Updating the natural history of hpv and anogenital cancer

10-Jun-2017 17:01

The suggested nomenclature for precancerous squamous lesions in the anogenital tract has shifted from intraepithelial neoplasia (IN terminology, graded 1, 2, or 3) to intraepithelial lesions (graded as low or high grade).[44] In this LAST high-grade squamous intraepithelial lesions (HSIL) include those formerly called cervical intraepithelial neoplasia CIN 3 and those called CIN 2 that have p16, an immunohistochemical marker of disease.Precancerous cervical lesions include HSIL and adenocarcinoma in situ (AIS).In most patients, treatment results in resolution of the wart(s).Untreated, anogenital warts can resolve spontaneously, remain unchanged, or increase in size or number.Screening is not recommended for other HPV-associated cancers, although some specialized clinics conduct anoscopy to identify precancerous anal lesions in men who have sex with men.[37] Anogenital warts are usually diagnosed by visual inspection, although biopsy may be helpful in some cases.

Pap testing is recommended every 3 years from 21–29 years of age.

For cervical biopsy results of low-grade squamous intraepithelial lesions (LSIL, also called CIN1), the preferred management may be to follow-up with repeat cytology to detect persistence or progression of the lesion.

For HSIL or AIS, there are several treatment options including removal of the area of abnormality (via laser, loop electrosurgical excisional procedure [LEEP], or cold knife conization) or destruction of the area of abnormality (via cryotherapy or laser vaporization).[46] Each approach has its indications, advantages, and disadvantages, but, importantly, cure rates are comparable.

Julia Gargano, Ph D; Elissa Meites, MD, MPH; Meg Watson, MPH; Elizabeth Unger, MD, Ph D; Lauri Markowitz, MD Genital human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.[1,2] An estimated 14 million persons newly infected every year, resulting in approximately estimated

Pap testing is recommended every 3 years from 21–29 years of age.

For cervical biopsy results of low-grade squamous intraepithelial lesions (LSIL, also called CIN1), the preferred management may be to follow-up with repeat cytology to detect persistence or progression of the lesion.

For HSIL or AIS, there are several treatment options including removal of the area of abnormality (via laser, loop electrosurgical excisional procedure [LEEP], or cold knife conization) or destruction of the area of abnormality (via cryotherapy or laser vaporization).[46] Each approach has its indications, advantages, and disadvantages, but, importantly, cure rates are comparable.

Julia Gargano, Ph D; Elissa Meites, MD, MPH; Meg Watson, MPH; Elizabeth Unger, MD, Ph D; Lauri Markowitz, MD Genital human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.[1,2] An estimated 14 million persons newly infected every year, resulting in approximately estimated $1.7 billion (estimates range from $800 million to $2.9 billion) in direct medical costs.[3] Although the vast majority of HPV infections cause no symptoms and are self-limited, persistent HPV infection can cause cervical cancer in women as well as other anogenital cancers, oropharyngeal cancer, and genital warts in men and women.[1] More than 200 HPV types have been identified, including approximately 40 that preferentially infect the genital mucosa.[4–6] Genital HPV types are categorized according to their epidemiologic association with cancer.[7] High-risk types (e.g., types 16 and 18) can cause low-grade cervical cell abnormalities, high-grade cervical cell abnormalities that are precursors to cancer, and cancers.[7–9] Nearly all cervical cancers are attributable to high-risk HPV types,[10] and approximately 70% of cervical cancer cases worldwide are caused by types 16 and 18.[11] HPV 16 infection is also responsible for most cases of other anogenital cancers, such as cancers of the vulva, vagina, penis, and anus, as well as cancers arising in some oropharynx subsites.[7] According to the International Agency for Research on Cancer (IARC), ten additional HPV types (31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) have sufficient evidence of carcinogenicity in humans based on their association with cervical cancer, and several types are classified as probably or possibly carcinogenic.[7] Other HPV types, including types 6 and 11, can cause genital warts, benign or low-grade cervical cell changes, and recurrent respiratory papillomatosis (RRP).[12] Among the cancer-related outcomes of HPV infection, invasive cervical cancer has been considered the most important worldwide, with over 500,000 new cases and 265,000 attributable deaths in 2012.[13] Though the vast majority of women with high-risk HPV infection do not develop cancer, persistent infection with high-risk HPV types is widely recognized as the primary causative factor for development of cervical cancer.[14–16] Most HPV infections are transient and asymptomatic, causing no symptoms.

More than 90% of new HPV infections, including those caused by high-risk HPV types, clear or become undetectable within 2 years, and clearance usually occurs in the first 6 months after infection.[16–18] Persistent infection with high-risk HPV is the most important risk factor for HPV-related diseases including cancer precursors and invasive cervical cancer.[16,18–21] Many aspects of the natural history of HPV are poorly understood, including the role and duration of naturally acquired immunity after HPV infection.

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Pap testing is recommended every 3 years from 21–29 years of age.For cervical biopsy results of low-grade squamous intraepithelial lesions (LSIL, also called CIN1), the preferred management may be to follow-up with repeat cytology to detect persistence or progression of the lesion.For HSIL or AIS, there are several treatment options including removal of the area of abnormality (via laser, loop electrosurgical excisional procedure [LEEP], or cold knife conization) or destruction of the area of abnormality (via cryotherapy or laser vaporization).[46] Each approach has its indications, advantages, and disadvantages, but, importantly, cure rates are comparable.Julia Gargano, Ph D; Elissa Meites, MD, MPH; Meg Watson, MPH; Elizabeth Unger, MD, Ph D; Lauri Markowitz, MD Genital human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.[1,2] An estimated 14 million persons newly infected every year, resulting in approximately estimated $1.7 billion (estimates range from $800 million to $2.9 billion) in direct medical costs.[3] Although the vast majority of HPV infections cause no symptoms and are self-limited, persistent HPV infection can cause cervical cancer in women as well as other anogenital cancers, oropharyngeal cancer, and genital warts in men and women.[1] More than 200 HPV types have been identified, including approximately 40 that preferentially infect the genital mucosa.[4–6] Genital HPV types are categorized according to their epidemiologic association with cancer.[7] High-risk types (e.g., types 16 and 18) can cause low-grade cervical cell abnormalities, high-grade cervical cell abnormalities that are precursors to cancer, and cancers.[7–9] Nearly all cervical cancers are attributable to high-risk HPV types,[10] and approximately 70% of cervical cancer cases worldwide are caused by types 16 and 18.[11] HPV 16 infection is also responsible for most cases of other anogenital cancers, such as cancers of the vulva, vagina, penis, and anus, as well as cancers arising in some oropharynx subsites.[7] According to the International Agency for Research on Cancer (IARC), ten additional HPV types (31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) have sufficient evidence of carcinogenicity in humans based on their association with cervical cancer, and several types are classified as probably or possibly carcinogenic.[7] Other HPV types, including types 6 and 11, can cause genital warts, benign or low-grade cervical cell changes, and recurrent respiratory papillomatosis (RRP).[12] Among the cancer-related outcomes of HPV infection, invasive cervical cancer has been considered the most important worldwide, with over 500,000 new cases and 265,000 attributable deaths in 2012.[13] Though the vast majority of women with high-risk HPV infection do not develop cancer, persistent infection with high-risk HPV types is widely recognized as the primary causative factor for development of cervical cancer.[14–16] Most HPV infections are transient and asymptomatic, causing no symptoms.More than 90% of new HPV infections, including those caused by high-risk HPV types, clear or become undetectable within 2 years, and clearance usually occurs in the first 6 months after infection.[16–18] Persistent infection with high-risk HPV is the most important risk factor for HPV-related diseases including cancer precursors and invasive cervical cancer.[16,18–21] Many aspects of the natural history of HPV are poorly understood, including the role and duration of naturally acquired immunity after HPV infection.

.7 billion (estimates range from 0 million to .9 billion) in direct medical costs.[3] Although the vast majority of HPV infections cause no symptoms and are self-limited, persistent HPV infection can cause cervical cancer in women as well as other anogenital cancers, oropharyngeal cancer, and genital warts in men and women.[1] More than 200 HPV types have been identified, including approximately 40 that preferentially infect the genital mucosa.[4–6] Genital HPV types are categorized according to their epidemiologic association with cancer.[7] High-risk types (e.g., types 16 and 18) can cause low-grade cervical cell abnormalities, high-grade cervical cell abnormalities that are precursors to cancer, and cancers.[7–9] Nearly all cervical cancers are attributable to high-risk HPV types,[10] and approximately 70% of cervical cancer cases worldwide are caused by types 16 and 18.[11] HPV 16 infection is also responsible for most cases of other anogenital cancers, such as cancers of the vulva, vagina, penis, and anus, as well as cancers arising in some oropharynx subsites.[7] According to the International Agency for Research on Cancer (IARC), ten additional HPV types (31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) have sufficient evidence of carcinogenicity in humans based on their association with cervical cancer, and several types are classified as probably or possibly carcinogenic.[7] Other HPV types, including types 6 and 11, can cause genital warts, benign or low-grade cervical cell changes, and recurrent respiratory papillomatosis (RRP).[12] Among the cancer-related outcomes of HPV infection, invasive cervical cancer has been considered the most important worldwide, with over 500,000 new cases and 265,000 attributable deaths in 2012.[13] Though the vast majority of women with high-risk HPV infection do not develop cancer, persistent infection with high-risk HPV types is widely recognized as the primary causative factor for development of cervical cancer.[14–16] Most HPV infections are transient and asymptomatic, causing no symptoms.

More than 90% of new HPV infections, including those caused by high-risk HPV types, clear or become undetectable within 2 years, and clearance usually occurs in the first 6 months after infection.[16–18] Persistent infection with high-risk HPV is the most important risk factor for HPV-related diseases including cancer precursors and invasive cervical cancer.[16,18–21] Many aspects of the natural history of HPV are poorly understood, including the role and duration of naturally acquired immunity after HPV infection.

Pap testing is recommended every 3 years from 21–29 years of age.For cervical biopsy results of low-grade squamous intraepithelial lesions (LSIL, also called CIN1), the preferred management may be to follow-up with repeat cytology to detect persistence or progression of the lesion.For HSIL or AIS, there are several treatment options including removal of the area of abnormality (via laser, loop electrosurgical excisional procedure [LEEP], or cold knife conization) or destruction of the area of abnormality (via cryotherapy or laser vaporization).[46] Each approach has its indications, advantages, and disadvantages, but, importantly, cure rates are comparable.Julia Gargano, Ph D; Elissa Meites, MD, MPH; Meg Watson, MPH; Elizabeth Unger, MD, Ph D; Lauri Markowitz, MD Genital human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.[1,2] An estimated 14 million persons newly infected every year, resulting in approximately estimated

Pap testing is recommended every 3 years from 21–29 years of age.

For cervical biopsy results of low-grade squamous intraepithelial lesions (LSIL, also called CIN1), the preferred management may be to follow-up with repeat cytology to detect persistence or progression of the lesion.

For HSIL or AIS, there are several treatment options including removal of the area of abnormality (via laser, loop electrosurgical excisional procedure [LEEP], or cold knife conization) or destruction of the area of abnormality (via cryotherapy or laser vaporization).[46] Each approach has its indications, advantages, and disadvantages, but, importantly, cure rates are comparable.

Julia Gargano, Ph D; Elissa Meites, MD, MPH; Meg Watson, MPH; Elizabeth Unger, MD, Ph D; Lauri Markowitz, MD Genital human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.[1,2] An estimated 14 million persons newly infected every year, resulting in approximately estimated $1.7 billion (estimates range from $800 million to $2.9 billion) in direct medical costs.[3] Although the vast majority of HPV infections cause no symptoms and are self-limited, persistent HPV infection can cause cervical cancer in women as well as other anogenital cancers, oropharyngeal cancer, and genital warts in men and women.[1] More than 200 HPV types have been identified, including approximately 40 that preferentially infect the genital mucosa.[4–6] Genital HPV types are categorized according to their epidemiologic association with cancer.[7] High-risk types (e.g., types 16 and 18) can cause low-grade cervical cell abnormalities, high-grade cervical cell abnormalities that are precursors to cancer, and cancers.[7–9] Nearly all cervical cancers are attributable to high-risk HPV types,[10] and approximately 70% of cervical cancer cases worldwide are caused by types 16 and 18.[11] HPV 16 infection is also responsible for most cases of other anogenital cancers, such as cancers of the vulva, vagina, penis, and anus, as well as cancers arising in some oropharynx subsites.[7] According to the International Agency for Research on Cancer (IARC), ten additional HPV types (31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) have sufficient evidence of carcinogenicity in humans based on their association with cervical cancer, and several types are classified as probably or possibly carcinogenic.[7] Other HPV types, including types 6 and 11, can cause genital warts, benign or low-grade cervical cell changes, and recurrent respiratory papillomatosis (RRP).[12] Among the cancer-related outcomes of HPV infection, invasive cervical cancer has been considered the most important worldwide, with over 500,000 new cases and 265,000 attributable deaths in 2012.[13] Though the vast majority of women with high-risk HPV infection do not develop cancer, persistent infection with high-risk HPV types is widely recognized as the primary causative factor for development of cervical cancer.[14–16] Most HPV infections are transient and asymptomatic, causing no symptoms.

More than 90% of new HPV infections, including those caused by high-risk HPV types, clear or become undetectable within 2 years, and clearance usually occurs in the first 6 months after infection.[16–18] Persistent infection with high-risk HPV is the most important risk factor for HPV-related diseases including cancer precursors and invasive cervical cancer.[16,18–21] Many aspects of the natural history of HPV are poorly understood, including the role and duration of naturally acquired immunity after HPV infection.

Cervical screening recommendations do not currently differ for unvaccinated women and those who have received HPV vaccination.

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Pap testing is recommended every 3 years from 21–29 years of age.For cervical biopsy results of low-grade squamous intraepithelial lesions (LSIL, also called CIN1), the preferred management may be to follow-up with repeat cytology to detect persistence or progression of the lesion.For HSIL or AIS, there are several treatment options including removal of the area of abnormality (via laser, loop electrosurgical excisional procedure [LEEP], or cold knife conization) or destruction of the area of abnormality (via cryotherapy or laser vaporization).[46] Each approach has its indications, advantages, and disadvantages, but, importantly, cure rates are comparable.Julia Gargano, Ph D; Elissa Meites, MD, MPH; Meg Watson, MPH; Elizabeth Unger, MD, Ph D; Lauri Markowitz, MD Genital human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.[1,2] An estimated 14 million persons newly infected every year, resulting in approximately estimated $1.7 billion (estimates range from $800 million to $2.9 billion) in direct medical costs.[3] Although the vast majority of HPV infections cause no symptoms and are self-limited, persistent HPV infection can cause cervical cancer in women as well as other anogenital cancers, oropharyngeal cancer, and genital warts in men and women.[1] More than 200 HPV types have been identified, including approximately 40 that preferentially infect the genital mucosa.[4–6] Genital HPV types are categorized according to their epidemiologic association with cancer.[7] High-risk types (e.g., types 16 and 18) can cause low-grade cervical cell abnormalities, high-grade cervical cell abnormalities that are precursors to cancer, and cancers.[7–9] Nearly all cervical cancers are attributable to high-risk HPV types,[10] and approximately 70% of cervical cancer cases worldwide are caused by types 16 and 18.[11] HPV 16 infection is also responsible for most cases of other anogenital cancers, such as cancers of the vulva, vagina, penis, and anus, as well as cancers arising in some oropharynx subsites.[7] According to the International Agency for Research on Cancer (IARC), ten additional HPV types (31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) have sufficient evidence of carcinogenicity in humans based on their association with cervical cancer, and several types are classified as probably or possibly carcinogenic.[7] Other HPV types, including types 6 and 11, can cause genital warts, benign or low-grade cervical cell changes, and recurrent respiratory papillomatosis (RRP).[12] Among the cancer-related outcomes of HPV infection, invasive cervical cancer has been considered the most important worldwide, with over 500,000 new cases and 265,000 attributable deaths in 2012.[13] Though the vast majority of women with high-risk HPV infection do not develop cancer, persistent infection with high-risk HPV types is widely recognized as the primary causative factor for development of cervical cancer.[14–16] Most HPV infections are transient and asymptomatic, causing no symptoms.More than 90% of new HPV infections, including those caused by high-risk HPV types, clear or become undetectable within 2 years, and clearance usually occurs in the first 6 months after infection.[16–18] Persistent infection with high-risk HPV is the most important risk factor for HPV-related diseases including cancer precursors and invasive cervical cancer.[16,18–21] Many aspects of the natural history of HPV are poorly understood, including the role and duration of naturally acquired immunity after HPV infection.Cervical screening recommendations do not currently differ for unvaccinated women and those who have received HPV vaccination.

.7 billion (estimates range from 0 million to .9 billion) in direct medical costs.[3] Although the vast majority of HPV infections cause no symptoms and are self-limited, persistent HPV infection can cause cervical cancer in women as well as other anogenital cancers, oropharyngeal cancer, and genital warts in men and women.[1] More than 200 HPV types have been identified, including approximately 40 that preferentially infect the genital mucosa.[4–6] Genital HPV types are categorized according to their epidemiologic association with cancer.[7] High-risk types (e.g., types 16 and 18) can cause low-grade cervical cell abnormalities, high-grade cervical cell abnormalities that are precursors to cancer, and cancers.[7–9] Nearly all cervical cancers are attributable to high-risk HPV types,[10] and approximately 70% of cervical cancer cases worldwide are caused by types 16 and 18.[11] HPV 16 infection is also responsible for most cases of other anogenital cancers, such as cancers of the vulva, vagina, penis, and anus, as well as cancers arising in some oropharynx subsites.[7] According to the International Agency for Research on Cancer (IARC), ten additional HPV types (31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) have sufficient evidence of carcinogenicity in humans based on their association with cervical cancer, and several types are classified as probably or possibly carcinogenic.[7] Other HPV types, including types 6 and 11, can cause genital warts, benign or low-grade cervical cell changes, and recurrent respiratory papillomatosis (RRP).[12] Among the cancer-related outcomes of HPV infection, invasive cervical cancer has been considered the most important worldwide, with over 500,000 new cases and 265,000 attributable deaths in 2012.[13] Though the vast majority of women with high-risk HPV infection do not develop cancer, persistent infection with high-risk HPV types is widely recognized as the primary causative factor for development of cervical cancer.[14–16] Most HPV infections are transient and asymptomatic, causing no symptoms.More than 90% of new HPV infections, including those caused by high-risk HPV types, clear or become undetectable within 2 years, and clearance usually occurs in the first 6 months after infection.[16–18] Persistent infection with high-risk HPV is the most important risk factor for HPV-related diseases including cancer precursors and invasive cervical cancer.[16,18–21] Many aspects of the natural history of HPV are poorly understood, including the role and duration of naturally acquired immunity after HPV infection.Cervical screening recommendations do not currently differ for unvaccinated women and those who have received HPV vaccination.