Lower Liver-Related Death in African-American
Women With Human Immunodeficiency
Virus/Hepatitis C Virus Coinfection, Compared
to Caucasian and Hispanic Women
Monika Sarkar,1Peter Bacchetti,2Audrey L. French,3Phyllis Tien,4Marshall J. Glesby,5
Marek Nowicki,6Michael Plankey,7Stephen Gange,8Gerald Sharp,9Howard Minkoff,10
and Marion G. Peters1for the Women’s Interagency HIV Study (WIHS)
Among individuals with and without concurrent human immunodeficiency virus (HIV),
racial/ethnic differences in the natural history of hepatitis C virus (HCV) have been
described. African Americans have lower spontaneous HCV clearance than Caucasians, yet
slower rates of liver fibrosis once chronically infected. It is not clear how these differences
in the natural history of hepatitis C affect mortality, in either HIV-positive or -negative
individuals. We conducted a cohort study of HIV/HCV coinfected women followed in the
multicenter Women’s Interagency HIV Study to determine the association of self-reported
race/ethnicity with all-cause and liver-related mortality. Survival analyses were performed
using Cox’s proportional hazards models. The eligible cohort (n 5 794) included 140
Caucasians, 159 Hispanics, and 495 African Americans. There were 438 deaths and 49
liver-related deaths during a median follow-up of 8.9 years and maximum follow-up of 16
years. African-American coinfected women had significantly lower liver-related mortality,
compared to Caucasian (hazard ratio [HR], 0.41; 95% confidence interval [CI]: 0.19-0.88;
P 5 0.022) and Hispanic coinfected women (HR, 0.38; 95% CI: 0.19-0.76; P 5 0.006).
All-cause mortality was similar between racial/ethnic groups (HRs for all comparisons:
0.82-1.03; log-rank test: P 5 0.8). Conclusions: African-American coinfected women were
much less likely to die from liver disease, as compared to Caucasians and Hispanics, inde-
pendent of other causes of death. Future studies are needed to investigate the reasons for
this marked racial/ethnic discrepancy in liver-related mortality. (HEPATOLOGY 2012;56:1699-
of transmission, hepatitis C virus (HCV) infection in
n the United States, at least 5 million people are
infected with hepatitis C, 80% of whom are esti-
mated to be viremic.1,2Because of shared modes
patients with human immunodeficiency virus (HIV) is
common. Approximately one third of HIV-positive
patients are coinfected with HCV, and this number
approaches 80% among those with injection drug use
Abbreviations: Ab, antibody; ALT, alanine aminotransferase; BMI, body mass index; CHC, chronic hepatitis C; CI, confidence interval; DM, diabetes mellitus;
GFR, glomerular filtration rate; HAART, highly active antiretroviral therapy; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HCV, hepatitis C virus;
HIV, human immunodeficiency virus; HR, hazard ratio; HTN, hypertension; IDU, injection drug use; IV, intravenous; NIH, National Institutes of Health; SNP,
single-nucleotide polymorphisms; WIHS, Women’s Interagency HIV Study.
From the1Department of Medicine, Division of Gastroenterology and Hepatology, University of California San Francisco, San Francisco, CA;2Department of
Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA;3Department of Medicine, CORE Center/Stroger Hospital of Cook County,
Chicago, IL;4Department of Medicine, Division of Infectious Diseases, University of California San Francisco, San Francisco, CA;5Department of Medicine, Division
of Infectious Diseases, Weill Cornell Medical College, New York, NY;6Department of Medicine, University of Southern California, Los Angeles, CA;7Department of
Medicine, Division of Infectious Diseases, Georgetown University, Washington, DC;8Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health,
Baltimore, MD;9Epidemiology Branch, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Division of Acquired Immune Deficiency
Syndrome, Bethesda, MD; and10Department of Obstetrics and Gynecology, Maimonides Medical Center, Brooklyn, NY.
Received March 14, 2012; accepted May 15, 2012.
The Women’s Interagency HIV Study is funded by the National Institute of Allergy and Infectious Diseases (UO1-AI-35004, UO1-AI-31834, UO1-AI-34994,
UO1-AI-34989, UO1-AI-34993, and UO1-AI-42590) and by the National Institute of Child Health and Human Development (UO1-HD-32632). The study
is cofunded by the National Cancer Institute, the National Institute on Drug Abuse, and the National Institute on Deafness and Other Communication Disorders.
Additional support was received through the National Institutes of Health (T32 DK060414; to M.S.).
(IDU).3Among patients with HIV, hepatitis C–related
liver disease remains the second leading cause of
death.4Data projecting liver-related mortality also
indicate that deaths from hepatitis C are continuing to
rise and remain an important cause of premature mor-
Racial/ethnic differences in the natural history of
hepatitis C have been well described. Spontaneous
HCV clearance is lower among African Americans,
compared to Caucasians and Hispanics, yet African
Americans appear to develop less fibrosis and inflam-
mation once chronically infected, compared to other
racial/ethnic groups.8-10It remains unclear how these
racial differences in the natural history of hepatitis C
may affect liver-related death, in either HCV monoin-
fection or in HIV/HCV-coinfected individuals.
Data on race and mortality in patients with chronic
HCV infection are conflicting. Several recent studies
have reported higher death rates among Caucasians
with chronic hepatitis C (CHC), compared to African
Americans, although one large study observed opposite
trends.11-14Most studies have also focused on male
predominant cohorts, with limited available data on
race and mortality among women with HCV or HIV/
Given conflicting previous data on race and mortal-
ity, and the absence of robust data in either female or
HIV-infected populations, we aimed to determine the
association between race/ethnicity and liver-related
death in a large cohort of HIV/HCV-coinfected
women followed in the Women’s Interagency HIV
Study (WIHS). The rich ethnic diversity and long-
term follow-up of WIHS participants has allowed us
Patients and Methods
Study Population. We conducted a cohort study of
women participating in the WIHS. The WIHS is a
National Institutes of Health (NIH)-funded, prospec-
tive, multicenter cohort of women at risk for, or cur-
rently diagnosed with, HIV. Enrollment in the WIHS
took place in two study cohorts: the first in 1994-
1995 and the second in 2001-2002.15Women in the
WIHS are seen twice-yearly and undergo detailed his-
tories, physical exams, structured interviews, and labo-
ratory testing. This study was approved by the WIHS
Executive Committee and the institutional review
boards at the six participating WIHS study sites. Study
eligibility included HIV/HCV coinfection at WIHS
study entry, as defined by detectable HCV RNA,
HCV antibody (Ab), and positive HIV western blot-
ting. Because of the small number of women who self-
reported as other than Caucasian, Hispanic, or African
American, these individuals were excluded from the
Predictor and Outcome Measures. The primary
predictor was race/ethnicity determined by self-report
at WIHS entry visit. We defined the African-American
group as non-Hispanic African Americans. The Cauca-
sian group was defined as non-Hispanic Caucasians.
The Hispanic group was defined as Hispanic Cauca-
sians, Hispanic African Americans, and other His-
panics. Our outcome of interest was primary liver-
related death, as determined by death certificate verifi-
cation. We also reported data on all-cause mortality.
Primary death certificate data were reviewed by two
clinicians to determine cause of death. In some cases,
there was supplemental information from medical re-
cord review, communication with the primary clini-
cian, or patient families. Primary liver-related deaths
included those resulting from hepatic decompensation
or hepatocellular carcinoma, although most death cer-
tificates simply recorded ‘‘hepatitis C’’ as the primary
cause of liver death, without further specification.
The following covariates were included in our sur-
vival analysis: age; substance abuse history, including
intravenous (IV) drugs, non-IV drugs, tobacco, and
alcohol; HIV-related factors, such as HIV RNA levels,
CD4 count, and highly active antiretroviral therapy
(HAART); liver-related factors, including HCV RNA
levels, HCV genotype, HCV treatment history, and
chronic hepatitis B virus (HBV); and comorbid fac-
tors, such as diabetes mellitus (DM), hypertension
(HTN), body mass index (BMI), glomerular filtration
rate (GFR), and cancer history.
Laboratory Assays. Plasma HIV RNA levels were
measured using the NASBA/NuciSens HIV RNA assay
(bioMerieux, Durham, NC) in laboratories certified by
Address reprint requests to: Monika Sarkar, M.D., Department of Medicine, Division of Gastroenterology and Hepatology, University of California San
Francisco, 513 Parnassus Avenue, Room S-357, San Francisco, CA 94143-0358. E-mail: firstname.lastname@example.org; fax: 415-476-0659.
View this article online at wileyonlinelibrary.com.
Potential conflict of interest: Nothing to report.
C 2012 by the American Association for the Study of Liver Diseases.
1700SARKAR ET AL.HEPATOLOGY, November 2012
the NIH National Institute of Allergy and Infectious
Diseases Virology Quality Assurance Certification Pro-
gram. HCV and HBV serologies were performed using
standard commercial assays and included hepatitis C
Ab by EIA 3.0 (Ortho Clinical Diagnostics, Raritan,
NJ) as well as hepatitis B surface antigen (HBsAg)
(Abbott Laboratories, Abbott Park, IL). HCV RNA
levels were measured by the COBAS Amplicor Moni-
tor 2.0 assay (Roche Diagnostics, Branchburg, NJ),
with a linear range of 600-700,000 IU/mL, or
COBAS Taqman (Roche Diagnostics), with a linear
range of 10-2.0 ? 108IU/mL.
compared using chi-square tests, t tests, and Kruskal-
Wallis’ tests, when appropriate. Cox’s regression models
were used to calculate the hazards ratios (HRs) and
95% confidence intervals (CIs) for factors associated
with all-cause and liver-related mortality. All survival
analyses used age as the time scale, with age at study
entry treated as a left-truncation time to reflect the
fact that only living women could be enrolled. This
automatically accounts for the important influence of
age on mortality risk and is a more biologically mean-
ingful time scale than time since study enrolment. All
variables that were measured repeatedly were analyzed
as time-varying covariates, with the most recent value
carried forward until a new measurement was made.
The only non-time-varying covariates were race/ethnic-
ity and HCV genotype, because these factors do not
change over time. The final multivariate model was
developed using forward selection of covariates, as well
as inclusion of covariates with high biological plausibil-
ity of an association with death. A Fine-Gray compet-
ing-risks analysis,16as well as a survival analysis of
non-liver-related death, was performed to assess the
possibility that racial/ethnic differences in liver-related
death could be attributed to a differential risk of non-
liver-related death among racial/ethnic groups. All
analyses were performed using STATA software (ver-
sion 11.0; StataCorp LP, College Station, TX).
We identified 794 women in the WIHS with con-
firmed CHC and HIV infection. Of these, 62.3%
(495 of 794) were African American, 20% were His-
panic (159 of 794), and 17.7% (140 of 794) were
Caucasian. Women were followed for up to 16 years,
with a median follow-up of 8.9 years. The median fol-
low-up for Caucasians, African Americans, and His-
panics was 9.0, 8.7, and 9.2 years, respectively. During
this time, there were 438 deaths from all causes,
including 49 liver-related deaths. Among primary
causes of death, HIV/AIDS (36.9%) was the most
common cause of death, followed by liver-related dis-
ease (11.2%) and homicides, suicides, and accidents
(9.0%). Approximately 55.8% (276 of 495) of African
Americans, 52.2% (83 of 159) of Hispanics, and
56.4% (79 of 140) of Caucasians died during follow-
up. Liver disease was the primary cause of death in
7.6% (21 of 276) of African Americans, 20.5% (17 of
Compared to Hispanics and Caucasians, African-
American women were older at study entry and time of
death. They were also more likely to have heavy alcohol
and tobacco use, to be diagnosed with hypertension,
and to be infected with HCV genotype 1. Compared
to Hispanics and African Americans, Caucasian women
were more likely to use IV drugs. There were no signif-
icant differences in median CD4 count, median HIV
viral load, or HAART use between racial/ethnic groups.
HCV treatment was uncommon, with similar percen-
tages between racial/ethnic groups (Table 1).
We first analyzed racial/ethnic differences in all-cause
mortality, which was similar between racial/ethnic
groups on both uni- and multivariate models (HRs for
all comparisons: 0.82-1.03; log-rank test: P ¼ 0.8).
These results contrasted markedly from our analysis of
liver-related mortality. On univariate analysis, there was
a trend toward lower risk of liver-related death among
African Americans, compared to Caucasians (HR, 0.48;
95% CI: 0.23-1.03; P ¼ 0.058) and a statistically sig-
nificantly lower risk of liver-related death among Afri-
can Americans, compared to Hispanics (HR, 0.44; 95%
CI: 0.22-0.87; P ¼ 0.019). On multivariate analysis,
adjusted for CD4 count and HIV RNA levels, we
observed even stronger racial/ethnic differences in liver-
related mortality, with an HR comparing African-Amer-
ican to Caucasian women of 0.41 (95% CI: 0.19-0.88;
P ¼ 0.022) and an HR comparing African-American to
Hispanic women of 0.38 (95% CI: 0.19-0.76; P ¼
0.006). Liver-related mortality was similar between
Caucasian and Hispanic coinfected women on uni- and
multivariate analyses (Table 2). These associations are
demonstrated graphically in an age-adjusted survival
curve, with a log-rank test of P ¼ 0.032 (Fig. 1).
Additional factors associated with liver-related mor-
tality on univariate analysis included CD4 count (HR,
0.78 per 2-fold increase; 95% CI: 0.67-0.91; P ¼
0.002) and HIV RNA level (HR, 1.47 per 10-fold
increase; 95% CI: 1.17.0-1.9; P ¼ 0.001), although
there was no significant association with HCV RNA
levels (HR, 1.44; 95% CI: 0.94-2.2; P ¼ 0.09). On
HEPATOLOGY, Vol. 56, No. 5, 2012 SARKAR ET AL.1701
multivariate analysis, HIV RNA levels were associated
with liver-related death (HR, 1.44; 95% CI: 1.11-1.9;
P ¼ 0.006) (Table 3).
We also assessed liver-related mortality after adjust-
ing for categories of factors that could affect risk of
death. We continued to observe marked racial/ethnic
differences in liver-related mortality after adjusting for
cardiovascular risk factors, HIV immune control, and
liver-related factors, suggesting that the observed
racial/ethnic differences were not explained by these
comorbid conditions (Table 4).
Importantly, we performed a competing-risks analy-
sis to determine whether the lower risk of liver-related
mortality among African-American women was the
result of African Americans dying at a higher rate
from non-liver-related diseases, as compared to other
racial/ethnic groups. In addition, we performed a sur-
vival analysis of non-liver-related mortality. The com-
peting-risks analysis estimated that African-American
HIV/HCV-coinfected women had a similar risk of
groups, as did the survival analysis of non-liver-related
mortality (HR, 1.01; 95% CI: 0.75 -1.36; P ¼ 0.95
versus Caucasians and HR, 1.18; 95% CI: 0.88-1.59;
P ¼ 0.27 versus Hispanics). Therefore, African-Ameri-
can women had a lower risk of liver-related mortality,
as compared to Hispanic and Caucasian coinfected
women, independent of other causes of death.
as other racial/ethnic
Table 1. Cohort Characteristics
(n ¼ 794)
(n ¼ 140)
(n ¼ 159)
(n ¼ 495)
Mean age at entry (6 SD)
Mean age at death (6 SD)
Tobacco use at entry, %
Ongoing tobacco use, %
IDU at entry, %
Ongoing IDU, %
Non IDU at entry, %
Ongoing non-IDU, %
Alcohol use at entry, %
Ongoing alcohol use, %
Median CD4 at entry (IQR)
Median nadir CD4 during study (IQR)
Last available CD4 (IQR)
Median log HIV RNA at entry (IQR)
Median log last available HIV RNA (IQR)
HAART use during study, %
Median log HCV RNA at entry (IQR)
Median log last available HCV RNA (IQR)
HCV treatment during study, %
HCV genotype 1, %
Chronic hepatitis B, %
Diabetes history, %
HTN history, %
Median BMI at entry (IQR)
Median GFR at entry (IQR)
Cancer history, %
SD, standard deviation; IQR, interquartile range.
Table 2. All-Cause and Liver-Related Mortality by Race/Ethnicity
Deaths From All Causes (n ¼ 438)
HR (95% CI)P Value
Liver-Related Deaths (n ¼ 49)
HR† (95% CI)P Value
HR (95% CI)P Value
HR‡ (95% CI)P Value
Hispanic (Ref) versus African American
*Age is the time scale, therefore all analyses account for the effect of age; see Statistical Analysis.
†Adjusted for BMI, CD4 count, GFR, HCV viral load, and HIV viral load.
‡Adjusted for CD4 count and HIV viral load.
1702 SARKAR ET AL.HEPATOLOGY, November 2012
Inthislarge cohortof HIV/HCV-coinfected
women, we investigated liver-related and all-cause
mortality. We observed marked differences in liver-
related death between racial/ethnic groups, whereas all-
cause mortality was similar between African-American,
Hispanic, and Caucasian coinfected women. African
Americans were approximately 60% less likely to die
from liver disease, as compared to Caucasian and His-
panic women. This relationship persisted after adjust-
ing for an extensive list of covariates that could possi-
bly affect risk of death.
A previous investigation of HIV/HCV-coinfected
veterans identified important racial differences in all-
cause mortality, with significantly higher mortality
among Caucasian coinfected males, compared to Afri-
can Americans. Interestingly, these differences were not
observed among HCV-monoinfected patients.14Unlike
our study, the Veteran study was predominantly male
and limited by its cross-sectional design, small number
of Hispanic patients, and inability to investigate liver-
related death. Although the Veteran study did report
important racial/ethnic differences in all-cause mortal-
ity among coinfected men, no previous data reflect
liver-related mortality trends among coinfected popula-
tions or in HIV/HCV-coinfected women.
The reasons for the marked racial/ethnic differences
in liver-related mortality in the current study certainly
warrant further investigation. When we adjusted for
many cofactors known to accelerate liver disease, such
as HIV immune status, obesity, and alcohol use, we
continued to observe significant differences between
racial/ethnic groups. Although African Americans are
less likely to spontaneously clear HCV, previous data
do suggest that once chronically infected, African
Americans tend to have less liver inflammation, as
measured by alanine aminotransferase (ALT) levels and
necroinflammatory scores on liver biopsy.10Sugimoto
et al. also investigated T-cell response in patients with
chronic HCV infection and found that African Ameri-
cans had a significantly more-robust T-cell response
than Caucasians, as well as higher platelet counts,
lower bilirubin, and lower ALT levels.17These results
were not due to alcohol use, gender differences, or
Fig. 1. Age-adjusted survival curve of liver-related mortality in HIV/
HCV-coinfected women during the WIHS. African-American (AA) women
had greater survival than Caucasian (Cauc) and Hispanic (Hisp)
women (log-rank test: P ¼ 0.032).
Table 3. Factors Associated With Liver-Related Mortality
Univariate Analysis* Multivariate Analysis†
VariableHR (95% CI)P Value HR (95% CI)P Value
Log HIV RNA
Log HCV RNA
HCV genotype 1
*Age is the time scale, therefore all analyses account for the effect of age;
see Statistical Analysis.
†Adjusted for CD4 count, HIV viral load, and race/ethnicity.
Table 4. Liver-Related Death Adjusted for Categories of Risk Factors
HR (95% CI)P Value
Factors HR† (95% CI)P Value
HR‡ (95% CI)P Value
HR§ (95% CI)P Value
Hispanic (Ref) versus
*Age is the time scale, therefore all analyses account for the effect of age; see Statistical Analysis.
†Adjusted for BMI, DM, HTN, and tobacco use.
‡Adjusted for CD4 count, HIV treatment, and HIV viral load.
§Adjusted for alcohol use, chronic HBV, and HCV viral load.
HEPATOLOGY, Vol. 56, No. 5, 2012 SARKAR ET AL. 1703
HCV genotype, which were evenly distributed between
African Americans and Caucasians. It is quite possible
that differential immunologic response to HCV may
account for differences in progression of HCV-related
liver disease between racial/ethnic groups.
African Americans may also have slower rates of liver
fibrosis than Caucasians or Hispanics once chronically
infected with hepatitis C. However, most studies on
this topic have been limited by small sample size, and
these differences have generally not reached statistical
significance.9,10,18,19Two studies have noted a signifi-
cantly increased rate of liver fibrosis in Hispanics, com-
pared to Caucasians and African Americans, after
adjusting for comorbid conditions that could accelerate
liver fibrosis.18,20Interestingly, these associations with
fibrosis progression are similar to the racial/ethnic
trends that we report for liver-related mortality, suggest-
ing that differential rates of fibrosis progression may
play an important role in explaining racial/ethnic dif-
ferences in HCV-related mortality.
Recent data suggest that single nucleotide polymor-
phisms (SNPs) may play an important role in differen-
tial rates of liver fibrosis. A study by Barreiro et al.
found that the CC genotype associated with the IL28B
SNP rs12979860 was predictive of cirrhosis in HIV/
HCV-coinfected patients.21Because the frequency of
the CC genotype is higher in Caucasians (39%) and
Hispanics (35%), as compared to Africans Americans
(16%),22these data could, in part, explain why African
Americans may have slower rates of liver fibrosis.
However, other studies investigating the association
between IL28B and fibrosis progression have been con-
flicting.23-25A genome-wide association study investi-
gating the role of IL28B is currently underway within
the WIHS to help further address differential rates of
liver fibrosis between racial/ethnic groups.
There were several limitations in the current study.
First, we analyzed only primary cause of death and
therefore may have underestimated the true prevalence
of liver-related death. Many patients with decompen-
sated liver disease may die from infectious complica-
tions, and these diagnoses may not have been coded as
liver-related events. We also lacked data on the severity
of liver disease, such as cirrhosis history or synthetic
functions tests (albumin and international normalized
ratio). However, liver-related deaths are often the result
of hepatic decompensation or liver cancer, both of
which were captured as liver-related events.4Additional
data on severity of liver disease or secondary causes of
death would likely have strengthened our findings.
There were important strengths of the current study,
most notably our ability to separately analyze liver-
related and non-liver-related deaths. This showed that
the lower risk of liver-related death among African-
American women was not simply the result of African
Americans dying at a higher rate from non-liver-
related deaths, as compared to Hispanics and Cauca-
sians. In addition, the primary cause of death was
abstracted from death certificates, which are often sub-
ject to misclassification and miscoding. However, death
data were ascertained in a similar fashion over time,
and any misclassification would have unlikely varied
by race. Finally, our survival analyses incorporated a
time-varying analysis of many time-dependent factors
that may have affected mortality risk. Alcohol use, for
example, was analyzed over time, rather than use at a
fixed time point in the study period. This statistical
method allowed us to capture the complex and chang-
ing effect of many risk factors for death over the
course of each participant’s lifetime.
In conclusion, we observed novel, important racial/
ethnic trends in this large cohort of HIV/HCV-coin-
fected women. Compared to Hispanic and Caucasian
women were much less likely to die from liver-related
disease, which did not appear to be the result of differ-
ential classification of cause of death. Previous data
have revealed racial/ethnic differences in immunologic
response to HCV, which may affect rates of liver fibro-
sis. Future studies incorporating fibrosis progression
may help us to better understand these marked racial/
ethnic discrepancies in liver-related mortality.
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