High Prevalence of Anal Human Papillomavirus–Associated Cancer Precursors in a Contemporary Cohort of Asymptomatic HIV-Infected Women
High Prevalence of Anal Human Papillomavirus- Associated Cancer Precursors in a Contemporary Cohort of Asymptomatic HIV-Infected Women
Isabelle Heard 1 2 4
Isabelle Etienney 0 2
Valérie Potard 2 6 7
Isabelle Poizot-Martin 2 5
Catherine Moore 2 9
Anne-Carole Lesage 0 2
Emmanuelle Ressiot 2 5
Catherine Crenn-Hebert 2 8
Jean-François Fléjou 2 3
Heather Cubie 2 9
Dominique Costagliola 2 7
Teresa M. Darragh 2 10
for the ANRS-C 2
VIHGY Study Group 2
0 Department of Proctology, Diaconesses-Croix Saint-Simon Group Hospitals
1 Groupe Hospitalier Pitié-Salpêtrière, Assistance Publique, Hôpitaux de Paris (AP-HP)
2 Received 18 September 2014; accepted 24 January 2015; electronically pub- lished 2 February 2015. papillomavirus humains, Institut Pasteur , 25-28 rue du Dr Roux, 75015 Paris , France
3 Department of Pathology, AP-HP-Hôpitaux Universitaires de l'Est Parisien, Hôpital Saint-Antoine , Paris , France
4 French Human Papillomavirus Reference Laboratory, Institut Pasteur
5 Aix Marseille Univ, Assistance Publique, Hôpitaux de Marseille , Sainte-Marguerite , Service d'Immuno-hématologie clinique, INSERM U912 (SESSTIM) , Marseille , France
6 INSERM Transfert , Paris
7 Sorbonne Universités, UPMC Univ Paris 06, UMR_S 1136
8 AP-HP-Hôpitaux Universitaires Paris Nord Val de Seine, Hôpital Mourier , Colombes
9 Scottish Human Papillomavirus Reference Laboratory , Edinburgh , United Kingdom
10 Department of Pathology, University of San Francisco , California
Background. Although human immunodeficiency virus (HIV)-infected women are at high risk for anal cancer, few data have been published on prevalence of and risk factors for anal precancer and potential screening strategies in this risk group. Methods. A cross-sectional anal screening study was nested in a gynecological cohort of HIV-infected women. Anal swab specimens were collected for cytology and human papillomavirus (HPV) testing. High-resolution anoscopy, with biopsy when indicated, was systematically performed. Results. Among the 171 enrolled women, median age was 47.3 years and 98% were receiving combination antiretroviral therapy. Median CD4+ count was 655 cells/µL and HIV load was <50 copies/mL in 89% of subjects. High-grade anal intraepithelial neoplasia or worse (HG-AIN+) was diagnosed in 12.9% (n = 21). In multivariable analysis, a history of cervical squamous intraepithelial lesion (odds ratio [OR], 4.2; 95% confidence interval [CI], 1.116.4) and anal HPV-16 infection (OR, 16.1; 95% CI, 5.4-48.3) was associated with increased risk of HG-AIN+. Abnormal anal cytology and HPV-16 infection performed best as a screening strategy for HG-AIN+ histology, with positive likelihood ratios of 3.4 (95% CI, 2.3-5.1) and 4.7 (95% CI, 2.5-8.7) and negative likelihood ratios of 0.2 (95% CI, .07-.8) and 0.4 (95% CI, .2-.9), respectively. Conclusions. HIV-infected women with a history of HPV-associated cervical disease are at increased risk for HG-AIN+ and should be offered anal cancer screening. Anal cytology and HPV-16 genotyping had the best screening performance. Anal cytology is easy to perform routinely; it may be the best candidate for screening for HG-AIN among HIV-infected women.
anal cancer screening; HIV; women; anal intraepithelial neoplasia; human papillomavirus
human papillomavirus (HPV)-associated genital
precancers or cancer is a known risk factor for anal
intraepithelial neoplasia (AIN) and cancer . Many studies
have now documented that people living with human
immunodeficiency virus (HIV)/AIDS, mainly men who
have sex with men (MSM), but also heterosexual men
and women, have an increased risk for anal cancer .
In HIV-infected women, the risk for anal cancer is
approximately 14 times higher than among HIV-positive
women diagnosed with AIDS , with the anal cancer
rate estimated at 30–36 per 100 000 person-years [3, 5].
Despite the introduction of combination antiretroviral
therapy (cART), there is no evidence of a declining incidence of
anal cancer .
Among HIV-infected women, several studies have documented
the course of HPV-associated cervical disease; however, few data
are available for anal disease . Rates of abnormal anal cytology
ranging between 10% and 42% have been reported in recent
studies [7, 8]. Poorly controlled HIV and concurrent cervical lesions
were reported as risk factors for high-grade anal lesions [9–11].
Hessol et al observed that HPV was more prevalent in the anus
than in the cervix, and that there was little correlation between
severity of anal and cervical disease . This suggests that natural
history might not be identical at these anatomical sites.
Effective screening for and treatment of cervical lesions have
dramatically decreased cervical cancer mortality . Routine
screening for anal cancer is not yet recommended in HIV-infected
individuals . Performances of cytology, high-resolution
anoscopy (HRA), and HPV testing have been evaluated primarily
among men .
The present study aimed to determine the prevalence of anal
HPV infection and related lesions and to assess the risk factors
for anal high-grade AIN or invasive cancer (HG-AIN+) in a
prospective cohort of HIV-infected women previously enrolled in a
cervical cancer screening study and subsequently followed for at
least 4 years. We also estimated the performance of available
The data presented are the results of a nested substudy, icube,
within the VIHGY cohort, a multicenter study of HIV-infected
women conducted in 5 sites within France, aimed at providing
longitudinal data on cervical HPV infection and related lesions.
Women were recruited for this substudy during their first
VIHGY visit in 2012 at 3 of the VIHGY hospital sites:
ParisPitié-Salpétrière, Colombes-Louis-Mourier, and
MarseilleSainte Marguerite. Women were eligible if they had no history
of anal cancer, and were invited to participate in a 2-step study:
(1) anal HPV specimen collection during the gynecological visit
and (2) to undergo an HRA at specialized anal dysplasia clinics.
The icube protocol and consent form were approved by the
institutional review board of Ile-de-France VI. Informed written
consent was obtained before anal HPV specimen collection and
before HRA. Previous medical history, the most recent CD4 cell
count, viral load, and current cART status were obtained from
the women’s medical record. Anal HPV samples were collected
prior to collection of the cervical specimen. Swabs were placed
into PreservCyt collection medium (Hologic).
To identify specific HPV genotypes, samples were tested
using HPV Linear Array (Roche Molecular Systems) according
to the manufacturer’s instructions. Linear Array allows
detection of high-risk HPV (HR-HPV) types 16, 18, 26, 31, 33, 35,
39, 45, 51, 52, 53, 56, 58, 59, 64, 66, 67, 68, 69, 70, 73, 82,
and IS39 and low-risk types 6, 11, 40, 42, 54, 55, 61, 62, 71,
72, 81, 83, 84, and CP6108.
Women attending HRA were asked to complete a short
questionnaire regarding anal disease history and sexual behavior.
Anal swab specimens were collected for cytology before the
physical examination, which included a digital anorectal
Two experienced clinicians (I. E. and A.-C. L.) had received
formal training at the University of California, San Francisco
Anal Neoplasia Clinic and trained the other anoscopists.
HRA was performed without knowledge of the cytology and
HPV results. Acetowhite areas were biopsied and processed
for histological examination.
Cervical cytology was read centrally. Anal cytology and
biopsies were read in local laboratories, blinded to the HPV result,
and then reviewed centrally (T. M. D.). Anal and cervical
cytology results were categorized according to the 2001 Bethesda
System terminology: negative; atypical squamous cells of
undetermined significance (ASC-US); low-grade squamous
intraepithelial lesion (LSIL); high-grade squamous intraepithelial lesion
(HSIL); atypical squamous cells, cannot exclude HSIL (ASC-H);
and cancer. Anal histology was reported as benign, low-grade
AIN (AIN1 and condyloma), HG-AIN (AIN2, AIN3), or
invasive cancer according to the most recent lower anogenital
squamous terminology recommendations . If no biopsy was
taken, histology was considered to be benign, provided that
the HRA was normal.
Baseline characteristics of the study population were described
and compared according to acceptance to undergo HRA, using
the χ2 test for categorical variables and the rank-sum test for
continuous variables. The reproducibility of anal cytology
diagnoses was assessed after classification in 2 categories: negative or
minor cytological abnormalities (negative, ASC-US, or LSIL) vs
significant cytological abnormalities (ASC-H, HSIL, or invasive
cancer). The agreement between cytologists was calculated
using κ with 95% confidence interval (CI). The κ values were
interpreted using Altman thresholds .
For the analyses of factors associated with HG-AIN+, a
composite endpoint of the most severe diagnosis on cytology or
histology was used. In the absence of histology, the grade was based
on cytology alone. If the anal cytology was unsatisfactory, and
the HRA was normal, those who were HPV negative were
categorized as benign. Women with unsatisfactory cytology and no
biopsy were excluded from the analyses if HR-HPV was
positive. HG-AIN+ was defined as histological HG-AIN+ or HSIL
on cytology, in the absence of biopsy.
Univariable and multivariable logistic regression models
were used for analysis of factors associated with HG-AIN+.
The following factors were assessed: age, sub-Saharan origin,
tobacco smoking, total number of sexual partners, history of anal
sex, anal sex in the last year, current CD4 cell count, nadir CD4
cell count, history of cervical LSIL or worse (LSIL+), history of
cervical HSIL or worse, concurrent cervical cytology result,
concurrent cervical HPV-16 infection, history of anal condyloma,
and concurrent anal infection with HPV-16 or with HR-HPV
excluding HPV-16. Variables with P < .15 in the univariable
analysis were considered for inclusion in the final backward
multivariable model in which P < .05 was considered as
significant. HR-HPV types were defined according to the 2009
International Agency for Research on Cancer classification of types,
which were at least “probably carcinogenic to humans”—that is,
HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68 .
Sensitivity, specificity, positive predictive value, negative
predictive value, positive likelihood ratio (PLR), and negative likelihood
ratio (NLR) of anal HR-HPV, HPV-16, cytological result, and
cytology combined with HPV-16 testing were calculated for
detection of HG-AIN+ histology. Statistical analyses were performed
using SAS software version 9 (SAS Institute, Cary, North Carolina).
Of the 352 women who had at least 1 VIHGY study visit in
2012, 319 (90.6%) accepted the invitation to the anal HPV
screening icube substudy. Of these 319 women, 171 (54%)
attended the HRA examination. The median time between
HPV testing and anal cytology/HRA was 48 days (interquartile
range, 20–130 days). These 171 women were significantly older
(47.3 vs 43.1 years; P = .0004) than the 148 remaining women
who did not attend HRA. The 171 women also had a significantly
higher median CD4+ cell count (655 vs 561; P = .005), more
received cART and had a viral load <50 copies/mL (89.3% vs
78.9%; P = .01), and had a longer time since HIV diagnosis (17
years vs 14; P = .03). Approximately one-third (36.8%) of the
171 women were born in sub-Saharan Africa (Table 1).
All 171 anal cytologies were reviewed centrally. The rate of
unsatisfactory cytology was 5.8% at the local laboratories and 12.3%
with the central pathology reader (κ = 0.61 [95% CI, .41–.82]).
Table 2 shows the comparison of the anal cytology results by
the cytopathologists at local laboratories vs central reader for
those considered adequate for evaluation by the central reviewer.
The κ was 0.61 (95% CI, .39–.83). The central cytopathologist was
more likely to interpret the cytology as ASC-H or more severe.
were infected with an HR-HPV type. HPV-16 was detected in
According to the centrally reviewed anal cytology, 29.3%
were abnormal, with ASC-US or LSIL in 28 (18.7%) women,
ASC-H or HSIL in 15 (10.0%) women, and anal carcinoma in
1 woman (0.6%) (Table 3). Of the 169 HRAs performed, no
lesions were detected in 100 women (59.2%); acetowhite areas
were biopsied in the remaining 69 women. Biopsy-proven
low-grade AIN was found in 18 women (28.1%), HG-AIN in
10 women (15.6%), and cancer in 1 woman. Patients were
treated according to clinical practice at each center, which included
surgical excision, infrared coagulation, and electrocautery. The
woman with anal squamous cell carcinoma was a 48-year-old
woman born in Africa. She received chemotherapy with
5fluorouracil, mitomycin, and pelvic irradiation of 45 Gy with
complete disappearance of the primary anal mass and inguinal
lymph node. Her disease has now been controlled for 2 years.
Risk Factors for HG-AIN+
The results of anal cytology, HRA, histology, and HPV testing
are shown in Table 4. Low-grade AIN was detected in 33 of the
163 women (20.2%; 16 histologically confirmed results and 17
LSIL cytology alone) and HG-AIN+ in 21 (12.9%; 11
histologically confirmed results and 10 HSIL cytology alone). Results of
univariable and multivariable analyses of factors associated with
HG-AIN+ are presented in Table 5. In the multivariable
analysis, histories of cervical LSIL+ (odds ratio [OR], 4.2 [95% CI,
1.1–16.4]) and concurrent anal HPV-16 infection (OR, 16.1
[95% CI, 5.4–48.3]) were independently associated with
HGAIN+. Number of sexual partners, history of anal sex, anal
sex in the last year, current CD4 count, and nadir CD4 count
<350 cells/µL were not significant.
Tests Characteristics for the Detection of HG-AIN+ Histology
As shown in Table 6, anal HR-HPV testing and anal cytology
combined with HPV-16 testing had the highest sensitivity for
detecting HG-AIN+ histology (91%). HPV-16 genotyping and anal
cytology (abnormal cytology being defined as ASC-US or more
severe) had sensitivities of 64% and 82%, respectively, with no
significant differences between the tests. HPV-16 testing had
the highest specificity (86%). Detection of HPV-16, anal
cytology, and anal cytology combined with HPV-16 testing had similar
ability to detect HG-AIN+ histology with a PLR of 4.7 for
HPV16, 3.4 for cytology, and 3.1 for anal cytology combined with
HPV-16 testing, and NLR of 0.4, 0.2, and 0.1, respectively.
Prevalence of Anal HPV–Associated Disease
The prevalence of HR-HPV infection was 57.9%. Infection with
multiple HPV types was found in 81 of 99 (81.8%) women who
In this contemporary cohort of HIV-infected women receiving
effective cART and with regular gynecological follow-up, the
prevalence of any anal lesions was 33.1%, with low-grade AIN
No HRA (n = 148)
HRA (n = 171)
Age, y, median (IQR)
Heterosexual Intravenous drug users Other Missing
Cigarette smoker at baseline
Total No. of sexual partners
History of anal sex
Anal sex in the last year
HIV clinical characteristics
Prior diagnosis of AIDS
Current cART use
cART and HIV load <50 copies/mL
cART and HIV load >50 copies/mL
CD4+ cell count
Median (IQR) cells/µL
Nadir CD4+ count
Median (IQR) cells/µL
Gynecological clinical characteristics
History of treatment of LSIL+
History of LSIL+
Concurrent cervical Pap test result
Anal clinical characteristics
Concurrent anal HPV-16 infection
History of anal condyloma
History of anal cytologic screening
in 20.2% and HG-AIN or cancer in 12.9%. Factors associated
with HG-AIN+ in multivariable analysis were a history of
cervical lesion (LSIL+) and concurrent anal HPV-16 infection.
Anal cytology, HPV-16 detection, and cytology combined
with HPV-16 testing were the best methods to identify women
with HG-AIN+ histology.
Table 2. Interrater Agreement for Anal Cytology Interpretation in Adequate Specimens
Negative or ASC-US
or LSIL, No.
ASC-H or HSIL or
Central Pathology Review Negative or ASC-US or LSIL No. (%)
Abbreviations: ASCC, anal squamous cell carcinoma; ASC-H, atypical
squamous cells, cannot exclude HSIL; ASC-US, atypical squamous cells of
undetermined significance; HSIL, high-grade squamous intraepithelial lesion;
LSIL, low-grade squamous intraepithelial lesion.
To our knowledge, our study is the first to provide
comprehensive data on HPV-associated anal disease among HIV-infected
women, as all patients underwent cytology, HPV testing, and
HRA to evaluate the prevalence and characteristics of anal
HPV-associated lesions. Random biopsies of patients with
Anal HPV (n = 171)
HPV-16 alone or with other genotypes
Infection with HR-HPV type other than 16
Multiple HPV infectiona
Anal cytology (by central review) (n = 150)
Negative ASC-US/LSIL ASC-H/HSIL ASCC
HRA (n = 169)
Identification of acetowhite areas
Anal histology (n = 64)
Abbreviations: AIN, anal intraepithelial neoplasia; ASCC, anal squamous
cell carcinoma; ASC-H, atypical squamous cells, cannot exclude HSIL;
ASCUS, atypical squamous cells of undetermined significance; HIV, human
immunodeficiency virus; HPV, human papillomavirus; HRA, high-resolution
anoscopy; HR-HPV, high-risk human papillomavirus; HSIL, high-grade
squamous intraepithelial lesion; LSIL, low-grade squamous intraepithelial lesion.
a Multiple HPV infection: infection with at least 2 different genotypes including
1 HR-HPV type.
normal HRA were not performed; thus, some lesions could
have been missed . Patients who agreed to participate in the
HRA substudy differed significantly from women enrolled only in
the anal HPV substudy. A history of cervical LSIL+ was more
frequent among them, and anal HPV-16 was detected twice as
frequently. Therefore, the prevalence of anal lesions in our study
might be overestimated, whereas the power to detect risk factors
and to evaluate the screening strategies was improved. Women
who attended HRA also differed in terms of age and total number
of sexual partners and had better HIV clinical characteristics.
However, none of these factors were risk factors for HG-AIN+.
The overall prevalence of anal lesions was 33.1%, similar to
what has been described in the Women’s Interagency HIV
Study . Similar to others, we also found the prevalence of
low-grade AIN to be twice as high as the prevalence of
HGAIN+ [7, 8, 19, 20]. Despite this, the prevalence of HG-AIN+
in our study population was lower than that of 30%–43% of
patients reported among HIV-infected MSM .
Although anal cancer is a growing problem in women, there
have been few studies evaluating anal cytology as a method of
screening for the prevention of anal cancer in women, whether
HIV infected or not. Interobserver agreement of anal cytology
has been evaluated primarily in men [22, 23]. In the current
study, when anal cytology was categorized as the clinically
relevant categories of negative or minor cytological abnormalities
vs significant cytological abnormality, we found good
agreement between cytopathologists at local sites and central review
with a κ at 0.61, similar to that previously reported in a study
involving men . The central review cytopathologist
upgraded 7 cases to HSIL that had a local diagnosis of negative or LSIL.
The κ value we report here for anal cytology is lower than that
(0.82 [95% CI, .76–.87]) for agreement between 2 raters for
liquid-based cervical cytology of samples collected among women
participating in the VIHGY cohort . The higher agreement
observed with cervical samples might be related to much greater
experience with sampling and interpreting cervical cytology
compared with anal cytology .
In multivariable analysis, risk factors for HG-AIN+ included
history of cervical lesion (low-grade or more severe, LSIL+) and
concurrent anal HPV-16 infection. The mechanism underlying
the relationship between a history of cervical LSIL+ and
HGAIN+ may reflect an initial HR-HPV infection of the cervix
with autoinoculation from the cervicovaginal compartment to
the anal canal, given the low rate of anal intercourse in our
population. Having had a high-grade cervical lesion is a risk factor
for anal cancer in the general population . Only cervical
LSIL+ was a risk factor in our study population, possibly due
to the fact that the women were frequently screened for cervical
lesions and that high-grade cervical lesions were previously
treated. As observed in HIV-infected MSM , HPV-16 was
associated with an increased risk of anal HG-AIN+. Similar to
Absence of Oncogenic HPV
Result of Anal Biopsy
Absence of Oncogenic HPV
Absence of lesion, n = 35
LSIL, n = 2
HSIL+, n = 1
Absence of lesion, n = 7
Absence of Oncogenic HPV
No Biopsy Absence of lesion, n = 1 LSIL, n = 1 0
Abnormal HRA (n = 69)
Missing No HG-AIN
Absence of lesion, Absence of lesion,
n = 1 n = 12
n = 10
0 HSIL+, n = 5
Missing HRA, n = 2
Presence of Oncogenic HPV
Result of Anal Biopsy
Missing Absence of lesion, n = 1 LSIL, n = 2
Unclassifiable, n = 1
Presence of Oncogenic HPV
Presence of Oncogenic HPV
what has been observed for the cervix , it is possible that
HG-AIN+ associated with HPV-16 has a higher risk of
progression to invasive carcinoma than those associated with non–
HPV-16/-18 subtypes. Although earlier studies showed that
CD4 count <200 cells/mL was a risk factor for anal cytological
abnormalities in women, in our study population and in a
recent article, neither CD4 count nor CD4 nadir was associated
with composite cytohistology HG-AIN+ [8, 29, 30]. In fact,
most of the prior studies were performed in the late 1990s,
when the CD4 count threshold for starting cART was lower
than at present (from <200 cells/µL in the early cART period
to currently >350 cells/µL). It is possible that the women
included in our study had less-severe immunodeficiency due to earlier
access to cART (only 2 of them had a CD4 count <200 cells/µL
at the time of the study) and that the repertoire of lymphocytes
required to successfully control oncogenic HPV infection was
less damaged . It has also been shown that anal cancer occurs
at all levels of immunosuppression . As previously reported
by others, we found that neither history of anal sex nor anal sex
in the past year were risk factors for HG-AIN+ [8, 9]. In women,
receptive anal intercourse may not be necessary to acquire anal
HPV infection, as hypothesized above.
HR-HPV and HPV-16 detection had sensitivities of 91% and
64% and specificities of 44% and 86%, respectively, for detecting
HG-AIN+ histology. In our study, the gynecologists, using a
similar procedure as for the anal cytology, collected the anal
Characteristics of Women No. No.
Age at baseline
18–39 y 30 4
40–49 y 84 8
≥50 y 49 9
Sub-Saharan Africa 60 5
Other 103 16
Cigarette smoker (8 missing)
No 104 12
Yes 51 9
Total No. of sexual partners (1 missing)
1–4 62 4
≥5 100 17
History of anal sex (4 missing)
No 101 10
Yes 58 10
Anal sex in the last year (4 missing)
No 148 17
Yes 11 3
≥500 cells/µL 115 13
350–500 cells/µL 35 5
<350 cells/µL 11 3
Nadir CD4+ count
≥350 cells/µL 32 2
<350 cells/µL 131 19
History of cervical lesion (LSIL+)
No 74 3
Yes 89 18
History of cervical lesion (HSIL+)
No 117 13
Yes 46 8
Concurrent cervical Pap test result (1 missing)
Negative 135 16
ASC-US/LSIL 25 3
ASC-H/HSIL/ICC 2 1
History of anal condyloma
No 143 14
Yes 20 7
No 152 17
Yes 11 4
No 136 7
Yes 27 14
Univariable (95% CI)
Table 5 continued.
Characteristics of Women
Univariable (95% CI)
Logistic Model .06
sample for HPV testing. They found it easy to perform, and it
was well accepted by participants (91% of women attending
their gynecology consultation participated). Anal cytology had
a high sensitivity (82%) for the identification of HG-AIN+
histology. A similar high sensitivity of anal cytology has also been
found in other populations such as non-HIV-infected women
with HPV-associated lesions of the lower genital tract and in
HIV-infected men [14, 32]. The specificity of anal cytology was
76%, lower than what has been described in HIV-uninfected
women (93%), but much higher than that reported in
HIVinfected men (47% [95% CI, 24%–71%]), although the reasons
are unclear . Collection of a specimen for anal cytology is
quite simple to do, fast and painless, usually performed in a
doctor’s office, and does not require the use of an anoscope.
Finally, anal cytology and HPV-16 testing, with a high PLR and
low NLR, are easy tests to perform and might therefore be the
optimum screening strategy for detection of HG-AIN+
histology among HIV-infected women, although at a higher cost.
Unlike cervical cancer, there are no guidelines for screening
and treatment of anal lesions. The success of screening
programs depends on a number of fundamental principles,
including that (1) the target disease should be a common form
of cancer with high associated morbidity and mortality; (2)
test procedures should be safe, acceptable, and relatively
inexpensive; and (3) an effective treatment should be available
. Our findings of a high prevalence of anal HPV–associated
High-Grade AIN or
ASC-US or worse
ASC-US or worse or
Negative cytology and
% (95% CI)
% (95% CI)
PLR (95% CI) NLR (95% CI)
disease in HIV-infected women support the need for enhanced
screening efforts among these women, particularly as no
decrease in the incidence of anal cancer has been observed, despite
the availability of cART . Because early diagnosis and
treatment of high-grade lesions may prevent progression to anal
cancer, all women diagnosed with HG-AIN+ should be
considered for treatment or at least be followed closely, as recently
proposed in men .
Anal cytology along with HPV-16 genotyping, having the best
screening performance, might be a useful strategy for identification
of anal lesions. Although the effectiveness of treatment of anal
HG-AIN+ has not been fully established, anal cytology and
HPV testing appear to be well accepted by both gynecologists
and patients; these tests could readily be offered to HIV-infected
women during their gynecological examination and may facilitate
the early detection and treatment of anal cancer and its precursors.
Acknowledgments. ANRS-C017 VIHGY Study Group: Scientific
committee: S. Franceschi, J. Palefsky, I. Heard, D. Costagliola, H. Cubie,
C. Bergeron, G. Carcelain, H. Foulot, C. Crenn-Hébert, R. Tubiana,
I. Poizot-Martin, A. Isabelle Richet, B. Lefebvre, C. Rousset Jablonski,
J. P. Viard, X. Sastre Garau. Study Group Collaborators: Hospital Pitié:
R. Tubiana, M. Bonmarchand, L. Cuccu; Hospital St-Antoine: B. Lefebvre,
A. Richet, D. Torchin, B. Carbonne, J. F. Fléjou, N. Hoyeau; Hospital Ste
Marguerite: I. Poizot, M.J. Ducassou, E. Ressiot, D. Figarella-Branger;
Hospital Louis Mourier: F. Meier, C. Crenn-Hébert, C. Gorbatchev; Hospital
Hôtel Dieu: C. Rousset-Jablonski, J. P. Viard; Hospital Diaconesses:
I. Etienney, A. Lesage. Methodology: INSERM U943: V. Potard, S. Taibi;
D. Costagliola. Virology: H. Cubie, C. Moore. Cytology-Histology:
Financial support. This work was supported by ANRS (France
REcherche Nord & Sud Sida-hiv Hépatites).
Potential conflicts of interest. I. P.-M. has received travel grants,
consultancy fees, honoraria, and study grants from Bristol-Myers-Squibb, Gilead
Sciences, Janssen-Cilag, Abbott, Merck Sharp & Dohme-Chibret, and ViiV
Healthcare. C. C.-H. has received consultancy fees from Bristol-Myers
Squibb. J.-F. F. has served on advisory boards for GlaxoSmithKline and
Genentech. H. C. has received diagnostic reagents for research and occasional
speaker’s expenses from Hologic and Roche. T. M. D. has received research
supplies for anal cytology from Hologic; has served on the advisory board
for OncoHealth; and has served on the advisory board and speaker’s bureau
for Roche. D. C. has received travel grants, consultancy fees, honoraria, and
study grants from Bristol-Myers Squibb, Gilead Sciences, Janssen-Cilag,
Merck Sharp & Dohme-Chibret, and ViiV Healthcare. All other authors
report no potential conflicts.
All authors have submitted the ICMJE Form for Disclosure of Potential
Conflicts of Interest. Conflicts that the editors consider relevant to the
content of the manuscript have been disclosed.
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