Medscape is available in 5 Language Editions – Choose your Edition here.


Lipodystrophy in HIV

  • Author: David T Robles, MD, PhD; Chief Editor: Dirk M Elston, MD  more...
Updated: Dec 08, 2014


HIV-associated lipodystrophy is a syndrome that occurs in HIV-infected patients 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. This article addresses both lipohypertrophy and lipoatrophy, with a focus on the morphologic changes and underlying pathophysiology of HIV-associated lipodystrophy. Note the image below.

Facial HIV-associated lipodystrophy in a patient r Facial HIV-associated lipodystrophy in a patient receiving highly active antiretroviral therapy.

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.

Lipodystrophy can be disfiguring cosmetically. Involvement of the face is most common and carries a social stigma that may reduce the quality of life of patients with HIV disease and may pose a barrier to treatment and reduce medical adherence.[1, 2]

The incidence of diabetes mellitus or atherosclerotic cardiovascular disease is increased secondary to hyperglycemia (from insulin resistance) or hyperlipidemia, respectively.

Other features of HIV lipodystrophy syndrome include hyperlipidemia, insulin resistance, hyperinsulinemia, and hyperglycemia. Consequently, patients with HIV lipodystrophy syndrome are at increased risk for the development of atherosclerosis and diabetes mellitus.

The following Medscape articles address other forms of lipodystrophy:

The following Medscape Resource Centers may be helpful as well:

For other discussions on management of HIV infection, see HIV Disease, Pediatric HIV Infection, and Antiretroviral Therapy for HIV Infection.

For patient education information, see the Sexually Transmitted Diseases Center, Cholesterol Center, and Statins Center, as well as HIV/AIDS, High Cholesterol, Cholesterol FAQs, and Atorvastatin (Lipitor).



Although the precise mechanisms underlying HIV lipodystrophy are not well understood, several hypotheses based on in vitro and human studies may explain the pathogenesis of the lipid changes that take place. Most experts currently believe that HIV type 1 (HIV-1) protease inhibitors (PIs) and nucleoside reverse transcriptase inhibitors (NRTIs), especially stavudine and zidovudine, are implicated.[3, 4, 5, 6, 7] Genetic factors in the patient may confer particular susceptibility.[8, 9] In addition, immunohistochemical components may play a role in the process of lipodystrophy in HIV patients.[10]

One mechanism in which PIs function is by down-regulating PPAR-gamma and C/EBP-alpha, which are key adipogenic transcription factors. Once these factors are down-regulated, there is an interruption with lipogenesis and adipocyte maturation. In addition, they create a large production of reactive oxygen species, which leads to the production of cytokines, macrophage recruitment, and inhibition of glucose transport 4 (GLUT-4), along with a deficiency in insulin signaling and the hormones leptin and adiponectin.[11] PIs have also been shown to activate endoplasmic reticulum stress pathways by depleting the calcium in adipocytes. In addition, they also interfere with the expression of regulator genes, CHOP, ATF4, and XBP, which further alters lipid metabolism and autophagy.[11]

PIs also 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.

NRTIs inhibit mitochondrial DNA (mtDNA) polymerase gamma, leading to mtDNA depletion, respiratory chain dysfunction, and reduced energy production, which, in turn, causes insulin resistance and secondary dyslipidemia.[12, 13] 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.[14]

Some PIs, particularly ritonavir, inhibit cytochrome P450 3A, a key enzyme in lipid metabolism. Ritonavir has also been shown to cause an extreme amount of apoptosis. On the other hand, atazanavir has been shown to cause apoptosis and autophagy. The PIs saquinavir, ritonavir, and nelfinavir directly inhibit the development of adipocytes from stem cells and increase the metabolic destruction of fat in existing adipocytes.

Taking genetics into account, a missense mutation in the resistin gene has been shown to have an association with hyperlipidemia, insulin resistance, and limb fat loss when combined with highly active antiretroviral therapy (HAART).[11] Other studies have shown that resistin can function as a useful biomarker for peripheral adipose tissue loss and may be the future of therapeutic strategies.[15]

In observation of immunohistochemical components, a 2014 cross-analytical study analyzed the cytokine expression from adipose tissue obtained in biopsies in 19 HIV patients experiencing lipodystrophy. As a result, tissue necrosis factor (TNF)–alpha and caspase-3 were more prominent in men than in women. In addition, the patients with lipodystrophy had less TNF-beta when being compared with the control group. Lastly, the group of individuals that experienced longer exposure to HIV and HAART had a positive association with levels of TNF-alpha.[10] As shown, sex differences lead toward different pathophysiologic outcomes, but more so, the elevation in cytokine production elevates the likelihood of developing lipodystrophy in HIV patients.

In another 2014 study focused on HIV patients with lipodystrophy, 21% of women and 37% of men were found to have growth hormone deficiencies (GHDs). Men who had GHD had higher amounts of visceral adipose tissue, subcutaneous adipose tissue, and trunk fat. Women who had GHD had significantly lower insulinlike growth factor-1 (IGF-1). Overall, adipose tissue distribution accounts for growth hormone sex differences; those with deficiencies have more problems with lipodystrophy.[16]

Evidence also suggests decreased insulin sensitivity and beta-cell dysfunction in patients with HIV-associated lipodystrophy.[17] 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 HAART regimens that include PIs. Stavudine has been particularly implicated in the apoptosis of adipocytes, affecting both dividing and differentiating cells.[18, 19]

In addition, HIV-1 may cause dyslipidemia and lipodystrophy in the absence of HAART, 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.[12, 20]

A 2006 study in HIV-positive patients on HAART found that resting energy expenditure and lipid oxidation were significantly higher in those with lipodystrophy than in those without lipodystrophy.[21]



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 proved 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.[22, 23]

In children with HIV, both thymidine analogue NRTIs and PIs are implicated in the development of lipodystrophy.[24] 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 lipohypertrophy are as follows:

  • Duration of antiretroviral therapy
  • Female sex
  • Higher body fat at onset of HAART
  • Higher triglyceride levels

Other reported risk factors associated with HIV-associated lipoatrophy are as follows:

  • Therapy with thymidine analogue NRTIs (eg, stavudine, zidovudine)
  • Lower pretreatment body mass index at onset of HAART
  • Longer duration of HIV infection
  • White race

Other reported risk factors associated with both lipohypertrophy and lipoatrophy are as follows[25] :

  • Duration of HAART therapy
  • Older age
  • Low CD4 count


United States statistics

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[26, 27] ; a 2007 meta-analysis found a prevalence rate of 14-40% in HIV-positive patients on highly active antiretroviral therapy (HAART).[28] 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 statistics

Rates of HIV-associated lipodystrophy vary according to country.[29, 30, 6] 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.

In 2014, among all people living with HIV worldwide, the prevalence of lipodystrophy ranges from 10-80%.[31]

Racial, sexual, and age-related differences in incidence

The risk of lipoatrophy is higher in whites (5.4 odds ratio) than in blacks. 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.[32] Increasing age is a risk factor in the development of this syndrome.



HIV-associated lipodystrophy progressively worsens as PI therapy is continued, and the discontinuation of PI therapy may result in regression.[33]

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 insulin resistance and hyperlipidemia is associated with excess morbidity and mortality. The incidences of diabetes mellitus and atherosclerotic cardiovascular disease are increased secondary to hyperglycemia (from insulin resistance) and hyperlipidemia, respectively.

Osteopenia of the lumbar spine may be present in patients with increased visceral fat accumulation.

Dorsocervical fat pad accumulation may result in neck pain and sleep apnea.


Clinical Presentation

HIV-associated lipodystrophy is a progressive disease; its severity is directly proportional to age, duration of disease, and length of protease inhibitor (PI) and/or nucleoside reverse transcriptase inhibitor (NRTI) treatment. On physical examination, abnormal fat accumulation (lipohypertrophy) findings are as follows:

  • The dorsocervical fat pad (commonly called "buffalo hump") becomes variably enlarged [34, 35, 36]
  • 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 [37]
  • Suprapubic fat pads (pubic lipomas) occur in nearly 10% of patients with lipodystrophy [38]
  • The development of multiple angiolipomas is associated with PI therapy [39]

Lipoatrophy findings are as follows:

  • Temporal wasting and loss of subcutaneous fat from the cheeks (buccal fat pad) produces an emaciated appearance with prominent nasolabial creases (see image below)
    Facial HIV-associated lipodystrophy in a patient r Facial HIV-associated lipodystrophy in a patient receiving highly active antiretroviral therapy.
  • Subcutaneous tissue is depleted from the arms, shoulders, thighs, and buttocks (peripheral wasting), with prominence of the superficial veins in these sites


Diagnostic considerations

Other problems to be considered in patients with lipodystrophy are as follows:

  • Seip-Berardinelli syndrome
  • Lawrence syndrome
  • Dunnigan syndrome
  • Kobberling syndrome
  • Barraquer-Simons syndrome
  • Abdominal carcinoma
  • Malnutrition

Other problems to be considered in patients with lipohypertrophy are as follows:

  • Cushing disease
  • Glucocorticoid therapy
  • Scleredema of diabetes mellitus
  • Launois-Bensaude syndrome

Other problems to be considered in patients with lipoatrophy are as follows:

  • HIV wasting syndrome [40]
  • Localized lipodystrophy
  • Malnutrition
  • Anorexia nervosa
  • Hyperthyroidism
  • Cancer cachexia
  • Severe chronic infection
  • Adrenal insufficiency


Generalized Lipodystrophy

Acquired Partial Lipodystrophy

Progressive Lipodystrophy

Localized Lipodystrophy



HIV-associated lipodystrophy is a clinical diagnosis. Although there is not a specific clinical protocol to make the diagnosis, advancements have been made that can aid in the assessment of lipodystrophy. A 2014 cross-sectional European study showed that anthropometric ratios (fat-mass ratio, waist-to-thigh ratio, waist-to-calf ratio, and arm-to-trunk ratio) are useful in making the diagnosis of lipodystrophy. Incorporating this method can lead to an accurate and earlier diagnosis.[41]

The only relevant laboratory studies are serum lipid assays. A skin or subcutaneous fat biopsy is not routinely performed to make a diagnosis of HIV lipodystrophy. Imaging studies are not generally necessary in the workup of HIV lipodystrophy. Dual energy x-ray absorptiometry scanning, CT scanning, and MRI are limited to research studies to objectively quantify fat abnormalities.[42]

MRI demonstrates the accumulation of visceral fat in the abdomen compared with subcutaneous fat. CT scanning demonstrates abnormal fat proliferation throughout the abdomen in a perivisceral distribution and little subcutaneous fat. Intra-abdominal organs are normal, and no ascites is seen. Dual-energy x-ray absorptiometry may demonstrate lumbar spine bone density reduction in association with increased visceral fat accumulation.[43]

Lipid panel

Because abnormal glucose and/or lipid metabolism may accompany HIV lipodystrophy, checking the lipid panel and assessing for glucose intolerance is important prior to initiating antiretroviral therapy. Some experts suggest checking these values again at 6 months and then, if the results are normal, yearly.

Hyperlipidemia findings are as follows:

  • Fasting cholesterol level – Greater than 200 mg/dL
  • Fasting triglyceride level - Greater than 150 mg/dL
  • Increased apolipoprotein c-III and apolipoprotein E levels

Hyperglycemia and/or hyperinsulinemia findings are as follows:

  • Diabetes - Fasting plasma glucose level of greater than 126 mg/dL or a 2-hour oral glucose tolerance test result of greater than 200 mg/dL
  • Impaired fasting glucose - Fasting plasma glucose level of 100-125 mg/dL
  • Impaired glucose tolerance - Two-hour oral glucose tolerance test result of 140-199 mg/dL

Treatment & Management

Lipodystrophy is often progressive and, in limited cases, may regress after the withdrawal of PI therapy. Withdrawal of thymidine analogues (eg, switching from protease inhibitors to efavirenz) has shown to be effective for reversing lipoatrophy.[24, 44]

Treatment of the underlying metabolic derangements of glucose and lipid metabolism is necessary. The evaluation and management of glucose intolerance, diabetes, and hyperlipidemia are discussed elsewhere (see Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Polygenic Hypercholesterolemia, and Hypertriglyceridemia).

Tesamorelin, a growth hormone–releasing factor analog, was approved by the US Food and Drug Administration (FDA) for treatment of HIV-associated lipodystrophy in November 2010. Approval was based on 2 studies that showed that visceral adipose tissue was significantly decreased from baseline at 26 weeks and sustained at 52 weeks.[45, 46, 47] These were multicenter, randomized, double-blind, placebo-controlled, phase 3 studies in 816 HIV-infected patients with excess abdominal fat associated with lipodystrophy.

For the treatment of hyperlipidemia, fibrates and/or statins, as well as dehydroepiandrosterone (DHEA) alone, improve the lipid profile.[48]

For treatment of hyperglycemia, metformin,[49] insulinlike growth factor–1,[50, 51] and DHEA improve glycemic control.

Studies of thiazolidinedione treatment for HIV lipodystrophy have yielded conflicting results. One randomized controlled trial demonstrated positive effects of rosiglitazone on lipoatrophy, insulin sensitivity, and metabolic indices[52] ; another randomized, controlled trial of rosiglitazone did not show a benefit for lipoatrophy or metabolic parameters.[53]

A meta-analysis of six placebo-controlled trials found that pioglitazone therapy was more effective than placebo for increasing limb fat mass in HIV lipoatrophy, but rosiglitazone was not significantly more effective.[54] A meta-analysis of 16 trials concluded that rosiglitazone should not be used in HIV-associated lipodystrophy; that pioglitazone may be safer, but any benefits appear small; and that metformin was the only insulin-sensitizer to demonstrate beneficial effects on insulin resistance, lipids, and body fat redistribution.[55]

An improvement in lipohypertrophy and/or lipoatrophy in individuals treated with human growth hormone,[56, 57] anabolic steroids, naltrexone, and a combination of DHEA and a cyclo-oxygenase inhibitor (eg, (indomethacin 100 mg/day, naprosyn 1000 mg/day) has been reported in some cases.

Lastly, a case report has shown that the use of oral contraceptive pills worsens hypertriglyceridemia; therefore, this is not the recommended method of birth control while dealing with lipodystrophy.[58]

Surgical procedures for lipodystrophy

A variety of plastic surgery procedures have been studied for the treatment of HIV-associated lipodystrophy.[59] For lipohypertrophy, the effects of treatment with liposuction or lipectomy are variable, and recurrence is common. Fat harvested during liposuction of the dorsocervical fat pad can be used for autologous fat transfer to facial areas exhibiting lipoatrophy.[60] Facial fat grafting is further addressed in Facial Fat Grafting.

For lipoatrophy, free flaps, lipotransfer, or commercial fillers or implants can be used to replace adipose tissue. Poly-L-lactic acid (Sculptra) has been used as a semipermanent injectable filler in these patients.[61] Sculptra is approved by the FDA for the treatment of facial lipoatrophy in HIV-positive patients. In addition, the use of polymethylmethacrylate (PMMA) has been proven to benefit those patients experiencing lipoatrophy. Individuals who experience the benefits of PMMA have improved quality of life and body image, which has been shown to aid in reducing depression and increasing the compliance of antiretroviral therapy.[62, 63]

Calcium hydroxylapatite (Radiesse) is a soft-tissue filler consisting of 30% calcium hydroxylapatite microspheres and 30% carboxylmethylcellulose. It is also FDA-approved for the treatment of facial lipoatrophy in HIV-positive patients.

Other filler options include injectable bovine and human collagens, hyaluronic acid,[64, 65] and autologous free fat transfer. See Soft Tissue Implants for more information.

Rare cases of persistent granulomatous inflammatory reactions to some fillers have been reported[66] ; thus, patients undergoing such treatment should understand possible risks.

Diet and activity

No specific dietary regimen is used in the management of HIV-associated lipodystrophy. Adequate nutrition and exercise may result in modest improvement in lipodystrophy and improve central obesity. A balanced low-fat, low-carbohydrate diet is preferable when hypertriglyceridemia is present.[67]

Exercise has been proven to improve insulin sensitivity. One study showed that progressive resistance training with an aerobic component may reduce trunk fat mass.[68] Physical activity has also been shown to yield metabolic improvements and a decreased risk of cardiovascular disease and mortality.[69]


Dermatologist consultation can be useful for an evaluation of the underlying causes of lipodystrophy and for consideration of surgical options. Plastic surgeons also may be considered for fillers, fat transfers, and liposuction.

Internal medicine or endocrinology specialist consultations help for an evaluation of the underlying causes of lipodystrophy and for the management of hyperlipidemia and hyperglycemia.

Infectious diseases specialist consultation is useful for the management of HIV infection.

Psychiatrist or psychologist consultation may be necessary because of the psychological impact of body shape changes.

Long-term monitoring

Follow-up laboratory testing should include assessments of the following:

  • Viral load and/or CD4+ T-cell counts to evaluate HIV-disease progression
  • Fasting lipid profile to evaluate hyperlipidemia
  • Fasting blood glucose and/or glucose tolerance test to evaluate hyperglycemia and insulin resistance

Patients should receive follow-up care every 3-6 months, and the aforementioned laboratory examinations should be performed as necessary.

Patients with HIV lipodystrophy may report feelings of anxiety, depression, loss of self-esteem, poor body image, and social and sexual dysfunction. It is important to ask about these issues and consider referral to a psychiatrist when appropriate.

Contributor Information and Disclosures

David T Robles, MD, PhD Dermatologist, Chaparral Medical Group

David T Robles, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.


Jacquiline Habashy, MSc Western University of Health Sciences College of Osteopathic Medicine of the Pacific

Jacquiline Habashy, MSc is a member of the following medical societies: American Osteopathic College of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.


Roy M Colven, MD Associate Professor of Medicine (Dermatology), Adjunct Associate Professor of Global Health, University of Washington School of Medicine; Section Head of Dermatology, Harborview Medical Center

Roy M Colven, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American Telemedicine Association, Phi Beta Kappa, and Washington State Medical Association

Disclosure: Nothing to disclose.

Ali Hendi, MD Assistant Professor, Department of Dermatology, Mayo Clinic College of Medicine at Jacksonville; Consulting Staff, Mayo Clinic

Disclosure: Nothing to disclose.

Suzan Obagi, MD Assistant Professor, Department of Dermatology, University of Pittsburgh School of Medicine

Disclosure: Nothing to disclose.

Jonathan M Olson, MD Fellow, Division of Dermatology, University of Washington Medical Center

Jonathan M Olson, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Jason Whalen, MD Dermatologist, University of Pittsburgh Medical Center

Disclosure: Nothing to disclose.

  1. Huang JS, Lee D, Becerra K, Santos R, Barber E, Mathews WC. Body image in men with HIV. AIDS Patient Care STDS. 2006 Oct. 20(10):668-77. [Medline].

  2. Reynolds NR, Neidig JL, Wu AW, Gifford AL, Holmes WC. Balancing disfigurement and fear of disease progression: Patient perceptions of HIV body fat redistribution. AIDS Care. 2006 Oct. 18(7):663-73. [Medline].

  3. Bogner JR, Vielhauer V, Beckmann RA, Michl G, Wille L, Salzberger B, et al. Stavudine versus zidovudine and the development of lipodystrophy. J Acquir Immune Defic Syndr. 2001 Jul 1. 27(3):237-44. [Medline].

  4. Bonnet E, Ruidavets JB, Tuech J, Ferrières J, Collet X, Fauvel J, et al. Apoprotein c-III and E-containing lipoparticles are markedly increased in HIV-infected patients treated with protease inhibitors: association with the development of lipodystrophy. J Clin Endocrinol Metab. 2001 Jan. 86(1):296-302. [Medline].

  5. Martinez E, Mocroft A, García-Viejo MA, Pérez-Cuevas JB, Blanco JL, Mallolas J, et al. Risk of lipodystrophy in HIV-1-infected patients treated with protease inhibitors: a prospective cohort study. Lancet. 2001 Feb 24. 357(9256):592-8. [Medline].

  6. Rakotoambinina B, Médioni J, Rabian C, Jubault V, Jais JP, Viard JP. Lipodystrophic syndromes and hyperlipidemia in a cohort of HIV-1-infected patients receiving triple combination antiretroviral therapy with a protease inhibitor. J Acquir Immune Defic Syndr. 2001 Aug 15. 27(5):443-9. [Medline].

  7. van der Valk M, Gisolf EH, Reiss P, Wit FW, Japour A, Weverling GJ, et al. Increased risk of lipodystrophy when nucleoside analogue reverse transcriptase inhibitors are included with protease inhibitors in the treatment of HIV-1 infection. AIDS. 2001 May 4. 15(7):847-55. [Medline].

  8. Bonnet E, Genoux A, Bernard J, Fauvel J, Massip P, Perret B. Impact of genetic polymorphisms on the risk of lipid disorders in patients on anti-HIV therapy. Clin Chem Lab Med. 2007. 45(7):815-21. [Medline].

  9. Domingo P, Mateo MG, Pruvost A, Torres F, Salazar J, Gutierrez MD, et al. Polymorphisms of Pyrimidine Pathway Enzymes Encoding Genes and HLA-B*40:01 Carriage in Stavudine-Associated Lipodystrophy in HIV-Infected Patients. PLoS One. 2013. 8(6):e67035. [Medline]. [Full Text].

  10. de Souza Dantas Oliveira SH, de Souza Aarão TL, da Silva Barbosa L, Souza Lisbôa PG, Tavares Dutra CD, Margalho Sousa L, et al. Immunohistochemical analysis of the expression of TNF-alpha, TGF-beta, and caspase-3 in subcutaneous tissue of patients with HIV lipodystrophy syndrome. Microb Pathog. 2014 Feb-Mar. 67-68:41-7. [Medline].

  11. Nolis T. Exploring the pathophysiology behind the more common genetic and acquired lipodystrophies. J Hum Genet. 2014 Jan. 59(1):16-23. [Medline].

  12. Oh J, Hegele RA. HIV-associated dyslipidaemia: pathogenesis and treatment. Lancet Infect Dis. 2007 Dec. 7(12):787-96. [Medline].

  13. Kakuda TN, Brundage RC, Anderson PL, Fletcher CV. Nucleoside reverse transcriptase inhibitor-induced mitochondrial toxicity as an etiology for lipodystrophy. AIDS. 1999 Nov 12. 13(16):2311-2. [Medline].

  14. Gentil C, Le Jan S, Philippe J, Leibowitch J, Sonigo P, Germain S, et al. Is oxygen a key factor in the lipodystrophy phenotype?. Lipids Health Dis. 2006 Oct 18. 5:27. [Medline].

  15. Arama V, Munteanu DI, Streinu Cercel A, Ion DA, Mihailescu R, Tiliscan C, et al. Lipodystrophy syndrome in HIV treatment-multiexperienced patients: implication of resistin. J Endocrinol Invest. 2014 Jun. 37(6):533-9. [Medline].

  16. Brigante G, Diazzi C, Ansaloni A, et al. Gender differences in GH response to GHRH+ARG in lipodystrophic patients with HIV: a key role for body fat distribution. Eur J Endocrinol. 2014 May. 170(5):685-96. [Medline].

  17. Haugaard SB, Andersen O, Vølund A, Hansen BR, Iversen J, Andersen UB, et al. Beta-cell dysfunction and low insulin clearance in insulin-resistant human immunodeficiency virus (HIV)-infected patients with lipodystrophy. Clin Endocrinol (Oxf). 2005 Mar. 62(3):354-61. [Medline].

  18. Stankov MV, Lücke T, Das AM, Schmidt RE, Behrens GM. Relationship of mitochondrial DNA depletion and respiratory chain activity in preadipocytes treated with nucleoside reverse transcriptase inhibitors. Antivir Ther. 2007. 12(2):205-16. [Medline].

  19. Cherry CL, Lal L, Thompson KA, McLean CA, Ross LL, Hernandez J, et al. Increased adipocyte apoptosis in lipoatrophy improves within 48 weeks of switching patient therapy from Stavudine to abacavir or zidovudine. J Acquir Immune Defic Syndr. 2005 Mar 1. 38(3):263-7. [Medline].

  20. Madge S, Kinloch-de-Loes S, Mercey D, Johnson MA, Weller IV. Lipodystrophy in patients naive to HIV protease inhibitors. AIDS. 1999 Apr 16. 13(6):735-7. [Medline].

  21. Sutinen J, Yki-Järvinen H. Increased resting energy expenditure, fat oxidation, and food intake in patients with highly active antiretroviral therapy-associated lipodystrophy. Am J Physiol Endocrinol Metab. 2007 Mar. 292(3):E687-92. [Medline].

  22. Moyle GJ, Sabin CA, Cartledge J, Johnson M, Wilkins E, Churchill D, et al. A randomized comparative trial of tenofovir DF or abacavir as replacement for a thymidine analogue in persons with lipoatrophy. AIDS. 2006 Oct 24. 20(16):2043-50. [Medline].

  23. Martin A, Smith DE, Carr A, Ringland C, Amin J, Emery S, et al. Reversibility of lipoatrophy in HIV-infected patients 2 years after switching from a thymidine analogue to abacavir: the MITOX Extension Study. AIDS. 2004 Apr 30. 18(7):1029-36. [Medline].

  24. Viganò A, Brambilla P, Cafarelli L, Giacomet V, Borgonovo S, Zamproni I, et al. Normalization of fat accrual in lipoatrophic, HIV-infected children switched from stavudine to tenofovir and from protease inhibitor to efavirenz. Antivir Ther. 2007. 12(3):297-302. [Medline].

  25. Schwenk A, Breuer JP, Kremer G, Römer K, Bethe U, Franzen C, et al. Risk factors for the HIV-associated lipodystrophy syndrome in a cross-sectional single-centre study. Eur J Med Res. 2000 Oct 30. 5(10):443-8. [Medline].

  26. Dieterich D. Incidence of body habitus changes in a cohort of 700 HIV-infected patients. Presented at: 36th Annual Meeting of Infectious Disease Society of America. November 12-15, 1998.

  27. Tsiodras S, Mantzoros C, Hammer S, Samore M. Effects of protease inhibitors on hyperglycemia, hyperlipidemia, and lipodystrophy: a 5-year cohort study. Arch Intern Med. 2000 Jul 10. 160(13):2050-6. [Medline].

  28. Waters L, Nelson M. Long-term complications of antiretroviral therapy: lipoatrophy. Int J Clin Pract. 2007 Jun. 61(6):999-1014. [Medline].

  29. Dong K, Flynn MM, Dickinson BP, et al. Changes in body habitus in HIV(+) women after initiation of protease inhibitor therapy. Presented at: 12th World AIDS Conference. 1998.

  30. Elwood W. Lipodystrophy: cause for concern with protease inhibitor therapy?. Reactions. 1998. 713:3-4.

  31. Alves MD, Brites C, Sprinz E. HIV-associated lipodystrophy: a review from a Brazilian perspective. Ther Clin Risk Manag. 2014. 10:559-66. [Medline]. [Full Text].

  32. Sorli Redó ML, Knobel Freud H, Montero M, Jericó Alba C, Guelar Grimberg A, Pedro-Botet Montoya J. [Sex influence in lipodystrophy of HIV-infected patients and its association with cardiovascular risk factors]. An Med Interna. 2007 Apr. 24(4):168-72. [Medline].

  33. Carr A, Samaras K, Thorisdottir A, Kaufmann GR, Chisholm DJ, Cooper DA. Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: a cohort study. Lancet. 1999 Jun 19. 353(9170):2093-9. [Medline].

  34. De Luca A, Murri R, Damiano F, Ammassari A, Antinori A. "Buffalo hump" in HIV-1 infection. Lancet. 1998 Jul 25. 352(9124):320. [Medline].

  35. Lo JC, Mulligan K, Tai VW, Algren H, Schambelan M. "Buffalo hump" in men with HIV-1 infection. Lancet. 1998 Mar 21. 351(9106):867-70. [Medline].

  36. Roth VR, Kravcik S, Angel JB. Development of cervical fat pads following therapy with human immunodeficiency virus type 1 protease inhibitors. Clin Infect Dis. 1998 Jul. 27(1):65-7. [Medline].

  37. Palella FJ Jr, Chmiel JS, Riddler SA, Calhoun B, Dobs A, Visscher B, et al. A novel pattern of lipoaccumulation in HIV-infected men. JAMA. 2006 Aug 16. 296(7):766-8. [Medline].

  38. Guaraldi G, Orlando G, Squillace N, Roverato A, De Fazio D, Vandelli M, et al. Prevalence of and risk factors for pubic lipoma development in HIV-infected persons. J Acquir Immune Defic Syndr. 2007 May 1. 45(1):72-6. [Medline].

  39. Dank JP, Colven R. Protease inhibitor-associated angiolipomatosis. J Am Acad Dermatol. 2000 Jan. 42(1 Pt 1):129-31. [Medline].

  40. Polsky B, Kotler D, Steinhart C. HIV-associated wasting in the HAART era: guidelines for assessment, diagnosis, and treatment. AIDS Patient Care STDS. 2001 Aug. 15(8):411-23. [Medline].

  41. Beraldo RA, Vassimon HS, Aragon DC, Navarro AM, Albuquerque de Paula FJ, Foss-Freitas MC. Proposed ratios and cutoffs for the assessment of lipodystrophy in HIV-seropositive individuals. Eur J Clin Nutr. 2014 Jul 30. [Medline].

  42. Gellett LR, Haddon L, Maskell GF. CT appearances of HIV-related lipodystrophy syndrome. Br J Radiol. 2001 Apr. 74(880):382-3. [Medline].

  43. Huang JS, Rietschel P, Hadigan CM, Rosenthal DI, Grinspoon S. Increased abdominal visceral fat is associated with reduced bone density in HIV-infected men with lipodystrophy. AIDS. 2001 May 25. 15(8):975-82. [Medline].

  44. Martínez E, García-Viejo MA, Blanco JL, Bianchi L, Buira E, Conget I, et al. Impact of switching from human immunodeficiency virus type 1 protease inhibitors to efavirenz in successfully treated adults with lipodystrophy. Clin Infect Dis. 2000 Nov. 31(5):1266-73. [Medline].

  45. Falutz J, Potvin D, Mamputu JC, et al. Effects of tesamorelin, a growth hormone-releasing factor, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension. J Acquir Immune Defic Syndr. 2010 Mar 1. 53(3):311-22. [Medline].

  46. Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. N Engl J Med. 2007 Dec 6. 357(23):2359-70. [Medline].

  47. Falutz J, Mamputu JC, Potvin D, et al. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010 Sep. 95(9):4291-304. [Medline].

  48. Baldini F, Di Giambenedetto S, Cingolani A, Murri R, Ammassari A, De Luca A. Efficacy and tolerability of pravastatin for the treatment of HIV-1 protease inhibitor-associated hyperlipidaemia: a pilot study. AIDS. 2000 Jul 28. 14(11):1660-2. [Medline].

  49. Hadigan C, Corcoran C, Basgoz N, Davis B, Sax P, Grinspoon S. Metformin in the treatment of HIV lipodystrophy syndrome: A randomized controlled trial. JAMA. 2000 Jul 26. 284(4):472-7. [Medline].

  50. Kuzuya H, Matsuura N, Sakamoto M, Makino H, Sakamoto Y, Kadowaki T, et al. Trial of insulinlike growth factor I therapy for patients with extreme insulin resistance syndromes. Diabetes. 1993 May. 42(5):696-705. [Medline].

  51. Moses AC, Morrow LA, O'Brien M, Moller DE, Flier JS. Insulin-like growth factor I (rhIGF-I) as a therapeutic agent for hyperinsulinemic insulin-resistant diabetes mellitus. Diabetes Res Clin Pract. 1995 Aug. 28 Suppl:S185-94. [Medline].

  52. Hadigan C, Yawetz S, Thomas A, Havers F, Sax PE, Grinspoon S. Metabolic effects of rosiglitazone in HIV lipodystrophy: a randomized, controlled trial. Ann Intern Med. 2004 May 18. 140(10):786-94. [Medline].

  53. Cavalcanti RB, Raboud J, Shen S, et al. A randomized, placebo-controlled trial of rosiglitazone for HIV-related lipoatrophy. J Infect Dis. 2007 Jun 15. 195(12):1754-61. [Medline].

  54. Raboud JM, Diong C, Carr A, et al. A meta-analysis of six placebo-controlled trials of thiazolidinedione therapy for HIV lipoatrophy. HIV Clin Trials. 2010 Jan-Feb. 11(1):39-50. [Medline].

  55. Sheth SH, Larson RJ. The efficacy and safety of insulin-sensitizing drugs in HIV-associated lipodystrophy syndrome: a meta-analysis of randomized trials. BMC Infect Dis. 2010 Jun 23. 10:183. [Medline]. [Full Text].

  56. Lo JC, Mulligan K, Noor MA, Schwarz JM, Halvorsen RA, Grunfeld C, et al. The effects of recombinant human growth hormone on body composition and glucose metabolism in HIV-infected patients with fat accumulation. J Clin Endocrinol Metab. 2001 Aug. 86(8):3480-7. [Medline].

  57. Wanke C, Gerrior J, Kantaros J, Coakley E, Albrecht M. Recombinant human growth hormone improves the fat redistribution syndrome (lipodystrophy) in patients with HIV. AIDS. 1999 Oct 22. 13(15):2099-103. [Medline].

  58. Patni N, Diaz EG, Cabral MD, Siqueira LM, Diaz A. Worsening hypertriglyceridemia with oral contraceptive pills in an adolescent with HIV-associated lipodystrophy: a case report and review of the literature. J Pediatr Endocrinol Metab. 2014 Nov 1. 27(11-12):1247-51. [Medline].

  59. Nelson L, Stewart KJ. Plastic surgical options for HIV-associated lipodystrophy. J Plast Reconstr Aesthet Surg. 2008. 61(4):359-65. [Medline].

  60. Davison SP, Timpone J Jr, Hannan CM. Surgical algorithm for management of HIV lipodystrophy. Plast Reconstr Surg. 2007 Dec. 120(7):1843-58. [Medline].

  61. Lafaurie M, Dolivo M, Porcher R, Rudant J, Madelaine I, Molina JM. Treatment of facial lipoatrophy with intradermal injections of polylactic acid in HIV-infected patients. J Acquir Immune Defic Syndr. 2005 Apr 1. 38(4):393-8. [Medline].

  62. Quintas RC, de França ER, de Petribú KC, Ximenes RA, Quintas LF, Cavalcanti EL, et al. Treatment of facial lipoatrophy with polymethylmethacrylate among patients with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS): impact on the quality of life. Int J Dermatol. 2014 Apr. 53(4):497-502. [Medline].

  63. Blashill AJ, Goshe BM, Robbins GK, Mayer KH, Safren SA. Body image disturbance and health behaviors among sexual minority men living with HIV. Health Psychol. 2014 Jul. 33(7):677-80. [Medline]. [Full Text].

  64. Gooderham M, Solish N. Use of hyaluronic acid for soft tissue augmentation of HIV-associated facial lipodystrophy. Dermatol Surg. 2005 Jan. 31(1):104-8. [Medline].

  65. Ritt MJ, Hillebrand-Haverkort ME, ten Veen JH. Local treatment of facial lipodystrophy in patients receiving HIV protease inhibitor therapy. Acta Chir Plast. 2001. 43(2):54-6. [Medline].

  66. Wildemore JK, Jones DH. Persistent granulomatous inflammatory response induced by injectable poly-L-lactic acid for HIV lipoatrophy. Dermatol Surg. 2006 Nov. 32(11):1407-9; discussion 1409. [Medline].

  67. Loonam CR, Mullen A. Nutrition and the HIV-associated lipodystrophy syndrome. Nutr Res Rev. 2012 Dec. 25(2):267-87. [Medline].

  68. Roubenoff R, Weiss L, McDermott A, Heflin T, Cloutier GJ, Wood M, et al. A pilot study of exercise training to reduce trunk fat in adults with HIV-associated fat redistribution. AIDS. 1999 Jul 30. 13(11):1373-5. [Medline].

  69. Jaggers JR, Prasad VK, Dudgeon WD, Blair SN, Sui X, Burgess S, et al. Associations between physical activity and sedentary time on components of metabolic syndrome among adults with HIV. AIDS Care. 2014. 26(11):1387-92. [Medline]. [Full Text].

Facial HIV-associated lipodystrophy in a patient receiving highly active antiretroviral therapy.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.