eMedicine Specialties > Dermatology > Diseases of the Subcutaneous Tissue

Lipodystrophy, HIV

Author: David T Robles, MD, PhD, Dermatologist, Kaiser Permanente Southern California
Coauthor(s): Jonathan M Olson, BS, University of Washington School of Medicine; Roy M Colven, MD, Associate Professor of Medicine (Dermatology), University of Washington School of Medicine; Section Head of Dermatology, Harborview Medical Center; Attending Physician, Department of Dermatology, Harborview Medical Center, Madison and Medical Specialties Clinics
Contributor Information and Disclosures

Updated: Dec 8, 2008

Introduction

Background

HIV-associated lipodystrophy is a syndrome that occurs in individuals with HIV infection who are being treated with antiretroviral medications. Although the term HIV-associated lipodystrophy refers to abnormal central fat accumulation (lipohypertrophy) and localized loss of fat tissue (lipoatrophy), some patients have only lipohypertrophy, some have only lipoatrophy, and, less commonly, a subset of patients exhibits a mixed clinical presentation. Because no uniform morphologic changes occur with HIV lipodystrophy, lipohypertrophy and lipoatrophy are considered distinct entities with different risk factors and metabolic processes underlying their development. In this article, both lipohypertrophy and lipoatrophy are addressed, with a focus on the morphologic changes and underlying pathophysiology of HIV-associated lipodystrophy.

Lipohypertrophy in this syndrome is characterized by the presence of an enlarged dorsocervical fat pad, circumferential expansion of the neck, breast enlargement, and abdominal visceral fat accumulation. Lipoatrophy is exemplified by peripheral fat wasting with loss of subcutaneous tissue in the face, arms, legs, and buttocks. Involvement of the face is most common and carries a social stigma that may negatively affect the quality of life of patients with HIV disease and may pose a barrier to treatment and reduce medical adherence. Other features of HIV lipodystrophy syndrome include hyperlipidemia, insulin resistance, hyperinsulinemia, and hyperglycemia. Patients with HIV lipodystrophy syndrome are at increased risk for the development of atherosclerosis and diabetes mellitus.

The following eMedicine articles address other forms of lipodystrophy:

The following Medscape Resource Centers may be helpful as well:

Pathophysiology

Although the precise mechanisms underlying this syndrome are not well understood, several hypotheses based on in vitro and human studies may explain the pathogenesis of the changes. Most experts presently believe that HIV type 1 (HIV-1) protease inhibitors (PIs) and nucleoside reverse transcriptase inhibitors (NRTIs), especially stavudine and zidovudine, are implicated as follows:

  • Decreased production of retinoic acid and triglyceride uptake: PIs have a high affinity for the catalytic site of HIV-1 protease, which shares a 60% sequence homology with 2 proteins involved in lipid metabolism, cytoplasmic retinoic acid–binding protein type 1 (CRABP-1) and low-density lipoprotein receptor–related protein (LDLR-RP). Inhibition of CRABP-1 impairs the production of retinoic acid, leading to decreased fat storage and adipocyte apoptosis with the subsequent release of lipids into the circulation. Inhibition of LDLR-RP results in hyperlipidemia secondary to the failure of hepatic and endothelial removal of chylomicrons and triglycerides from the circulation. 
  • Inhibition of mitochondrial DNA (mtDNA) polymerase gamma: NRTIs inhibit mtDNA polymerase gamma, leading to mtDNA depletion, respiratory chain dysfunction, and reduced energy production, which, in turn, causes insulin resistance and secondary dyslipidemia.1,2 Interestingly, mtDNA is depleted only at normal oxygen levels—hypoxic adipocytes do not take up triglycerides and are resistant to mtDNA-induced damage, except after treatment with NRTIs.3
  • Inhibition of lipid metabolism: Some PIs, particularly ritonavir, inhibit cytochrome P450 3A, a key enzyme in lipid metabolism. 
  • Prevention of the development of adipocytes: Saquinavir, ritonavir, and nelfinavir (all PIs) directly inhibit the development of adipocytes from stem cells and increase the metabolic destruction of fat in existing adipocytes.
Evidence also suggests decreased insulin sensitivity and beta-cell dysfunction in patients with HIV-associated lipodystrophy. Additionally, researchers have found that estrogen receptor expression is down-regulated in the subcutaneous adipose tissue of these patients. This is due to the effects of highly active antiretroviral therapy (HAART) regimens including PIs. Stavudine has been particularly implicated in the apoptosis of adipocytes, affecting both dividing and differentiating cells.4

In addition, HIV-1 may cause dyslipidemia and lipodystrophy in the absence of HAART therapy, via impaired cholesterol efflux from macrophages and increased tumor necrosis factor-alpha, which modulates free fatty acid metabolism and lipid oxidation and attenuates insulin-mediated suppression of lipolysis.1
 
A 2006 study found that resting energy expenditure and lipid oxidation were significantly higher in HIV-positive patients (on HAART) with lipodystrophy, compared with HIV-positive controls without lipodystrophy, also on HAART.5

Frequency

United States

Wide variation exists in the literature regarding the prevalence of HIV lipodystrophy. Various studies show the prevalence rate of this syndrome is 2-60% in all patients who are HIV positive; a 2007 meta-analysis found a prevalence rate of 14-40% in HIV-positive patients on HAART.6 In untreated patients with HIV infection, a 4% prevalence rate is reported. The incidence of associated new-onset hypercholesterolemia, hypertriglyceridemia, and hyperglycemia is 24%, 19%, and 5%, respectively.

International

Rates of HIV-associated lipodystrophy vary according to country. A prospective cohort study in England demonstrated a 17% prevalence rate after an 18-month follow-up. Variations in the reported prevalence rates are related to a variety of many factors, including age, genetics, HIV medications, and case definition.

Mortality/Morbidity

To the authors’ knowledge, no studies have been conducted to determine the morbidity and mortality from the body morphologic changes of HIV-associated lipodystrophy per se. However, the syndrome associated with insulin resistance and hyperlipidemia is associated with excess morbidity and mortality. 

Race

The risk of lipoatrophy is increased in whites (5.4 odds ratio) compared with blacks.

Sex

Women are at a higher risk of lipodystrophy than men (1.9 relative risk). Women are more likely to report fat accumulation in the abdomen and breasts and hypertriglyceridemia, whereas men are more likely to describe fat depletion from the face and extremities along with hypertension and hypercholesterolemia.7

Age

Increasing age is a risk factor in the development of this syndrome.

Clinical

History

  • HIV-associated lipodystrophy is a progressive disease; its severity is directly proportional to age, duration of disease, and length of PI and/or NRTI treatment.
  • Lipodystrophy can be disfiguring cosmetically, and the physical findings may stigmatize the individual as one with HIV disease; patients are more likely to have decreased body image and quality of life.8
  • The incidence of diabetes mellitus or atherosclerotic cardiovascular disease is increased secondary to hyperglycemia (from insulin resistance) or hyperlipidemia, respectively.

Physical

Pertinent physical findings:

  • Abnormal fat accumulation (lipohypertrophy)  
    • The dorsocervical fat pad (commonly called "buffalo hump") becomes variably enlarged.
    • The circumference of the neck expands by 5-10 cm.
    • Breast hypertrophy occurs.
    • Central truncal adiposity results from abdominal visceral fat accumulation ("Crix belly" [referring to Crixivan, the trade name for indinavir, a PI] or "protease paunch").
    • Symmetric and asymmetric lipomatoses may occur. A rare pattern of lipoaccumulation involving bandlike lipomatosis tissue symmetrically from the breasts, laterally to the axillae, has been reported.9
    • Suprapubic fat pads (pubic lipomas) occur in nearly 10% of patients with lipodystrophy.10
    • The development of multiple angiolipomas is associated with PI therapy.11
  • Lipoatrophy
    • Temporal wasting and loss of subcutaneous fat from the cheeks (buccal fat pad) produces an emaciated appearance with prominent nasolabial creases.
    • Subcutaneous tissue is depleted from the arms, shoulders, thighs, and buttocks (peripheral wasting), with prominence of the superficial veins in these sites.

Causes

Part of the early difficulty in establishing the risk factors for HIV-associated lipodystrophy has been agreement on a case definition. Fat accumulation and lipoatrophy are clinically distinct and appear to have separate risk factors. Because most patients are taking a regimen of combined antiretroviral medications, identifying a specific class of antiretroviral associated with lipodystrophy has proven difficult. Despite this, the most common culprits of HIV-associated lipodystrophy appear to be those regimens containing PIs and thymidine analogue NRTIs. 

  • Lipodystrophy associated with PIs occurs 2-12 months after starting PI therapy. 
  • Previous reports have shown that ritonavir-saquinavir combinations have a stronger association with abnormal fat accumulation than indinavir or nelfinavir. One study revealed that switching from other PIs to nelfinavir led to an improvement in lipodystrophy symptoms.
  • The association between ritonavir and hypertriglyceridemia is stronger than that with other PIs. 
  • An increased risk of lipodystrophy is reported with the addition of NRTIs (eg, stavudine) to PI treatment compared with treatment with only PIs.
  • Of the NRTIs, the thymidine analogues stavudine (d4T) and zidovudine (ZDV, previously known as AZT) are mostly directly implicated in lipodystrophy, particularly lipoatrophy; switching to a different NRTI such as tenofovir or abacavir can produce demonstrable increases in limb fat and can improve lipid profiles.12,13
  • In children with HIV, both thymidine analogue NRTIs and PIs are implicated in the development of lipodystrophy.14
  • Lipodystrophy has been reported in individuals with HIV infection who have never been treated with PIs; possible mechanisms are noted in Pathophysiology.
  • Other reported risk factors associated with HIV-associated lipodystrophy are as follows:   
    • Lipohypertrophy  
      • Duration of antiretroviral therapy
      • Female gender
      • Higher body fat at onset of HAART
      • Higher triglyceride levels 
    • Lipoatrophy 
      • Therapy with thymidine analogue NRTIs (eg, stavudine, zidovudine)
      • Lower pretreatment body mass index at onset of HAART
      • Longer duration of HIV infection
      • White race
    • Both 
      • Duration of HAART therapy
      • Increased age
      • Low CD4 count

More on Lipodystrophy, HIV

Overview: Lipodystrophy, HIV
Differential Diagnoses & Workup: Lipodystrophy, HIV
Treatment & Medication: Lipodystrophy, HIV
Follow-up: Lipodystrophy, HIV
Multimedia: Lipodystrophy, HIV
References
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Further Reading

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Keywords

lipohypertrophy, lipoatrophy, lipodystrophy, human immunodeficiency virus, HIV, antiretroviral medication, protease inhibitor, highly active antiretroviral therapy, HAART

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Contributor Information and Disclosures

Author

David T Robles, MD, PhD, Dermatologist, Kaiser Permanente Southern California
David T Robles, MD, PhD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Jonathan M Olson, BS, University of Washington School of Medicine
Disclosure: Nothing to disclose.

Roy M Colven, MD, Associate Professor of Medicine (Dermatology), University of Washington School of Medicine; Section Head of Dermatology, Harborview Medical Center; Attending Physician, Department of Dermatology, Harborview Medical Center, Madison and Medical Specialties Clinics
Roy M Colven, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Telemedicine Association, Phi Beta Kappa, and Washington State Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist  Speaking and teaching

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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