Management of Hepatitis C Virus Infection in Heavy Drinkers
Charlotte E. Costentin1,†, Jean-Baptiste Trabut1,†*, Vincent Mallet1,2,3, Stéphane Darbeda1, Véronique Thépot1,
Bertrand Nalpas1,4, Béatrice Badin de Montjoye5, Béatrice Lavielle1, Anaïs Vallet-Pichard1,3, Philippe Sogni1,2,3and
1Unité d’Hépatologie et d’Addictologie, Hôpital Cochin, Assistance Publique des Hôpitaux de Paris, 27 rue du faubourg Saint Jacques, 75014 Paris, France,
2Université Paris Descartes, Paris, France,3INSERM U-1016, Paris, France,4Département de l’Alcool et des Addictions, INSERM, Paris, France and
5Centre Cassini, Hôpital Cochin
*Corresponding author: E-mail: email@example.com
†C.E.C. and J.-B.T. have equally contributed and are the joint first authors.
(Received 27 December 2012; first review notified 7 February 2013; in revised form 12 February 2013; accepted 14 February 2013)
Abstract — Aim: Optimal management of hepatitis C virus (HCV) infection is controversial in heavy drinkers. We compared the
management of HCV infection of heavy drinkers with that of patients without a history of alcohol abuse. Methods: In a retrospective
case–control study, 69 HCV-infected heavy drinkers [daily alcohol consumption at referral above 60 g/day, hereafter ‘alcohol group’]
were compared with matched HCV-infected patients with low alcohol consumption (<40 g/day, ‘control group’). Results: Patients of
the ‘alcohol group’ were younger (42 vs. 45 years, P=0.05), more often male (69.6 vs. 56.5%, P=0.11) and had been infected by
intravenous drug use (85.5 vs. 45.0%, P<0.0001). The percentage of patients with a recommendation for treatment according to the
French 2002 consensus (bridging fibrosis or genotype 2 or 3) was 52 of 69 (75.4%) in both groups, while the proportion of patients
treated was higher in the control group (71.0 vs. 44.9%, P=0.002). In the ‘alcohol group’, patients had better access to treatment if
they were employed or consumed 170 g/day or less at first referral. Sustained virological response (SVR) was obtained in 10 of 31
patients (32.3%) of the ‘alcohol group’ vs. 8 of 31 patients (25.8%) of the control group matched for genotype and type of treatment
(P=0.58). Conclusion: Heavy drinkers are less often considered for antiviral therapy compared with patients without a history of
alcohol abuse. However, once treatment is actually initiated, SVR rates are comparable with those achieved in non-drinkers despite
the continuation of alcohol consumption during therapy in some patients.
Chronic infection with the hepatitis C virus (HCV) is a
leading cause of liver disease worldwide. Among chronic
HCV carriers, however, only a fraction will eventually
develop life-threatening complications such as cirrhosis, liver
failure or hepatocellular carcinoma. A variety of co-factors—
related to host characteristics, co-morbidities or lifestyle—
affect the long-term outcome of HCV infection. Heavy
alcohol consumption is one of the most important of those
co-factors with a significant influence on the natural history
of HCV infection (Safdar and Schiff, 2004).
Heavy alcohol consumption is common in patients with
chronic hepatitis C and has a synergistic effect on fibrosis
progression. Prevalence of HCV infection is higher in heavy
drinkers (8 to 45%) (Parés et al., 1990; Caldwell et al.,
1993; Mendenhall et al., 1993; Fong et al., 1994; Befrits
et al., 1995; Coelho-Little et al., 1995; Srugo et al., 1998)
than in the general population (<1% in France as in most
western countries; Meffre et al., 2010). The higher preva-
lence of HCV infection in heavy drinkers is likely to be
mainly related to the common intravenous drug use history,
which hasbeen switched
(McHutchison et al., 1992; Mendenhall et al., 1993; Verbaan
et al., 1993; Fong et al., 1994; Befrits et al., 1995; Galperim
et al., 2006). An association has consistently been shown
between high alcohol consumption and advanced fibrosis
stage (Parés et al., 1990; Laskus et al., 1992; Caldwell et al.,
1993; Fong et al., 1994; Befrits et al., 1995; Coelho-Little
et al., 1995; Ostapowicz et al., 1998; Nevins et al., 1999;
Khan and Yatsuhashi, 2000; Harris et al., 2001; Fabris et al.,
2004; Hutchinson et al., 2005), especially when gender, age
and suspected length of the disease are taken into account
(Pessione et al., 1998; Pol et al., 1998; Wiley et al., 1998).
Regarding antiviral treatment, several studies have reported
that a history of excessive alcohol consumption was associated
with a lower rate of HCV eradication in patients receiving an
interferon-based regimen (Okazaki et al., 1994;Mochida et al.,
1996; Ohnishi et al., 1996; Loguercio et al., 2000; Tabone
et al., 2002). It has been hypothesized, in accordance with in
vivo data, that ethanol could have a direct impact on HCV rep-
lication and on interferon signal transduction (Pessione et al.,
1998; Loguercio et al., 2000; Osna et al., 2005; McCartney
et al., 2008). Guidelines, therefore, recommend a 6-month
period of abstinence before initiation of antiviral therapy in
HCV-infected patients (Dhumeaux et al., 2003; Sherman
et al., 2007). However, data evaluating the real impact of
ongoing alcohol consumption during interferon-based therapy
are scarce and, to date, no study has demonstrated the benefi-
cial effect of protracted abstinence before the introduction of
antiviral therapy. On the one hand, in most studies reporting a
negative impact of alcohol consumption on the outcome of
interferon therapy, patients had stopped using alcohol before
the beginning of antiviral therapy and were supposed to remain
abstinent throughout treatment (Okazaki et al., 1994; Mochida
et al., 1996; Ohnishi et al., 1996; Tabone et al., 2002). On the
other hand, Anand et al. (2006) have shown that the negative
impact of alcohol consumption on antiviral therapy might be
entirely attributable to low adherence and premature termin-
ation of the treatment. Taken together, those data suggest that
abstinence per se is not sufficient to improve the efficacy of
antiviral treatment in patients with a history of heavy alcohol
C.E.C. and J.-B.T. have equally contributed and are the joint first
Alcohol and Alcoholism Vol. 48, No. 3, pp. 337–342, 2013
Advance Access Publication 21 March 2013
© The Author 2013. Medical Council on Alcohol and Oxford University Press. All rights reserved
use and that efforts should also focus on the improvement of
adherence to treatment.
It is, therefore, crucial to get more data on the manage-
ment of HCV among alcoholics. The aim of this retrospect-
ive case–control study was to compare the management of
HCV infection in a cohort of patients with heavy alcohol
consumption at the time of referral with that in a cohort of
HCV-infected patients without any history of alcohol abuse.
PATIENTS AND METHODS
This was a retrospective case–control study including
patients with HCV infection with a current history of alcohol
abuse (case, hereafter ‘alcohol group’) and without a history
of alcohol abuse (control). All patients have been referred to
our Liver Unit between 1991 and 2009.
The inclusion criteria in the ‘alcohol group’ were: chronic
HCV infection defined by detectable HCV RNA for at least
6 months; alcohol consumption ≥60 g/day for at least 1 year
at the time of first referral; no previous antiviral treatment
and available fibrosis evaluation performed at first referral,
either with a liver biopsy or with a non-invasive test such as
liver stiffness measurement or validated biomarkers (e.g.
FibroTest®) according to the recommendations of the French
health authorities (Fontaine et al., 2007).
Two control groups were constituted, for comparison with
the ‘alcohol group’, in order to evaluate access to antiviral
therapy (‘control/access group’) and response to treatment
(‘control/response group’), respectively. The inclusion cri-
teria in both control groups were identical to those in the
‘alcohol group’ (chronic HCV infection, fibrosis evaluation
and no previous antiviral treatment) except for alcohol con-
sumption that had to be below 40 g/day without previous
periods of alcohol abuse. In each control group, patients
were matched with those of the ‘alcohol group’ on a 1/1
ratio. In the ‘control/access group’, patients were matched
according to stage of fibrosis (F0–1 vs. F2–3 vs. F4, in the
METAVIR scoring system), period of the first evaluation
(before 1998 vs. 1998 to 2001 vs. after 2001), genotype (1
or 4 vs. 2 or 3) and, when possible, gender and age. In the
‘control/response group’, patients were matched to the
treated patients of the ‘alcohol group’ according to type of
antiviral therapy (standard interferon monotherapy vs. stand-
ard interferon associated to ribavirin vs. pegylated interferon
associated to ribavirin), genotype (1 vs. 2 or 3 vs. 4) and,
when possible, to stage of fibrosis, gender and age.
Altogether, 69 patients were included in the ‘alcohol
group’ [69.9% male, median age: 42 years] and in the
‘control/access group’ (56.5% male, median age: 45 years).
The 31 treated patients of the ‘alcohol group’ (77.4% male,
median age: 42 years) were matched to the 31 patients of the
‘control/response group’ (67.4% male, median age: 42 years).
The following data were recorded at the time offirst referral:
age, gender, route of HCV transmission, hepatitis B virus
status [positivity or negativity HBs antigen (HBsAg) and of
anti-HBc antibodies (HBcAb)], co-infection with HIV, aspar-
tate transaminase (AST), alanine transaminase and gamma
glutamyl transpeptidase (GGT) levels and, indication for anti-
viral treatment. Indication for antiviral treatment was defined
according to the French 2002consensus as follows
(Dhumeaux et al., 2003): bridging fibrosis (i.e. METAVIR fi-
brosis stage ≥2) or genotype 2 or 3 whatever the fibrosis stage.
In the ‘alcohol group’, data related to employment, housing,
opiate substitution therapy and the existence of comorbidities
(psychiatric diseases, diabetes, obesity and cardiovascular or
neurological diseases) were also collected. During the follow-
up, the number of antiviral treatment courses and, for each of
them, the drugs used and their duration were recorded in both
groups. Sustained virological response (SVR) was defined by
undetectable HCV RNA 6 months after the end of therapy.
All the patients were followed by a hepatologist during all
the period covered by the study. In the ‘alcohol group’,
patients had an additional specific follow-up by a multidis-
ciplinary team comprising an addiction specialist, a psych-
ologist and a social worker. The high incidence of
psychiatric co-morbidities in this group and the management
of interferon side effects also justified a joint follow-up with
a psychiatrist for the majority of the patients. In the ‘control
groups’, the need for psychosocial support was assessed on a
case-by-case basis. Approval of the study was obtained from
the local ethical board.
Quantitative parameters were described using median and
interquartile range (IQR), while qualitative parameters were
described as percentages. Quantitative values were compared
using the Mann–Whitney test. Dichotomous parameters were
compared using the χ2test. The Fisher exact test was used
when the sample was too small to use the χ2test. Logistic
binary regression was used for multivariate analyses after
continuous variables were categorized (below or above the
median). The statistical significance level was <5%. All tests
were done using ‘BiostaTGV’ (http://marne.u707.jussieu.fr/
biostatgv/) except for multivariate analyse that was done with
the SPSS software.
The ‘alcohol group’ included 69 patients with excessive
alcohol consumption and chronic HCV infection. To evalu-
ate access to treatment, they were compared with 69 patients
group’). As shown in Table 1, patients in the ‘alcohol group’
were younger (42 vs. 45 years, P =0.05) and more frequently
infected through intravenous drug use (85.5 vs. 45.0%,
P <0.0001). No patient was HBsAg positive and the pres-
ence of anti-HBcAb was more common in the ‘alcohol
group’ (54.7 vs. 35.5%, P =0.03). Five patients were
co-infected with HIV in the alcohol group and one in the
‘control/access group’ (P= 0.09). Patients were mainly
infected with genotype 1 (50.7% in ‘alcohol group’ vs.
56.5% in ‘control/access group’), and genotype 3 (34.8 vs.
29.0%). Median alcohol consumption in the ‘alcohol group’
was 170 g/day (IQR: 115–250) at the time of referral.
There was no difference in terms of fibrosis stage, as
patients were matched according to this criterion: percentage
of patient with significant fibrosis, i.e. METAVIR ≥F2, was
63.8% in both groups. Percentage of cirrhosis was 43.4 and
37.7% in the ‘alcohol group’ and in the ‘control/access
338 Costentin et al.
group’, respectively (P=0.49). Median AST and GGT levels
were higher in the ‘alcohol group’ (Table 1).
Access to treatment
As shown in Table 1, fewer treatments were initiated in the
‘alcohol group’ than in the ‘control/access group’ (44.9 vs.
71.0%, P =0.002). Among the patients with an indication for
antiviral therapy, the rate of treatment initiation was also
lower in the ‘alcohol group’ than in the ‘control/access
group’ (53.8 vs. 88.5%, P =0.0001). A lower rate of treat-
ment initiation in the ‘alcohol group’ was also observed
among patients with advanced fibrosis (56.8 vs. 93.2%,
Patients in the ‘alcohol group’ were more likely to receive
treatment if their alcohol consumption at first referral was
below 170 g/day (OR =3.40, P =0.002) and/or if they were
currently employed (OR =3.20,
remaining significantly associated with treatment initiation in
multivariate analysis (Table 2).
In the ‘alcohol group’, the reasons for not treating despite
indication (24 patients) were the following (several patients
had more than one reason): mild fibrosis (METAVIR F1) in
patients with genotype 3 (n= 4), absence of sustained abstin-
ence (n=11), psychiatric disorders (n= 5), patient’s refusal
(n=5) and loss to follow-up (n=5). Among the six patients
of the ‘control/access group’ who did not receive treatment
despite indication, the reasons not to treat were mild fibrosis
in patients with genotype 3 (n=3), patient’s refusal (n=2)
and loss to follow-up (n= 1).
After one treatment failure, a second treatment was
initiated in 50% of the ‘alcohol group’ and in 64.1% in the
‘control/access group’ (P=0.30). At the end of follow-up,
there was a non-significant trend toward a lower rate of viral
clearance in the ‘alcohol group’ than in the ‘control/access
group’ (17.4 vs. 24.6%, P =0.29).
Table 2. Factors associated with access to antiviral therapy among
HCV-infected heavy drinkers (‘alcohol group’)
Odds ratio (CI 95%)
for access to therapy
Alcohol consumption (n=68)
Opiate substitution (n=64)
Psychiatric comorbidities (n=65)
Somatic comorbidities (n=68)
1.04 (0.41; 2.76)0.89
1.50 (0.53; 4.27)0.45
0.75 (0.27; 2.04) 0.57
0.47 (0.16; 1.35) 0.05
3.20 (1.14; 8.98)0.02
0.45 (0.15; 1.30) 0.13
3.40 (1.27; 9.10) 0.002
0.62 (0.20; 1.64)0.29
0.95 (0.31; 2.86) 0.93
1.59 (0.61; 4.16) 0.34
‘Antiviral therapy’ denotes interferon-based regimen against HCV infection.
The ‘P’ is given for univariate analysis. Both ‘alcohol consumption ≤170 g/
day’ and ‘employment’ remained significantly associated with access to
antiviral therapy in multivariate analysis (P<0.05).
HCV, hepatitis C virus; CI, confidence interval.
Table 1. Baseline characteristics and access to antiviral treatment in
HCV-infected heavy drinkers (‘alcohol group’) compared with
HCV-infected patients without a history of alcohol abuse (‘control/access
group’ (N=69) P
Male, n (%)
Median age, years (IQR)
Median alcohol consumption
Positive HBsAg, n (%)
Positive HBcAb, n (%)
Drug users, n (%)
HIV infection, n (%)
Genotype, n (%)
Median AST, IU (IQR)
Median ALT, IU (IQR)
Median GGT, IU (IQR)
Fibrosis ≥2a, n (%)
Indication for antiviral
treatment, n (%)
Treated (total)b, n (%)
Treated (with indication)b, n
Reasons not to treat despite indication
Minimal fibrosis, n
Absence of abstinence, n
Psychiatric diseases, n
Patient’s refusal, n
Loss to follow-up, n
Treated (with advanced
fibrosis), n (%)
First treatment failure, n (%)
Second treatment, n (%)
0 (0) 0 (0)1
25/44 (56.8) 41/44 (93.2)0.00008
Patients were matched for stage of fibrosis, genotype and, when possible, for
gender and age. ‘Antiviral therapy’ denotes interferon-based regimen against
HCV, hepatitis C virus; IQR, interquartile range; IU, international units;
AST, aspartate transferase; ALT, alanine transferase; GGT, gamma glutamyl
aAccording to METAVIR scoring system.
b‘Total’ includes patients treated according to the French 2002 consensus
(Dhumeaux et al., 2003) and patients treated outside the recommendations;
‘with indication’ includes only patients with an indication according to the
French 2002 consensus; ‘with advanced fibrosis’ includes only patients with
fibrosis ≥2 (METAVIR).
cThis comparison was made without matching patients for the genotype or
the type of treatment. Results with this matching are provided in Table 3.
Hepatitis C management in heavy drinkers 339
Response to treatment
Each of the 31 patients of the ‘alcohol group’ was matched
with a control patient according to the type of treatment
received and to their genotype (‘control/response group’).
‘Alcohol group’ and ‘control/response group’ were also com-
parable according to other clinical characteristics (gender,
age and stage of fibrosis, Table 3). Three patients of the
alcohol group were lost to follow-up before the assessment
of SVR. Those cases were considered treatment failures. The
rate of SVR was similar in both groups (32.3% in the
‘alcohol group’ vs. 25.8% in the ‘control/response group’,
P =0.58). In the ‘alcohol group’, rate of premature treatment
discontinuation was 12.9 vs. 10.0% in the ‘control/response
group’ (P =1.00).
Alcohol consumption during antiviral treatment
In the subgroup of 31 patients who received antiviral
therapy, abstinence had been obtained before initiation of
antiviral therapy in 23 patients but the length of abstinence
was less than 6 months in 18 (Table 4). Twelve of those
patients remained abstinent throughout the treatment. Eight
patients did not stop alcohol consumption before initiation of
antiviral therapy but most lowered their consumption during
treatment. Among the 19 patients who consumed alcohol
while on therapy, 9 consumed less than 40 g/day and 10 con-
sumed 40 g/day or more.
There was a non-significant trend for a higher rate of SVR
in patients who stopped alcohol consumption before treat-
ment and among those who remained abstinent (Table 4).
‘High’ alcohol consumption (≥40 g/day) during therapy was
not associated with a decrease of the SVR rate (3/10, 30%).
In this cohort, 11 patients (35.5%) were abstinent 1 year
This observational study compared the management of HCV
infection in a group of patients with heavy alcohol consump-
tion at the time of first referral (‘alcohol group’) with that in
a group of patients with hepatitis C but no history of alcohol
abuse. We observed that patients in the ‘alcohol group’ were
less likely to receive antiviral therapy than patients without a
history of alcohol abuse, even in the case of advanced liver
disease with definite indication to treatment. However,
patients of the ‘alcohol group’ who received antiviral treat-
ment had a similar rate of SVR compared with controls.
In our study, failure to achieve sustained abstinence was
the main reason to postpone treatment despite indication.
This is in accordance with guidelines that recommend pro-
tracted abstinence before the introduction of antiviral treat-
ment (Dhumeaux et al., 2003; Sherman et al., 2007). It
should be emphasized, however, that most treatments were
introduced after short-term abstinence (<6 months) and that
some patients were treated despite ongoing alcohol consump-
tion. Our results also show that it remains difficult to con-
sider antiviral treatment in very heavy drinkers (≥170 g/day
at first referral).
Besides alcohol consumption, reasons not to treat were
absence of patient’s adherence to the therapeutic project
(treatment’s refusal or loss to follow-up) and psychiatric co-
morbidities. We also found that unemployed patients were
less likely to be treated. It illustrates the fact that management
of hepatitis C in heavy drinkers requires a global multidiscip-
linary approach, including hepatologists, addiction specialists,
psychiatrists as well as psychosocial support. This kind of
management was systematically proposed to all patients of the
‘alcohol group’ in this study, as our liver unit has a long
experience of both hepatitis C treatment and alcohol addiction
care. It might partly explain why, in our study, the rate of
treatment initiation in heavy drinkers was higher than that
reported by Anand et al. in a similar population setting
(45 vs. 23%) but in a different country (Anand et al., 2006).
Our multidisciplinary approach probably also explains why
we achieved similar SVR rates in our alcohol group compared
with the control group. Several studies have reported lower
rates of SVR in this population setting, and it has been
hypothesized that ethanol could directly impair the antiviral
activity of interferon (Okazaki et al., 1994; Mochida et al.,
1996; Ohnishi et al., 1996; Loguercio et al., 2000; Tabone
et al., 2002; McCartney et al., 2008). However, three studies
Table 4. Sustained virological response according to alcohol consumption
during antiviral treatment in the 31 treated patients of the ‘alcohol group’
Alcohol withdrawal before treatment:
Alcohol withdrawal for more than 6 month before treatment:
Total abstinence during treatment:
SVR, sustained virological response.
denotes interferon-basedregimen againstHCV
Table 3. Response to HCV therapy in HCV-infected heavy drinkers
(‘alcohol group’) compared with HCV-infected patients without a history of
alcohol abuse (‘control/response group’)
Male, n (%)
Age (years), median (IQR)
Genotype, n (SVR)
Fibrosis, n (%)
Treatment received, n (% SVR)
Interferon and ribavirin
discontinuation, n (%)
SVR, n (%)
15 (SVR: 26.7%)
12 (SVR: 33.3%)
4 (SVR: 50.0%)
15 (SVR: 20.0%)
12 (SVR: 33.3%)
4 (SVR: 33.3%)
8 (SVR: 0%)
3 (SVR: 66.7%)
20 (SVR: 40.0%)
8 (SVR: 12.2%)
3 (SVR: 0%)
20 (SVR: 35.0%)
4 (12.9%)3 (10%) 1.00
10 (32.3)8 (25.8)0.58
Patients were matched for genotype, treatment received and, when possible,
stage of fibrosis, gender and age.
HCV, hepatitis C virus; IQR, interquartile range; SVR, sustained virological
340 Costentin et al.
recently reported results comparable with ours with satisfac-
tory SVR rates in patients with a history of alcohol abuse
(Bruggmann et al., 2010; Le Lan et al., 2012; Russell et al.,
2012) probably due to a better rate of treatment completion.
For example, Anand et al reported a 40% rate of treatment dis-
continuation among recent heavy drinkers, although only
patients who managed to stop their alcohol consumption were
considered for antiviral treatment in this study (Anand et al.,
2006).In our study, we observed a lower rate of treatment dis-
continuation (13%) in the alcohol group, including abstinent
and non-abstinent patients receiving antiviral treatment. Le
Lan et al. also reported a low rate of treatment discontinuation
(16%) in a similar population including abstinent and non-
abstinent patients (Le Lan et al., 2012).
Reporting antiviral treatment outcomes among patients
with ongoing alcohol consumption during therapy is also of
interest. In the ‘alcohol group’, two thirds of the patients
consumed alcohol during antiviral therapy, whether they had
begun treatment without prior withdrawal or resumed alcohol
consumption during therapy. Compared with the ‘control
group’, alcohol consumption (even above 30 g/day) did not
clearly impact on the rate of SVR. There was, however, a
trend toward a better outcome in patients who remained ab-
stinent throughout treatment. In the same line of evidence,
Le Lan et al. have reported a significantly higher rate of
SVR in former heavy drinkers who remained abstinent
throughout antiviral therapy compared with patients with
ongoing alcohol consumption (Le Lan et al., 2012).
It is noteworthy that most heavy drinkers at the beginning
of the study had reduced their consumption before initiation
of therapy or during treatment. Moreover, in more than
one-third of the patients, antiviral therapy had led to sus-
tained abstinence. Management of chronic hepatitis C could
influence the patient’s awareness of his addiction, as knowl-
edge of HCV infection and antiviral treatment have both
been shown to conduct patients to reduce their alcohol con-
sumption (Nalpas et al., 2001; Russell et al., 2012). Thus, to
start with the management of chronic hepatitis C instead of
waiting for a substantial length of abstinence that might
never be obtained could be a strategy to get the patient
involved in a process of change and to reduce his alcohol
It is important to bear in mind that interferon can modulate
the immune system and hence induce flare-ups of acute alco-
holic hepatitis (Zylberberg et al., 1999). As a consequence,
antiviral treatment in heavy drinkers with advanced liver
disease must be cautiously evaluated. Nevertheless, we
believe that the so-called ‘6-months rule’ of abstinence from
alcohol before considering antiviral treatment recommended
by the French 2002 consensus (Dhumeaux et al., 2003) is
excessive. In the present study, most of the patients had
started antiviral treatment before achieving this duration of
abstinence with satisfactory results in terms of SVR.
Our work has limitations. First, it was a retrospective
study without formalized data collection. This could have
biased the evaluation of alcohol consumption and the ana-
lysis of its interactions with treatment efficacy. Second, the
number of patients studied was insufficient to draw definite
conclusion from subgroups analyses. For example, despite
the fact that the rate of SVR was more than 2-fold higher in
former heavy drinkers who had remained completely abstin-
ent during antiviral therapy than in patients who had
consumed alcohol during therapy, this difference did not
reach statistical significance. Third, the study was not con-
trolled for the type of intervention received by heavy drin-
kers and the conclusions we draw on the positive impact of
our multidisciplinary approach is mainly based on a compari-
son with previously published data. We cannot exclude that
confounding factors could have biased such a comparison.
Fourth, we do not provide data on the evolution of liver
disease after antiviral treatment. If clinical benefits associated
with HCV eradication in heavy drinkers have never been
specifically studied, epidemiological data clearly show the
harmful effect of ongoing HCV infection in this population.
For example, while the odds ratio associated with heavy
drinking alone are 9 and 7 for decompensated cirrhosis and
hepatocellular carcinoma, respectively, the corresponding
figures are 147 and 109 in patients with both heavy drinking
and HCV infection (Corrao and Aricò, 1998; Donato et al.,
2002). As a consequence, one may speculate that successful
antiviral treatment is likely to have a positive impact on the
rate of liver-related clinical events in this population.
In conclusion, although alcohol abstinence must remain the
primary target in the care of heavy drinkers infected with
HCV, our work suggests that it should be, per se, neither a
sufficient nor an indispensable prerequisite for the introduc-
tion of antiviral therapy. First, we have shown that a multidis-
ciplinary approach including psychosocial support might
improve access to treatment, completion of therapy as well as
the rate of SVR in HCV-carriers with a history of alcohol
abuse. Second, it seems possible, with such an approach, to
achieve SVR in some patients with ongoing alcohol consump-
tion during treatment. Moreover, antiviral therapy can be a
starting point for change leading the patient to abstinence or at
least to reduce his alcohol consumption. Additional work is
obviously needed on these topics, but our results should
already encourage all professionals involved in the manage-
ment of patients struggling with alcohol to screen for HCV in-
fection and to consider this population for antiviral treatment.
Conflict of interest statement. None declared.
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