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8/3/2019 Gua 2006 Seguimiento mujeres con lesiones cervicales por VPH
1/17Copyright @ 2007 American Society for Colposcopy and Cervical Pathology. Unauthorized reproduction of this article is prohibited.
2006 Consensus Guidelines for the
Management of Women With
Cervical Intraepithelial Neoplasiaor Adenocarcinoma In Situ
Thomas C. Wright Jr., MD,1 L. Stewart Massad, MD,2 Charles J. Dunton, MD,3
Mark Spitzer, MD,4 Edward J. Wilkinson, MD,5 Diane Solomon, MD;6
for the 2006 American Society for Colposcopy and
Cervical PathologyYsponsored Consensus Conference1Department of Pathology, College of Physicians and Surgeons of Columbia University,New York, NY, 2Department of Obstetrics and Gynecology, Washington University School
of Medicine, St Louis, MO, 3Department of Obstetrics and Gynecology, Lankenau Hospital,Wynnewood, PA, 4Department of Obstetrics and Gynecology, Brookdale University Hospitaland Medical Center, Brooklyn, NY, 5Department of Pathology, University of Florida College
of Medicine, Gainesville, FL, and6National Institutes of Health and National Cancer Institute,Bethesda, MD
h Abstract
Objective. To provide updated consensus guidelinesfor the management of women with cervical intraepithe-lial neoplasia (CIN) or adenocarcinoma in situ (AIS).
Participants. A group of 146 experts including repre-sentatives from 29 professional organizations, federalagencies, and national and international health organiza-tions met on September 18Y19, 2006, in Bethesda, MD, todevelop the guidelines.
Major Changes in the Guidelines. The management ofwomen with CIN grade 1 (CIN 1) has been modifiedsignificantly. In the earlier guidelines, managementdepended on whether the colposcopic examination wassatisfactory and treatment using ablative or excisionalmethods was acceptable for women with CIN 1. In the
new guidelines, cytological follow-up is the only recom-mended management option, regardless of whether thecolposcopic examination is satisfactory, for women withCIN 1 who have a low-grade referral cervical cytology.Treatment of CIN 1 is particularly discouraged in adoles-cents. The basic management of women in the generalpopulation with CIN 2,3 underwent only minor modifica-tions, but options for the conservative management ofadolescents with CIN 2,3 have been expanded. Moreover,management recommendations for women with biopsy-confirmed AIS are now included.
Conclusion. Updated evidenced-based guidelineshave been developed for the management of womenwith CIN or AIS. These guidelines reflect recent changes inour understanding of human papillomavirusYassociateddiseases of the cervix and the potential impact oftreatment on future pregnancies. h
Key Words: cervical intraepithelial neoplasia, treatment,
loop electrosurgical excision procedure, cryotherapy, adeno-
carcinomas in situ of the cervix
Cervical cancer, once one of the leading causes ofcancer death in women in the United States, is nowrelatively uncommon. This decline is frequently attrib-
uted to cervical cancer screening programs, but the
appropriate management of women with cervical
Reprint requests to: Thomas C. Wright Jr., MD, Room 16-404 P&S Bldg,
630 W 168th St, New York, NY 10032. E-mail: [email protected]
These evidenced-based Consensus Guidelines reflect recent changes in
our understanding of how to manage women with cervical intraepithelial
neoplasia and adenocarcinoma in situ of the cervix.
These guidelines were developed with funding from the American
Society for Colposcopy and Cervical Pathology and the National Cancer
Institute. Its contents are solely the responsibility of the authors and the
American Society for Colposcopy and Cervical Pathology and do not
necessarily represent the official views of the National Cancer Institute.
2007, American Society for Colposcopy and Cervical Pathology
Journal of Lower Genital Tract Disease, Volume 11, Number 4, 2007, 223Y239
8/3/2019 Gua 2006 Seguimiento mujeres con lesiones cervicales por VPH
2/17Copyright @ 2007 American Society for Colposcopy and Cervical Pathology. Unauthorized reproduction of this article is prohibited.
intraepithelial neoplasia (CIN) is as critical a component
of cervical cancer prevention programs as screening and
managing abnormal screening test results. Cervical
intraepithelial neoplasia is a relatively common pro-
blem, especially in women of reproductive age. Labora-tory surveys from the mid-1990s from the College of
American Pathologists suggest that more than 1 million
women are diagnosed each year with low-grade cervical
intraepithelial lesions, referred to as CIN grade 1 (CIN
1), and that approximately 500,000 are diagnosed with
high-grade cervical cancer precursor lesions, referred to
as CIN 2,3 [1]. Since the mid-1990s, the rate of
abnormal cervical cytology has increased in the United
States, suggesting that the number of women with CIN is
continuing to increase [1]. A report from the Kaiser
Permanente Northwest health plan indicates a some-
what lower rate of CIN among women enrolled in a
prepaid health plan, with a projected annual incidence
per 1,000 women of 1.2 for CIN 1 and 1.5 for CIN 2,3
[2]. Improper management of CIN can increase risk of
cervical cancer on the one hand and can result in
complications from overtreatment on the other. It is
becoming increasingly clear that loop electrosurgical
excision, which is widely used to treat CIN, produces a
small, but significant, negative impact on subsequent
pregnancy [3, 4].
Approximately 5 years ago, the American Society for
Colposcopy and Cervical Pathology (ASCCP) joinedother professional societies and federal and international
organizations to develop the 2001 Consensus Guidelines
for Managing Women with Cervical Intraepithelial
Neoplasia [5]. The goal was to improve the care of
women with CIN by weighing the best available
evidence and developing consensus management guide-
lines. Since 2001, considerable new information has
become available on the natural history of CIN, par-
ticularly in adolescents and young women [6Y8]. Our
understanding of how to manage women with cervical
adenocarcinoma in situ (AIS), a human papillomavirus
(HPV)Yassociated precursor to invasive cervical adeno-carcinoma, also has progressed. Therefore, in 2005,
the ASCCP and its partner organizations (listed in
Appendix A), began the process of revising the 2001
Consensus Guidelines. This culminated in a consensus
conference held at the National Institutes of Health in
September 2006. This report provides the recommenda-
tions developed with respect to managing women with
CIN and AIS. Recommendations for managing women
with abnormal cervical cancer screening tests appear in
an accompanying article [9].
GUIDELINE DEVELOPMENT PROCESS
The process used to develop the 2006 guidelines was
similar to that for the 2001 guidelines and is described in
depth elsewhere [5, 9]. Guidelines were developed
through a multistep process. Nationally recognized
experts in cervical cancer prevention were recruited to
working groups. These groups met initially to define
areas where modifications to the existing guidelines
might be needed, establishing each as a research
question. They then performed literature reviews and
retrieved and rated articles published since 2000 on each
question. They next conducted Internet-based discus-
sions open to the professional community at large that
focused on the research questions. The working groups
presented draft guidelines and supporting evidence to
the full Consensus Conference, which voted on each,with revision as needed. All guidelines were passed by
at least 66% of participants.
The terminology utilized for the new guidelines is
identical to that used previously, as is the 2-part rating
system and is provided in the Table 1. The terms
recommended, preferred, acceptable, and unacceptable
Table 1. Rating the Recommendations
Strength of recommendationa
A Good evidence for efficacy and substantial clinical
benefit support recommendation for use
B Moderate evidence for efficacy or only limited
clinical benefit supports recommendation for use
C Evidence for efficacy is insufficient to support a
recommendation for or against use, but
recommendations may be made on other grounds
D Moderate evidence for lack of efficacy or for adverse
outcome supports a recommendation against use
E Good evidence for lack of efficacy or for adverse
outcome supports a recommendation against use
Quality of evidencea
I Evidence from at least 1 randomized controlled trial
II Evidence from at least 1 clinical trial without
randomization, from cohort or case-control
analytic studies (preferably from more than one
center), or from multiple time-series studies,
or dramatic results from uncontrolled experiments
III Evidence from opinions of respected authorities based
on clinical experience, descriptive studies, or reports
of expert committees
Terminology used for recommendationsb
Recommended Good data to support use when only one option
is available
Preferred Option is the best (or one of the best) when there are
multiple other options
Acceptable One of multiple options either when there are data
indicating that another approach is superior or when
there are no data to favor any single option
Unacceptable Good data against use
aModified from Gross et al. [89] and Kish [90].bTheassignment of these terms representsan opinion ratifiedby voteby the ConsensusConference.
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are used in the guidelines to describe various interven-
tions. For example, in some clinical situations, there are
multiple management options that have reasonable
evidence of efficacy, but, based on less-defined issues
such as costs or patient convenience, one approach maybe Bpreferred.[ The letters A through E are used to
indicate Bstrength of recommendation[ for or against the
use of a particular option. The strength of the
recommendation is based on consideration of several
criteria, including potential for harm if an intervention
did not occur, potential complications of a given
intervention, as well as the Bquality of the evidence.[
Therefore, an exact correlation does not exist between
Bstrength of the recommendation[ and the Bquality of
the evidence.[ Quality of evidence is designated using
Roman numerals I to III as defined in Table 1. A number
of terms that are used in the guidelines were specifically
defined at the beginning of the Consensus Conference,
and those definitions are provided in Appendix B.
2006 CONSENSUS GUIDELINES
General Comments
Although the 2006 Consensus Guidelines are Bevidenced
based,[ in many instances there was a limited amount of
evidence available on which to base recommendation for
a particular management decision, or the evidence
which was available to inform the development of a
guideline was quite limited. This resulted in instances in
which the guidelines had to be based on either relatively
small descriptive studies or simply on expert opinion. It
is also important to recognize that although the 2006
Consensus Guidelines are designed to provide guidance
to clinicians caring for women with cervical cancer
precursors in the United States, management approaches
will frequently need to be individualized to take into
account individual patients clinical findings and pre-
ferences. Guidelines should never be considered a
substitute for clinical judgment, and it is impossible to
develop guidelines comprehensive enough to apply to allclinical situations. Finally, both clinicians and patients
need to realize that although cervical cancer can often be
prevented through a program of screening and treatment
of cervical cancer precursor lesions, no screening or
treatment modality is perfect, and unfortunately, inva-
sive cervical cancer can develop in women who
participate in such programs.
The histological classification incorporated into
these guidelines is a 2-tiered system that applies the
terms CIN 1 to low-grade lesions and CIN 2,3 to high-
grade precursors. Cytological low-grade squamous
intraepithelial lesion (LSIL) is not equivalent to
histological CIN 1, and cytological high-grade squa-
mous intraepithelial lesion (HSIL) is not equivalent to
histological CIN 2,3.Treatment Methods. Both ablative treatment meth-
ods that destroy the affected cervical tissue in vivo and
excisional modalities that remove the affected tissue are
widely utilized for treating CIN lesions [10]. Ablative
methods include cryotherapy, laser ablation, electro-
fulguration, and cold coagulation. Ablative methods are
usually recommended only for women who have a
satisfactory colposcopic examination and in whom
invasive cervical cancer has been ruled out through a
combination of colposcopy and endocervical sampling
with cytological correlation [11, 12]. Pretreatment
endocervical sampling can help identify women with
occult invasive cervical cancer [13]. In one study of 391
women undergoing a diagnostic excisional conization,
none of the women with a negative endocervical
curettage before conization were found to have an
occult invasive lesion in the conization specimen,
whereas all of the 17 found to have invasive disease
had a positive endocervical sampling [13]. Studies of
patients diagnosed with invasive disease after ablative
therapy have found that many either did not have an
endocervical sampling before treatment or underwent
an ablative procedure despite having a positive endo-cervical sampling [14].
Excisional methods that provide a tissue specimen for
pathological examination include cold-knife conization,
loop electrosurgical excision procedures (widely referred
to as LEEP or LLETZ [large loop excision of the
transformation zone]), laser conization, and electrosur-
gical needle conization. Excisional methods are con-
sidered preferable in situations where invasive cervical
cancer cannot be ruled out through a combination of
colposcopy and endocervical sampling with cytological
correlation and in situations where the risk of occult
cervical cancer is high. Examples include women withunsatisfactory colposcopic examinations, positive endo-
cervical curettage, and large lesions with a high-grade
colposcopic appearance [12]. It is also often recom-
mended that women with posttreatment recurrence of
CIN 2,3 be treated using an excisional as opposed to an
ablative method [12]. Many recurrent or persistent CIN
lesions are found in the endocervical canal, where they
are not colposcopically visible and therefore are not
suitable for ablative therapy. Cold-knife conization was
the original conservative method for treating CIN, but
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today, cold-knife conization has been largely replaced by
other excisional methods that do not require general
anesthesia. Cold-knife conization is also associated with
a higher rate of complications, and there is clear
evidence that it produces pregnancy-related morbidity.Therefore, today, cold-knife conization is usually
restricted to selected patients such as older women in
whom there is a suspicion of microinvasion or those who
have glandular neoplasia that can be located deep in the
endocervical canal [15]. Hysterectomy is a radical
procedure which is infrequently used today for the
treatment of intraepithelial lesions [15]. Hysterectomy
carries a substantially greater risk of morbidity, and even
mortality, when compared with excisional and ablative
procedures. This usually outweighs any potential benefit
of using hysterectomy as primary therapy for women
with CIN 2,3.
Simple outpatient excisional methods such as loop
excision offer the potential to be used as part of a Bsee-
and-treat[ approach in which both evaluation and
treatment are performed at the same visit [16]. See-
and-treat has a number advantages, especially for
women with an HSIL referral cytology, most of whom
will eventually undergo treatment irrespective of the
findings at colposcopy. Performing a loop excision at the
time at the initial colposcopic examination reduces the
number of office visits, reduces the potential for women
being lost to follow-up before treatment, and is thoughtto reduce patient anxiety while they wait for biopsy
results [15]. It does, however, result in some over-
treatment of women without CIN 2,3. This can be
minimized by only performing see-and-treat when
women have an HSIL referral cytology [12]. One study
of see-and-treat found that when limited to women
referred with HSIL cytology, 84% of the treated patients
had histologically identified CIN 2,3 in the loop excision
specimens [17]. Another study reported that 94% of
loop excisions specimens obtained using a see-and-treat
approach in women referred with HSIL had histologi-
cally identified CIN 2,3 [18].All of the treatment methods listed above are widely
utilized for treating CIN lesions, and each of the
different modalities has its proponents [19]. Only a
relatively limited number of randomized trials have
directly compared the different treatment modalities. A
Cochrane Database Systematic Review evaluated 28
individual trials that in aggregate compared a total of 7
treatment modalities [10]. Many of the trials were not
randomized controlled trials. Data were extracted from
the published reports by 2 investigators independently.
The primary conclusion of the Cochrane Review was
that there is no significant difference in the success rate
of the different modalities [10]. Other reviews have also
concluded that both ablative and excisional modalities
have a similar efficacy with respect to eliminating CINand reducing a womans risk of future invasive cervical
cancer [15, 20Y22]. It should be cautioned, however,
that the number of randomized controlled trials directly
comparing any 2 treatment modalities is limited, and
most trials are only powered to identify large differences
in outcomes. Moreover, there are difficulties inherent in
interpreting the pooled data for very diverse trials that
have different enrollment criteria, depth of excision, and
other variables associated with treatment [12].
Several randomized clinical trials and clinical case
series have directly compared the efficacy of cold-knife
conization with loop excisional procedures in women
requiring conization [23, 24]. These trials have reported
equivalent success rates and comparable rates of
complications for both methods. It remains unclear,
however, whether there is a significant difference
between cold-knife conization and loop excision with
respect to pathologic margins. Some, but not all, studies
have found that pathologic margins are less frequently
involved by CIN and are easier to interpret when cold-
knife conization is used [23, 25Y27].
It has been recognized for some time that cold-knife
conization increases a womans risk of future pretermlabor, low-birth-weight infant, and cesarean section
[28]. Other treatment methods such as loop excision
were thought to have no adverse effects on future
pregnancies since most of the studies published in the
early 1990s showed little impact on obstetric outcomes.
This has changed. Over the last few years, several large
retrospective series have reported that all forms of
excisional procedures present obstetrical risks [3, 15,
29Y31]. A recent systematic review of the published
literature on obstetric outcomes after treatment of CIN
found that all types of excisional procedures result in
pregnancy-related morbidity [3]. Loop excision wasfound to have a significant association with preterm
delivery (11% risk in treated women versus 7% risk in
untreated women), low-birth-weight infants (8% in
treated women versus 4% in untreated women), and
premature rupture of membranes (5% in treated women
versus 2% in untreated women). Although there were no
significant increases in neonatal intensive care unit
admissions or perinatal mortality in women who had
undergone loop excision versus those who had not,
nonsignificant increases were observed. In most studies,
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ablative methods have not been shown to be associated
with a similar adverse effect on pregnancy outcome;
however, it is difficult to measure small effects on
pregnancy outcome [3, 30, 31]. A large record linkage
study from Finland that evaluated national data on8,210 subsequent singleton births among 25,827
women who had been treated for CIN has recently
reported that any form of treatment including ablative
methods and loop excision increases the risk of preterm
delivery [32]. Thus, it is possible that ablative methods
may also have an adverse effect on future pregnancies.
Of interest, a recent Australian study showed that both
treated and untreated women with CIN were at
increased risk for preterm birth compared with the
general population, suggesting that treatment may be a
proxy for other risks [31].
There are no accepted nonsurgical therapies for CIN
[33]. Several topical agents have been either evaluated or
are in clinical trials, but none has been proven as
effective as excision or ablation. Similarly, although
there is considerable interest in therapeutic HPV
vaccines, none has been proven effective [34].
These considerations indicate that the decision as to
which therapeutic option to use in an individual patient
depends on considerations such as patient age, parity,
desire for future childbearing, preferences, prior cytol-
ogy and treatment history, and history of default from
follow-up, operator experience, and nonvisualization ofthe transformation zone.
Posttreatment Follow-up. The reported treatment
failure rate using either ablative or excisional methods
varies between 1% and 25% [10, 20, 35Y37].
Systematic reviews indicate overall pooled failure
rates of 5% to 15% for the different modalities,
with no significant difference between the modalities
[20]. Most failures occur within 2 years after treat-
ment [35, 38]. In addition to developing recurrent/
persistent CIN, women who have been treated for CIN
2,3 remain at increased risk for developing invasive
cervical cancer for a protracted period [22, 39]. Arecent systematic review reported that the incidence of
invasive cervical disease in treated women remains
about 56 per 100,000 for at least 20 years after
treatment, substantially greater than that in the general
US population (5.6/100,000 woman-years) [22, 40].
Therefore, decades-long follow-up is essential.
A number of posttreatment follow-up protocols have
been recommended [41, 42]. These include cytology,
colposcopy, combinations of cytology and colposcopy,
and testing for high-risk (oncogenic) types of HPV,
performed at a variety of intervals. None of the follow-
up protocols has been evaluated in randomized clinical
trials, and because the various follow-up approaches are
so different, it is difficult to compare them [38].
Systematic reviews of the performance of high-riskHPV DNA testing for posttreatment follow-up have
found that its performance is quite good and exceeds
that of cytological follow-up [38, 42]. Overall, the
pooled sensitivity of high-risk HPV testing for identify-
ing recurrent/persistent CIN reaches 90% by 6 months
after treatment and has been shown to remain at this
level for at least 24 months. In contrast, the pooled
sensitivity of cytology is approximately 70% [38]. In
some studies, but not others, use of a combination of
HPV testing and cytology resulted in an increased
sensitivity [38].
Special Populations. Adolescents (aged 13Y20 years)
and young women are considered a Bspecial population.[
There is a very low risk for invasive cervical cancer in this
group, but cytologically diagnosed squamous intraepithe-
lial lesions are common [2, 43]. Squamous intraepithelial
lesions in adolescents have a very high rate of sponta-
neous regression [8].
Pregnant women are another special population. The
risk of progression of CIN 2,3 to invasive cervical cancer
during pregnancy is minimal, and the rate of sponta-
neous regression postpartum is relatively high [44, 45].
In fact, many oncologists follow early-stage cervicalcancer during pregnancy until fetal viability is achieved
[46]. Treatment of CIN during pregnancy is associated
with a high rate of complications including severe
intraoperative hemorrhage [47]. Moreover, there is a
high rate of incomplete excision which results in a high
rate of recurrence or persistence [48, 49]. Therefore,
treatment for CIN during pregnancy should be avoided,
and the only indication for therapy of cervical neoplasia
in pregnant women is invasive cancer.
Cervical Intraepithelial Neoplasia Grade 1
It is important for clinicians to recognize that bothhistopathology and cytology are relatively poor pre-
dictors of the biological potential of an individual lesion.
Based on biomarkers as well as biological behavior
during long-term follow-up, it is now clear that some
lesions that are histologically and cytologically low-
grade have biological features of a high-grade lesion.
Moreover, some lesions that are histologically and
cytologically high-grade behave biologically like low-
grade lesions, with substantial rates of regression [50].
Nevertheless, the histological diagnosis of CIN remains
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the standard for determining clinical management.
Literature cited at the time of the 2001 Consensus
Conference recognized that CIN 1 represents a hetero-
geneous group of lesions [51]. This heterogeneity is due to
several factors including the poor reproducibility of ahistological diagnosis of CIN 1 [52]. In the National
Cancer Institutes ASCUS/LSILTriage Study (ALTS), it was
found that less than half of lesions diagnosed as CIN 1 by
the clinical site pathologists were subsequently classified as
CIN 1 when reviewed by a study pathologist [52]. In most
instances, this was attributable to lesions initially classified
as CIN 1 being Bdowngraded[ to normal by the study
pathologists. This occurred in 41% of cases. Nonconcor-
dance in the opposite direction was less common, but did
occur. Twelve percent of CIN 1 lesions were Bupgraded[
by the study pathologist to CIN 2,3. There also is more
heterogeneity with respect to associated HPV types for
CIN 1 lesions than for CIN 2,3 lesions.
Although most CIN 1 lesions are associated with
high-risk types of HPV, the distribution of high-risk
types in CIN 1 is different than that seen in CIN 2,3 [53].
A meta-analysis of HPV types associated with CIN 1
found that HPV-16 was the single most common
genotype identified. HPV-16 is found in 26.3% of all
HPV-positive CIN 1 [53]. HPV-31, -51, and -53 were the
next most commonly identified HPV types. Each type is
identified in 10% to 12% of CIN 1 lesions. CIN 1
lesions can also be associated with low-risk types ofHPV [53]. However, HPV-6 or -11 was detected in only
12% of the HPV DNAYpositive CIN 1. In addition to
being heterogeneous with respect to HPV types, CIN 1
lesions are also heterogeneous with respect to ploidy
status and other markers of neoplasia [54].
Low-grade cervical lesions have a high rate of
spontaneous regression in the absence of treatment. A
prospective study of Brazilian women with a cytological
result of LSIL found that more than 90% regressed
within 24 months [55]. Another study from the Nether-
lands found that over a 4-year period all women with
LSIL who were infected with nonYhigh-risk types ofHPV regressed to normal cytology, as did 70% of those
infected with high-risk types of HPV [56]. Even higher
rates of regression occur in adolescents and young
women. Moscicki et al. [8] found that 91% of
adolescents and young women with LSIL spontaneously
cleared their lesions with 36 months, irrespective of
associated HPV type.
Recent data suggest that CIN 1 uncommonly
progresses to CIN 2,3, at least within 24 months of
being diagnosed. In ALTS, the risk for having a CIN 2,3
lesion identified during the subsequent 2 years after
initial colposcopy was nearly identical in women with a
histological diagnosis of CIN 1 (13%) and in women
whose initial colposcopy and biopsy were negative
(12%) [57]. The risk of having an undetected CIN 2,3or AIS lesion is expected to be greater in women with
CIN 1 preceded by an HSIL or atypical glandular cells
(AGC) cytology result than for women with CIN 1
preceded by an ASC or LSIL cytology result. CIN 2,3 is
identified in 84% to 97% of women with HSIL cytology
evaluated using a LEEP [17, 18, 58]. Therefore, in the
2006 guidelines, separate recommendations are made
for women with CIN 1 preceded by an HSIL or AGC
cytology result.
Recommended Management of Women With CIN 1.
CIN 1 PRECEDED BY ASC-US, ASC-H, OR LSIL CYTOLOGY. The
recommended management of women with a histologi-
cal diagnosis of CIN 1 preceded by an ASC-US (atypical
squamous cells of undetermined significance), ASC-H
(atypical squamous cells, cannot exclude HSIL), or LSIL
cytology is follow-up with either HPV DNA testing
every 12 months or repeat cervical cytology every 6 to
12 months (BII) (Figure 1). If the HPV DNA test is
positive or if repeat cytology is reported as ASC-US or
greater, colposcopy is recommended. If the HPV test is
negative or 2 consecutive repeat cytology tests are Bnega-
tive for intraepithelial lesion or malignancy,[ return to
routine cytological screening is recommended (AII).If CIN 1 persists for at least 2 years, either continued
follow-up or treatment is acceptable (CII). If treatment is
selected and the colposcopic examination is satisfactory,
either excision or ablation is acceptable (AI). A
diagnostic excisional procedure is recommended if the
colposcopic examination is unsatisfactory, the endocer-
vical sampling contains CIN, or the patient has been
previously treated (AIII).
Treatment modality should be determined by the
judgment of the clinician and should be guided by
experience, resources, and clinical value for the specific
patient (A1). In patients with CIN 1 and an unsatisfac-tory colposcopic examination, ablative procedures are
unacceptable (EI). Podophyllin or podophyllin-related
products are unacceptable for use in the vagina or on the
cervix (EII). Hysterectomy as the primary and principal
treatment for histologically diagnosed CIN 1 is unac-
ceptable (EII).
CIN 1 PRECEDED BY HSIL OR AGC-NOS CYTOLOGY. Either a
diagnostic excisional procedure or observation with
colposcopy and cytology at 6 month intervals for one
year is acceptable for women with a histological
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diagnosis of CIN 1 preceded by HSIL or AGC-NOS
(atypical glandular cells not otherwise specified) cytol-
ogy, provided in the latter case that the colposcopic
examination is satisfactory and endocervical sampling is
negative (Figure 2) (BIII). In this circumstance, it is also
acceptable to review the cytological, histological, and
colposcopic findings; if the review yields a revised
interpretation, management should follow guidelines
for the revised interpretation (BII).
If observation with cytology and colposcopy is
elected, a diagnostic excisional procedure is recom-
mended for women with repeat HSIL cytological results
at either the 6- or 12-month visit (CIII). After 1 year of
observation, women with 2 consecutive Bnegative for
intraepithelial lesion or malignancy[ results can return
to routine cytological screening. A diagnostic excisional
procedure is recommended for women with CIN 1
preceded by an HSIL or AGC-NOS cytology in whom
the colposcopic examination is unsatisfactory, except in
special populations (e.g., pregnant women) (BII).
CIN 1 in Special Populations.
ADOLESCENT WOMEN. Follow-up with annual cytolo-
gical assessment is recommended for adolescents
with CIN 1 (Figure 3) (AII). At the 12-month
follow-up, only adolescents with HSIL or greater
on the repeat cytology should be referred to colpo-
scopy. At the 24-month follow-up, those with an
ASC-US or greater result should be referred to
Figure 1.
Figure 2.
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colposcopy (AII). Follow-up with HPV DNA testing
is unacceptable (EII).
PREGNANT WOMEN. The recommended management of
pregnant women with a histological diagnosis of CIN 1
is follow-up without treatment (BII). Treatment of
pregnant women for CIN 1 is unacceptable (EII).
Cervical Intraepithelial Neoplasia Grade 2,3
In the 2001 Consensus Guidelines, a decision was made
to utilize CIN 2,3 as the threshold for treatment
decisions. CIN 2,3 includes lesions previously referred
to as moderate dysplasia (i.e., CIN 2) and severe
dysplasia/carcinoma in situ (i.e., CIN 3) [54]. There
are a number of reasons for combining CIN 2 with CIN
3 for treatment decisions. Follow-up studies have shown
that despite marginal relative differences in behavior,
both of these lesions are more likely to persist or
progress than to regress [50, 59, 60]. A systematic
review of published follow-up studies found that 43% of
untreated CIN 2 lesions regress in the absence of
treatment, whereas 35% will persist, and 22% willprogress to carcinoma in situ or become invasive [60].
For CIN 3 lesions, the rates of regression, persistence,
and progression were 32%, 56%, and 14%, respec-
tively. Another reason for combining CIN 2 with CIN 3
for clinical management decisions is that a histological
diagnosis of CIN 2 is poorly reproducible [61, 62]. In
ALTS, only 43% of lesions histologically diagnosed as
CIN 2 by the clinical site pathologists were subsequently
classified as CIN 2 when reviewed by a study pathologist
[62]. Twenty-seven percent of all lesions originally
diagnosed as CIN 2 were upgraded to CIN 3 by the
study pathologists. Nonconcordance in the opposite
direction was also common. The study pathologists
downgraded 29% of lesions initially classified as CIN 2
to CIN 1 or normal.
Although CIN 2 lesions are more likely to regress
during long-term follow-up than are CIN 3 lesions,
CIN 2 and CIN 3 lesions share a number of biological
characteristics usually associated with true cervical
cancer precursors [54]. In contrast to CIN 1 lesions,
almost all CIN 2 and CIN 3 lesions are monoclonal
proliferations of cells that show evidence of genetic
instability [54, 63]. The majority of CIN 2 and CIN 3
lesions are aneuploid and have loss of heterozygosity
at nonrandom chromosomal loci that may be asso-
ciated with neoplastic development [54, 64]. CIN 2
and CIN 3 lesions also have much less heterogeneity
with respect to associated HPV types than do CIN 1
lesions. A meta-analysis recently reported that just 5
high-risk types of HPV (16, 18, 31, 33, and 58) are
associated with 75% of high-grade cervical lesions[65]. Therefore, CIN 2 is generally utilized as the
threshold for treatment in the United States to provide
an added measure of safety [54, 62].
Treatment of Women With Biopsy-Confirmed CIN
2,3. There is widespread agreement that treatment of
CIN 2,3 reduces both incidence and mortality from
invasive cervical cancer. To be effective, treatment
needs to remove the entire transformation zone,
rather than selectively targeting the colposcopically
identified lesion [66]. As discussed previously, data
Figure 3.
230 & W R I G H T E T A L .
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from clinical trials have generally failed to show
significant differences in outcome after treatment
using different modalities. Therefore, both ablative
and excisional methods can be utilized to treat
women with biopsy-confirmed CIN 2,3 and asatisfactory colposcopic examination. However, exci-
sional methods allow pathological assessment of the
excised tissue and should reduce the risk that a
microinvasive or occult invasive carcinoma is treated
as a noninvasive lesion. This is particularly an issue
for women with large high-grade lesions or lesions
extending into the endocervical canal and for women
who have been previously treated for CIN. Up to 7%
of women with an unsatisfactory colposcopic exam-
ination and CIN 2,3 have an occult carcinoma
detected when they undergo a diagnostic excisional
conization [13, 23]. Therefore, a diagnostic excisional
conization that allows pathological assessment of the
excised tissue should be used in these instances.
Pathologic margin status is generally considered to be
a risk factor for the development of recurrent or
persistent CIN [67Y70]. When performed at the time
of a diagnostic excisional procedure, endocervical
sampling correlates with endocervical margin status
and a positive endocervical sampling is predictive of
residual disease [13, 70]. Rates of recurrent or persistent
CIN when the margin is involved have ranged from 10%
to 33% in recent studies [68, 71Y
74]. Although anumber of studies have reported that recurrent or
persistent CIN is more frequent in women with involved
resection margins, relatively few studies have been able
to control for other variables that might account for the
higher failure rates in these patients. The few studies that
have utilized multivariate analysis to adjust for other
potential contributing factors have found that margin
status is not an independent predictor of residual disease
[75, 76]. It must be emphasized that most women withinvolved margins will not develop recurrent or persistent
CIN and that up to 40% of all women undergoing loop
excision have pathologic margin involvement [77, 78].
Based on these considerations, it is generally recom-
mended that women with positive margins be counseled
about their elevated risk for recurrent or persistent CIN,
but that in most instances they should be closely
followed up rather than receive immediate treatment
[72Y74]. For cases in which further treatment is decided
upon, repeat excision offers a balance between the risk
of treatment complications and the desire to eradicate
potential residual CIN. Hysterectomy may be appro-
priate in selected instances.
Recommended Management of Women With CIN 2,3.
INITIAL M ANAGEMENT. Both excision and ablation are
acceptable treatment modalities for women with a
histological diagnosis of CIN 2,3 and satisfactory
colposcopy, except in special circumstances (see below)
(Figure 4) (AI). A diagnostic excisional procedure is
recommended for women with recurrent CIN 2,3 (AII).
Ablation is unacceptable and a diagnostic excisional
procedure is recommended for women with a histolo-
gical diagnosis of CIN 2,3 and unsatisfactory colpo-scopy (AII). Observation of CIN 2,3 with sequential
cytology and colposcopy is unacceptable, except in
special circumstances (see below) (EII). Hysterectomy is
unacceptable as primary therapy for CIN 2,3 (EII).
Figure 4.
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FOLLOW-UP AFTER TREATMENT. Acceptable posttreat-
ment management options for women with CIN 2,3
include HPV DNA testing at 6 to 12 months (BII).
Follow-up using either cytology alone or a combination
of cytology and colposcopy at 6 months intervals is alsoacceptable (BII). Colposcopy with endocervical sam-
pling is recommended for women who are HPV DNA
positive or have a repeat cytology result of ASC-US or
greater (BII). If the HPV DNA test is negative or if 2
consecutive repeat cytology tests are Bnegative for
intraepithelial lesion or malignancy,[ routine screening
for at least 20 years commencing at 12 months is
recommended (AI). Repeat treatment or hysterectomy
based on a positive HPV DNA test is unacceptable (EII).
If CIN 2,3 is identified at the margins of a diagnostic
excisional procedure or in an endocervical sample
obtained immediately after the procedure, reassessment
using cytology with endocervical sampling at 4 to 6
months posttreatment is preferred (BII). Performing a
repeat diagnostic excisional procedure is acceptable
(CIII). Hysterectomy is acceptable if a repeat diagnostic
procedure is not feasible.
A repeat diagnostic excision or hysterectomy is
acceptable for women with a histological diagnosis of
recurrent or persistent CIN 2,3 (BII).
CIN 2,3 in Special Populations.
ADOLESCENT AND YOUNG WOMEN. For adolescents and
young women with a histological diagnosis of CIN 2,3not otherwise specified, either treatment or observation
for up to 24 months using both colposcopy and cytology
at 6-month intervals is acceptable, provided colposcopy
is satisfactory (Figure 5) (BIII). When a histological di-
agnosis of CIN 2 is specified, observation is preferred
but treatment is acceptable. When a histological diag-
nosis of CIN 3 is specified or when colposcopy is
unsatisfactory, treatment is recommended (BIII).
If the colposcopic appearance of the lesion worsensor if HSIL cytology or a high-grade colposcopic lesion
persists for 1 year, repeat biopsy is recommended (BIII).
After 2 consecutive Bnegative for intraepithelial lesion or
malignancy[ results, adolescents and young women
with normal colposcopy can return to routine cytologi-
cal screening (BII). Treatment is recommended if CIN 3
is subsequently identified or if CIN 2,3 persists for 24
months (BII).
PREGNANT WOMEN. In the absence of invasive disease or
advanced pregnancy, additional colposcopic and cyto-
logical examinations are acceptable in pregnant women
with a histological diagnosis of CIN 2,3 at intervals no
more frequent than every 12 weeks (BII). Repeat biopsy
is recommended only if the appearance of the lesion
worsens or if cytology suggests invasive cancer (BII).
Deferring re-evaluation until at least 6 weeks postpar-
tum is acceptable (BII). A diagnostic excisional proce-
dure is recommended only if invasion is suspected (BII).
Unless invasive cancer is identified, treatment is unac-
ceptable (EII). Re-evaluation with cytology and colpo-
scopy is recommended no sooner than 6 weeks
postpartum (CIII).
Adenocarcinoma In Situ
Adenocarcinoma in situ (AIS) is much less commonly
encountered than is CIN 2,3. In 1991Y1995, the
overall incidence of squamous carcinoma in situ of
Figure 5.
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the cervix in white women in the United States was
41.4 per 100,000, whereas the incidence of AIS was
only 1.25 per 100,000 [40]. Although the overall
incidence of AIS remains rather low, the incidence
increased by approximately 6-fold from the 1970s to
1990s [40].
Management of women with AIS is both challen-
ging and controversial. Many of the assumptions
that are used to justify conservative management
approaches in women with CIN 2,3 lesions do notapply to AIS. For example, the colposcopic changes
associated with AIS can be minimal, so it can be
difficult to determine the extent of a lesion. AIS
frequently extends for a considerable distance into the
endocervical canal, making complete excision dif-
ficult. AIS is also frequently multifocal and frequently
has Bskip lesions.[ Thus, negative margins on a
diagnostic excisional specimen do not necessarily
mean that the lesion has been completely excised.
Because of these considerations, hysterectomy con-
tinues to be the treatment of choice for AIS in women
who have completed childbearing. However, AIS oftenoccurs in women who wish to maintain their fertility.
A number of studies have now clearly demonstrated
that an excisional procedure is curative in the
majority of these patients. The failure rate after an
excisional procedure (e.g., recurrent/persistent AIS or
invasive adenocarcinoma) ranges from 0% to 9%
[79Y83]. A comprehensive review of the published
literature conducted in 2001 identified 16 studies that
included a total of 296 women with AIS who had
been treated with a diagnostic excisional procedure
[82]. The overall failure rate was 8% [82]. Margin
status is one of the most clinically useful predictors of
residual disease [84Y87]. Recent data suggest that
endocervical sampling at the time of an excisional
biopsy is also predictive of residual disease [84].
Some, but not all, studies have suggested that there is
an increased recurrence rate as well as an increase in
positive margins when a loop excision procedure, as
opposed to cold-knife conization, is used [81, 82, 88].
Irrespective of conization method, clinicians shouldremember that margin status and interpretability of
the margins are important for future treatment
planning and management. Moreover, it should be
emphasized that a diagnostic excisional procedure is
required in all women with AIS before making any
subsequent management decisions.
Recommended Management of Women With Adeno-
carcinoma In Situ. Hysterectomy is preferred for
women who have completed childbearing and have a
histological diagnosis of AIS on a specimen from a
diagnostic excisional procedure (Figure 6) (CIII).
Conservative management is acceptable if futurefertility is desired (AII). If conservative management is
planned and the margins of the specimen are involved
or endocervical sampling obtained at the time of
excision contains CIN or AIS, re-excision to increase
the likelihood of complete excision is preferred. Re-
evaluation at 6 months using a combination of cervical
cytology, HPV DNA testing, and colposcopy with
endocervical sampling is acceptable in this circumstance.
Long-term follow up is recommended for women who do
not undergo hysterectomy (CIII).
Figure 6.
2006 Consensus GuidelinesVHistology & 233
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Acknowledgments
The authors thank all of the participants and formal
observers to the 2006 Consensus Conference who
worked so hard to develop the guidelines. Their names
and organizations can be viewed at www.asccp.org. The
authors also thank Ms Kathy Poole for administrative
support during the development of the guidelines and Dr
Anna Barbara Moscicki who chaired the Adolescent
Working Group.
Text for this article was first published in Wright TC Jr,
Massad LS, Dunton CJ, Spitzer M, Wilkerson EJ,
Solomon D. 2006 Consensus guidelines for the manage-
ment of women with cervical intraepithelial neoplasia
or adenocarcinoma in situ. Am J Obstet Gynecol
2007;197:340Y45. Elsevier/2007.
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APPENDICES
Appendix A: Participants and ParticipatingOrganizations
Organizer: American Society for Colposcopyand Cervical Pathology (ASCCP) (Also onhttp://www.asccp.org/consensus.shtml)Participants.
Fadi Abdul-Karim, MD, University Hospitals of Cleveland, Cleveland, OH
Ronald D. Alvarez, MD, University of Alabama, Birmingham, AL*
Barbara Apgar, MD, MS, University of Michigan, Ann Arbor, MI*
Raheela Ashfaq, MD, University of Texas Southwestern, Dallas, TX* ,
R. MarshallAustin, MD, PhD,Magee-Womens Hospital of the University of
Pittsburgh, Pittsburgh, PA*
Mark M. Bajorek, MD, Oregon Health Sciences University, Portland, OR
Jonathan Berek, MD, Stanford University School of Medicine, Los Angeles,
CA*,
Monique Bertrand, MD, London Health Sciences Center, London, Ontario,
Canada*
Marluce Bibbo, MD, Thomas Jefferson University Hospital, Philadelphia,
PA*
George Birdsong, MD, Grady Health System, Atlanta, GA
Lori A. Boardman, MD, ScM, Brown University Women and Infants
Hospital, Providence, RI*
Fredrik F. Broekhuizen, MD, Medical College of Wisconsin, Milwaukee,WI
Carol L. Brown, MD, Memorial Sloan-Kettering Cancer Center, New York,
NY*,
S. C. Peter Bryson, MD, Queens University, Kingston, Ontario, Canada
Louis Burke, MD, Beth Israel/Deaconess Medical Center, Harvard Medical
School, Boston, MA
Robert A. Burger, MD, University of California Irvine, Irvine, CA*,
Philip Castle, PhD, MPH, National Cancer Institute, Bethesda, MD*
David Chhieng, MBA, MD, University of Alabama, Birmingham, AL
Carmel Cohen, MD, Columbia University, New York, NY*
Terrance Colgan, MD, Mount Sinai Hospital, Toronto, Ontario, Canada*
Terri Cornelison, MD, National Cancer Institute, Bethesda, MD*
J. Thomas Cox, MD, University of CaliforniaYSanta Barbara, Santa Barbara,
CA*
William Creasman, MD, Medical University of South Carolina, Charleston,
SC
Christopher P. Crum, MD, Harvard Medical School, Boston, MA*
Vanessa Cullins, MD, Planned Parenthood Federation of America, New
York, NY
Teresa M. Darragh, MD, University of CaliforniaYSan Francisco, San
Francisco, CA
Diane D. Davey, MD, University of Kentucky, Lexington, KY*
Gordon D. Davis, MD, Maricopa Medical Center, St Josephs Hospital and
Medical Center, Phoenix, AZ
Linda Dominguez, CNP, RN, Planned Parenthood of New Mexico,
Albuquerque, NMRebecca K. Donohue, PhD, RN, CS, Simmons College, Boston, MA
Charles Dunton, MD, Lankenau Hospital, Wynnewood, PA*
Juan C. Felix, MD, LAC-USC Medical Center, Los Angeles, CA
Francisco Garcia, MD, MPH, University of Arizona Health Sciences Center,
Tucson, AZ*
Kim R. Geisinger, MD, Wake Forest University School of Medicine, Winston
Salem, NC
Melvin V. Gerbie, MD, Northwestern University Medical School, Chicago, IL*
Michael A. Gold, MD, University of Oklahoma Health Sciences Center,
Oklahoma City, OK*
David L. Greenspan, MD, Maricopa Medical Center, St Josephs Hospital
and Medical Center, Phoenix, AZ*
Benjamin Greer, MD, University of Washington Medical Center, Seattle,
WA*
Richard Guido, MD, Magee-Womens Hospital of the University of
Pittsburgh, Pittsburgh, PA*
Fernando Guijon, MD, University of Manitoba, Winnipeg, Manitoba, CanadaHope K. Haefner, MD, University of Michigan, Ann Arbor, MI*
Kenneth D. Hatch, MD, University of Arizona Health Sciences Center,
Arizona Cancer Center, Tucson, AZ*,
Thomas J. Herzog, MD, Columbia University, New York, NY*,
Christine Holschneider, MD, UCLA School of Medicine, Los Angeles, CA
Beth C. Huff, MSN, NP, Vanderbilt University Medical Center, Nashville, TN
Warner K. Huh, MD, University of Alabama at Birmingham, Birmingham, AL*
Verda J. Hunter, MD, Gynecologic Resource Center for Gynecologic
Oncology, Kansas City, MO
Mujtaba Husain, MD, Wayne State University, Detroit, MI
Jose A. Jeronimo, MD, National Cancer Institute, Bethesda, MD
Howard W. Jones, III, MD, Vanderbilt University, Nashville, TN*
Beth Jordan, MD, Association of Reproductive Health Professionals,
Washington, DC
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Thomas M. Julian, MD, University of Wisconsin, Madison, WI
Barbara F. Kelly, MD, AF Williams Family Medical Center, Denver, CO
Valerie J. King, MD, MPH, Oregon Health and Science University, Portland,
OR
Walter Kinney, MD, University of CaliforniaYDavis, Permanente Medical
Group, Sacramento, CA*
Marina Kondratovich, PhD, Food and Drug Administration, Rockville, MDEdwardR. Kost, MD,BrookeArmy Medical Center, Fort SamHouston, TX*,
Burton A. Krumholz, MD, Long Island, NY*,
Robert J. Kurman, MD, Johns Hopkins Hospital, Baltimore, MD
Hershel W. Lawson, MD, Centers for Disease Control and Prevention,
Atlanta, GA*
Neal M. Lonky, MD, MPH, Kaiser Permanente, Yorba Linda, CA*
Silvana Luciani, PhD, Pan-American Health Organization, Washington, DC
L. Stewart Massad, MD, Washington University School of Medicine, St
Louis, MO*
Edward J.Mayeaux,MD, Louisiana State University Health Sciences Center,
Shreveport, LA*
Alexander Meisels, MD, Laval University, Quebec City, Quebec, Canada
Kathleen McIntyre-Seltman, MD, Magee Womens Hospital, Pittsburgh, PA*
Anna-Barbara Moscicki, MD, University of CaliforniaYSan Francisco, San
Francisco, CA*
Carolyn Y. Muller, MD, University of New Mexico, Albuquerque, NM
Gary R. Newkirk, MD, Family Medicine Spokane, Spokane, WA
Hextan Y. S. Ngan,MBBS, MD, International Federation of Gynecology and
Obstetrics (FIGO), Hong Kong
Kenneth L. Noller, MD, Tufts University School of Medicine, Boston, MA*
Dennis M. OConnor, MD, Clinical Pathology Associates, Inc, Louisville, KY*
Edward Partridge, MD, University of Alabama at Birmingham, Birmingham, AL*
Diane M. Provencher, MD, CHUM-Hopital Notre-Dame, Montreal, Quebec,
Canada
Stephen Raab, MD, Allegheny General Hospital, Pittsburgh, PA
Eddie Reed, MD, Centers for Disease Control and Prevention, Atlanta, GA
Max Robinowitz, MD, Food and Drug Administration, Rockville, MD
William Rodgers, MD, University of Maryland Medical System, Baltimore, MD*
Mary Rubin, RNC, PhD, CRNP, University of CaliforniaYSan Francisco, San
Francisco, CA*
Mona Saraiya, MD, MPH, Centers for Disease Control and PreventionVUS
Public Health Service, Atlanta, GA
Debbie Saslow, PhD, American Cancer Society, Atlanta, GA*,
Mark Schiffman, MD, MPH, National Cancer Institute, Bethesda, MD*VolkerSchneider, MD, InternationalAcademy of Cytology, Freiburg, Germany
Karen Shea, MSN, CRNP, Planned Parenthood Federation, New York, NY
Mark Sherman, MD, National Cancer Institute, Bethesda, MD*
Mary Sidawy, MD, George Washington University, Washington, DC
Diane Solomon, MD, National Cancer Institute, Bethesda, MD*
Mark Spitzer, MD, Brookdale University Hospital and Medical Center,
Brooklyn, NY*
Mark Stoler, MD, University of Virginia Health Sciences Center, Charlottes-
ville, VA*
Pamela Stratton, MD, National Institutes of Child Health and Human
Development, Rockville, MD
Cornelia Trimble, MD, Johns Hopkins University, Baltimore, MD*
Edward G. Trimble, MD, MPH, National Cancer Institute, Bethesda, MD*
Leo B. Twiggs, MD, University of Miami School of Medicine, Miami, FL*
Elizabeth R. Unger, MD, PhD, Centers for Disease Control and Prevention
(CEVC), Atlanta, GA
Jeffrey Waldman, MD, Planned Parenthood Shasta-Diablo, Concord, CA*Alan G. Waxman, MD, Unversity of New Mexico, Albuquerque, NM*
Claudia L. Werner, MD, University of Texas Southwestern, Dallas, TX*
Edward Wiesmeier, MD, UCLA, Los Angeles, CA
David C. Wilbur, MD, Massachusetts General Hospital, Boston, MA
Edward J. Wilkinson, MD, Universityof Florida College of Medicine,Gainesville, FL*
Cheryl Wiseman, MPH, CT, Centers for Medicaid and Medicare Services,
Baltimore, MD
Jason D. Wright, MD, Columbia University, New York, NY*,
Thomas C. Wright, MD, Columbia University, New York, NY*
*Conference participants who were members of the working groups.Members of working groups who were unable to attend the conference.Designated delegates who participated in the public comment review periods anddelegate conference calls but were unable to attend the conference.
Formal Observers*.
Shaheen Ahmed, MD, Blue Springs, MO
Andrea Abati, MD, National Cancer Institute, Bethesda, MD
Edward A. Barker, MD, Medical Laboratory Associates, Seattle, WA
Henry W. Buck, MD, University of Kansas, Lawrence, KS
Catherine Copenhaver, MD, Bethesda, MD
Julia Corrado, MD, Food and Drug Administration, Rockville, MD
Maria L. Diaz, MD, Davie, FL
Mary C. Eiken, SGO National Office, Chicago, IL
Tremel Faison, Food and Drug Administration, Rockville, MD
Sarah Feldman, MD, MPH, Harvard Medical School, Cambridge, MA
Lisa Flowers, MD, Emory University School of Medicine, Atlanta, GA
Patricia Lynn Fontaine, MD, MS, University Family PhysiciansYNorth
Memorial Clinic, Minneapolis, MN
Julia C. Gage, MPH, Health Resources and Services Administration,
Rockville, MD
Chad A. Hamilton, MD, Stanford University Medical Center, Stanford, CA
Vivien W. Hanson, MD, University of Washington School of Public Health,
Seattle, WA
Robert D. Hilgers, MD, University of Louisville, Louisville, KY
Thomas M. Kastner, MD, Mayo Clinic, Rochester, MN
Jill Koshiol, PhD, National Cancer Institute, Bethesda, MD
Aimee R. Kreimer, PhD, National Cancer Institute, Bethesda, MD
Michelle D. Lavey, MS-FNP, Rockville, MD
Ronald D. Luff, MD, Quest Diagnostics, Teterboro, NJ
Louise E. Magruder, Food and Drug Administration, Rockville, MD
Sheila F. Mahoney, CNM, MPH, National Institute of Child Health and
Human Development, Bethesda, MD
William J. Mann, Jr, MD, Jersey Shore University Medical Center, Neptune,
NJ
Linda McWey-Price, MD, Carilion New River Valley Medical Center,
Christiansburg, VA
Gabriele Medley, AM, MBBS, FRCPA, FIAC, University of Melbourne,
Victoria, Australia
Melissa A. Merideth, MD, MPH, National Institute of Health, Bethesda, MD
Brigitte E. Miller, MD, Wake Forest University Baptist Medical Center,
Winston-Salem, NC
Mary F. Mitchell,ACOGYDepartment of Practice Activities, Washington, DC
Mary L. Nielsen, MD, University of Kansas School of Medicine, Wichita, KS
Catherine Platt, MD, Arlington, VAMarianne U. Prey, MD, Quest Diagnostics Incorporated, St Louis, MO
Mahboobeh Safaeian, MD, MPH, National Cancer Institute, Bethesda, MD
Ellen E. Sheets, MD, Cytyc Corporation, Malborough, MA
Mario G. Sideri, MD, European Institute of Oncology, Milan, Italy
Albert Singer, MD, Whittington Hospital, London, UK
Diane R. Smith, NP, Arlington, VA
Karen K. Smith-McCune, MD, UCSF Comprehensive Cancer Center, San
Francisco, CA
Nancy J. Swick, MSN, CRNP, Santa Rosa Memorial Hospital, Santa Rosa, CA
Candice A. Tedeschi, OGNP, North ShoreYLIJ Health Systems, Lake Success, NY
Leslie A. Tyska, MD, California State Polytechnic University, Pomona, CA
Joanne P. Walenga, RN, Rockville, MD
Amy J. Wendel, SCT, MP, Mayo Clinic, Rochester, MN
Donald S. Wiersma, MD, Potomac, MD
Barbara A. Winkler, MD, Quest Diagnostics Incorporated, Teterboro, NJ
Meggan Zsemlye, MD, University of New Mexico, Albuquerque, NM
*All observers were either members or employees of the participating organizationsand federal agencies.
Participating Organizations
American Academy of Family Physicians, American
Cancer Society, American College Health Association,
American College of Obstetricians and Gynecologists,
American Social Health Association, American Society for
Clinical Pathology, American Society for Colposcopy and
Cervical Pathology, American Society of Cytopathology,
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17/17
Association of Reproductive Health Professionals,
Centers for Disease Control and PreventionVDivision
of Viral and Rickettsial Disease, Centers for Disease
Control and PreventionVDivision of Cancer Preven-
tion and Control, Centers for Disease Control andPreventionVDivision of Laboratory Systems, Centers
for Medicaid and Medicare Services, College of
American Pathologists, Food and Drug Administra-
tion, International Academy of Cytology, International
Federation for Cervical Pathology and Colposcopy,
International Federation of Gynecology and Obstetrics,
International Gynecologic Cancer Society, International
Society of Gynecological Pathologists, National Cancer
Institute, National Association of Nurse Practitioners in
Womens Health, Papanicolaou Society of Cytopathol-
ogy, Pan-American Health Organization, Planned Par-
enthood Federation of America, Society of Canadian
Colposcopists, Society of Gynecologic Oncologists,
Society of Gynecologic Oncologists of Canada, and
Society of Obstetricians and Gynaecologists of Canada.
Appendix B: Definitions of Terms
Colposcopy is the examination of the cervix, vagina,
and, in some instances, the vulva, with the colposcope
after the application of a 3% to 5% acetic acid solution
coupled with obtaining colposcopically directed biopsies
of all lesions suspected of representing neoplasia.
Endocervical samplingincludes obtaining a specimen
for either histological evaluation using an endocervicalcurette or a cytobrush or for cytological evaluation using
a cytobrush.
Endocervical assessment is the process of evaluating
the endocervical canal for the presence of neoplasia
using either a colposcope or endocervical sampling.
Endometrial sampling includes obtaining a specimen
for histological evaluation using an endometrial biopsy
or a Bdilatation and curettage[ or hysteroscopy.
Diagnostic excisional procedure is the process of
obtaining a specimen from the transformation zone and
endocervical canal for histological evaluation and
includes laser conization, cold-knife conization, loop
electrosurgical excision (i.e., LEEP), and loop electro-
surgical conization.
Satisfactory colposcopy indicates that the entire
squamocolumnar junction and the margin of any visible
lesion can be visualized with the colposcope.
Adolescent women are women 13 to 20 years of age
(i.e., from 13th to 21st birthdays).
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