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099-46
HIV-Associated Facial Lipoatrophy
Julia James, MD,* Alastair Carruthers, MD,* and Jean Carruthers, MD †
*Division of Dermatology and †Department of Ophthalmology, University of British Columbia, Vancouver,
British Columbia, Canada
background. HIV-infected individuals are living long, healthy
lives. They are now concerned with less life-threatening prob-
lems, especially lipodystrophy.
objective. To review the current state of our knowledge
about lipodystrophy in HIV-infected individuals.
methods. The literature was reviewed and analyzed for rele-
vant information. In addition, our clinical experience of manag-
ing such individuals was utilized.
results. Lipodystrophy and facial lipoatrophy and their rela-
J. JAMES, MD, A. CARRUTHERS, MD, AND J. CARRUTHERS, MD HAVE INDICATED NO SIGNIFICANT INTEREST
WITH COMMERCIAL SUPPORTERS.
HIV-ASSOCIATED LIPODYSTROPHY syndrome has
only recently been recognized, nevertheless there have
been numerous reports describing the changes in body
shape and associated metabolic disturbances. The con-
dition is characterized by fat loss and/or redistribution,
insulin resistance, and proatherogenic hyperlipidemia.
This is distinct from HIV wasting syndrome, which is
predominantly due to loss of muscle mass.
Some investigators believe that there is a link be-
tween HIV lipodystrophy and the introduction of HIV
protease inhibitors, both of which were reported in
the literature from 1997 onwards. The encouraging
clinical, virologic, and immunologic effects of protease
inhibitors mean that there has been some tolerance of
side effects, however, some studies show that lipodys-
trophy has a prevalence of up to 83% and causes no-
ticeable disfigurement.1–6 This syndrome is a major
cause for concern, as the alteration in appearance has
a huge impact on these individuals’ lives, especially
now that more successful HIV treatment has reduced
the anxiety associated with living with HIV.
Lipodystrophy Syndrome
The lipodystrophies are a rare group of inherited or
acquired disorders that are characterized by regional
Address correspondence and reprint requests to: Alastair Carruthers,
MD, Carruthers Dermatology Center, Suite 820, 943 West Broadway,
Vancouver, BC, Canada V524E1, or e-mail: alastair@carruthers.net.
© 2002 by the American Society for Dermatologic Surgery, Inc. • Published by Blackwell Publishing, Inc.
ISSN: 1076-0512/02/$15.00/0 • Dermatol Surg 2002;28:979–986
tionship to HIV-infection are discussed. Their differences are
noted. The spectrum of appearance in individuals with facial li-
poatrophy is described and a severity scale suggested which
should be of value in assessing the results of treatment.
conclusion. Lipodystrophy and lipoatrophy are intimately
related to infection with HIV. In consequence, facial lipoatro-
phy is a major stigma for HIV-infected individuals and can
have dramatic effects on their self-esteem and socialization. Ef-
fective treatment is essential.
or generalized loss of subcutaneous fat. Lipodystrophy
is uncommon in individuals who are not infected with
HIV.
HIV-associated lipodystrophy syndrome can in-
clude fat loss and/or fat accumulation in distinct re-
gions of the body. Characteristically there is increased
fat around the abdomen, dorsocervical fat pad en-
largement (buffalo hump), and sometimes breast hy-
pertrophy.3,5,7,8 Fat is lost from the limbs, buttocks,
and face, especially the nasolabial regions, the tem-
ples, and when severe, the eye sockets.7,9 The fat wast-
ing in the limbs leads to prominence of the subcutane-
ous veins, and that of the face and buttocks leads to
marked hollowing and wrinkling of the skin.
Other manifestations of HIV-associated lipodystro-
phy syndrome include insulin resistance, hyperglyce-
mia, hypertriglyceridemia, hypercholesterolemia, and
low levels of high-density lipoprotein (HDL).2,5,10 In-
dividuals with these metabolic disturbances have the
potential to develop premature type 2 diabetes melli-
tus and coronary artery disease.11
Association of Lipodystrophy With
Protease Inhibitors
The introduction of protease inhibitors as antiretrovi-
ral therapy represents a major development in HIV
treatment. When used in combination with other anti-
retroviral drugs, protease inhibitors improve the
CD4 cell count and reduce plasma viral load further
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980 james et al.: hiv-associated facial lipoatrophy
than reverse transcriptase inhibitors or antiviral nucle-
oside analogs alone, dramatically changing the clinical
course of HIV disease. Therefore the use of highly ac-
tive antiretroviral therapy (HAART) has become stan-
dard practice in the treatment of all stages of HIV in-
fection.
Recently, fat redistribution and metabolic effects
such as insulin resistance and hyperlipidemia have
been considered as possible side effects of protease in-
hibitor use.2,12,13 There are several better-known ad-
verse effects of protease inhibitors, for instance, renal
calculi and gastrointestinal intolerance with indinavir;
diarrhea, nausea and perioral paresthesia with ritonavir;
and diarrhea with nelfinavir.13
Prevalence of lipodystrophy in HIV-infected patients
taking protease inhibitors has been documented in
many studies. Carr and Cooper14 performed two stud-
ies and found that 64% of patients receiving protease
inhibitor therapy developed lipodystrophy, whereas
only 3% of protease inhibitor-naïve patients developed
it. One year later the same authors reported 83% and
4%, respectively.6 They estimated that the mean time to
lipodystrophy was 10 months after commencing pro-
tease inhibitor treatment. Ho et al.1 found that 24% of
patients who had taken indinavir for more than 3
months developed facial lipoatrophy. Those taking nu-
cleoside reverse transcriptase inhibitors (NRTIs) and
those who had been on indinavir for less than 3 months
did not develop facial lipoatrophy.1
Lipodystrophy has not been found to be more likely
in those with a family history of diabetes mellitus.2
There is also no significant association of lipodystro-
phy with age, sex, body mass index (BMI), ethnicity,
route of HIV transmission, CD4 cell count, viral load,
history of AIDS-defining illness, or concomitant anti-
retroviral treatment.1,2,15
Several studies have compared the prevalence of lipo-
dystrophy in protease inhibitor-treated patients with
that in NRTI-treated patients. Bonnet et al.15 found
that 47% of patients on protease inhibitors developed
lipodystrophy compared to none of the NRTI-treated
group, but the sample of patients taking only NRTIs
was very small. Mallal et al.16 studied a larger group
of patients and established that 54% of protease inhib-
itor-treated patients developed lipodystrophy, whereas
only 13% of NRTI-treated protease inhibitor-naïve
patients did. NRTIs predisposed to slowly progressive
fat loss that is accelerated when a protease inhibitor is
added. Therefore protease inhibitors are the primary
influence in lipodystrophy, but they may act synergis-
tically with NRTIs.16
Carr et al.17 observed lipodystrophy in patients tak-
ing protease inhibitors, NRTIs, and those taking both.
There was no significant difference in physical or body
composition parameters between patients with NRTI-
Dermatol Surg 28:11:November 2002
lipodystrophy syndrome and those with protease in-
hibitor-associated lipodystrophy syndrome. However,
NRTI-lipodystrophy syndrome had more recent onset
symptoms and weight loss, higher lactate and alanine
aminotransferase, and lower albumin, cholesterol, triglyc-
erides, glucose, and insulin compared to protease inhib-
itor-associated lipodystrophy syndrome. They concluded
that both protease inhibitors and NRTIs contribute
to lipodystrophy syndrome, particularly if associated
with lactic acidemia, but have some distinguishable
clinical and metabolic effects.17
These studies show that lipodystrophy is more com-
mon in HIV-infected patients taking NRTIs or protease
inhibitors than in untreated individuals. It would appear
that protease inhibitors have more of an effect than
NRTIs, but they may act synergistically. The prevalence
of abnormal fat redistribution has been shown to be up
to 83%, but there is no conclusive evidence to show
whether it is due to HAART or part of the HIV disease
process. Further research is needed to understand HIV-
associated lipodystrophy in the era of HAART, which
has been accompanied by increased survival of HIV-
infected individuals and reduced complications.
Pathogenesis of Lipodystrophy
The underlying mechanisms of HIV-related lipodys-
trophy are not known. One hypothesis proposes that
protease inhibitors bind to and inhibit proteins in-
volved in lipid metabolism. There is homology be-
tween the amino acid sequences of the catalytic site of
HIV protease, which protease inhibitors bind to, and
two proteins involved in lipid metabolism regulation:
low-density lipoprotein receptor-related protein (LRP)
and cytoplasmic retinoic acid binding protein type 1
(CRABP-1). Protease inhibitor binding of LRP exacer-
bates hyperlipidemia by reducing postprandial chylo-
micron clearance. When protease inhibitors bind to
CRABP-1, retinoic acid cannot bind and less cis-9-ret-
inoic acid is produced leading to reduced differentia-
tion and increased apoptosis of peripheral adipocytes
with impaired fat storage and lipid release. Cyto-
chrome P-450 3A is the enzyme required to convert
retinoic acid to cis-9-retinoic acid, and protease inhib-
itors potently inhibit it, therefore exacerbating the
dysfunction of peripheral adipocytes.18
It has been postulated that central and dorsocervi-
cal adipocytes may be more metabolically active than
the peripheral ones. The impaired peripheral fat stor-
age and hyperlipidemia associated with protease in-
hibitor treatment would then lead to preferential cen-
tral accumulation of fat.12
More recently, lipoatrophy has been attributed to
mitochondrial toxicity induced by NRTIs. Some patients
treated only with NRTIs develop peripheral lipoatro-
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Dermatol Surg 28:11:November 2002
phy, and dorsocervical/abdominal fat accumulation,
with lactic acidemia. NRTIs deplete mitochondrial DNA
(mtDNA) and induce toxicity by inhibiting mtDNA
polymerase . The resulting apoptosis or complement
(C3) deficiency can lead to abnormal fat distribution.19
A recent study by Côté et al.20 measured mtDNA from
blood cells using polymerase chain reaction (PCR). Sig-
nificantly decreased levels of mtDNA were found in
HIV-positive patients treated with NRTIs, particularly
Stavudine, who had lactic acidemia and lipodystrophy.20
There are several other possible mechanisms for the
development of lipodystrophy in HIV-infected patients.
Accumulation of fat may occur as a refeeding effect as-
sociated with increased appetite following suppression
of HIV replication with antiretroviral therapy, but this
does not explain the lipoatrophy. There may be a corre-
lation between urinary free cortisol and accumulation
of central fat through an inappropriate hormonal stress
response and increased sensitivity of the central adipo-
cytes. Lipodystrophy may develop if there is parallel in-
creased release of catecholamines, which elevate resting
metabolic rate and enhance lipolysis.21,22
The insulin resistance that is often associated with
lipodystrophy is probably due to the increased circu-
lating lipids, which interfere with glucose uptake and
impair islet-cell secretion, leading to impaired glucose
tolerance. Insulin resistance has been shown to accom-
pany the loss of peripheral fat in lipodystrophy, and is
linked with elevated levels of the soluble type 2 tumor
necrosis factor- receptor (sTNFR-2). High levels of
sTNFR-2 can be used as an indicator of immune acti-
vation and are associated with the course of HIV in-
fection and with insulin resistance in obesity. This
suggests that inflammation may contribute to the patho-
genesis of lipodystrophy and insulin resistance.10
Risk factors for developing lipodystrophy may in-
clude low body weight before treatment, elevated trig-
lyceride and C-peptide, and low HDL levels after 1
year of therapy, total duration of HAART, and the use
of certain antiretroviral agents or combinations of drugs.6
Despite these insights into the pathogenesis of HIV-
associated lipodystrophy, further research is needed to
clarify the situation. It can be seen from the hypothe-
ses discussed above that the causes of lipodystrophy
and metabolic abnormalities seen in HIV infection are
probably multifactorial.
Facial Lipoatrophy Severity Scale
Facial lipoatrophy presents to varying degrees and it is
helpful to be able to classify the severity in order to de-
cide on a treatment regime. Currently there is no pub-
lished facial lipoatrophy severity scale, however, we
propose a system for the classification of facial lipoat-
rophy based on the effects on the cheeks (see Figure 1).
james et al.: hiv-associated facial lipoatrophy 981
Grade 1 is mild and localized facial lipoatrophy, and
the appearance is almost normal. Grade 2 has deeper
and longer central cheek atrophy, with the facial mus-
cles (especially zygomaticus major) beginning to show
through. In grade 3 facial lipoatrophy, the atrophic
area is even deeper and wider with the muscles clearly
showing. In grade 4, atrophy covers a wide area and ex-
tends up toward the orbit. The facial skin lies directly
on the muscles over a wide area. Grades 3 and 4 are
clearly abnormal and the quality of life for these pa-
tients is typically lower than that of normal individuals.
Psychologic Effects of Facial Lipoatrophy
There is very little in the literature on this subject, de-
spite the enormous psychosocial impact that facial li-
poatrophy has on HIV-infected patients. However,
Collins et al.23 carried out a survey of HIV-infected
patients with lipodystrophy syndrome to find out
what they perceived were the psychologic and social
effects of lipodystrophy. The questions concentrated
on body changes related to fat redistribution and not
the metabolic effects. It was found that individuals
with lipodystrophy had poor body image and low self-
esteem, became socially withdrawn, found their sexual
relationships were adversely affected, were often forced
into disclosing their HIV status due to facial lipoatro-
phy, commonly were depressed, often thought the doc-
tor found their lipodystrophy to be less important than
they did, were noncompliant with HAART due to lipo-
dystrophy, and the costs of supplements and surgery
had an economic impact on them. Many patients found
that coping with lipodystrophy was harder than just
living and surviving with HIV.23
The psychologic and social impact of lipodystrophy
syndrome on HIV-infected individuals is quite consid-
erable and it adversely affects their quality of life. The
changes to the body lower self-esteem and body im-
age, leading to social and sexual problems, and quite
often anxiety and depression follow. These patients
have previously coped with HIV infection, and in the
era of HAART, new hope is placed on the success of
these therapies, but the adverse effects are discourag-
ing. Patients must weigh the benefits and risks of anti-
retroviral therapy if they see no definitive treatment
for facial lipoatrophy and other features of fat redistri-
bution.
Lipodystrophy Treatment Options
There are no established methods of treatment for li-
podystrophy syndrome, but several experimental treat-
ments have been undertaken for various components
of it. Exercise can decrease central fat accumulation,
but this can worsen peripheral lipoatrophy. Another
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982 james et al.: hiv-associated facial lipoatrophy Dermatol Surg 28:11:November 2002

Figure 1. Facial lipoatrophy severity scale. Grade 1: mild and localized facial lipoatrophy. Grade 2: deeper and longer atrophy, with the fa-
cial muscles beginning to show through. Grade 3: atrophic area is even deeper and wider, with the muscles clearly showing. Grade 4: li-
poatrophy covers a wide area, extending up toward the eye sockets, and the facial skin lies directly on the muscles.
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Dermatol Surg 28:11:November 2002
Figure 1. Continued.
approach to reduce abdominal and dorsocervical fat
accumulation is liposuction. The dorsocervical fat ac-
cumulations are more fibrous compared to patients
having liposuction for reasons other than HIV-associ-
ated lipodystrophy, but the results are generally good.
The fat does not often reappear and patients are on
the whole highly satisfied.24,25
It may be possible to improve lipodystrophy by
switching patients from protease inhibitors, if they are
the suspected cause, to nonnucleoside reverse tran-
scriptase inhibitors (NNRTIs). Partial improvement has
been observed in body shape and metabolic abnormal-
ities in such patients approximately 6 months after
stopping protease inhibitors, with no significant change
in CD4 count or viral load.26 Alterations in body
shape may also improve with recombinant human
growth hormone (rHGH). When administered subcu-
taneously, lean tissue is augmented and destruction of
fat is promoted, however, circulating lipid levels are
not reduced. Lipoatrophy may be worsened and hy-
perglycemia can be precipitated, especially if rHGH is
given parenterally.27
One treatment strategy that would seem wise to try
for patients with lipodystrophy and high blood lipid
levels is lipid-lowering agents. Statins and/or fibrates
are effective at lowering cholesterol and triglycerides
in some, but not all patients with HIV-associated lipo-
dystrophy.28 Fibrates occasionally induce gallstones,
rash, erectile dysfunction, and gastrointestinal symp-
toms. Adverse effects of statins include hepatotoxicity,
gastrointestinal upset, and myopathy. The majority of
the statins interact with cytochrome P-450 3A, which
is inhibited by protease inhibitors, occasionally lead-
ing to hepatitis and myositis with combined use.29
Dose reductions of statins are required when adminis-
james et al.: hiv-associated facial lipoatrophy 983
tered with protease inhibitors, but there are insuffi-
cient data to calculate how far the dose should be re-
duced, and no data for other antiretroviral agents.
Insulin resistance due to HIV-associated lipodystro-
phy can be improved with antidiabetic agents in order
to reduce the risk of cardiovascular events. These
drugs enhance the sensitivity of peripheral tissues to
insulin, resulting in increased muscle and liver re-
sponses. Hadigan et al.30 found that compared to pla-
cebo, metformin therapy resulted in significant de-
creases in insulin levels, BMI, and diastolic blood
pressure in HIV-infected patients with glucose intoler-
ance and lipodystrophy. There were no serious ad-
verse effects, such as raised lactate levels or liver dys-
function, which can occur with troglitazone.
Some individuals with lipodystrophy use anabolic
steroids; although they only increase muscle mass, the
fat redistribution is masked by the enlarged muscle
bulk. It would appear that serum lipids and insulin
levels are not worsened through use of anabolic ste-
roids,31 but facial lipoatrophy continues to deteriorate.32
A novel proposal for treatment of lipodystrophy is
leptin replacement therapy. This appears to return
lipid levels and insulin resistance to normal, and to
promote weight loss. However, although fat is lost from
the abdomen, leptin cannot normalize the lipoatrophy
in other parts of the body, such as the face.33
Facial lipoatrophy is a prominent element of HIV–
associated lipodystrophy syndrome that is not greatly
improved with any of the treatment strategies described
above. One of the first treatments for lipoatrophy of
the nasolabial regions was injection of liquid silicone.
Since the 1960s, facial lipoatrophy has been treated
with small, regular injections of silicone into the deep
dermis and fat over several months.34–36 Only 1–2 ml
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984 james et al.: hiv-associated facial lipoatrophy Dermatol Surg 28:11:November 2002

are injected at a time to produce a gradual and even fi-
broplastic reaction, as larger injections appear to result
in migration of the silicone and visible inclusion cysts.
This use of silicone oil is not approved in the United
States or Canada. At the time of writing, there are no
publications on the use of injectable silicone in the
treatment of HIV-associated facial lipoatrophy.
Collagen implant therapy became the favored alter-
native to silicone injections when the FDA licensed
Zyderm (bovine collagen) for implant therapy in
1981.37 Skin testing for an allergic response is neces-
sary before starting treatment, and then several ses-
sions of injections are required at 2- to 4-week inter-
vals.38 Approximately 1 ml is injected into the dermis
at a time, as greater amounts can result in multiple
small papules or beading at the site.39 The soft tissue
augmentation produced by collagen does not last as
long as that produced by silicone injections, as the col-
lagen is rapidly degraded and longevity is measured in
weeks compared to months for silicone. Along with
the expense of the product, another disadvantage of col-
lagen implants is the reported adverse reactions. Local-
ized hypersensitivity reactions occur in some patients,
even following a negative skin test, and long-term gran-
ulomatous reactions with or without arthralgia may
also occur several months after implantation.40–42
Another substance that has been used for soft tissue
augmentation is injectable lyophilized particulate hu-
man fascia lata (Fascian). It is harvested from human
cadavers, then processed and sterilized ready for re-
constitution and injection.43 Fascian is human-derived
and so pretesting for an allergic response is not neces-
sary. One study quotes 0.02% rate of allergic reac-
tions following Fascian injection, so it can be seen that
the allergenicity is very low.44 The grafts are reported
to last longer than the effects of collagen injections
and there are few reported adverse effects. Cymetra is
micronized Alloderm, which is preserved human der-
mis. It has been available in the United States since
1995, but there are no published reports of its use for
treatment of facial lipoatrophy. Both Fascian and Cy-
metra share some of the problems seen with bovine
collagen, in other words, the lack of permanence of re-
sponse and the expense of the treatment.
Autologous fat has been used as a volume replace-
ment agent for many years. It has been used success-
fully in those whose lipoatrophy is not caused by HIV,
and also in the HIV-related condition with fat being
removed from the abnormal deposits and injected into
the face. However, in our experience, the excess fat
deposits on the abdomen and dorsal neck do not usu-
ally accompany the facial lipoatrophy and, indeed, the
facial lipoatrophy-affected individuals usually do not
have sufficient fat for realistic donor harvesting. In
other words, the fat available for transplantation is
minimal. Finally, since these individuals have a condi-
tion that produces a degree of fat loss throughout the
body, it does not appear logical to use an augmenting
agent that is likely to disappear in the future, with our
current HIV management.
Treatment of HIV-associated facial lipoatrophy should
use permanent augmenting agents since it is not antici-
pated that this process is reversible. The two perma-
nent injectable agents that are available in North
America are silicone oil, which has been mentioned
above, and Artecoll. Artecoll is a mixture of poly-
methylmethacrylate (PMMA) beads mixed in bovine
collagen which is used as a delivery vehicle. While the
bovine collagen disappears, there is some fibroplasia
around the beads and therefore the permanent volume
is approximately 50–60% of the injected volume. This
contrasts with injectable silicone, which increases in
size and produces a final volume of perhaps 200% of
the injected volume. Artecoll has been used extensively
in Europe and in Canada but its reported use in HIV-
associated lipoatrophy is currently limited.
Polytetrafluoroethylene (PTFE) has been used as a
permanent filling substance for facial lines and wrin-
kles, especially deeper skin creases and folds. It is an
extremely inert biomaterial, being nonallergenic, non-
carcinogenic, and having no foreign-body response.45
The structure is highly porous to allow the penetration
of cells and vessels once implanted, with minimal in-
flammatory reaction.46 There are two commonly used
forms of PTFE for insertable augmentation, GoreTex
and SoftForm. SoftForm is a hollow tube with a spe-
cial implantation device, whereas GoreTex can be
formed into tubes, strips, and patches. Typically the

Table 1. Universal Precautions of the Centers for Disease Control52

1. Use barrier precautions to prevent skin and mucous membrane exposure, including gloves, masks, and protective eyewear during procedures likely to
generate blood droplets, and gowns or aprons during procedures likely to generate splashes.
2. Hands and skin surfaces should be washed immediately and thoroughly if contaminated by blood or body fluids.
3. All health care workers should take precautions to prevent injuries caused by needles, scalpels, and other sharp instruments. Needles should not
be recapped, bent, or broken or removed from disposable syringes. After use, they should be placed in puncture-resistant containers.
4. Mouthpieces, resuscitation bags, or ventilation devices should be available in areas where resuscitation is predictable.
5. Health care workers with exudative lesions or weeping dermatitis should refrain from direct patient contact.
6. Because of the risk of prenatal transmission, pregnant health care workers should be especially familiar with universal precautions.
Licensed to Andressa Thomazzoni - andressathomazzoni123@gmail.com - 046.377.099-46
Dermatol Surg 28:11:November 2002
implants are inserted into the desired position through
small incisions under local anesthetic.47,48 Adverse ef-
fects include foreign body reactions, incorrect posi-
tioning, implant visibility, and infection.49,50 So far
there are no publications on the use of PTFE materials
in HIV-associated facial lipoatrophy.
Although HIV-associated lipodystrophy remains diffi-
cult to treat while maintaining the efficacy of antiret-
roviral therapy, there are several promising treatments
for various components of the syndrome. The success-
ful resolution of facial lipoatrophy seems to be hardest
to achieve, but there are several methods of treatment
available, and the use of a permanent agent would be
most desirable. The injection of silicone oil alone or in
combination with PTFE implants would seem to have
the most potential for alleviating this distressing prob-
lem. We are preparing a manuscript documenting our
experience combining PTFE with injectable silicone oil
in the management of HIV-related facial lipoatrophy.
Operating Precautions for Health
Care Professionals
HAART improves longevity in HIV-infected individu-
als, resulting in more of these patients requiring sur-
gery for HIV- and non-HIV-related conditions. A
study performed several years ago found that 15% of
patients who died of AIDS had undergone surgery at
least once during the time that they were infected with
HIV.51 There is some risk to health care workers dur-
ing surgical procedures, but HIV is not the greatest
risk. The risk of viral infection from needlestick inju-
ries is 0.3% for HIV, 3.0% for hepatitis C, and 30.0%
for hepatitis B.52 The risk of becoming infected with
HIV may be even lower when the patient is know to
be HIV positive, as health care professionals use more
care when handling the patient and have immediate
access to prophylaxis should exposure occur. In addi-
tion, many of these individuals are on treatment and
therefore have low or undetectable viral levels.
Exposure to HIV can be avoided through strict in-
fection control procedures, including universal pre-
cautions. Operating theater policy should contain pre-
cautions appropriate to the care of high-risk patients,
but be applicable to the care of all patients. The level
of precautions necessary depends on local factors,
such as HIV prevalence in a given area and the type of
surgery performed. Universal precautions recommend
that blood and body fluid safety measures be used for
all patients (see Table 1).53 These infection control
measures apply in the dermatology operating theater
as for any other, but further precautions include glov-
ing for minor procedures and use of face shields or
goggles to protect against bloody procedures.54
james et al.: hiv-associated facial lipoatrophy 985
Exposure can occur despite the presence of univer-
sal precautions, so it is important to have effective
prophylaxis available for health care workers. Chemo-
prophylaxis with zidovudine reduces the risk of infec-
tion by 80%, as long as the recipient does not have a
strain of HIV that is resistant to zidovudine. As this is
becoming increasingly more common, a combination
of zidovudine and lamivudine taken for 4 weeks is rec-
ommended. In those exposed to a source with likely
resistant HIV, a protease inhibitor such as indinavir
can be added.55
Conclusion
Lipodystrophy syndrome, characterized by fat redis-
tribution, hyperlipidemia, and insulin resistance is fre-
quently seen in HIV-infected individuals. Often it seems
to relate to protease inhibitor therapy, but additional
research is needed to determine the pathogenesis. Pa-
tients with lipodystrophy must weigh the impact the
syndrome has on their lives against the benefits of
HAART, which clearly decreases complications of HIV
and improves survival.
Management of HIV-associated lipodystrophy must
be specific for each patient. The central fat accumula-
tion can be reduced through exercise, liposuction, and
administration of rHGH, and the metabolic abnor-
malities moderated through switching from protease
inhibitors to NNRTIs and use of lipid-lowering or an-
tidiabetic agents. Facial lipoatrophy is difficult to treat
successfully, although we report elsewhere the success-
ful management of these individuals with a combina-
tion of GoreTex implants and silicone oil injections.
Further studies are required to determine the best ap-
proaches to treatment of HIV-associated facial lipoat-
rophy and to find the best antiretroviral strategies for
managing these complications.
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