Condyloma Acuminatum in Rochester, Minn, 1950-1978

Chuang, Tsu‐Yi

doi:10.1001/archderm.1984.01650400051012

Cited by 126 publications

(7 citation statements)

References 13 publications

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“…In a study from Rochester, Minnesota, the number of cases diagnosed increased each year from 1950 to 1975, with an annual incidence from 1975 through 1978 of 106.5 cases per 100 000 population [12]. British investigators reported an increase in men from 39.8 to 66.9 cases and in women from 20.3 to 34.6 per 100 000 population between 1971 and 1978 [13].…”

Section: Epidemiology Of Genital Human Papillomavirus Infectionmentioning

confidence: 99%

“…British investigators reported an increase in men from 39.8 to 66.9 cases and in women from 20.3 to 34.6 per 100 000 population between 1971 and 1978 [13]. The peak ages of occurrence range from 15 to 29 years [12][13][14]. Factors associated with an increased incidence of genital warts include exposure to multiple sexual partners and younger age at onset of sexual activity [12][13][14].…”

Section: Epidemiology Of Genital Human Papillomavirus Infectionmentioning

confidence: 99%

“…The peak ages of occurrence range from 15 to 29 years [12][13][14]. Factors associated with an increased incidence of genital warts include exposure to multiple sexual partners and younger age at onset of sexual activity [12][13][14]. The infectivity rate of the virus is approximately 65% following an incubation period ranging from 3weeks to 8 months with a mean of 3 months after contact with an infected partner [15].…”

Section: Epidemiology Of Genital Human Papillomavirus Infectionmentioning

confidence: 99%

“…Multiple sexual partners and onset of sexual activity at an early age are associated with an increased incidence of both HPV infection and CIN [19]. The mean age for women who have cervical or genital HPV infection is 19 years [12][13][14]. The mean age for women who have classical CIN is 30.8 years [35].…”

Section: Natural History and Sequelae: Cervical Carcinomamentioning

confidence: 99%

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Cervical carcinoma as a sexually transmitted disease: human papillomavirus and its possible etiologic role

Benson

1987

Adv Contracept

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Historical perspectiveBeginning in the late 15th century, genital warts, and in fact many unexplained genital lesions, were attributed to an outbreak of syphilis occurring in Europe during the time [1]. Gonorrhea was later proposed as an etiology of genital warts. It was not until the discovery of the gonococcus in 1879 that this was refuted. The then new theory proposed that warts resulted from genital irritation caused by secretions 'disordered through venery', and led to the coining of the term venereal warts [1]. The viral etiology of skin warts was recognized in 1949 and it was not until 20 years later that viral particles were demonstrated microscopically in genital and anal warts [1].Rubin, in 1910, while examining histologic specimens from patients, noted abnormal cellular morphologic changes in clinically normal appearing tissue [2]. He proposed the concept that not only tissue invasion but also intrinsic cellular morphology could be determinants of neoplastic transformation [2]. The significance of lesions that were not invasive but were morphologically abnormal was hotly debated over the ensuing two decades until the concept of carcinoma in situ was introduced by Broder in 1932 [3]. The perfection and widespread use of the Papanicolao u (Pap) smear established the importance of these early lesions on a mass scale. Structure and biology of human papillomavirusHuman papillomavirus (HPV), the etiologic agent of genital warts, is a nonenveloped DNA virus with an icosahedral capsid of 50-55 n in diameter containing 72 capsomeres [4]. The HPV genome exists in three forms within virions and infected cells: (1) a covalenfly closed circular supercoiled form; (2) an open circular form; and (3) a linear form [4]. All forms may exist as non-integrated plasmids in both benign and malignant lesions although DNA hybridization studies have also demonstrated integrated HPV genome within host cell nuclei. 103 Advances in Contraception. ISSN 0267-4874.

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Section: Epidemiology Of Genital Human Papillomavirus Infectionmentioning

confidence: 99%

Section: Epidemiology Of Genital Human Papillomavirus Infectionmentioning

confidence: 99%

Section: Epidemiology Of Genital Human Papillomavirus Infectionmentioning

confidence: 99%

Section: Natural History and Sequelae: Cervical Carcinomamentioning

confidence: 99%

See 2 more Smart Citations

Cervical carcinoma as a sexually transmitted disease: human papillomavirus and its possible etiologic role

Benson

1987

Adv Contracept

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“…Antagonism between HPV types was first suggested by Evans et al (1992) , who found decreased risk of development of cervical squamous intraepithelial lesions in women with anogenital wart history. Although early case-control studies reported that women with condyloma have an increased risk of cervical cancer (Chuang et al , 1984 ), a cohort study of women with condylomas found no evidence of excess cervical cancer risk, despite shared sexual risk factors (Sigurgeirsson et al , 1991 ). Also, it has been reported that there is little excess cervical cancer risk among HPV-16 seropositive women in populations with a high prevalence of sexually transmitted disease (STD), but there are highly elevated risks in populations with low STD prevalence (Dillner et al , 1997 ).…”

Section: Introductionmentioning

confidence: 99%

Serological evidence for protection by human papillomavirus (HPV) type 6 infection against HPV type 16 cervical carcinogenesis

Silins

Wang

Lundqvist

et al. 1999

Journal of General Virology

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New Concepts of Condyloma Acuminata in Children

Bender¹

1986

Arch Dermatol

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Dermatologists and pediatricians are experiencing an epidemic of condyloma acuminata in both adults and children.1-4 The presentation of a child with anogenital wart disease raises many issues and all too often, great anxiety. Not only does the clinician face the often difficult task of treating these recalcitrant warts, but the issue of sexual child abuse must be seriously considered. Dermatologists are often consulted as experts by legal authorities regarding the possibility of sexual child abuse and, unfortunately, accurate, reliable information regarding human papillomavirus (HPV) biology in the pediatric age group has been lacking. This confusion and ignorance may impede the appropriate investigation of a family by police, legal, and psychology/ social work professionals. Though the physician is often motivated to report a case of suspected sexual child abuse, there may be a reluctance to do so because of the erroneous belief that a large percentage of anogenital warts in children are transmitted by nonvenereal routes. Misconceptions exist regarding the epidemiology of anogenital warts in adults, See also p 1129. and very little information has been gathered to date regarding this problem in children. Therefore, the dermatologist often "hedges" when answering the queries of police, lawyers, psychologists, social work¬ ers, and the courts. In my own experience, this can result in the reluctance of the courts to make certain critical decisions regarding the child in question, because the suspicion of sexual abuse cannot be "proven." More clinicians are becoming aware of the associ¬ ation between certain HPV types and genital neopla-

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Condyloma Acuminatum in Rochester, Minn, 1950-1978

Cited by 126 publications

References 13 publications

Cervical carcinoma as a sexually transmitted disease: human papillomavirus and its possible etiologic role

Cervical carcinoma as a sexually transmitted disease: human papillomavirus and its possible etiologic role

Serological evidence for protection by human papillomavirus (HPV) type 6 infection against HPV type 16 cervical carcinogenesis

New Concepts of Condyloma Acuminata in Children

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