HIV/AIDS MAJOR ARTICLE

Anemia in HIV Infection: Clinical Impact

and Evidence-Based Management Strategies
Paul A. Volberding,1,a Alexandra M. Levine,2,a Douglas Dieterich,4 Donna Mildvan,5 Ronald Mitsuyasu,3
and Michael Saag,6 for the Anemia in HIV Working Groupb
1
University of California, San Francisco, and 2Keck School of Medicine, University of Southern California, and 3CARE Center, University
of California, Los Angeles; 4Mt. Sinai School of Medicine, New York, New York; 5Beth Israel Deaconess Medical Center, Boston, Massachusetts;
and 6University of Alabama at Birmingham

Anemia in human immunodeficiency virus (HIV)–infected patients can have serious implications, which vary
from functional and quality-of-life decrements to an association with disease progression and decreased sur-
vival. In 2002, 16 members of the Anemia in HIV Working Group, an expert panel of physicians involved in
the care of HIV-infected patients that met first in 1998, reconvened to assess new data and to translate these
data into evidence-based treatment guidelines. The group reached consensus on the prevalence of anemia in
the highly active antiretroviral therapy era; the risk factors that are independently associated with the devel-
opment of anemia; the impact of anemia on quality of life, physical functioning, and survival; the impact of
the treatment of hepatitis C virus coinfection on anemia in HIV-infected patients; evidence-based guidelines
for treatment of anemia in HIV-infected patients, including the therapeutic role of epoetin alfa; and directions
for future research.

Anemia is an important clinical problem in patients
with HIV infection and those with AIDS. In 1998, the
Anemia in HIV Working Group issued a consensus
statement addressing the impact of anemia on HIV-
infected individuals, as well as treatment strategies and
future research directions. The Anemia in HIV Working
Group reconvened in 2002 to evaluate recently available
Received 16 July 2003; accepted 6 December 2003; electronically published 27
April 2004.
Financial support: The consensus conference and associated logistics were
supported by an educational grant from Ortho Biotech Products. Ortho Biotech
Products provided support in convening the meeting and obtained the services of
an independent company (The Spellman Group) to assist with transcription and
summarization of the meeting discussion.
a
Consensus conference co-chairs.
b
Members of the Anemia in HIV Working Group are listed at the end of the
text.
Reprint or correspondence: Dr. Paul A. Volberding, Veterans Administration
Hospital, 4150 Clement St., San Francisco, CA 94121 (paul.volberding@med.
va.gov).
Clinical Infectious Diseases 2004; 38:1454–63
 2004 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2004/3810-0020$15.00
data and to determine the implications of those data
for patient management.
The consensus statement that follows is based on
evidence in the published literature, clinical experience,
and the expert opinion of the panel. The chairpersons
selected panelists from among the participants in the
1998 Anemia in HIV Working Group meeting and
other experts who are involved in HIV study and who
specialize in the hematological complications of the
disease.
WHAT CAUSES ANEMIA
IN HIV-INFECTED PERSONS?
An obvious cause of anemia in patients with HIV in-
fection is blood loss. Blood loss may be associated with
such conditions as neoplastic disease (e.g., Kaposi sar-
coma in the gastrointestinal tract) or gastrointestinal
lesions that accompany opportunistic cytomegalovirus
infection. Other than blood loss, the pathophysiology
of HIV-associated anemia may involve 3 basic mech-

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 Table 1. Drugs that commonly cause myelo-
suppression in HIV-infected patients.
Antiretrovirals
Zalcitabine
Zidovudine
Antiviral agents
Ganciclovir
Foscarnet
Cidofovir
Antifungal agents
Flucytosine
Amphotericin
Anti–Pneumocystis carinii agents
Sulfonamides
Trimethoprim
Pyrimethamine
Pentamidine
Antineoplastic agents
Cyclophosphamide
Doxorrubicin
Methotrexate
Paclitaxel
Vinblastine
Liposomal doxorubicin
Liposomal daunorubicin
Immune response modifiers: IFN-a
NOTE. From [3].
anisms: decreased RBC production, increased RBC destruction,
and ineffective RBC production.
Decreased RBC production. Decreased RBC production
may be a consequence of infiltration of the bone marrow by
neoplasm [1] or infection [2], use of myelosuppressive medi-
cations (table 1) [3], HIV infection itself [3], a decreased pro-
duction of endogenous erythropoietin, a blunted response to
erythropoietin [4], or hypogonadism. [5]
Increased RBC destruction (i.e., hemolysis). Increased or
premature RBC destruction in the spleen or the circulator sys-
tem may occur in patients with HIV infection. Hemolytic ane-
mia may result from RBC autoantibodies, hemophagocytic syn-
drome, disseminated intravascular coagulation, thrombotic
thrombocytopenic purpura, or glucose-6-phosphate dehydrog-
enase deficiency [3, 6–11]. Hemolysis may also develop as a
consequence of the use of various medications [12].
Ineffective RBC production. Anemia may result from nu-
tritional deficiencies—most commonly, deficiencies in iron,
folic acid, or vitamin B12. In patients with HIV disease, folic
acid deficiency is generally caused by either dietary deficiency
or jejunal pathology [3]. Vitamin B12 deficiency may result from
malabsorption in the ileum or from gastric pathology caused
by an array of infections or other conditions that affect the
gastric mucosa in HIV-infected patients [13].
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WHAT FACTORS ARE ASSOCIATED WITH
ANEMIA IN HIV-INFECTED PERSONS?
Individuals with HIV infection who are significantly more likely
to develop anemia include women and African American per-
sons [14–18]. There is also evidence of increased risk of anemia
in association with zidovudine use, CD4 cell counts of !200
cells/mL, increased virus load, and a number of additional fac-
tors (table 2) [15, 16, 18–22].
Sex. In the Anemia Prevalence Study Group [16], which
involves nearly 10,000 patients, there was a 71% greater prev-
alence of anemia among women than among men when anemia
was defined as a hemoglobin level of !12 g/dL in women and
of !13 g/dL in men (P !.0001). Both the Women’s Interagency
HIV Study (WIHS) [15] of 2625 women and the Human Im-
munodeficiency Virus Epidemiology Research (HER) Study
[19] of 1186 women corroborate these findings. Presumably,
the increased prevalence of anemia in female HIV-infected per-
sons, compared with male individuals, reflects the overall higher
prevalence of anemia in female persons, which may be largely
attributed to menstrual blood loss and to the drains on iron
stores that occur with pregnancy and delivery.
Race. Multivariate analyses in several major studies, in-
cluding the Anemia Prevalence Study, the WIHS [15], and the
HER study [19], found that HIV-positive patients who were
African American demonstrated a higher prevalence of anemia
than that found in other races. In the most recent report from
the Anemia Prevalence Study Group [16], for example, the
prevalence of anemia in HIV-infected persons was 39% among
African American women, 19% among white women, 31%
among African American men, and 12% among white men
(figure 1). African American individuals with HIV infection
may be at particular risk for the development of anemia, in
part as a result of the presence of inherited hematologic dis-
orders, such as sickle cell disease and thalessemia. Dietary fac-
tors may also be involved [23].
Table 2. Risk factors currently associated with
anemia in HIV infection.
History of clinical AIDS
CD4 cell count of !200 cells/mL
Plasma virus load
Women
Black race
Zidovudine use
Increasing age
Lower body mass index
History of bacterial pneumonia
Oral candidiasis
History of fever
NOTE. From [15, 16, 18, 22].
HIV/AIDS • CID 2004:38 (15 May) • 1455

Figure 1. Prevalence of anemia, by race, in a cohort of 969 HIV-
infected patients [16]. Anemia was defined as a hemoglobin level of !12
g/dL for women and !13 g/dL for men.
Zidovudine treatment. Zidovudine treatment is associated
with bone marrow suppression and an increased risk of de-
veloping anemia [21, 24–28]. The HER study [19] demon-
strated that, although the use of zidovudine was associated with
an increased risk of anemia (defined as a hemoglobin level of
!12 g/dL) in the pre-HAART era (1993–1996), use of zido-
vudine during the HAART era (1996–2000) was not signifi-
cantly associated with anemia. In contrast, the WIHS recorded
the presence of anemia (defined as a hemoglobin level of !10
g/dL or a physician’s diagnosis) in 41.6% of subjects receiving
zidovudine therapy, compared with 34.3% of those not receiv-
ing zidovudine (P ! .01) [15].
Worsening HIV disease parameters. Low CD4 cell counts
Figure 2. Kaplan-Meier progression to death for patients in the EuroSIDA study, according to baseline hemoglobin level, in multivariate analysis
[20]. Normal was defined as a hemoglobin level of 114 g/dL for men and 112 g/dL for women; mild anemia was defined as a hemoglobin level of
8–14 g/dL for men and 8–12 g/dL for women; and severe anemia was defined as a hemoglobin level of !8 g/dL for both men and women.
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(!200 cells/mL) and higher HIV-1 RNA levels in plasma have
each been independently associated with an increased risk of
anemia in multivariate analyses [15, 18–20].
WHAT IS THE SIGNIFICANCE OF ANEMIA
IN HIV-INFECTED PERSONS?
Although no causal relationship has been documented, retro-
spective analyses have found an association between anemia at
baseline, decreased survival, and increased disease progression
in patients with HIV infection [17, 20, 29, 30]. In the EuroSIDA
study [20], for example, the 12-month survival rate was 96.9%
among nonanemic patients, compared with 84.1% among pa-
tients with anemia at baseline (defined as a hemoglobin level
of !12 g/dL for women and of !14 g/dL for men; P ! .0001),
and it was 59.2% among those with severe anemia (defined as
a hemoglobin level of !8 g/dL for both men and women;
P ! .0001) (figure 2).
In the Multistate Adult and Adolescent Spectrum of HIV
Disease Surveillance Project, Sullivan et al. [17] analyzed the
medical records of 32,867 individuals with HIV infection. The
median duration of survival was significantly shorter in persons
with anemia (defined as a hemoglobin level of !10 g/dL) than
in those without anemia, regardless of baseline CD4 cell count.
Among individuals with CD4 cell counts of ⭓200 cells/mL, the
relative risk of death was 148% higher in those who developed
anemia. Among patients whose baseline CD4 cell counts were
!200 cells/mL, the risk of death was increased by 56% in the
presence of anemia. Survival rates improved markedly among
subjects recovering from anemia.

Figure 3. Prevalence of anemia during HAART in a cohort of 1624
patients in the EuroSIDA study [20]. No anemia was defined as a he-
moglobin level of 114 g/dL for men and 112 g/dL for women; mild anemia
was defined as a hemoglobin level of 8–14 g/dL for men and 8–12 g/
dL for women; and severe anemia was defined as a hemoglobin level of
!8 g/dL for both men and women.
WHAT IS THE IMPACT OF ANEMIA IN HIV-
INFECTED PERSONS ON QUALITY OF LIFE
AND PHYSICAL FUNCTIONING?
Impact of fatigue. Fatigue is a common symptom of HIV
infection and is associated with impaired physical functioning,
psychological distress, and decrements in quality of life [31,
32]. Although the etiology of HIV-related fatigue may be mul-
tifactorial [33], anemia is considered an important contributing
factor or underlying cause [31].
In a pre-HAART study of 112 patients (62 of whom were
HIV seropositive and 50 of whom were HIV seronegative) by
Darko et al. [34], 50% of HIV-positive subjects (who at that
time had disease classified as CDC stage IV) reported that fa-
tigue interfered with their daily activities, whereas none of the
comparison subjects (whose disease was classified as CDC stage
III or who were HIV negative) reported problems with fatigue.
Employment problems and sleep disturbances were shown to
contribute to morbidity and disability in the HIV-infected
group. In a later study of 427 patients by Breitbart et al. [31],
52.7% of subjects responded positively to both the “lack of
energy” item on the Memorial Symptom Assessment Scale and
the “persistent or frequent fatigue” item on the AIDS-specific
Physical Symptom Checklist and were subsequently classified
as having fatigue. Serum hemoglobin levels (available from a
subset of 176 fatigued patients) were significantly lower than
in nonfatigued patients (P ! .02 ). A substudy of 148 patients
from the ongoing multinational INITIO trial of 913 antiret-
roviral therapy–naive patients revealed an independent rela-
tionship between low baseline levels of hemoglobin and overall
quality of life [35].
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Impact of correction of anemia. Correction of anemia in
patients with HIV infection has been associated with mean-
ingful improvements in quality of life and physical functioning.
Abrams et al. [36] evaluated epoetin alfa treatment (100–300
U/kg 3 times per week) in 221 HIV-positive patients with ane-
mia (defined as a hemoglobin level of ⭐11 g/dL). Of these
patients, 207 subjects for whom both baseline and follow-up
measurements were available demonstrated significant (P !
.01) and sustained improvement in hemoglobin levels (mean
increase, 2.5 g/dL). Small increases in the hemoglobin level (up
to 2 g/dL) were associated with a beneficial effect on total
quality of life (as measured by the Functional Assessment of
HIV Infection scale), whereas increases of ⭓2 g/dL were sig-
nificantly associated with greater improvement in quality of life
score (P ! .05).
In a recent study, Grossman et al. [37] randomly assigned
269 HIV-infected patients with anemia (defined as a hemoglo-
bin level of !12 g/dL) to receive 16 weeks of treatment with
epoetin alfa at either 100 U/kg 3 times per week or 40,000 U
once per week. Quality of life was measured using 2 instru-
ments: the Linear Analog Scale Assessment (LASA) and the
validated Medical Outcomes Study HIV Health Survey (MOS-
HIV). Significant increases from the baseline level in mean
hemoglobin levels (P ! .0001) and in quality of life scores
(P ! .0001) were demonstrated for both dosage regimens.
In a recently completed study of 709 evaluable HIV-positive
patients with anemia (defined as a hemoglobin level of ⭐11 g/
dL) who received epoetin alfa (40,000 U once per week), the
mean change in hemoglobin level from baseline was statistically
significant (P ! .05) as early as week 4, with a mean increase
of 2.7 g/dL achieved by week 8 [38]. Each 1-g/dL increase in
hemoglobin level was associated with a 6.4-point increase in
the LASA energy/fatigue score, resulting in an overall mean
improvement of 41% (P ! .001). The MOS-HIV energy/fatigue
score improved by a mean of 37% (P ! .001). The greatest
Table 3. Treatable causes of anemia in HIV-infected patients.
Nutritional deficiencies (malnutrition and malabsorption)
Anemia of chronic disease
Myelosuppressive drugs (e.g., zidovudine, antimicrobials, and anti-
neoplastic agents)
Hypogonadism
Vitamin B12 , iron, or folate deficiency
Hemophagocytic histocytosis
Myelofibrosis or myelodysplasia
Neoplasia (e.g., non-Hodgkin lymphoma)
Opportunistic bone marrow infections (e.g., infection with cyto-
megalovirus, parvovirus B19, Mycobacterium avium complex, or
Cryptococcus neoformans)
NOTE. From [57].
HIV/AIDS • CID 2004:38 (15 May) • 1457
 Figure 4. Simplified diagnostic approach to anemia in HIV-infected individuals [39]. AZT, zidovudine; ddC, dideoxycytidine; DIC, disseminated
intravascular coagulation; HB, hemoglobin; MCV, mean cell volume; TTP, thrombotic thrombocytopenic purpura.
improvements in quality of life occurred when hemoglobin
levels increased from a baseline level of 11–13 g/dL.
WHAT IS THE EFFECT OF HAART
ON THE PREVALENCE OF ANEMIA
IN HIV-INFECTED PERSONS?
Although the prevalence of severe anemia has decreased since
the introduction of HAART, mild-to-moderate anemia contin-
ues to be common [39–42]. A subset of 1624 patients was
evaluated as part of the EuroSIDA study [20]. Before HAART
was initiated, mild anemia (defined as a hemoglobin level of
!12 g/dL for women and of !14 g/dL for men) was present in
64% of subjects, and severe anemia (defined as a hemoglobin
level of !8 g/dL for both women and men) was present in 1.5%
of subjects (figure 3). After 6 months of HAART therapy, mild
anemia was present in 52% of subjects, and severe anemia was
present in 1.2%. After 12 months, further improvements were
recorded, with 45.6% of patients demonstrating mild anemia
and 0.6% demonstrating severe anemia [20].
Even with use of HAART, anemia remains strongly and con-
sistently associated with HIV disease progression [20]. Studies
have shown that, as hemoglobin levels decrease, the risk of
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disease progression increases [17, 20, 29, 43, 44]. In a EuroSIDA
study cohort of 2027 HIV-infected patients, Lundgren et al.
[29] examined the relative hazard of clinical progression be-
tween patients who were anemic and those with normal he-
moglobin levels (114 g/dL in men and 112 g/dL in women).
The relative hazard of clinical progression was 2.2 among men
with hemoglobin levels 8–14 g/dL and women with levels of
8–12 g/dL. The relative hazard of clinical progression was 7.1
in men and women with hemoglobin levels of !8 g/dL [29].
In a study of 19,213 patients by Sullivan et al. [17], the risk of
death increased by 148% in patients with a hemoglobin level
of !10 g/dL and a CD4 cell count of ⭓200 cells/mL (P ! .001).
A study of 2348 patients reported by Moore et al. [43] dem-
onstrated an increase in the rate of death of 206% in persons
with a hemoglobin level 8.0–9.4 g/dL and of 290% in those
with a hemoglobin level of !6.5 g/dL (P ! .001). A 158% in-
crease in the rate of death was reported by Levine et al. [44]
in a study of 1525 patients with a hemoglobin level of !12 g/
dL (P p .007). Mocroft et al. [20] found similar results, with
a 1-g/dL decrease in most-recent hemoglobin measurement re-
sulting in an increased risk of death of 57% (P ! .001). In the
National Institutes of Health–sponsored WIHS, the develop-
ment or persistence of anemia in HIV-positive subjects was
 Figure 5. Linear Analog Scale Assessment for determining quality of life
independently associated with a decreased duration of survival
(P ! .0001) [45]. Determination of whether a cause-and-effect
relationship exists between correction of anemia and improved
survival is an important area for future research.
WHAT ARE THE CURRENT
TREATMENT GUIDELINES FOR ANEMIA
IN HIV-INFECTED PERSONS?
Address correctable causes of anemia. The clinical evaluation
of an HIV-infected person with anemia should attempt to iden-
tify treatable underlying causes, including hypogonadism (table
3). A simplified approach to the assessment of anemia in pa-
tients with HIV infection is illustrated in figure 4. To the extent
possible, treatable causes should be corrected. In patients whose
anemia is severe, transfusion should be considered for allevi-
ation of acute symptoms.
Use of HAART. HAART use may result in improvement
of existing anemia. A multivariate analysis of the WIHS study
found that HAART was significantly associated with correction
of anemia; improvement was noted within 6 months, and a
greater resolution occurred after a longer duration of HAART
use (P ! .0001) [45].
Use of epoetin alfa. In multiple controlled and uncon-
trolled studies, epoetin alfa has been proven safe and effective
for the treatment of anemia in HIV infection. In an early,
combined analysis of four 12-week, randomized, double-blind,
multicenter, controlled clinical trials [22], epoetin alfa (100–
200 U/kg 3 times per week) significantly improved hematocrit
levels (P ⭐ .05) in patients with AIDS who were receiving zi-
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dovudine, with endogenous erythropoietin levels of ⭐500 IU/
L. An increase of 11 g was seen by week 2, with furthers in-
creases of 12 g by week 4. Treatment was also associated with
significant reductions in transfusion requirements (P ! .003)
and improvements in overall quality of life. As has been de-
scribed previously, more recent clinical studies of anemic pa-
tients with HIV infection have found that epoetin alfa may also
be administered once per week (40,000 U), resulting in im-
provements comparable to those associated with thrice-weekly
administration [37, 38].
Consensus recommendations. The Anemia in HIV Work-
ing Group concluded that the following evidence-based treat-
ment strategies should be implemented for anemia in HIV-
infected patients:
• Monitor hemoglobin levels routinely (e.g., concurrently
with each CD4 cell count determination). Ask patients
whether they are fatigued and determine whether there is
impairment of physical functioning. Assess quality of life
on an ongoing basis using such measures as the LASA (figure
5) or MOS-HIV.
• If the hemoglobin level is lower than normal (!14 g/dL in
men and !12 g/dL in women), or if the patient shows symp-
toms of anemia, rule out or correct treatable causes.
• Initiate HAART if warranted.
• If correctable causes of anemia have been ruled out and the
hemoglobin level is !13 g/dL in men and !12 g/dL in
women, initiate epoetin alfa therapy at a dosage of 40,000
U once per week.
• Anticipated benefits of epoetin alfa treatment weighed
HIV/AIDS • CID 2004:38 (15 May) • 1459
 Figure 6. Guidelines for dose titration of epoetin alfa for anemic, HIV-positive patients [46]. Hb, hemoglobin.
against its cost must be considered by the clinician in the
absence of data from rigorous cost-benefit analyses.
• Continue epoetin alfa therapy until symptoms have re-
solved and hemoglobin levels of ⭓13 g/dL for men or ⭓12
g/dL for women are achieved, then maintain hemoglobin
levels by dosage titration or increasing the dosing interval
(figure 6).
WHAT IS THE IMPACT OF TREATMENT FOR
HEPATITIS C VIRUS (HCV) INFECTION ON
ANEMIA IN HIV-INFECTED PERSONS?
HCV coinfection is estimated to occur in ∼30% of HIV-infected
individuals in the United States [12]. Ribavirin in combination
with IFN or pegylated interferon IFN is the standard of care
for treatment of HCV infection, but it has been shown to cause
anemia, frequently leading to dosage reduction and potentially
suboptimal outcomes [14, 47].
When treating patients with ribavirin-related anemia, he-
moglobin levels should be monitored, and epoetin alfa should
be added to the treatment regimen in the presence of anemia.
In patients with HCV infection alone, epoetin alfa (40,000 U
once per week) has been shown to effectively treat anemia
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associated with ribavirin therapy, to allow maintenance of ri-
bavirin dose, and to reduce discontinuation rates, and it may
also improve quality of life [48–52]. The relative percentage of
patients who are able to tolerate optimal doses of ribavirin can
be expected to increase by 40%–50% with receipt of epoetin
alfa therapy [50, 51]. Studies of the utility of epoetin alfa therapy
for patients infected with both HIV and HCV are currently in
progress.
WHAT ARE THE DIRECTIONS
FOR FUTURE RESEARCH ON ANEMIA
IN HIV-INFECTED PERSONS?
Future research should focus on furthering understanding of
the causes of anemia, its long-term consequences and prog-
nostic importance, the impact of various HAART regimens
on the prevalence of anemia, and optimal dosing strategies
for the use of epoetin alfa in special populations. Emerging
data suggest that epoetin alfa has effects beyond erythropoi-
esis. There is evidence, for example, that epoetin alfa has
antiapoptotic effects in multiple cell lines, which may have a
positive impact on the immunologic response in patients with
HIV infection [53, 54]. Moreover, in animal studies, epoetin
 alfa has been shown to cross the blood-brain barrier and to
protect neurons and astrocytes from injury [55]. A recent
pilot study of patients demonstrated benefit in acute ischemic
stroke, with an improvement in clinical outcome at 1 month
[56]. It is thus conceivable that epoetin alfa may one day
prove useful in the treatment of neurologic conditions, in-
cluding stroke and cognitive dysfunction.
Cost-benefit analyses are needed to determine the impact of
treatment of anemia in HIV-infected patients with epoetin alfa
and/or alternative therapies. Factors involved in cost-benefit
studies should include identification of the predictors of a re-
sponse to therapy, determination of optimal doses and schedule
of treatment, calculation of the associated costs of treatment,
and consideration of any effects of therapy on the natural his-
tory of HIV infection.
CONCLUSIONS
Despite use of lower dosages of zidovudine and the introduc-
tion of HAART, mild-to-moderate anemia still occurs in a sub-
stantial portion of HIV-infected persons and is associated with
increased mortality, increased disease progression, and reduced
quality of life. Female sex, African American race, medications
used for treatment of HIV infection, high HIV-RNA levels, and
low CD4 cell count are risk factors for the development of
anemia in HIV-infected persons. The Anemia in HIV Working
Group agreed that guidelines for the treatment of anemia
should be updated. Hemoglobin levels and functional status
should be monitored in a systematic manner on an ongoing
basis. When anemia is present, treatable causes should be cor-
rected. HAART should be initiated at hemoglobin levels of !14
g/dL for men and !12 g/dL for women if other criteria for
institution of HAART are met. If correctable causes have been
excluded, epoetin alfa should be added if hemoglobin levels
decrease to !13 g/dL in men and !12 g/dL in women or if
anemia does not improve after 6 months of HAART. Admin-
istration of epoetin alfa once per week is appropriate for the
treatment of chronic anemia. Future research on epoetin alfa
in HIV-infected patients, beyond its effects on erythropoiesis,
is warranted.
THE ANEMIA IN HIV WORKING GROUP
Cochairmen are Paul Volberding (University of California, San
Francisco, San Francisco Veterans Affairs Medical Center) and
Alexandra Levine (University of Southern California Keck
School of Medicine and Norris Cancer Hospital, Los Angeles).
Other members of the Working Group are Richard Chaisson
(Johns Hopkins University, Baltimore), Terri Creagh (Clinical
Epidemiology Research, Atlanta), Douglas Dieterich (Mt. Sinai
School of Medicine, New York), Howard Grossman (Columbia
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University and St. Luke’s Roosevelt Hospital Center, New York),
Donna Mildvan (Infectious Diseases, Beth Israel Medical Cen-
ter, and Albert Einstein College of Medicine, New York), Ronald
Mitsuyasu (University of California, Los Angeles, CARE Cen-
ter), Michael Saag (AIDS Outpatient Clinic, University of Al-
abama at Birmingham), Victoria Sharp (Center for Compre-
hensive Care, St. Luke’s–Roosevelt Hospital Center, New York),
Renslow Sherer (Rush Medical Center, Cook County Hospital,
Chicago), and Patrick Sullivan (HIV Vaccine Trials Network,
Seattle).
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