Topic: Disease Progression
M. Lee; H. Yang; C. Liu; S. You; P. Chen; C. Chen
Background
and aims:
Chronic hepatitis C virus (HCV) infection is an
important risk predictor of hepatocellular carcinoma (HCC). But the cumulative
HCC incidence associated with chronic HCV infection has rarely been examined by
community-based long-term follow-up studies.
Aim:
This prospective study aimed to evaluate the impacts
of HCV on HCC in
Methods:
A total of 19,565 residents who were
HBsAg-seronegative and free of liver cirrhosis or HCC at entry were enrolled during
1991 to 1992. There were 1,041 anti-HCV-seropositives and 18,524
anti-HCV-seronegatives. They were followed until
Results:
During the follow-up of 246,154 person-years, the
cumulative HCC incidence per 100,000 person-years was 26 for
anti-HCV-seronegative participants, 290 for anti-HCV-seropositives with
undetectable HCV RNA, 464 for anti-HCV- seropositives with detectable genotype
1 HCV RNA, and 370 for anti-HCV- seropositives with detectable genotype non-1
HCV RNA. Compared with anti-HCV- seronegative participants as the referent
group, the HRadj (95% CI) was 8.0 (4.3-14.7) for anti-HCV-seropositives with
undetectable HCV RNA, 6.6 (3.9-11.2) for anti-HCV-seropositives with detectable
genotype 1 HCV RNA, and 6.2 (3.3-11.7) for anti-HCV-seropositives with
detectable genotype non-1 HCV RNA after adjustment for age, gender, cigarette
smoking and serum ALT level at study entry. The HRadj (95% CI) was 2.7
(1.7-4.1) and 7.6 (4.4-13.1), respectively, for serum ALT levels of 16-45 and
>45 IU/L compared with ALT level <15 IU/L. Cigarette smoking was also
associated with an increased HCC risk with an HRadj
(95% CI) of 1.7 (1.0-2.8). In the stratification analyses, the
age-gender-adjusted HRadj (95% CI) for the anti-HCV- seropositives with
undetectable HCV RNA, anti-HCV-seropositives with detectable genotype 1 HCV
RNA, and anti-HCV-seropositives with detectable genotype non-1 HCV RNA was 25.7
(7.3-90.9), 10.7 (3.3-34.6) and 11.3 (3.3-39.7), respectively, for those with
ALT levels at entry >45 IU/L. The corresponding figures were 5.2 (2.2-12.0),
9.8 (5.3-18.2), and 7.5 (3.2-17.5) for those with ALT levels at entry < 45
IU/L.
Conclusion:
HCV infection, elevated serum ALT levels, and
cigarette smoking are important HCC risk predictors for HBsAg-seronegatives in
Topic: HIV/HCV Coinfection
135. Liver-related mortality in human immunodeficiency
virus-infected patients between 1995 and 2005 in the French GERMIVIC Joint
Study Group Network (MORTAVIC 2005 Study in collaboration with MORTALITE 2005,
ANRS-EN19)
E. Rosentha1, D. Salmon; C. Lewden; F. Bonnet; T. May;
P. Morla; M. François; C. Burty; E. Jougla; D. Costagliola; G. Chêne, P. Cacoub
Objective:
To determine mortality due to end-stage liver disease(ESLD) and the profile of patients who died from ESLD
in a nationwide population of HIV-infected patients and the evolution over a
10-years period.
Design and
methods:
All departments of internal medicine and infectious
diseases from the GERMIVIC Study Group prospectively recorded all deaths in
HIV-infected patients during 2005. Fifty six departments, following around
35,000 HIV-infected patients, participated in the study. Results were compared
with those of previous surveys conducted using similar methodology in 1995,
1997, 2001 and 2003.
Results:
Among 364 deaths documented during 2005, 142 (39.0%)
were related to AIDS, 64 (17.6%) to ESLD, 55 (15.1%) to cancers neither related
to HIV nor hepatitis viruses, 20 (5.5%) to cardiovascular diseases and 83
(22.8%) to other causes. Mortality due to ESLD represented 28.8% of non
AIDS-related deaths. Patients dying from ESLD had chronic hepatitis due to
virus C in 79.6% of cases and 46.6% of these patients had high alcohol
consumption (> 30g/day)(table 1). In the Germivic
survey, the proportion of ESLD-deaths has increased: 5% in 1995, 6.6% in 1997,
14.3% in 2001, 12.6% in 2003 and 17.6% in 2005, p<0.01. The proportion of
hepatocellular carcinoma as a cause of death increased over this 10-years
period (4.7% in 1995 vs 31.2% in 2005, p<0.01). Treatment of hepatitis C in
patients who died from ESLD was more frequent in 2005 (37.5%) than in 1995
(19.0%), p<0.01.
Conclusions:
In HIV-HCV coinfected patients, the proportion of
HCV-ESLD is still increasing and it constitutes a leading cause of mortality in
this population.
|
|
1995 |
1997 |
2001 |
2003 |
2005 |
|
Sex, male, no (%) |
15 (71.4) |
30 (83.3) |
30 (78.9) |
22 (81) |
53 (83) |
|
Mean age, y (range) |
41 (26-66) |
42 (31-62) |
42 (32-69) |
42 (36-54) |
45 (35-68) |
|
Injection drug use, no (%) |
6 (28.5) |
14 (38) |
29 (76.3) |
26/26 (100) |
39/63 (61.9) |
|
Alcohol consumption > 30g/day, no (%) |
6 (28.5) |
16 (44.4) |
19 (50) |
16 (59.2) |
28/60 (46.6) |
|
HBsAg positive, no (%) |
8 (38.1) |
15 (41.7) |
8 (21.1) |
2 (7.4) |
17 (26.5) |
|
HCC, no (%) |
1 (4.7) |
4 (11.1) |
9 (25) |
4 (14.8) |
20 (31.2) |
|
Anti-HCV treatment, no (%) |
4 (19) |
3 (8.3) |
10 (26.3) |
12 (44.4) |
24 (37.5) |
|
CD4 count (cells/mm3), median (IQR) |
113 (27-257) |
131 (46-306 |
158 (72-303) |
132 (66-350) |
239 (110-355) |
|
HAART, no (%) |
0 |
15 (41.6) |
28 (73.6) |
23 (85) |
58 (90.6) |
ESLD,
end-stage liver disease; HCV, hepatitis C virus; HCC, hepatocellular carcinoma;
HAART, highly active antiretroviral therapy
Topic: HIV/HCV Coinfection
A. Monto; S. Currie; L. M. Dove; D. Tracy; S. George;
A. Myers; J. C. Ryan1; T. L. Wright
Background:
HIV coinfection may accelerate the complications of
hepatitis C virus (HCV) infection. Much of this perception, however, has been
based on retrospective case series or short-term prospective follow-up.
Aim:
To explore mortality and liver-related complications
in a prospective cohort of American inner-city injection drug users, followed at an urban county and a veterans hospital,
who have chronic HCV.
Methods:
350 patients were enrolled beginning in 1997 and have
been followed for a mean of 4.8 years. 176 patients (49.7%)are
chronically coinfected with HIV and hepatitis C, and 174 patients had chronic
HCV infection alone. Causes of death were determined by the investigators, and
were attributed to HIV, end-stage liver disease (ESLD) or drugs only when this
was unequivocal. Cirrhosis was defined by histology or overt clinical or
radiological evidence of cirrhosis.
Results:
Overall, 48 HIV-HCV coinfected and 34 HCV monoinfected
patients died during follow-up, but coinfected patients did not have
statistically-significantly increased death than the group overall (O.R. 1.54,
95% CI 0.94-2.54, p=0.09), data shown in Table. Similar proportions of
coinfected patients were also found to develop cirrhosis, 29 (16%), as compared
to monoinfected patients, 31 (18%, t-test p=NS). HAART was not protective
against death in coinfected patients: 34/48 (71%) of coinfected patients who
died had regularly received HAART, 29% had not (t-test p=NS).
Conclusions:
HIV-HCV coinfected and HCV monoinfected patients, when
followed prospectively, have similar rates of death or cirrhosis. End-stage
liver disease and HIV are competing causes of death in coinfected patients.
Reported high rates of ESLD-associated death in coinfected patients alive today
should be interpreted with caution, and compared to those in similar groups of
HCV monoinfected patients. As the HAART era continues, morbidity and mortality
in HIV-positive patients may approach that of their HIV-negative counterparts.
|
HIV-HCV |
Deaths |
Overall |
48 (27%) |
|
|
|
HIV-Assoc |
7 (4%) |
|
|
|
Other |
18 (10%) |
|
|
|
ESLD-Assoc |
12(7%) |
|
|
|
Drug-related |
0 (0%) |
|
|
|
Unknown |
11 (6%) |
|
|
Cirrhosis |
|
29 (16%) |
|
HCV |
Deaths |
Overall |
34 (19%) |
|
|
|
Other |
16 (9%) |
|
|
|
ESLD-Assoc |
6 (3%) |
|
|
|
Drug-related |
1 (1%) |
|
|
|
Unknown |
11 (6%) |
|
|
Cirrhosis |
|
31 (18%) |