHPV types frequentlyDiseaseassociatedPlantar and common warts1,2,4Flat or plane warts3,10Butcher’s wart7,2Bowen’s diseaseGenital16Extragenital2,3,4,16Condylomata acuminta6,11Bowenoid papulosis16,34,37,42Intraepithelial neoplasiaLow grade6,11High grade16,18Respiratory papillomatosis6,11Adapted from Table 1 in epidemiology of human papillomavirus infection (Ref. 5Palefsky JM Epidemiology of human papillomavirus infections.UpToDate. 2012; Google Scholar). Open table in a new tab Adapted from Table 1 in epidemiology of human papillomavirus infection (Ref. 5Palefsky JM Epidemiology of human papillomavirus infections.UpToDate. 2012; Google Scholar). The vast majority of HPV acquisition occurs via direct person-to-person transmission. Indeed, anogenital HPV is estimated to be the most common sexually transmitted infection in the United States (6Weinstock H Berman S Cates Jr, W Sexually transmitted diseases among American youth: Incidence and prevalence estimates, 2000.Perspect Sex Reprod Health. 2004; 36: 6-10Crossref PubMed Scopus (1267) Google Scholar). HPV can also be acquired by infants during the passage through the birth canal of HPV-infected mothers—this is likely the mode of viral transmission in children who later develop recurrent respiratory papillomatosis (7Merckx M Liesbeth WV Arbyn M et al.Transmission of carcinogenic human papillomavirus types from mother to child: A meta-analysis of published studies.Eur J Cancer Prev. 2012; Google Scholar,8Shah KV Stern WF Shah FK Bishai D Kashima HK Risk factors for juvenile onset recurrent respiratory papillomatosis.Pediatr Infect Dis J. 1998; 17: 372-376Crossref PubMed Scopus (100) Google Scholar). Most persons infected with HPV are asymptomatic so transmission of the infection from individuals without visible lesions is common. In addition, anogential HPV can be seen concurrently with cutaneous warts or oral mucosal disease, suggesting that auto-infection can occur from one site to another (9Eversole LR Laipis PJ Green TL Human papillomavirus type 2 DNA in oral and labial verruca vulgaris.J Cutan Pathol. 1987; 14: 319-325Crossref PubMed Scopus (32) Google Scholar,10Hernandez BY Shvetsov YB Goodman MT et al.Genital and extra-genital warts increase the risk of asymptomatic genital human papillomavirus infection in men.Sex Transm Infect. 2011; 87: 391-395Crossref PubMed Scopus (18) Google Scholar). To date, there have been no reports of HPV acquired through organ transplantation. Once HPV has infected epithelial cells, it evades the host immune response by various mechanisms. These include a prolonged infection cycle, a relative lack of inflammatory response during viral replication, and downregulation of the interferon response. In addition, HPV infection rarely causes viremia. Infection is localized to the mucosal and cutaneous surfaces and away from the vascular and lymphatic systems where adaptive immune responses are initiated (11Stanley MA Immune responses to human papilloma viruses.Indian J Med Res. 2009; 130: 266-276PubMed Google Scholar,12Stanley MA Epithelial cell responses to infection with human papillomavirus.Clin Microbiol Rev. 2012; 25: 215-222Crossref PubMed Scopus (266) Google Scholar). Nevertheless, at least 80–90% of genital HPV infections clear spontaneously over time. Histologic analysis of regressing warts show a CD4+ T cell-dominated Th1 response. Resolution of the lesions depends on a successful cell-mediated immune response against early viral proteins (12Stanley MA Epithelial cell responses to infection with human papillomavirus.Clin Microbiol Rev. 2012; 25: 215-222Crossref PubMed Scopus (266) Google Scholar,13de Jong A van der Burg SH Kwappenberg KM et al.Frequent detection of human papillomavirus 16 E2-specific T-helper immunity in healthy subjects.Cancer Res. 2002; 62: 472-479PubMed Google Scholar). Failure to develop effective cell mediated immunity (CMI) results in an inability of the host to clear or control the HPV infection, leading to persistent infection, and resulting in an increased probability of cancer. The importance of CMI was highlighted in a recent systematic review of population-based registry studies in HIV/AIDS and in transplant recipients. The investigators demonstrated a similar pattern of significantly increased incidence of all HPV-related cancers in both populations (14Grulich AE van Leeuwen MT Falster MO Vajdic CM Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: A meta-analysis.Lancet. 2007; 370: 59-67Abstract Full Text Full Text PDF PubMed Scopus (1724) Google Scholar). This suggests that immune deficiency likely plays the most important role in the increased risk of HPV-associated neoplasia. Among HIV-infected patients, the risk of HPV-associated cancers is increased in those with higher HIV viral load and is inversely related to CD4+ count (15Ahdieh L Munoz A Vlahov D Trimble CL Timpson LA Shah K Cervical neoplasia and repeated positivity of human papillomavirus infection in human immunodeficiency virus-seropositive and -seronegative women.Am J Epidemiol. 2000; 151: 1148-1157Crossref PubMed Scopus (113) Google Scholar, 16Palefsky JM Minkoff H Kalish LA et al.Cervicovaginal human papillomavirus infection in human immunodeficiency virus-1 (HIV)-positive and high-risk HIV-negative women.J Natl Cancer Inst. 1999; 91: 226-236Crossref PubMed Scopus (405) Google Scholar, 17Vernon SD Holmes KK Reeves WC Human papillomavirus infection and associated disease in persons infected with human immunodeficiency virus.Clin Infect Dis. 1995; 21: S121-S124Crossref PubMed Scopus (41) Google Scholar). Similarly, in a single-center review of renal transplant recipients over 40 years, T cell depleting induction with antithymocyte globulin was an independent risk factor for the development of anogenital cancer. This again suggests an association between the degree of immunosuppression and the probability of HPV-related malignancy (18Meeuwis KA Melchers WJ Bouten H et al.Anogenital malignancies in women after renal transplantation over 40 years in a single center.Transplantation. 2012; 93: 914-922Crossref PubMed Scopus (48) Google Scholar). As a result of impaired cell-mediated immunity, transplant recipients experience an increased frequency of extensive, sometimes treatment-refractory cutaneous and anogenital warts (19Euvrard S Kanitakis J Chardonnet Y et al.External anogenital lesions in organ transplant recipients. A clinicopathologic and virologic assessment.Arch Dermatol. 1997; 133: 175-178Crossref PubMed Google Scholar,20Euvrard S Kanitakis J Cochat P Cambazard F Claudy A Skin diseases in children with organ transplants.J Am Acad Dermatol. 2001; 44: 932-939Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar) and are at a higher risk for neoplastic transformation in cervical and anogenital HPV infections (21Paternoster DM Cester M Resente C et al.Human papilloma virus infection and cervical intraepithelial neoplasia in transplanted patients.Transplant Proc. 2008; 40: 1877-1880Crossref PubMed Scopus (55) Google Scholar,22Penn I Cancers of the anogenital region in renal transplant recipients. Analysis of 65 cases.Cancer. 1986; 58: 611-616Crossref PubMed Scopus (302) Google Scholar). HPV is associated with both benign and premalignant/malignant neoplasms in a variety of sites (Table 2).Table 2:Clinical manifestations of HPVLocalizationBenignPremalignant/MalignantSkinCutaneous wartsPotential role in squamous cell carcinoma of the skinAnogenitalAnogenital wartsCIN, cervical cancer, AIN, anal cancer, vulvar and penile carcinomaRespiratory tractRespiratory papillomatosisNo clearly established link to malignant respiratory neoplasmHead and neckNone establishedSquamous cell carcinoma of head and neck Open table in a new tab Cutaneous warts are skin lesions of characteristic appearance and include common warts, deep plantar and flat warts. The prevalence of warts in transplant patients corresponds with the duration of immunosuppressive therapy, increasing to 50–92% in patients who are more than 4–5 years after transplantation (23Dyall-Smith D Trowell H Dyall-Smith ML Benign human papillomavirus infection in renal transplant recipients.Int J Dermatol. 1991; 30: 785-789Crossref PubMed Scopus (50) Google Scholar). Ultraviolet light is also believed to be an important risk factor for the development of cutaneous warts in transplant recipients, as most lesions appear in sun-exposed areas (24Boyle J MacKie RM Briggs JD Junor BJ Aitchison TC Cancer, warts, and sunshine in renal transplant patients. A case-control study.Lancet. 1984; 1: 702-705Abstract PubMed Scopus (244) Google Scholar). Anogenital warts, also known as condyloma acuminata, are one of the most common sexually transmitted diseases worldwide. They are caused by low-risk HPV types, most commonly types 6 and 11. However, at least 18 other HPV types have been associated with anogenital warts, including types 16 and 18, which are more commonly associated with malignant lesions (25Gormley RH Kovarik CL Human papillomavirus-related genital disease in the immunocompromised host: Part II.J Am Acad Dermatol. 2012; 66 (17 e1, quiz 99–900.): 883Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar,26Wiley DJ Douglas J Beutner K et al.External genital warts: Diagnosis, treatment, and prevention.Clin Infect Dis. 2002; 35: S210-S224Crossref PubMed Scopus (289) Google Scholar). These exophytic, typically flesh- or gray-colored lesions are frequently multifocal, involving different parts of the anogenital tract simultaneously. In women, external anogenital warts are often associated with cervical lesions (27Moscicki AB Hills N Shiboski S et al.Risks for incident human papillomavirus infection and low-grade squamous intraepithelial lesion development in young females.JAMA. 2001; 285: 2995-3002Crossref PubMed Scopus (484) Google Scholar). Patients with anogenital warts, especially those who are immunosuppressed, are often also infected with high-risk HPV types. Therefore, immunosuppressed patients with anogenital warts will require monitoring and screening for HPV-mediated malignancies. A French study of organ transplant recipients reported a prevalence of anogenital warts of 1.8% (19Euvrard S Kanitakis J Chardonnet Y et al.External anogenital lesions in organ transplant recipients. A clinicopathologic and virologic assessment.Arch Dermatol. 1997; 133: 175-178Crossref PubMed Google Scholar). The oncogenic role of HPV infection has been most firmly established in the pathogenesis of CIN and cervical cancer. Persistent HPV infection, particularly with types 16 and 18, may lead to progressive deregulation of the replication of epithelial cells and potential malignant transformation (28Rodriguez AC Schiffman M Herrero R et al.Rapid clearance of human papillomavirus and implications for clinical focus on persistent infections.J Natl Cancer Inst. 2008; 100: 513-517Crossref PubMed Scopus (393) Google Scholar). HPV infection also causes AIN and anal cancer with similar high risk HPV-types as those implicated in cervical neoplasia (3Tilston P Anal human papillomavirus and anal cancer.J Clin Pathol. 1997; 50: 625-634Crossref PubMed Scopus (65) Google Scholar). An increasing number of studies have investigated the epidemiology of cervical and AIN among transplant recipients. In a Scottish study in the late 1980s, CIN and high-risk HPV types 16 and 18 were present more frequently in renal transplant recipients compared to age-matched controls (29Alloub MI Barr BB McLaren KM Smith IW Bunney MH Smart GE Human papillomavirus infection and cervical intraepithelial neoplasia in women with renal allografts.Br Med J. 1989; 298: 153-156Crossref PubMed Scopus (196) Google Scholar). In a more recent study from Italy, 7% of 151 transplant recipients were found to have CIN (21Paternoster DM Cester M Resente C et al.Human papilloma virus infection and cervical intraepithelial neoplasia in transplanted patients.Transplant Proc. 2008; 40: 1877-1880Crossref PubMed Scopus (55) Google Scholar). One of the largest reports to date is a retrospective Dutch single center study of 1023 women who underwent renal transplants between 1968 and 2008. Of these patients, a total of 16 anogential malignancies (1.6%) were noted, including six vulvar, five cervical and six anal carcinomas (18Meeuwis KA Melchers WJ Bouten H et al.Anogenital malignancies in women after renal transplantation over 40 years in a single center.Transplantation. 2012; 93: 914-922Crossref PubMed Scopus (48) Google Scholar). Investigators found detectable HPV in 22/24 malignant and precancer lesions, and 54.5% of these were HPV type 16. Using cancer registry data from the general Dutch population, the authors estimated that these kidney transplant patients had increased risks of 5-fold for cervical, 41-fold for vulvar and 122-fold for anal carcinoma. Another review of 453 women who received renal transplants from 1990 to 2008 in South Korea revealed an incidence of 58.1 cervical carcinomas per 100 000 patient-years, which was 3.5-fold higher than the general population (29Alloub MI Barr BB McLaren KM Smith IW Bunney MH Smart GE Human papillomavirus infection and cervical intraepithelial neoplasia in women with renal allografts.Br Med J. 1989; 298: 153-156Crossref PubMed Scopus (196) Google Scholar). There is also a high burden of HPV-associated anal precancer lesions among transplant recipients. Ogunbiyi et al. showed a high proportion of AIN in renal transplant recipients who presented for elective lower gastrointestinal or genitourinary surgeries compared to matched controls (20% vs. 1%; Ref. 30Ogunbiyi OA Scholefield JH Raftery AT et al.Prevalence of anal human papillomavirus infection and intraepithelial neoplasia in renal allograft recipients.Br J Surg. 1994; 81: 365-367Crossref PubMed Scopus (137) Google Scholar). Patel and others collected anal cytology and performed anal HPV polymerase chain reaction (PCR) in 108 renal transplant recipients (68 men and 40 women). They reported a 5.8% prevalence of AIN, with risk factors as follows: oncogenic HPV infection, duration of immunosuppression, a previous history of genital warts and receptive anal intercourse (31Patel HS Silver AR Levine T Williams G Northover JM Human papillomavirus infection and anal dysplasia in renal transplant recipients.Br J Surg. 2010; 97: 1716-1721Crossref PubMed Scopus (40) Google Scholar). Similar results were found in a systematic review of 32 000 transplant recipients from Danish, Finnish, Swedish, Canadian and Australian cohort studies. This study demonstrated a twofold increased risk of cervical cancer compared to the general population, and a nearly fivefold excess risk for anal cancer (14Grulich AE van Leeuwen MT Falster MO Vajdic CM Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: A meta-analysis.Lancet. 2007; 370: 59-67Abstract Full Text Full Text PDF PubMed Scopus (1724) Google Scholar). Particularly striking was the 22-fold excess risk of vulvar and vaginal cancers. Compared to the general population, carcinomas of the anogenital region occurred at an earlier average age (41 years) in transplant recipients and were frequently multifocal. Over 40% of transplant recipients with anogenital carcinomas reported a prior history of anogenital warts (32Penn I Post-transplant malignancy: The role of immunosuppression.Drug Saf. 2000; 23: 101-113Crossref PubMed Scopus (346) Google Scholar). SCC of the skin occur 65–250 times more frequently in transplant recipients than in the general population, and are often characterized by earlier age of onset, multiple lesions, a rapid course and more frequent node metastases than in the general population (33Euvrard S Kanitakis J Claudy A Skin cancers after organ transplantation.N Engl J Med. 2003; 348: 1681-1691Crossref PubMed Scopus (1323) Google Scholar). Using degenerate PCR, a high prevalence (65–81%) of a variety of HPV DNA types has also been consistently demonstrated in premalignant skin lesions and in skin cancers of transplant recipients (34Harwood CA Surentheran T McGregor JM et al.Human papillomavirus infection and non-melanoma skin cancer in immunosuppressed and immunocompetent individuals.J Med Virol. 2000; 61: 289-297Crossref PubMed Scopus (387) Google Scholar). Another study reported high-risk HPV in 46.2% of the SCC epithelium in renal transplant recipients compared to 23.5% in the immunocompetent control group (35Reuschenbach M Tran T Faulstich F et al.High-risk human papillomavirus in non-melanoma skin lesions from renal allograft recipients and immunocompetent patients.Br J Cancer. 2011; 104: 1334-1341Crossref PubMed Scopus (46) Google Scholar). HPV was highly prevalent (>94%) in DNA analysis of eyebrow hairs in renal transplant patients, both with SCC and without SCC, although the presence of HPV DNA and the corresponding antibodies for the same HPV type was associated with increased risk of SCC (36Proby CM Harwood CA Neale RE et al.A case-control study of betapapillomavirus infection and cutaneous squamous cell carcinoma in organ transplant recipients.Am J Transplant. 2011; 11: 1498-1508Abstract Full Text Full Text PDF PubMed Scopus (104) Google Scholar). While the results of these studies are intriguing, it is not clear to what extent HPV contributes to the development of skin cancer among transplant recipients (37Ho WL Murphy GM Update on the pathogenesis of post-transplant skin cancer in renal transplant recipients.Br J Dermatol. 2008; 158: 217-224Crossref PubMed Scopus (73) Google Scholar). Interestingly, sirolimus, an immunosuppressant with antineoplastic and antiviral properties, may have a protective effect against skin cancers compared to other immunosuppressive agents. A cohort of 1000 renal transplant recipients on sirolimus regimens had a similar incidence of skin cancers compared with the general population (38Kahan BD Knight R Schoenberg L et al.Ten years of sirolimus therapy for human renal transplantation: The University of Texas at Houston experience.Transplant Proc. 2003; 35: 25S-34SCrossref PubMed Scopus (85) Google Scholar). However, HPV infection was not examined in this cohort, and the potential benefit of the antiviral effect of sirolimus in this setting remains speculative. There is increasing evidence that HPV is implicated in the pathogenesis of some head and neck cancers. This is especially seen in neoplasms arising from the base of the tongue and tonsillar region, and is not typically associated with smoking or alcohol consumption as seen in other head and neck cancers. D’Souza et al. (39D’Souza G Kreimer AR Viscidi R et al.Case-control study of human papillomavirus and oropharyngeal cancer.N Engl J Med. 2007; 356: 1944-1956Crossref PubMed Scopus (2108) Google Scholar) conducted a case-control study and showed that seropositivity for HPV-16 (odds ratio 32.2) and the presence of an HPV oral infection (odds ratio 14.6) had strong associations with oropharyngeal cancer. Of note, HPV-associated head and neck cancer appears to have a better prognosis compared to those not associated with HPV (40Ang KK Harris J Wheeler R et al.Human papillomavirus and survival of patients with oropharyngeal cancer.N Engl J Med. 2010; 363: 24-35Crossref PubMed Scopus (4807) Google Scholar). HPV infection in the oral cavity is not rare. One large cross sectional study (41Gillison ML Broutian T Pickard RK et al.Prevalence of oral HPV infection in the United States, 2009–2010.JAMA. 2012; 307: 693-703Crossref PubMed Scopus (826) Google Scholar) showed a prevalence of oral HPV infection in the general population in the United States of 6.9%, with more men than women infected (10.1% vs. 3.6%). There are no published studies that explicitly investigate the association between oral HPV infection and head and neck cancer in transplant recipients. However, the prevalence of oral HPV infection is known to be higher in renal transplant recipients compared to immunocompetent patients (42Rose B Wilkins D Li W et al.Human papillomavirus in the oral cavity of patients with and without renal transplantation.Transplantation. 2006; 82: 570-573Crossref PubMed Scopus (31) Google Scholar). In one systematic review, transplant recipients were found to have a threefold excess risk of oropharyngeal cancer (14Grulich AE van Leeuwen MT Falster MO Vajdic CM Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: A meta-analysis.Lancet. 2007; 370: 59-67Abstract Full Text Full Text PDF PubMed Scopus (1724) Google Scholar). It is likely that the increased rate of head and neck cancer is partly attributable to more persistent HPV infection in transplant recipients. Further studies are needed to clarify this relationship. HPV can also cause a benign upper airway neoplasm called recurrent respiratory papillomatosis. The most frequently affected population is young children. Babies acquire HPV (typically HPV types 6 and 11) through contact with infected secretions in the birth canal. Lesions can also be adult-onset, occurring as a sequelae of HPV infection acquired sexually (43Tasca RA Clarke RW Recurrent respiratory papillomatosis.Arch Dis Child. 2006; 91: 689-691Crossref PubMed Scopus (50) Google Scholar). It has been proposed that there is a relationship between HPV and SCC or adenocarcinomas of the lungs. However, studies are conflicting (44Klein F Amin Kotb WF Petersen I Incidence of human papilloma virus in lung cancer.Lung Cancer. 2009; 65: 13-18Abstract Full Text Full Text PDF PubMed Scopus (123) Google Scholar,45Koshiol J Rotunno M Gillison ML et al.Assessment of human papillomavirus in lung tumor tissue.J Natl Cancer Inst. 2011; 103: 501-507Crossref PubMed Scopus (79) Google Scholar). Whether there is a more substantial role of HPV in the pathogenesis of pulmonary neoplasms among transplant recipients remains to be determined. A thorough clinical inspection of the entire genital tract is sufficient to diagnose most external anogenital warts. Bright light and magnification with a hand lens or colposcope may assist in the diagnosis (Figure 1). All women with external anogenital warts must have a speculum examination for possible vaginal and cervical lesions. For men and women with recurrent perianal warts and/or a history of receptive anal intercourse, evaluation for intra-anal warts is recommended (46von Krogh G Lacey CJ Gross G Barrasso R Schneider A European guideline for the management of anogenital warts.Int J STD AIDS. 2001; 12: 40-47Crossref PubMed Scopus (54) Google Scholar). If urinary symptoms are prominent, the distal urethra and meatus should be visually examined and a referral for urethroscopy should be considered. Providers should have a low threshold to biopsy any genital warts that have an atypical appearance. This is because high-grade squamous epithelial neoplastic lesions are common and may be clinically indistinguishable from genital warts among immunocompromised patients (47Sillman FH Sentovich S Shaffer D Ano-genital neoplasia in renal transplant patients.Ann Transplant. 1997; 2: 59-66PubMed Google Scholar). Using dilute (3–5%) acetic acid solutions (i.e. “acetowhite test”) may be of help in delineating the extent of disease before biopsy; however, routine use of the test for screening individuals for HPV infection is not recommended due to poor sensitivity and specificity (32Penn I Post-transplant malignancy: The role of immunosuppression.Drug Saf. 2000; 23: 101-113Crossref PubMed Scopus (346) Google Scholar) in predicting active disease. Patients with anogenital warts and their sex partners should be screened for other sexually transmitted diseases including gonorrhea, chlamydia, syphilis, trichomonas, hepatitis B virus infection and HIV infection (48Workowski KA Berman S Sexually transmitted diseases treatment guidelines, 2010.MMWR Recomm Rep. 2010; 59: 1-110PubMed Google Scholar). The Papanicolau (Pap) smear is the backbone of the screening strategy for early diagnosis of HPV-related cervical atypia and cancer. The implementation of regular Pap tests has reduced the rate of invasive cervical cancer by approximately 70% since the 1950s. Molecular diagnostic methods to detect HPV have become more widely available in the last few years. These methods include in situ hybridization on cell smears or histological sections, DNA hybrid capture and PCR on clinical specimens. A high viral load of HPV 16 has been shown to be associated with development of carcinoma in situ (49Josefsson AM Magnusson PK Ylitalo N et al.Viral load of human papilloma virus 16 as a determinant for development of cervical carcinoma in situ: A nested case-control study.Lancet. 2000; 355: 2189-2193Abstract Full Text Full Text PDF PubMed Scopus (328) Google Scholar,50Ylitalo N Sorensen P Josefsson AM et al.Consistent high viral load of human papillomavirus 16 and risk of cervical carcinoma in situ: A nested case-control study.Lancet. 2000; 355: 2194-2198Abstract Full Text Full Text PDF PubMed Scopus (293) Google Scholar). There are now multiple FDA-approved tests to detect high-risk HPV DNA. See Table 3 for recommendations for HPV co-testing in immunocompetent and the immuncompromised women. Detection and typing of HPV have no proven benefit in the diagnosis and management of anogenital warts and is therefore not recommended (50Ylitalo N Sorensen P Josefsson AM et al.Consistent high viral load of human papillomavirus 16 and risk of cervical carcinoma in situ: A nested case-control study.Lancet. 2000; 355: 2194-2198Abstract Full Text Full Text PDF PubMed Scopus (293) Google Scholar). When the diagnosis is in doubt, consider referral to a practitioner experienced in the diagnosis of anogenital warts. See below for the incorporation of molecular methods in screening.Table 3:Guidelines for cervical cancer screening for different populationsImmunocompetent womenUS PreventiveAmerican College ofAmerican CancerServices TaskObstetricians andHIV positiveSolid organSociety (52Saslow D Solomon D Lawson HW et al.American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer.CA Cancer J Clin. 2012; 62: 147-172Crossref PubMed Scopus (953) Google Scholar)Forces (53Moyer VA Screening for cervical cancer: U.S. Preventive Services Task Force recommendation statement.Ann Intern Med. 2012; 156 (W312.): 880-891Crossref PubMed Scopus (761) Google Scholar)Gynecologists (54Screening for cervical cancer.Obstet Gynecol. 2012; 120: 1222-1238Crossref PubMed Google Scholar)women (55Kaplan JE Benson C Holmes KH Brooks JT Pau A Masur H Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: Recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America.MMWR Recomm Rep. 2009; 58 (quiz CE1–4.): 1-207Google Scholar)transplant recip" @default.
• W1505068903 created "2016-06-24" @default.
• W1505068903 creator A5039296570 @default.
• W1505068903 creator A5066236820 @default.
• W1505068903 date "2013-03-01" @default.
• W1505068903 modified "2023-09-27" @default.
• W1505068903 title "Human Papillomavirus in Solid Organ Transplantation" @default.
• W1505068903 cites W1508101372 @default.
• W1505068903 cites W1521484533 @default.
• W1505068903 cites W1571240917 @default.
• W1505068903 cites W1836464928 @default.
• W1505068903 cites W1965416300 @default.
• W1505068903 cites W1966171384 @default.
• W1505068903 cites W1968370860 @default.
• W1505068903 cites W1972517554 @default.
• W1505068903 cites W1972549270 @default.
• W1505068903 cites W1978092173 @default.
• W1505068903 cites W1986673775 @default.
• W1505068903 cites W1989473625 @default.
• W1505068903 cites W1990736061 @default.
• W1505068903 cites W1991658798 @default.
• W1505068903 cites W2000282244 @default.
• W1505068903 cites W2000476016 @default.
• W1505068903 cites W2004098973 @default.
• W1505068903 cites W2009914893 @default.
• W1505068903 cites W2013606441 @default.
• W1505068903 cites W2014132336 @default.
• W1505068903 cites W2014252872 @default.
• W1505068903 cites W2014968338 @default.
• W1505068903 cites W2025019929 @default.
• W1505068903 cites W2026996973 @default.
• W1505068903 cites W2029671223 @default.
• W1505068903 cites W2030613580 @default.
• W1505068903 cites W2031782896 @default.
• W1505068903 cites W2042166143 @default.
• W1505068903 cites W2045849258 @default.
• W1505068903 cites W2048473430 @default.
• W1505068903 cites W2051560054 @default.
• W1505068903 cites W2053197313 @default.
• W1505068903 cites W2060068145 @default.
• W1505068903 cites W2064378910 @default.
• W1505068903 cites W2066707055 @default.
• W1505068903 cites W2077351947 @default.
• W1505068903 cites W2081047239 @default.
• W1505068903 cites W2083611746 @default.
• W1505068903 cites W2088909920 @default.
• W1505068903 cites W2089150671 @default.
• W1505068903 cites W2092094752 @default.
• W1505068903 cites W2093901599 @default.
• W1505068903 cites W2094510719 @default.
• W1505068903 cites W2097555726 @default.
• W1505068903 cites W2101196984 @default.
• W1505068903 cites W2103959246 @default.
• W1505068903 cites W2105348246 @default.
• W1505068903 cites W2106677962 @default.
• W1505068903 cites W2110664940 @default.
• W1505068903 cites W2110888002 @default.
• W1505068903 cites W2111636713 @default.
• W1505068903 cites W2114986710 @default.
• W1505068903 cites W2123299572 @default.
• W1505068903 cites W2125223938 @default.
• W1505068903 cites W2126246455 @default.
• W1505068903 cites W2127043059 @default.
• W1505068903 cites W2130505310 @default.
• W1505068903 cites W2132185636 @default.
• W1505068903 cites W2132640627 @default.
• W1505068903 cites W2133408276 @default.
• W1505068903 cites W2136103754 @default.
• W1505068903 cites W2136171269 @default.
• W1505068903 cites W2136236728 @default.
• W1505068903 cites W2138469341 @default.
• W1505068903 cites W2139736159 @default.
• W1505068903 cites W2141274038 @default.
• W1505068903 cites W2147519428 @default.
• W1505068903 cites W2148422519 @default.
• W1505068903 cites W2148643959 @default.
• W1505068903 cites W2148933413 @default.
• W1505068903 cites W2149179336 @default.
• W1505068903 cites W2153979400 @default.
• W1505068903 cites W2158872827 @default.
• W1505068903 cites W2169767104 @default.
• W1505068903 cites W2174023915 @default.
• W1505068903 cites W2174935414 @default.
• W1505068903 cites W4213084120 @default.
• W1505068903 cites W4232170885 @default.
• W1505068903 cites W4232841342 @default.
• W1505068903 cites W4234566842 @default.
• W1505068903 cites W4247724132 @default.
• W1505068903 cites W4302312636 @default.
• W1505068903 doi "https://doi.org/10.1111/ajt.12142" @default.
• W1505068903 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23465011" @default.
• W1505068903 hasPublicationYear "2013" @default.
• W1505068903 type Work @default.
• W1505068903 sameAs 1505068903 @default.
• W1505068903 citedByCount "23" @default.
• W1505068903 countsByYear W15050689032013 @default.
• W1505068903 countsByYear W15050689032015 @default.
• W1505068903 countsByYear W15050689032016 @default.

• next