Current perspectives on the management and prevention
of antiretroviral-associated lipoatrophy
David Richard Phillips1and Phillip Hay1,2*
1Courtyard Clinic, St George’s Hospital NHS Trust, Blackshaw Road, Tooting, London SW17 0QT, UK;2Centre
for Infection, St George’s, University of London, London, UK
Lipoatrophy (LA) is a common and now well-recognized complication of highly active antiretroviral
therapy (HAART). Over the last decade as knowledge of the mechanisms behind LA has developed,
several antiretroviral drugs, in particular, have emerged as the likely agents responsible for this com-
plication. This has been supported by studies comparing alternative HAART regimens and by those in
which HAART regimens have been modified with a resulting impact on LA. In this article, we review
the evidence underlying the current perspectives on the development of LA and the strategies
employed to manage or avoid it.
Keywords: lipoatrophy, lipodystrophy, HAART, HIV, antiretrovirals
Highly active antiretroviral therapy (HAART) has markedly
reduced the morbidity and mortality of those infected with the
human immunodeficiency virus (HIV), transforming the infec-
tion into a chronic disease. However, with more patients survi-
ving on antiretroviral (ARV) medications, long-term toxicities
of these medications have become prominent issues for
HIV management in the developed world.1Lipoatrophy (LA),
initially described alongside visceral fat accumulation, insulin
resistance and dyslipidaemia as the lipodystrophy syndrome, is
one such complication that has even been a cause for caution over
early initiation of HAART. Mild LA may manifest as increased
muscle definition and venous prominence in the limbs or face.
Severe LA can cause facial disfigurement or pain as fat cushioning
is lost from bony prominences, e.g. the buttocks. Facial LA is
particularly stigmatizing because for some it discloses their HIV
status. LA may contribute to failure in adherence to ARVs or
delay initiation of ARVs in those needing to start them.
Mechanism of LA
Initially, protease inhibitors (PIs) were associated with the meta-
bolic disturbances of the ‘lipodystrophy syndrome’ and impli-
cated in all aspects of lipodystrophy. However, substantial
evidence has accumulated implicating nucleoside reverse tran-
scriptase inhibitors (NRTIs), particularly the thymidine ana-
logues (tNRTIs), as those responsible for LA.2–5Recent studies
disregard PIs in the aetiology of LA, e.g. Moyle et al.6demon-
strated little benefit in removing PIs from a HAART regimen
compared with the greater benefit from removing tNRTIs.
A growing body of evidence from larger ‘switch studies’
(Table 1) where a tNRTI is replaced by another ARV endorses
the role of tNRTIs in LA.7–15
NRTIs inhibit mitochondrial g-DNA polymerase thereby
reducing replication of mitochondrial DNA (mtDNA).16,17
Reduction of mtDNA has been demonstrated in adipocytes of
patients with LA, suggesting an organ-specific disturbance of
mtDNA.9,18Cohorts taking the tNRTI stavudine have consist-
ently reported a high incidence of LA and since stavudine is a
potent inhibitor of g-DNA polymerase in vitro, mitochondrial
toxicity has gained credibility as the mechanism behind LA.
In vitro g-DNA polymerase is also inhibited by didanosine and
zidovudine, while lamivudine, emtricitabine, tenofovir diso-
proxil fumarate and abacavir show little inhibition. This is the
rationale for examining NRTI switching to resolve or prevent
LA. Although zidovudine is a relatively weak inhibitor of
g-DNA polymerase, it is converted into stavudine-triphosphate
in some human cells and is well correlated with LA.18–20
For established LA, management involves switching ARV
drugs, using non-ARV pharmacological agents or employing
reconstructive-cosmetic techniques. The majority of this article
outlines the basis behind each of these approaches.
Measurement and interpretation of intervention
studies on LA
Data on LA can appear to be confusing. LA improvements with
an ARV switch in one study may appear contradicted by
another. The methods by which LA is evaluated may be partly
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Table 1. An overview of the major trials that have studied the association of particular ARVs with LA
Ref. Acronym and yearStudy design
8 MITOX 2004 randomized, open, switch; patients on AZT or
d4T regimen randomized to:
† continue AZT or d4T (n ¼ 57) or
† switch AZT/d4T for ABC (n ¼ 54)
104 14 in AZT/d4T group
12 in ABC group
DEXA (n ¼ 77) AZT/d4T group mean limb fat
gain: 490+1380 g
switch to ABC group mean limb
fat gain: 1260+2020 g
9 TARHEEL 2004 randomized, open, switch; patients on HAART
had d4T switched for:
† ABC (n ¼ 86) or
† AZT (n ¼ 32)
48 25 in total, groups not
DEXA median % change in arm fat
ABC group: 38 (237 to 174)
AZT group: 17 (246 to 132)
11RAVE 2006 randomized, open, switch; 105 patients on d4T
or AZT regimen with LA switched to:
† TDF (n ¼ 52) or
† ABC (n ¼ 53) regimen
48 1 in TDF group
3 in ABC group
DEXAlimb fat gain:
TDF group: 329 g
ABC group: 483 g
14 ABCDE 2007randomized, open; 237 patients HAART-
naive started either:
† ABC-3TC-EFV (n ¼ 115) or
† d4T-3TC-EFV (n ¼ 122)
9640 in ABC group
59 in d4T group
DEXA (n ¼ 57)
‘moderate to severe’ LA reported:
ABC group 4.8%, d4T group
mean change in limb fat:
ABC group: þ913 g (gain)
d4T group: 21579 g (loss)
randomized, open, switch; 333 patients on
3TC-based HAART switched to:
† TDF-FTC (166) or
† ABC-3TC (167)
4822 of 166 from
32 of 167 from
(47 of total 333):
TDF-FTC ¼ 24
ABC-3TC ¼ 23
mean limb fat gain from baseline:
TDF-FTC: 164 g
ABC-3TC: 132 g
randomized, open, switch; 234 patients on
† continue regimen (n ¼ 117) or
† switch to TDF-FTC-EFV (n ¼ 117)
48 NADEXA (n ¼ 74) intention
to treat analysis
median change in limb fat from
TDF-FTC-EFV: þ261 g
AZT-3TC-EFV: 2187 g
26 GS934 2007 randomized, open; 509 patients HAART-
naive started either:
† TDF-FTC-EFV (n ¼ 255) or
† AZT-3TC-EFV (n ¼ 254)
144144 week DEXA
data not available:
TDF-FTC ¼ 207
AZT-3TC ¼ 216
DEXA (n ¼ 86)median actual limb fat (for those
with 48 week data):
TDF group: 8.3 kg
AZT group: 4.9 kg
AZT, zidovudine; 3TC, lamivudine; FTC, emtricitabine; d4T, stavudine; ABC, abacavir; TDF, tenofovir disoproxil fumarate; EFV, efavirenz; open, open-label study; naive, all entrants ARV-naive at
baseline; switch, all entrants on ARVs at baseline; NA, not available.
to blame. Some studies report subjective improvements in LA
by patient report or physician assessment;10however, many
trials now use objective measures, e.g. dual energy X-ray
absorptiometry (DEXA). This allows accurate and consistent
quantitative assessments of subcutaneous fat. However, the
detection of fat changes to the nearest gram may be unaccompa-
nied by subjective improvements in LA,6,8which is the purpose
of intervention. Mean limb fat for a man is ?8 kg. Severe LA
can reduce this by half, so with annual fat restoration at
0.4–0.7 kg,8,11return to pre-morbid composition may take
several years using switch strategies alone. So even after the
withdrawal of ARVs associated with LA, recovery may take a
long time and therefore the length of trial follow-up is important.
Similarly, measurable improvement in LA depends on the sever-
ity of LA prior to intervention, which, in turn, depends on the
duration of time for which an offending drug is taken. In the
SWEET study (summarized in Table 1) median limb fat increased
at 48 weeks in subjects switching to tenofovir disoproxil fumarate/
emtricitabine (Truvada) by 0.5, 0.2, 0.1 and ,0.05 kg in subjects
with a total exposure to zidovudine/lamivudine (Combivir) of
,1.5, 1.5–3.0, 3.0–4.5 and 4.5–10 years, respectively, suggesting
that recovery is likely to be better in subjects with a short exposure
to zidovudine/lamivudine.21This is compounded by the greater
amount of limb fat at baseline in those with shorter zidovudine/
lamivudine exposure: median limb fat in the respective groups was
5.69, 6.38, 3.75 and 3.57kg, respectively.
HIV infection and AIDS-related diseases themselves bring
about ill-health and wasting. This may take time to halt and
reverse despite initiation of HAART. So in early treatment, fat
loss may continue despite the use of non-LA-associated drugs.
Conversely, as health and nutrition improves on treatment, there
can be a short-term gain in body fat compared with the pre-
morbid state of relative cachexia, despite taking drugs associated
with later onset LA.
Switching ARV therapy
From the time stavudine became implicated in the aetiology of
LA, small cohort studies emerged, in which patients replaced sta-
vudine with another ARV resulting in improvement in LA.22–25
Then followed several large randomized ‘switch studies’
(Table 1) substituting stavudine9and also zidovudine with other
ARVs allowing restoration of limb fat while maintaining virolo-
gical control, further supporting the role of tNRTIs in LA.8,11,12
The TARHEEL study demonstrated improvement in LA even in
patients replacing stavudine with zidovudine, another tNRTI
(n ¼ 32). This apparent contradiction may be explained by
recognizing that the 86 patients switched to the non-tNRTI aba-
cavir experienced significantly greater subjective and objective
improvements in LA than patients in the zidovudine group.9
This does not exonerate zidovudine as cause of LA but suggests
that stavudine is a more potent toxin. Furthermore, we do not
know whether these patients may have just improved to a new
set point of less severe LA compared with those continuing to
take stavudine. It is more likely that these data support the hier-
archy of potency of tNRTIs in causing LA over other NRTIs
that do not. While earlier studies used abacavir, results
from RAVE and long-term data from GS934 have shown teno-
fovir disoproxil fumarate to be just as adequate a substitute to
tNRTIs.11,26The time required for LA to improve is variable
and depends on the tNRTI and severity of LA at entry to the
study as well as the LA assessment method (described above).
Some investigators have reported subjective benefit as early as
24 weeks following ARV switching,22whereas others found
only objective improvements by week 48.11In MITOX, it took
104 weeks before significant subjective benefits were reported in
the switch group.8
Several groups have investigated the effects of complete NRTI
sparing. In M03-613, following 24 weeks of induction with
zidovudine-lamivudine-efavirenz, 74 patients switched to the PI
lopinavir (boosted with ritonavir). At 96 weeks, this group
had 2.3 kg greater limb fat compared with those continuing
on zidovudine-lamivudine-efavirenz.27ANRS 108 randomized
switched to a non-NRTI (NNRTI) þ PI and 50 continued on
their original regimen. At week 48, significant improvements in
limb fat were found, yet limited to those switching away from a
tNRTI at baseline; viral suppression was maintained in all
groups.28With a similar 1:1 switch, ACTG-A5116 randomized
236 treatment-experienced patients but found high rates of virolo-
gical failure and treatment discontinuations due to toxicity in the
NNRTI þ PI group.29Since patients with established LA are
likely to have prior exposure and a degree of resistance to the
NNRTI and PI drug classes, NRTI-sparing HAART may be risky
or non-viable options better suited to treatment-naive patients.
A step further could involve complete cessation of HAART.
Histological markers of LA have been shown to improve by 6
months following HAART cessation; however, no subjective
improvements in LA were seen.30A 25% gain in limb fat by
week 48 (n ¼ 16) was shown on a 1-week-on–1-week-off
HAART schedule (containing zidovudine or stavudine), but a
third of cases failed virologically.31Ultimately, studies such as
SMART, demonstrating excess morbidity and mortality in sub-
jects undergoing structured treatment interruptions, render such
strategies unacceptably hazardous.32
NRTI-based HAART. Fifty
Non-ARV pharmacological interventions
Modifying HAART regimens can risk virological escape or drug
toxicity. ARV options for drug-experienced patients or those in a
resource-poor setting may be limited, and some patients, satisfied
with virological efficacy, wish to remain on their ARV regimens.
Furthermore, subjective improvement in LA following ARV
switching can take years.8,11,21Therefore, other therapies have
been investigated to be administered alongside or instead of
ARV switching. There are controversial results over the benefits
of thiazolidinediones or statins, showing no or modest improve-
ments in LA confined to those stopping offending drugs.33–36
Some have shown significant improvement in LA using recombi-
nant human growth hormone (rhGH) after 12 weeks of therapy,
but limb fat returned to baseline levels shortly after rhGH dis-
continuation.36,37Uridine is thought to counteract pyrimidine
depletion caused by tNRTI inhibition of g-DNA polymerase.
One randomized controlled trial has shown an average 900 g
increase in limb fat after 12 weeks of uridine supplementation in
patients taking tNRTIs.38
Cosmetic approaches to LA involve injection of natural or syn-
thetic compounds into areas of fat loss.39Permanent fillers last
up to 5 years40but demand considerable technical skill and can
give an unnatural look as the facial contour changes with age.41
They are unsuitable for patients who anticipate fat regain follow-
ing ARV switching. The semi-permanent agent poly-L-lactic
acid42(Newfillw) lasts ?2 years and is the only FDA-licensed
agent for the treatment of facial LA. Confirmed safety and effi-
cacy43,44along with ease of use has made it the leading cosmetic
treatment for facial LA in the UK.
What about patients yet to experience LA, either being ARV-
naive or on HAART with as yet no apparent features of LA:
should we avoid or pre-emptively switch away from ARVs
implicated in LA? With the now minimal use of stavudine in the
developed world, the real question is: are we so certain LA is
inevitable with zidovudine that we should avoid it? Despite all
the evidence discussed in favour of this, prominent studies still
emerge, which appear not to support the central role of tNRTIs
in the pathogenesis of LA. However, the methodology of these
studies makes it difficult to draw valid conclusions. ACTG
5005s, a substudy of ACTG 384, reported no LA in the
zidovudine-lamivudine-efavirenz group at week 144.45This was
a censored on-treatment subanalysis of a study whose primary
aim was not to evaluate the development of LA. This type of
analysis disregards dropouts (in this case up to 40%) leaving
comparison of small subgroups. The population was biased to
those remaining on the initial regimen and so ignored many sub-
jects who had been exposed to zidovudine. The apparent lack of
significant LA in the remaining small groups could be partly (as
previously discussed) down to the relative fat gain as a result
of improvements in general health following initiation of
HAART. ACTG 5142 showed LA to be associated with NNRTI
(efavirenz) use compared with a PI (lopinavir) and in some even
on a non-tNRTI backbone.46However, regimen switching was
allowed in ACTG 5142 and analysis was intention-to-treat, i.e.
subjects were grouped for analysis according to the drug they
were assigned at week 0. Exposure to zidovudine will have
occurred even in some subjects stated as commencing with
non-tNRTI regimens explaining why LA was reported in these
groups. One final comment regards the differential rates of
reported LA in NNRTI versus PI groups even after controlling
for tNRTI usage. A reasonable conclusion is that while tNRTIs
are central in the aetiology of LA, the modulating effect of PIs
and NNRTIs has not been elucidated fully. Ultimately, a ran-
domized study relating LA to cumulative exposure of ARVs is
required. Study GS934 meets this purpose: the tenofovir diso-
proxil fumarate group had normal limb fat (8.3 kg) at week 144
compared with almost 50% lower levels (4.9 kg) in the zidovudine
group (Figure 1), strongly associating zidovudine with LA.26
Data are convincing that newer non-tNRTIs do not lead to LA
and that switching away from tNRTIs associated with LA leads
to a slow recovery of fat loss. In the developing world where
tNRTIs play a major role in the limited ARV repertoire, we can
at least aim to opt for less toxic tNRTIs while anticipating wider
access to new generic drugs. In the developed world, where
options to switch ARVs are available, it is better to pre-empt
than await the clinical manifestations of LA. Even for those with
resistant virus, the availability of new ARV agents means that
tNRTIs are now rarely essential to achieve virological suppres-
sion and can be avoided. The data from GS934 and switch
studies are compelling: we cannot justify continuing to put
patients at very high risk of developing potentially irreversible
LA by the continued use of tNRTIs.
We wish to thank Dr J. Arribas and the GS934 study group for
their kind permission to reproduce a figure from their work in
P. H. has received reimbursement for attending conferences, fees
for speaking, consultancy fees, funds for research other than
directly for this work, reimbursement to his unit for clinical
trials from Abbott, Boehringer-Ingelheim, BMS, Gilead, GSK,
Pfizer, Roche and Tibotec. D. R. P. has received reimbursement
for attending conferences from the same companies.
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aWilcoxon Rank Sum test for comparison between treatment arms.
bWilcoxon Signed Rank test for change from week 48 within treatment.
FTC/TDF + EFV (n)
AZT/3TC + EFV (n)
$P < 0.001b
*P = 0.035a
+P < 0.001a
Figure 1. Data from GS934 comparing tenofovir disoproxil fumarate (TDF)
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