Current HIV Research, 2011, 9, 339-345 339
1570-162X/11 $58.00+.00 © 2011 Bentham Science Publishers
Gender Differences in Liver Fibrosis and Hepatitis C Virus-Related
Parameters in Patients Coinfected with Human Immunodeficiency Virus
Julio Collazos*,1, José Antonio Cartón2 and Víctor Asensi2
Infectious Disease Units of 1hospital de Galdácano-Usánsolo, Vizcaya, and 2hospital Central de Asturias, Oviedo, Spain
Abstract: Objectives: To evaluate gender differences in liver fibrosis and hepatitis C virus-related parameters in patients
coinfected with human immunodeficiency virus.
Methods: Transversal study of 782 patients who underwent a complete clinical and laboratory evaluation. Fibrosis was
measured by transient elastometry (TE) and by commonly used laboratory-derived fibrosis indexes.
Results: Men were older, had higher rates of alcohol abuse, higher HCV viral load and liver tests, lower platelet values,
poorer CDC clinical stages, longer duration of HCV infection, shorter time on successful antiretroviral therapy (ART) and
had appreciably more advanced fibrosis than women. Multivariate analysis revealed that male gender (P<0.0001), longer
time since HCV acquisition (P<0.0001), alcohol abuse (P<0.0001), HCV genotype 3 (P=0.01), shorter time on successful
ART (P=0.005) and worse CDC clinical stages (P=0.03) were independently associated with significant or higher stages
of fibrosis. Male gender was also independently predictive of advanced or higher stages of fibrosis (P=0.06) or cirrhosis
(P=0.02). In patients with no alcohol abuse, men had worse fibrosis parameters than women (P<0.01 for each), but these
differences decreased in patients with alcohol abuse and became non-significant.
Conclusions: HIV-HCV-coinfected women have more favorable HCV virological and clinical profile than men and,
particularly, lower degrees of fibrosis. Alcohol abuse seemed to result more deleterious in women than in men. The
reportedly poorer outcomes of liver disease in HIV-HCV-coinfected patients, as compared with their HCV-monoinfected
counterparts, could be ameliorated by addressing these cofactors, some of them preventable or treatable.
Keywords: Antiretroviral therapy, female, gender differences, HCV infection, hepatic fibrosis, HIV infection, male, transient
and hepatitis C virus (HCV) constitutes a substantial
problem today, representing a major cause of death in these
patients since the generalization of potent antiretroviral
therapy (ART). In fact, there is a general agreement that
HIV-coinfected patients experience more rapid progression
of liver fibrosis than their HCV monoinfected counterparts
[1-6]. In addition, the large number of coinfected patients,
particularly among intravenous drug users (IDU), in whom
the prevalence of HCV infection is higher than 90% [7,8],
and the high rate of cirrhosis among these patients, involving
up to one-third of them according to some series [7,9,10],
reinforces the public health repercussions of this combined
Co-infection with human immunodeficiency virus (HIV)
immunological parameters of men and women have been
reported in HIV infection, women showing more favorable
profiles than men . Therefore, a different behavior
according to gender regarding HCV infection might also
occur. Some studies, usually carried out in HCV
monoinfected patients and focused to other objectives, have
tangentially reported differences in the progression of HCV-
related hepatic fibrosis in men and women. Some of these
reports suggest that women have a more favorable course
Different behaviors in the clinical, virological and
*Address correspondence to this author at the Infectious Disease Unit,
Hospital de Galdácano-Usánsolo, 48960 Vizcaya, Spain; Tel: +34 94 400
7005; Fax: +34 94 400 7133; E-mail: email@example.com
than men [2,12-14], although other authors failed to find
differences [4,9,10,15], and other studies found different
patterns depending on if the patients were coinfected or not
with HIV  or had a history of alcohol abuse [3,16].
Furthermore, other factors such as HIV, the patients’
immunological status and ART, could interact with HCV
dynamics and liver effects, adding further complexity to the
evaluation of any parameter related to HCV infection.
noteworthy the lack of studies specifically focused on the
behavior of HCV infection according to gender either in
HCV-monoinfected or HCV-HIV-coinfected patients. On the
other hand, considering the risks and inconveniences of liver
biopsy, non-invasive methods have been developed for the
evaluation of liver fibrosis, including transient elastometry
(TE) and diverse indexes calculated from laboratory results
such as APRI , Forns  and FIB-4 . Therefore, we
carried out an extensive evaluation of a large population of
HIV-HCV-coinfected patients with active HCV infection,
who underwent TE measurements. This evaluation included
the recording of many data, particularly those related to HIV
infection and its treatment, as these aspects may influence
the course of HCV infection.
Given the contradictory findings published, it is
clinical and laboratory characteristics in men and women
coinfected with HIV-HCV, in order to evaluate possible
gender differences in parameters related to HCV infection,
paying special attention to liver fibrosis issues measured by
TE and by other commonly used indexes.
The aim of this study was to analyze demographic,
340 Current HIV Research, 2011, Vol. 9, No. 5 Collazos et al.
prospectively at the two main hospitals of Asturies,
Northwestern Spain, during the period October 2007-
November 2009. Patients were considered for inclusion if
they were older than 18 years, were infected with HIV and
had active HCV co-infection confirmed by plasma RNA
detection. All patients underwent measurements of liver
stiffness by TE and, simultaneously, relevant clinical and
laboratory data were recorded. Pregnant patients, and those
in whom the performance of TE was technically difficult
were excluded. Also, patients with an acute episode of
cytolysis or cholestasis at the time of evaluation were
excluded, as these disturbances could influence TE
measurements. Patients who had cleared HCV infection,
either spontaneously or as a result of anti-HCV therapy, or
that were receiving anti-HCV therapy at the time of
evaluation were not considered for this study.
The patients for this cross-sectional study were recruited
data were recorded, including HCV, HIV and immunological
parameters, liver fibrosis indexes, history of alcohol abuse,
HBsAg, hepatitis delta virus coinfection, and ART received.
For the purpose of this study, alcohol abuse was considered
if the patient reported an intake >50 g/day during at least 5
years. Regarding HCV infection, the date of the first HCV
positive serology was recorded, but this date clearly does not
represent the true date of infection. Considering that the vast
majority of patients acquired the infection through IDU, the
very high prevalence of HCV infection among these patients
and the common sharing of needles in Spain, particularly
when most of these patients initiated the habit, we also
registered a more realistic estimated date of infection, which
was established at one year after the initiation in IDU.
A number of sociodemographic, clinical and laboratory
its duration and efficacy. Antiretroviral therapy was
considered successful if the patient had good adherence and
the HIV viral load was <400 copies/ml. Otherwise it was
considered suboptimal. Time under successful or suboptimal
ART was also gathered.
Antiretroviral drug history was also recorded, as well as
(EchoSens, Paris, France). The TE value finally considered
was the median of at least 10 measurements, carried out on
the right lobe, and were expressed as kilo Pascals (kPa). The
success rate was calculated as the number of validated
measurements divided by the total number of assessments.
The measurements were considered representative of liver
stiffness only if the interquartile range of all validated
measurements was <30% of the median value, with a success
Liver stiffness was evaluated by TE using FibroScan
different TE cut-offs: mild or no fibrosis (<7.2 kPa),
significant fibrosis (7.2-9.3 kPa), advanced fibrosis (9.4-13.9
kPa) and cirrhosis (>13.9 kPa). These cut-off points were
selected because they have been validated against liver
biopsies and are commonly used [20-24], although no
general consensus about the exact cut-off points exists.
Patients were divided into four groups according to
out by the demonstration of specific antibodies by EIA.
Quantification of HIV and HCV RNA was performed by
Serologic diagnosis of both HIV and HCV was carried
quantitative PCR (detection limits 50 copies/ml for HIV and
40 UI/ml for HCV) and the HCV genotype was determined
by line-probe-assay. Routine blood and biochemical
parameters were measured by standardized laboratory
used indexes derived from these analytical results, such as
APRI (calculated from AST and platelets) , Forns
(calculated from age, platelets, GGT and total cholesterol)
, and FIB-4 (calculated from age, AST, ALT and
Apart from TE, fibrosis was also evaluated by commonly
laboratory, therapeutic and fibrosis data evaluated in this
study were collected on a standardized form, and were later
entered into a computer database to be analyzed.
The sociodemographic, clinical, viroimmunological,
according to the Kolmogorov-Smirrnov test, non-parametric
tests were used. Categorical variables were compared with
the chi-square test or the Fisher’s exact test as appropriate.
Continuous variables were reported as the median and
interquartile (IQ) range and their comparisons between
groups were carried out with the Mann-Whitney U test.
Stepwise logistic regressions were used to evaluate the
parameters predictive of the diverse strata of fibrosis.
Statistical calculations were performed with the SPSS 16.0
software (Chicago, Illinois). A P value<0.05 for a two-sided
test was considered statistically significant.
As most variables did not follow a Gaussian distribution
men, with a median age of 44.0 years (IQ range 39.7-47.4).
Most patients (95.0%) had acquired the infection though
IDU. At the time of evaluation patients had an estimated
HCV infection dating since 23.3 years earlier (IQ range
19.1-26.8), their CD4 counts were 458 cells/?l (IQ range
291.3-656.5) and 86.8% of them were receiving ART.
Undetectable HIV viral load was attained in 70.8% of the
patients, and the viral load of the remainder patients was
3.58 log10 copies/ml (IQ range 2.28-4.59). Median HCV
viral load was 6.13 log10 UI/ml (IQ range 5.73-6.60). The
predominant HCV genotypes were 1 (62.0%) and 3 (23.5%).
Twenty-six patients (3.3%) had also active coinfection with
hepatitis B virus (HBV), and in 7 of the 18 patients (38.9%)
with HBV coinfection who had the test performed, hepatitis
delta infection was also found.
The study group was composed of 782 patients, 72.0%
women. Men were older, had higher rates of smoking habit
and alcohol abuse, poorer CDC clinical stages, higher HCV
viral load, longer estimated duration of HCV infection, lower
platelet values and higher levels of AST, ALT and GGT.
Table 2 describes the past and present ART of the patients.
Women were treated with successful ART longer and
received current non-nucleoside reverse transcriptase
inhibitor therapy and didanosine more commonly and
lopinavir/ritonavir and saquinavir less commonly than men.
Table 3 shows the fibrosis parameters evaluated by TE and
other indexes. As depicted in the table, men had appreciably
Table 1 shows the baseline parameters in men and
Gender Differences in HIV-HCV Coinfection Current HIV Research, 2011, Vol. 9, No. 5 341
and consistently more advanced fibrosis parameters than
women in each of the tests evaluated.
male gender, alcohol abuse, HCV genotype 3, duration of
Multivariate logistic regression analysis revealed that
HCV infection, CDC clinical stages and time on ART were
independently associated with significant o higher stages of
fibrosis (Table 4). On the contrary, age (P=0.07), current
CD4 counts (P=0.4), nadir CD4 count (P=0.9), active HBV
Age (yr) 44.3 [40.0-47.5] 43.3 [38.5-46.5] 0.006
Infected through intravenous drug use 539 (95.7%) 204 (93.2%) 0.1
Current intravenous drug use 120 (21.5%) 42 (19.4%) 0.5
Current tobacco use 488 (87.6%) 173 (79.7%) 0.005
Current cannabis use 167 (30.0%) 73 (33.6%) 0.3
< 30 g/day 363 (65.2%) 166 (76.5%)
30-50 g/day 120 (21.5%) 32 (14.7%)
Current alcohol intake
>50 g/day 74 (13.3%) 19 (8.8%)
Alcohol abuse (>50 g/day during ? 5 years) 195 (35.0%) 41 (18.9%) <0.0001
Time since HIV infection (yr) 15.1 [10.2-19.1] 15.3 [10.4-18.4] 0.6
Undetectable HIV viral load 395 (70.4%) 157 (71.7%) 0.7
HIV viral load* (log10 copies/ml) 3.63 [2.33-4.75] 3.15 [2.18-4.15] 0.09
Nadir CD4 (cells/?l) 200 [79-313] 201 [95-300.8] 0.7
Current CD4 (cells/?l) 443 [291.8-643.5] 502 [302-741] 0.08
Increase in CD4 from nadir (cells/?l) 218 [76.3-402.8] 268.5 [96-456] 0.06
A 276 (58.7%) 112 (56.6%)
B 53 (11.3%) 36 (18.2%)
Clinical CDC stage
C 141 (30.0%) 50 (25.3%)
Hepatitis virus-related parameters
Time since estimated HCV infection (yr) 23.8 [19.5-27.7] 23.0 [18.2-25.8] 0.002
Time since the first positive HCV test (yr) 12.8 [8.6-16.7] 13.1 [8.8-16.4] 0.8
HCV viral load (log10 UI/ml) 6.18 [5.78-6.62] 5.98 [5.49-6.50] 0.0001
1 362 (64.3%) 123 (56.2%)
2 11 (2.0%) 3 (1.4%)
3 126 (22.4%) 58 (26.5%)
4 64 (11.4%) 35 (16.0%)
Past treatment with anti-HCV therapy 63 (11.2%) 30 (13.7%) 0.3
Hepatitis B virus coinfection (HBsAg +) 20 (3.6%) 6 (2.7%) 0.6
Hepatitis delta virus coinfection (only if HBsAg +) 6 (37.5%) 1 (50.0%) 0.7
Fibrosis indexes-related laboratory parameters
Platelet count/?l 176000 [133000-218000] 192000 [149000-248000] 0.0008
Alanine aminotransferase (IU/ml) 61 [40-102.5] 42 [29-69] <0.0001
Aspartate aminotransferase (IU/ml) 52 [36-82] 41 [31-62] <0.0001
Gammaglutamyl transpeptidase (IU/ml) 86 [49-173] 77 [36-141] 0.003
Cholesterol (mg/dl) 169 [142-197] 170 [149-198] 0.1
Values are expressed as median [IQ range] for continuous variables or n (% of those for whom the data are available) for discrete variables.
*Only in those patients with detectable viral load.
342 Current HIV Research, 2011, Vol. 9, No. 5 Collazos et al.
infection (P=0.1), HCV viral load (P=0.2), HIV suppression
(P=0.9), time on protease inhibitors (P=0.9), time on non-
nucleoside reverse transcriptase inhibitors (P=0.8) and time
on nucleoside/nucleotide analogues-based ART (P=0.7) did
not reach the statistical significance level. Male gender was
also predictive of fibrosis when evaluating advanced or
higher stages of fibrosis (OR 1.52, 95% CI 0.98-2.35,
P=0.06) or cirrhosis (OR 1.85, 95% CI 1.09-3.12, P=0.02).
intake on fibrosis in men and women, we compared
separately the genders depending on the history of alcohol
intake. In patients with no history of alcohol abuse there
were highly significant differences between men and women
for each fibrosis parameter: TE median 7.2 (IQ range 5.6-
11.2) vs 5.9 (4.8-8.6), P<0.0001, APRI 0.70 (0.43-1.46) vs
0.55 (0.34-0.95), P=0.0002, Forns 5.60 (4.30-7.10) vs 4.90
(3.65-6.16), P<0.0001, FIB-4 1.44 (1.01-2.52) vs 1.32 (0.89-
1.88), P=0.01, respectively. However these differences
decreased in the group with alcohol abuse and all of them
became non-significant (TE P=0.1, APRI P=0.1, Forns
P=0.4 and FIB-4 P=0.6).
To evaluate the possible differential effect of alcohol
sociodemographic, clinical, virological, therapeutic and
In our study we found that there were significant
between men and women in several
laboratory parameters. Regarding HCV infection, men had
higher HCV viral load, longer time of infection, and higher
rates of genotype 1 infection. Importantly, fibrosis
parameters, evaluated by laboratory-derived indexes and TE,
were significantly and consistently worse in men than in
women, differences that were confirmed in the multivariate
analysis for different stages of fibrosis.
and homogeneous population, specifically devoted to
evaluate gender differences in liver fibrosis. Some studies
occasionally described certain particular aspects of HCV
infection according to gender. In this regard, it has been
reported that male gender was independently associated with
an increased risk of severe liver disease and fibrosis
progression in HCV infection [2,12-14]. On the contrary,
other authors found that the histological and clinical
progression of liver disease was independent of gender
[9,10,15], and others described an association of fibrosis
with male gender in the univariate analysis that did not reach
statistical significance in the multivariate analysis . Also,
a study on mono- and coinfected patients did not find
gender-associated differences in time to onset of cirrhosis
among HIV-HCV coinfected patients, although males had a
shorter median risk/hazard to cirrhosis than females among
HCV monoinfected patients . However, our large study
found convincing evidence that men with HIV-HCV
To our knowledge, this is the first study, based on a large
Men Women P Value
ART naïves 53 (9.5%) 21 (9.6%) 1
Total time on ART (yr) 7.88 [3.0-11.0] 7.75 [2.51-11.42] 0.8
Time on protease inhibitors–based ART (yr) 4 [1-7] 3 [0.92-6] 0.1
Time on non-nucleoside analogues-based ART (yr) 1 [0-4] 1 [0-4.62] 0.4
Time on nucleoside/nucleotide analogues-based ART (yr) 0 [0-3] 1 [0-4] 0.4
Time on successful ART (yr) 5 [2-8.75] 6 [2-10] 0.06
Time on suboptimal ART (yr) 2 [0-5] 1 [0-4] 0.01
Proportion of time of follow-up on ART (%) 55.0 [24.0-78.5] 55.3 [26.6-77.1] 0.8
Proportion of time of follow-up on successful ART (%) 33.5 [9.9-57.0] 36.9 [14.7-63.1] 0.1
Proportion of time on ART since the onset of IDU (%) 32.1 [12.7-45.0] 33.4 [11.6-47.5] 0.37
Proportion of time on successful ART since the onset of IDU (%) 18.7 [5.6-33.2] 25.7 [8.2-38.4] 0.01
Time on the current ART regimen 2.17 [1.03-3.86] 2.03 [0.81-3.57] 0.4
Current ART 484 (86.6%) 191 (87.2%) 0.8
Current protease inhibitor therapy 266 (48.4%) 87 (41.0%) 0.07
Current non-nucleoside reverse transcriptase inhibitor therapy 178 (32.4%) 89 (42.0%) 0.01
Current therapy with other regimens/no ART 120 (21.8%) 42 (18.9%) 0.5
Current treatment with lopinavir/ritonavir 158 (29.9%) 42 (21.0%) 0.02
Current treatment with efavirenz 117 (22.0%) 66 (33.0%) 0.002
Current treatment with saquinavir 30 (5.7%) 3 (1.5%) 0.02
Current treatment with didanosine 118 (22.3%) 62 (31.0%) 0.02
Current treatment with any other specific drug - - NS
Values are expressed as median [IQ range] for continuous variables or n (% of those for whom the data are available) for discrete variables.
ART denotes antiretroviral therapy, and IDU intravenous drug use.
Gender Differences in HIV-HCV Coinfection Current HIV Research, 2011, Vol. 9, No. 5 343
coinfection had more advanced fibrosis than women overall
and in each of the fibrosis strata analyzed.
Table 4. Factors Independently Associated with Significant
or Higher Stages of Fibrosis
OR 95% CI P Value
Male gender 2.75 1.77-4.25 <0.0001
Alcohol abuse 4.48 2.66-7.58 <0.0001
Time since hepatitis C virus acquisition 1.11 1.07-1.16 <0.0001
Time on antiretroviral therapy 1.14 1.06-1.22 0.0002
Time on optimal antiretroviral therapy 0.89 0.82-0.97 0.005
C vs A 1.89 1.18-3.03 0.008
Clinical CDC stage
C vs B 1.66 0.87-3.18
3 vs 1 2.20 1.33-3.65 0.002
3 vs 2 1.65 0.27-10.0 0.6
Hepatitis C virus genotype
3 vs 4 2.54 1.27-5.10
study could be at least partially explained by the effects of
hormonal factors at the cellular and molecular level. Thus,
previous studies in animal models showed that estradiol
suppresses hepatic fibrosis by inhibiting hepatic stellate cell
proliferation and collagen synthesis [25-27] and estradiol
The differences in the degree of fibrosis found in our
treatment increases hepatic estrogen receptor levels and
mRNA expression preventing the development of fibrosis
[27,28]. Similarly, studies in humans also suggest that the
decrease in estrogens in postmenopausal women  and
free testosterone in men  are associated with higher
degrees of fibrosis.
abuse, adds further complexity in the interpretation of the
results. Thus, some authors found that fibrosis progression in
HCV infection was slower in females compared with males
but, in contrast, fibrosis progression was more rapid in
females in alcoholic liver disease . In fact, a large study
using population-based mortality data found that HCV-
related premature deaths were more common in men in the
absence of alcohol abuse, but as alcohol seems to have a
stronger effect in females, the gender difference diminished
in patients with alcohol abuse . Our results also support a
different effect of alcohol in men and women, as there were
highly significant differences between genders in fibrosis
parameters in patients with no history of alcohol abuse,
whereas these differences decreased greatly, and became
non-significant, in patients with alcohol abuse.
The presence of concomitant factors, such as alcohol
as an intake >50 g during ?5 years, was independently
associated with significant fibrosis. These findings are in
agreement with previous reports that consistently have
described the deleterious effect of alcohol in disease
progression of HCV-infection [2,4,10,15,16].
We also found that a history of alcohol abuse, as defined
slows fibrosis progression in HIV-HCV-coinfected patients
[5,31-34]. However, other authors found similar rates of
On the other hand, it is generally accepted that ART
Fibrosis Parameters in Men and Women
Men Women P Value
Transient elastometry values (kPa) 8.1 [6.1-14.5] 6.1 [4.9-9.8] <0.0001
No or minimal fibrosis 215 (38.2%) 133 (60.7%)
Significant fibrosis 111 (19.7%) 26 (11.9%)
Advanced fibrosis 87 (15.5%) 27 (12.3%)
Cirrhosis 150 (26.6%) 33 (15.1%)
Significant or higher stages of fibrosis 348 (61.8%) 87 (39.7%) <0.0001
Advanced or higher stages of fibrosis 236 (41.9%) 60 (27.4%) 0.0002
Cirrhosis 150 (26.6%) 33 (15.1%) 0.0006
Annual fibrosis progression index* (since the first positive HCV test) 0.76 [0.49-1.65] 0.56 [0.35-1.11] <0.0001
Annual adjusted fibrosis progression index* (since the estimated date of infection) 0.38 [0.29-0.68] 0.31 [0.23-0.48] <0.0001
Annual stage of fibrosis index§ 0.091 [0.05-0.134] 0.058 [0.041-0.111] <0.0001
Laboratory liver fibrosis indexes
APRI index 0.78 [0.46-1.64] 0.57 [0.35-1.01] <0.0001
Forns index 5.88 [4.74-7.41] 5.11 [3.82-6.50] <0.0001
FIB-4 index 1.65 [1.12-2.84] 1.40 [0.97-2.12] 0.0006
Values are expressed as median [IQ range] for continuous variables or n (% of those for whom the data are available) for discrete variables.
*Fibrosis progression indexes were calculated by dividing the transient elastometry value by the number of years elapsed since the event.
§Calculated by dividing the stage of fibrosis by the number of years elapsed since the estimated date of infection.
344 Current HIV Research, 2011, Vol. 9, No. 5 Collazos et al.
progression in ART treated and untreated patients , and a
recent study found significantly higher rates of significant
fibrosis in the univariate analysis in coinfected patients
receiving ART in comparison with untreated patients,
differences that were not confirmed in the multivariate
analysis . Interestingly we found that although the time
on ART was predictive of significant or higher stages of
fibrosis, perhaps reflecting the effect of time on fibrosis
progression, the period on optimal ART, as evaluated by
good adherence and HIV suppression, was independently
associated with milder fibrosis. This observation could
account for some discrepancies observed in the literature
when considering only ART, but not its quality, and
reinforces the importance of optimal control of HIV to
prevent the progression of HCV-related liver disease.
between HCV genotype 3 and higher degrees of fibrosis.
This association is in agreement with some studies
[12,24,35], although others did not find such a relationship
[4,9,14], and another large study found a trend towards a
protective effect of genotype 4 as compared with the
remainder genotypes . Our observation of the deleterious
effect of genotype 3 on fibrosis progression has practical
implications, because of the better response to therapy of this
genotype in comparison with the more common genotype 1,
and emphasizes the importance of treating all patients with
this genotype and no contraindications for anti-HCV therapy.
Another interesting finding of our study was the association
of the clinical CDC stage C with more fibrosis, perhaps
reflecting a poorer control of the HCV infection in patients
with worse clinical status.
Remarkably, we also found an independent relationship
acquisition was independently associated with higher stages
of fibrosis, probably as a result of longer periods of exposure
to HCV. We also observed higher HCV viral loads in men
than in women, observation that is in agreement with other
Not unexpectedly we also found that the time since HCV
somewhat higher TE values than women , which, to
some extent, could explain the differences observed in our
study. However, we also found highly significant differences
between men and women in each of the other fibrosis
indexes analyzed, which are unrelated to TE. Also, a study
on healthy living organ donors focused to identify the “true
normal” values of FibroScan did not find differences
between genders . Consequently, any possible bias of
gender in the TE measurements would result in minimal
differences, which does not seem to account for the clear
differences observed in our series.
It has been reported that apparently healthy men have
and homogeneous characteristics of the population analyzed,
the extensive data recorded from each case, focused to
immunological and therapeutic aspects, and the homogeneity
in the evaluation of the patients, which allow us to draw
reliable conclusions. On the contrary, limitations include
possible mistakes in the gathering and introduction of such
an amount of information, and inexactitudes in the
retrospective data. However, precautions were taken to avoid
bias and mistakes as much as possible and, in addition, such
limitations would affect evenly and similarly to both groups.
Advantages of our study include the large sample size
Therefore, the possible influence of such potential errors and
biases in the results, if any, would be minimal.
more favorable HCV virological parameters than men, as
well as lower degrees of fibrosis, as evaluated by TE and
commonly used laboratory-derived
investigations, particularly in animal models, suggest that
hormonal factors may be responsible at least partially for
these gender differences. HCV genotype 3 infection, CDC C
clinical stage, suboptimal ART, time since HCV infection
and alcohol abuse, are also cofactors independently
associated with liver fibrosis in these patients, the last being
seemingly more harmful in women than in men. The
reportedly poorer outcome of liver disease in HIV-HCV
coinfected patients, as compared with their HCV
monoinfected counterparts, could be ameliorated by
addressing these cofactors, some of them preventable or
We conclude that HIV-HCV coinfected women have
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Received: November 22, 2010
Revised: July 21, 2011 Accepted: July 25, 2011