original article
Wien Klin Wochenschr (2010) 122: 237–242
DOI 10.1007/s00508-010-1364-7
© Springer-Verlag 2010
Printed in Austria
Antiviral treatment of chronic hepatitis C in clinical routine
Andreas Maieron1, Sigrid Metz-Gercek2, Franz Hackl3, Alexander Ziachehabi1, Harri Fuchsteiner1,
Christoph Luger2, Helmut Mittermayer2, Rainer Schöfl1
1
Internal Medicine IV, Department of Gastroenterology and Hepatology, Elisabethinen Hospital Linz, Linz, Austria
2
Department of Hygiene, Microbiology and Tropical Medicine, Elisabethinen Hospital Linz, Linz, Austria
3
Department of Gastroenterology and Endoscopy/Hepatology, Diakonissen Hospital Linz, Linz, Austria
Received October 8, 2009, accepted after revision March 4, 2010
Hepatitis C Therapie: Ergebnisse in der klinischen
Routine
Zusammenfassung. Einleitung: Mit der heute zur Ver-
fügung stehenden Standardtherapie der chronischen
Hepatitis C bestehend aus pegyliertem Interferon und Ri-
bavirin erreichen in randomisierten und kontrollierten
Studien bis 60% der Patienten eine dauerhafte Viruselimi-
nation (SVR). Die Reproduzierbarkeit der Ergebnisse in
der klinischen Praxis ist unklar, deshalb untersuchten wir
alle konsekutiven, therapienaiven Patienten an unserer
Abteilung um die Wirksamkeit der Standardtherapie in der
klinischen Routine zu überprüfen.
Material und Methodik: Insgesamt wurden 219 Patien-
ten mit pegyliertem Interferon Alpha (2a oder 2b) und Ri-
bavirin (800–1200 mg/Tag) in den Jahren 2000 und 2006
behandelt. 34.8% der Genotyp 1/4/6 und 18.4 % der Geno-
typ 2/3 Patienten wiesen eine Fibrose Grad 3 oder 4 auf.
Die Patienten wurden gemäß der gängigen Ein- und
Ausschlusskriterien für klinische Studien in zwei Gruppen
geteilt. Die Therapieergebnisse dieser beiden Gruppen
wurden getrennt analysiert.
Ergebnisse: 44.3 % der Patienten erreichten eine dauer-
hafte Viruselimination. Jene mit einer niedrigen Fibrose
(F0 – F2) erreichten in 52.5 % und jene mit einer Fibrose
F3 – F4 erreichten in 20.8 % einen SVR. Die SVR-Rate für
Patienten mit Genotyp 1/4/6 betrug 35.4 % (SVR: F0 – F2
47.7; F3 – F4 19.6 %) und für Genotyp 2/3 67.8 %. In der
Gruppe der Patienten, mit ungünstigen Voraussetzungen
für die Therapie war die SVR-Rate signifikant niedriger
(32.4 % vs. 50 %; p = 0.017), zudem war in dieser Gruppe die
Non-Responder-Rate deutlich erhöht (30.9 % vs. 13.8 %).
Schlussfolgerung: Bis zu einem Drittel der Patienten
weisen ungünstige, zu schlechteren Therapieergebnissen
führende, Voraussetzungen, für eine antivirale Therapie
Correspondence: Andreas Maieron, Internal Medicine 4, Depart-
ment of Gastroenterology and Hepatology, Elisabethinen Hospital,
Fadingerstraße 1, 4010 Linz, Austria,
E-mail: andreas.maieron@elisabethinen.or.at
wkw 7–8/2010 © Springer-Verlag
Wiener klinische Wochenschrift
The Middle European Journal of Medicine
auf. Der Therapieerfolg ist durch Patientenselektion,
Schweregrad der zu Grunde liegenden Lebererkrankung
und Anteil der Patienten mit fortgeschrittener Leberer-
krankung beeinflusst.
Summary. Objective: Pegylated interferon plus ribavirin is
the standard treatment for chronic hepatitis C. Sustained
virological response (SVR) rates of up to 60% are reported
in randomized controlled trials, but it is unclear whether
the results from such trials are reproducible in the clinical
routine setting. We investigated consecutive treatment-
naïve chronic hepatitis C patients at our center to examine
the efficacy of treatment with pegylated interferon plus
ribavirin in clinical routine.
Materials and methods: Between 2000 and 2006 we
treated a total of 219 patients with pegylated interferon
alpha (2a or 2b) and ribavirin (800–1200 mg/d). Among
them, 34.8% of patients infected with HCV genotypes 1/4/6
and 18.4% of those with genotypes 2/3 had advanced fi-
brosis or cirrhosis (F3–F4). For analysis of outcome we
subdivided our series into two groups of patients: those
who fulfilled standard inclusion criteria in randomized
controlled trials and those who did not.
Results: The overall SVR rate was 44.3%. In patients with
F0–F2 an SVR was achieved in 52.5%; in those with F3–F4
the SVR rate was 20.8%. In patients infected with genotypes
1/4/6 the SVR rate was 35.4% (SVR: F0–F2 47.7%; F3–F4
19.6%); in those with genotypes 2/3 the rate was 67.8%. The
SVR rate in patients with unfavorable baseline factors was
significantly lower (32.4% vs. 50%; P = 0.017) and they were
more likely to be non-responders (30.9% vs. 13.8%).
Conclusion: In everyday clinical practice, up to one-
third of patients show unfavorable baseline factors for an-
tiviral therapy, resulting in worse therapeutic outcome.
Differences in therapeutic outcome are influenced by pa-
tient selection and by the proportion and severity of the
underlying liver disease.
Key words: Chronic hepatitis C, treatment outcome, clin-
ical practice, Austria, pegylated interferon.
Antiviral treatment of chronic hepatitis C in clinical routine 237
 original article
Background
Chronic hepatitis C is a major public health problem and
one of the leading causes of end-stage liver disease and
death in Europe and the USA [1, 2]. There are numerous
multinational randomized controlled trials (RCTs) of com-
bination therapy with pegylated interferon (PEG-IFN) and
ribavirin that show sustained virological response (SVR)
rates of 56% [3], 63% [4] and even higher (around 60% in
groups of patients unselected with regard to HCV geno-
type and 80–90% in selected groups) [5]. It remains unclear
whether these results can be reproduced in clinical rou-
tine, since these trials have been conducted in pre-se-
lected patient groups: patients in clinical trials are better
motivated, have less co-morbidity and might suffer from
less advanced disease, thus explaining better results. Data
from treating patients in clinical routine are sparse. We re-
port our single center experience of antiviral treatment
with PEG-IFN plus ribavirin in treatment-naïve patients
with chronic hepatitis C.
Methods
Patients
Between September 1992 and December 2006 we identified 1319
patients who tested positive for HCV RNA. Beginning in 2000, we
analyzed all patients whose HCV PCR status was still positive at
that time (n = 620) and who underwent treatment with PEG-IFN
and ribavirin (n = 407). We report our results from consecutive
treatment-naïve patients of the period 2000–2006 (n = 219). Abso-
lute contraindications for therapy at our center were: decompen-
sated liver disease, hepatocellular carcinoma, co-infection with
hepatitis B and/or HIV, leukocyte count <2500 cells/mm3, plate-
let count <50,000 cells/mm3, severe psychiatric disease, ongoing
substance abuse (active intravenous drug usage) including exces-
sive alcohol consumption (>100 g/day), age over 70 years, poorly
controlled diabetes (HbA1c > 8.5), poorly controlled coronary
heart disease, chronic pulmonary disease (stage > 2), immuno-
logically mediated disease, poorly controlled epilepsy and
patients with a high risk of anemia. All patients had a positive
anti-HCV antibody test and tested positive for HCV RNA 8 weeks
before the start of treatment. Only after physical examination,
laboratory tests, provision of extensive information about effects
and side effects and obtaining the patient’s consent was the treat-
ment started in outpatient care. Patients’ characteristics and HCV
genotype distribution are shown in Tables 1 and 2. A liver biopsy
was performed in 171 of the 219 patients (133 patients with geno-
types 1, 4 or 6; 38 patients with genotypes 2 or 3): 53 of the patients
(30.1%) had advanced fibrosis or liver cirrhosis (F3 or F4).
For analysis of outcome we subdivided our series into two
groups of patients: those who fulfilled strict treatment criteria ac-
cording to drug labeling used in RCTs and those who did not but
were still treated. In contrast to RCTs, patients in our clinic were
Table 1. Baseline patient characteristics
Characteristics Total HCV genotype 1, 4, or 6
Histology n = 219 n = 160 F0–F2: n = 87
Age (years) mean ± SD 45.2 ± 10 46.3 ± 10 43.5 ± 10.1
Sex: M/F, n/n (% male) 147/72 (67) 117/43 (73) 65/22 (75)
BMI mean ± SD 25.4 ± 4.2 25.9 ± 4.0 25.2 ± 3.8
238 Antiviral treatment of chronic hepatitis C in clinical routine
treated up to the age of 70 (RCT up to 65), with a thrombocyte
count between 50,000 and 100,000 cells/mm3 (RCT > 100,000 cells/
mm3), hemoglobin level between 10 and 12 g/dl (RCT: women >
12 g/dl; men > 13 g/dl), leucocyte count between 2500 and
3000 cells/mm3 (RCT > 3000 cells/mm3), history of major depres-
sion (RCT: mild depression), diabetes mellitus requiring insulin
therapy (RCT: no insulin therapy), and a normal transaminase
level (RCT: >1.5 times the upper limit of normal). In total, 151 of
our patients (59%) fulfilled strict treatment criteria equivalent to
those usually used in RCTs [6, 7].
Treatment
For patients with genotypes 1, 4 or 6 the regimen of HCV treat-
ment was 48 weeks with 180 μg PEG-IFN alpha 2a (n = 91) or 1.5 μg
per kg body weight PEG-IFN alpha 2b (n = 69) once a week com-
bined with body-weight-adjusted ribavirin ranging from 1000 to
1200 mg per day. For genotypes 2 and 3 the regimen was 24 weeks
with 180 μg PEG-IFN alpha 2a (n = 33) or 1.5 μg per kg body weight
PEG-IFN alpha 2b (n = 26) once a week combined with 800 mg of
ribavirin per day. HCV PCR was performed at week 12 and all
patients with at least a 2-log drop in viral load were approved to
continue treatment. SVR was defined as a negative HCV PCR
6 months after completing treatment.
The primary endpoint was SVR, defined as undetectable HCV
RNA at week 48 for patients with HCV genotypes 2 or 3 and at
week 72 for patients with genotypes 1, 4 or 6. Patients were mon-
itored routinely every four weeks, including physical examina-
tion and laboratory testing. Doses were reduced according to
drug approval criteria; it was recorded when patients had less
than 80% of the recommended dosage over less than 80% of the
time [8].
Statistics
Data were grouped and analyzed according to age, BMI, HCV
genotype, histology staging according to the Metavir score (no
cirrhosis: F0–F2, advanced fibrosis/cirrhosis: F3–F4), different
sets of treatment criteria and therapy regime (PEG-IFN: 2a vs. 2b).
Statistical analysis was performed on an intent-to-treat popula-
tion. All variables were analyzed descriptively. The Mann–
Whitney U-test was used for significance testing of quantitative
variables and the Chi-squared test for qualitative comparison.
SPSS 13.0 software was used for calculations. If the cell count of
tables was below five, we dichotomized the testing variables and
used the Chi-squared test for 2 × 2 tables.
Results
A total of 219 treatment-naïve patients were analyzed.
Histological data were available from 171 patients.
In our intent-to-treat analysis we found an overall SVR
rate of 44.3%. The distribution of overall outcome, accord-
ing to METAVIR staging and viral load, is shown in Fig. 1.
In total, 57 patients (26%) discontinued treatment early:
HCV genotypes 2, 3
F3–F4: n = 46 n = 59 F0–F2: n = 31 F3–F4: n = 7
50.5 ± 8.2 42.3 ± 9.7 42.7 ± 9.8 45.0 ± 10.4
32/14 (70) 30/29 (51) 15/16 (48) 6/1 (86)
27.2 ± 4.5 24.3 ± 4.0 24.4 ± 4.7 24.0 ± 2.9
© Springer-Verlag 7–8/2010 wkw
 original article

Table 2. Distribution of HCV genotypes
HCV genotype n
1b 101
1a 41
2 15
3 44
4 17
6 1
Total 219
lack of viral elimination in 42 (19%); side effects in 15 (7%).
The side effects included major depression (6 patients),
lab abnormalities (5 patients) and severe infection (4 pa-
tients). The dosage of ribavirin and/or PEG-IFN was
reduced to less than 80% of the recommended dosage over
less than 80% of the time in only three patients (one leuco-
cytopenia, two anemias) and none of them achieved SVR.
The regular medical checkups during therapy included
evaluation of adverse events and adherence to therapy.
Antidepressants were used in up to 20%.
Characteristics and therapeutic outcome for HCV
genotypes 1/4/6
Overall, 160 of the patients (73.1%; m = 117; f = 43) carried
HCV genotypes 1, 4 or 6. Their median age was 47.6 ± 10.2
years and median BMI 26 ± 4. Histological staging was per-
formed in 132 patients: 65.2% had fibrosis F0–F2 and 34.8%
were considered cirrhotic with fibrosis scores F3 and F4
according to the METAVIR score [9].
Their overall SVR rate was 35.4%. Relapse occurred in
24.7%, non-response in 25.9%, a breakthrough in 3.2%;
3.8% were lost and 7.0% discontinued therapy because of
typical and severe side effects: septicemia in two patients
(Staphylococcus aureus [10], Staphylococcus hominis [1]),
cerebral seizures in two and suspicion of malignant lym-
phoma in one. Patients with significant fibrosis (F3–F4)
were less likely to achieve SVR (Fig. 2). Patients with a low
viral count showed a significantly different outcome
(P < 0.001) than those with a high viral load (Fig. 2). Highly
viremic patients were less likely to achieve an SVR and
were more likely to experience a relapse or not to respond
at all.
Patients with less severe fibrosis (F0–F2) had signifi-
cantly lower BMI (P = 0.015) than patients with more
fibrosis (F3–F4: 25.2 ± 3.8 vs. 27.2 ± 4.5) and showed a sig-
nificantly different therapeutic outcome (P < 0.03; Fig. 2).
Those with advanced fibrosis (F3–F4: 50.7 ± 8.7 years) were
significantly older (P < 0.0001) than non-cirrhotic patients
(F0–F2: 44.3 ± 10.2 years).
Therapeutic outcome for patients with HCV genotype 1
is shown in Fig. 2. Patients with HCV genotype 4 showed a
very favorable SVR rate of 64.7% compared with patients
infected with genotype 1 (31.7%).
Characteristics and therapeutic outcome for patients
with HCV genotype 2/3
In total, 59 patients had HCV genotypes 2 or 3; sex distri-
bution was equal (m = 30, 50.8%; f = 29, 49.2%). Patients in-
fected with these genotypes (median age 44.0 ± 9.7) were
significantly younger (P = 0.004) than patients with geno-
types 1, 4 or 6 (median age 47.6 ± 10.2) and their BMI was
significantly lower (genotypes 1, 4, 6: 26.0 ± 4; genotypes 2
or 3: 23.5 ± 4.5; P = 0.006). Histological data were available
in 38 patients (64.4%): 81.6% had absent or mild fibrosis
(F0–F2); 18.4% were considered to have cirrhosis (F3–F4).
In patients infected with genotypes 2 or 3 the overall SVR
rate was 67.8%. Relapse, non-response and discontinuation

100%

SVR
90%
relapse
non-responder
80%
breakthrough
discontinued therapy
70%
lost

60%

50%

40%

30%

20%

10%

0%
Overall (n = 219) F0–F2 (n = 118) F3–F4 (n = 53) Viral load <500,000 (n = 64) Viral load >500,000 (n = 76)

Fig. 1. Overall outcome according to METAVIR staging and viral load. SVR sustained virological response

wkw 7–8/2010 © Springer-Verlag Antiviral treatment of chronic hepatitis C in clinical routine 239
 original article

100%

SVR
90%
relapse
non-responder
80%
breakthrough
discontinued therapy
70%
lost

60%

50%

40%

30%

20%

10%

0%
Genotype 1 G 1/4/6 F0–F2 (n = 86) G 1/4/6 F3–F4 (n = 46) G 1/4/6 Viral load <500,000 G 1/4/6 Viral load >500,000

Fig. 2. Overall outcome for genotype 1 and genotype 1/4/6 according to METAVIR staging and viral load. SVR sustained virological response

Table 3. Therapeutic outcome according to HCV Table 4. Therapeutic outcome according to type
genotypes 2 and 3 of interferon
Outcome HCV genotypes 2, 3 (%) Outcome PEG-IFN 2a PEG-IFN 2b
plus ribavirin (%) plus ribavirin (%)
SVR 67.8
SVR 42.7 46.3
Relapse 22.0
Relapse 25.0 23.2
Non-responder 1.7
Non-responder 17.7 21.1
Breakthrough 0
Breakthrough 2.4 2.1
Discontinued therapy 8.5
Discontinued therapy 9.7 4.2
Lost 0
Lost 2.4 3.2
SVR sustained virological response.
PEG-IFN pegylated interferon; SVR sustained virological response.

of therapy was found in 22.0%, 1.7% and 8.5%, respectively

(Table 3). No breakthrough or loss to follow-up was observed
in this subgroup. Because of the low number of patients, sta-
tistical subgroup analysis was deemed inappropriate.
Therapeutic outcome in relation to treatment criteria
Comparison of the subgroups of patients suitable and not
suitable for inclusion in RCTs revealed striking differences.
In the non-eligible group, the mean age was higher (mean
49.2 vs. 45.7 years), more than twice the number of pa-
tients suffered from advanced fibrosis (56.5% vs. 26.3%)
and the therapeutic outcome was much worse. The SVR
rate in this group was significantly lower (32.4% vs. 50%;
P = 0.017) and they were more likely to be non-responders
(30.9% vs. 13.8%).
Therapeutic outcome in relation to treatment regime
Comparison of the two treatment regimes (PEG-IFN 2a +
ribavirin; n = 124 vs. PEG-IFN 2b + ribavirin; n = 95) did not
reveal any significant relation between treatment outcome
and the type of interferon used (P = 0.72, Table 4). The treat-
ment groups were comparable according to age (P = 0.97),
sex (P = 0.82), HCV genotype (P = 0.97), BMI (P = 0.88) and
fibrosis score (P = 0.98). Even in a subgroup analysis of
highly viremic patients there was no difference in thera-
peutic outcome according to the type of PEG-IFN.
Discussion
We present data on consecutive treatment-naïve hepatitis
C patients at a single center who received at least one dose
of PEG-IFN plus ribavirin. There is reason to believe that
differences in therapeutic outcome are influenced by pa-
tient selection and the proportions and severity of under-
lying liver disease [11–14]. Only 69% of our patients could
have participated in an RCT, therefore our overall results
(SVR rate 44.3%) differ in many respects from data re-
ported from large RCTs [3, 4] where SVR rates range from
56 to 63%, similar to the rate achieved in those of our pa-
tients who could have participated in an RCT (50%). With
an SVR rate of 32.4% the other patients are in a much worse

240 Antiviral treatment of chronic hepatitis C in clinical routine © Springer-Verlag 7–8/2010 wkw

position. Even when we compare our results with a large
multicenter Austrian study where we recruited a greater
number of patients a difference in outcome is notable.
Ferenci et al. report SVR rates of 51% [15]. Furthermore, a
study by Foster et al. [16] showed that depending on the re-
spective patient profile the probability of a single patient
achieving SVR ranges from a startling 7 to 97%. Although
Marotta et al., when analyzing the combined results of six
different studies, report that SVR rates in community-
based treatment settings are similar to those in RCT
settings, closer examination of the data finds that, for ex-
ample, in the WIN-R trial the SVR rates for patients with
HCV genotype 1 ranged from 29 to 34% [17]. Disappoint-
ing results are also reported from the Birmingham group,
with SVR rates of 28% for HCV genotype 1 [18].
Among our patients we had up to 58% with a high viral
load. In large RCTs the rates of high viral load ranged be-
tween 41 [3] and 42% [7]. In addition, in subgroups of pa-
tients with cirrhosis or advanced fibrosis data are not as
promising. In the present study the overall SVR rates were
lower in patients with advanced fibrosis or cirrhosis
(20.8%) than in patients without cirrhosis (52.5%). In sub-
group analyses from large RCTs, SVR was achieved in
about 30–50% of patients with advanced fibrosis or com-
pensated cirrhosis [7, 19], which is in contrast to our SVR
rate. In a study by Abergel et al. [20] in patients with cirrho-
sis, overall SVR rates of 44.5% were reported for all HCV
genotypes (SVR in genotypes 1, 4 and 5 was only 25%).
Helbling et al. [21] reported SVR rates of 52% and with a
standard regimen in cirrhotic patients with all HCV geno-
types. In the Hadziyannis et al. trial [4] the SVR rate in the
cirrhosis group was 28%, whereas Fried et al. [3] reported
43% for cirrhotic patients. Reasons for the discrepancy
might be our negative selection of patients in relation to
age (our data: 45.2y, Fried: 42.5y, Manns [7]: 43y) and the
higher proportion of our patients (31%) having more ad-
vanced liver disease and co-morbidity.
Overall, 52.9% of our patients with cirrhosis or advanced
fibrosis tested negative for HCV RNA at the end of treat-
ment, but there was a relapse rate of 32.1%. Berg et al. re-
ported a reduction in the relapse rate of 24% in patients
who did not show a negative HCV RNA at week 12 and
continued treatment for 72 weeks instead of 48 weeks [22].
Similar data were reported by Sánchez-Tapias and Ferenci
et al., who reported relapse rates of up to 48% in patients
treated for 48 weeks, but only 26% in patients treated for 72
weeks [15, 23]. Thus patients with advanced fibrosis/cir-
rhosis who test positive for HCV RNA at week 12 benefit
from a longer treatment regimen [24].
Depending on the respective study, SVR rates for pa-
tients with HCV genotype 1 range from 34 [25] to 50% [3, 6,
7]. This is to some extent confirmed by reports from Borroni
et al. [26] and Shehab et al. [27], but again the composition
of the patient cohorts differ from ours (F3/F4: Shehab 21%;
our patients 35%). The overall SVR rate in our patients with
HCV genotypes 1, 4 or 6 was 35.4%. This is in contrast to
published evidence, again indicating the different compo-
sition of the analyzed patient group [4, 7, 22]. Early reports
on treatment of patients with HCV genotype 4 indicate
wkw 7–8/2010 © Springer-Verlag
original article
poor response rates; recent reports show SVR rates of up to
60% [28]. We can confirm these data with similar results
(our data: SVR rate 64.7%). Again, also for HCV genotypes
1/4/6, our F3–F4 patients had a significantly lower SVR
rate than those without advanced fibrosis/cirrhosis (19.6%
vs. 47.7%). This is in clear contrast to previously published
data from both Hadziyannis et al. [4], with 28 to 41% de-
pending on the ribavirin dosage, and Lee et al. [29], with
34%. In a recent analysis of a patient cohort similar to ours
by Bruno et al. [30], 28% of patients with HCV genotype 1
and biopsy-proven cirrhosis showed viral eradication. In
our patient collective, 32.9% showed a primary non-re-
sponder status or discontinued therapy because of severe
side effects. This highlights that patients in community set-
tings, compared with RCTs, seem to suffer from more ad-
vanced disease and more co-morbidity, making treatment
more difficult and outcomes worse.
In patients infected with HCV genotypes 2 or 3 the SVR
rates also depend on liver fibrosis, as shown in the studies
of Hadziyannis et al. and Andriulli et al. [4, 31]. The overall
SVR rate in patients with genotypes 2 or 3 in our sample
was 67.8%, which is lower than reported in previous RCTs
(76–93%) [2, 3, 8, 25, 32] but similar to “real world” data
from Lee et al. (73%) [29]. As we showed earlier, up to one-
third of our patients would not qualify for RCTs, because of
advanced liver disease and co-morbidity, and therefore
the SVR rates in our sample differ from published RCT re-
sults. As shown in the study by Zeuzem et al. [33], patients
with a high viral load had a significantly lower SVR rate
(70%) than patients with low viral load (86%). In our pa-
tients we observed a relapse rate of 22%, compared to 13%
[2], and one might speculate that this is due to the higher
number of patients with high viral load in our cohort.
Surprisingly, the proportion of our patients who were
lost to follow-up (2.7%) was similar to those in the studies
of Fried et al. and Hadziyannis et al. [3, 4], and only half of
those (5%) in the clinical practice data of Lee et al. [29].
Our rate of premature discontinuation (31.5%) was also
similar to that reported by Fried et al. (26%) and
Hadziyannis et al. (32%) – and lower than the 44% pub-
lished by Lee et al. We therefore suspect that our patients
were as well motivated to finish treatment as patients in
RCTs. The higher rate of discontinuation and loss observed
by Lee et al. could be due to a higher number of patients
with insufficient virological response or lower motivation.
Conclusion
Treatment outcome in patients with chronic hepatitis C is
influenced by host factors such as fibrosis, BMI, age and
co-morbidities and also by virus-related features such as
genotype and viral load. With this in mind, we need to ac-
knowledge the fact that many patients show unfavorable
baseline factors for antiviral therapy, resulting in worse
therapeutic outcome.
Conflict of interest
We confirm that all authors have read and approved the
content of the manuscript and it has not been published or
Antiviral treatment of chronic hepatitis C in clinical routine 241
 original article
submitted for publication elsewhere. None of the authors
has a competing interest to declare.
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