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Acquired Partial Lipodystrophy Treatment & Management

  • Author: George T Griffing, MD; Chief Editor: George T Griffing, MD  more...
Updated: Dec 16, 2015

Medical Care

In general, treatment for acquired partial lipodystrophy is limited to cosmetic, dietary, or medical options.

Currently, no effective treatment exists to halt the progression of lipodystrophy.

Thiazolidinediones have been used in the management of various types of lipodystrophies. They bind to peroxisome proliferator-activator receptor gamma (PPAR-gamma), which stimulates the transcription of genes responsible for growth and differentiation of adipocytes.[31] Several case reports have suggested a beneficial effect from treatment with rosiglitazone or pioglitazone on fat distribution in acquired partial lipodystrophy[32, 33] ; however, preferential fat gain was in the lower body.

Following the online publication of a meta-analysis,[34] the Food and Drug Administration issued an alert on May 21, 2007, to patients and health care professionals warning that rosiglitazone could potentially cause an increased risk of myocardial infarction (MI) and heart-related deaths. A thiazolidinedione derivative, rosiglitazone is an antidiabetic agent that improves glycemic control by improving insulin sensitivity. The drug is highly selective and is a potent agonist for PPAR-gamma. Activation of PPAR-gamma receptors regulates insulin-responsive gene transcription involved in glucose production, transport, and utilization, thereby reducing blood glucose concentrations and hyperinsulinemia. Potent PPAR-gamma agonists have been shown to increase the incidence of edema. A large-scale phase III trial (RECORD) has been underway to study the cardiovascular outcomes of rosiglitazone.

As of September 2010, the FDA is requiring a restricted access program to be developed for rosiglitazone under a risk evaluation and mitigation strategy (REMS). Patients currently taking rosiglitazone and benefiting from the drug will be able to continue if they choose to do so. Rosiglitazone will only be available to new patients if they are unable to achieve glucose control on other medications and are unable to take pioglitazone, the only other thiazolidinedione.

For more information, see the FDA’s Safety Alert on Avandia. Additionally, responses to the controversy, including the following articles, can be viewed at Heartwire news (the, from WebMD): 1) Rosiglitazone increases MI and CV death in meta-analysis, 2) The rosiglitazone aftermath: Legitimate concerns or hype?, and 3) RECORD interim analysis of rosiglitazone safety: No clear-cut answers.

Direct drug therapy is administered according to the associated condition. Membranoproliferative glomerulonephritis and the presence of renal dysfunction largely determine the prognosis of acquired partial lipodystrophy. Standard guidelines for the management of renal disease should be followed. The course of membranoproliferative glomerulonephritis in acquired partial lipodystrophy has not been significantly altered by treatment with corticosteroids or cytotoxic medications. Recurrent bacterial infections, if severe, might be managed with prophylactic antibiotics.

Metreleptin, a recombinant analogue of human leptin, has recently been approved to treat the metabolic derangements of lipodystrophy. Leptin is an adipocyte-derived hormone, which is decreased in lipodystrophy, leading to insulin resistance, dyslipidemia, and other metabolic problems. Metreleptin replaces this deficiency, thus improving insulin resistance, hyperglycemia, dyslipidemia, and hepatic steatosis. Acquired partial lipodystrophy has relatively higher leptin levels and less metabolic derangements. Therefore, the indications for metreleptin are less than for other forms of lipodystrophy.[35, 36, 37, 38]


Surgical Care

The purpose of surgery is mainly cosmetic. According to guidelines from the American Academy of Dermatology, lipodystrophy is one of the indications for fat transplant.

Several facial reconstruction techniques have been used, with variable success, to restore facial contour. However, surgical intervention cannot restore adipose tissue distribution in other affected areas.

The literature is controversial regarding these procedures. The best approach is to individualize the treatment options based on the patient's condition and requirements. These procedures are not recommended for prepubertal children.

Procedures may include the transposition of facial muscles, adipose tissue transplantation (liposuction), and the insertion of silicone or other implants.



Early consultation with a nephrologist or an endocrinologist is very important if renal or metabolic complications are suggested.



No evidence in the literature favors any specific diets in this group of patients. A low-fat, high-carbohydrate diet can be detrimental with regard to triglyceride levels, and weight gain should be avoided to reduce the risk of worsening metabolic status. However, children with this syndrome should be permitted normal food intake to allow for normal growth.



Regular exercise should be encouraged to help improve metabolic status.

Contributor Information and Disclosures

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Nutrition, American Society for Bone and Mineral Research, International Society for Clinical Densitometry, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Amir E Harari, MD Staff Physician, Endocrinology Division, Instructor, Department of Clinical Medicine, Naval Medical Center at San Diego

Amir E Harari, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Clinical Endocrinologists, American College of Physicians, Endocrine Society

Disclosure: Nothing to disclose.


Waleed Aldhahi, MD, FRCPC Clinical Research Fellow, Department of Endocrinology, Joslin Diabetes Center, Harvard University

Disclosure: Nothing to disclose.

Robert A Gabbay, MD, PhD Associate Professor of Medicine, Division of Endocrinology, Diabetes and Metabolism, Laurence M Demers Career Development Professor, Penn State College of Medicine; Director, Diabetes Program, Penn State Milton S Hershey Medical Center; Executive Director, Penn State Institute for Diabetes and Obesity

Robert A Gabbay, MD, PhD is a member of the following medical societies: American Association of Clinical Endocrinologists, American Diabetes Association, and Endocrine Society

Disclosure: Novo Nordisk Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching

Irina Lendel, MD Clinical Instructor in Endocrinology, Division of Endocrinology, Diabetes, and Metabolism, Milton S Hershey Medical Center

Disclosure: Nothing to disclose.

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Fat distribution in acquired partial lipodystrophy.
Model of the adipocyte destruction in acquired partial lipodystrophy showing complement activation at the adipocyte surface resulting in adipocyte lysis. Adipocytes synthesize C3, factor B, and factor D (adipsin), which allows C3bBb to be formed locally, but which usually does not result in the activation of the terminal lytic part of the complement pathway (C5-9).The IgG antibody, C3Nef, prevents the alternative complement C3-convertase C3Bb from dissociative inactivation, resulting in adipocyte lysis. Adipocytes synthesize factor D, the limiting component of the alternative complement pathway, which cleaves C3-bound factor B to its active enzymatic form. Factor D is expressed to a higher extent in the fat cells of the upper half of the body compared with the lower half, and it is possibly this regional difference that accounts for the restriction of fat loss to the head, arms, and trunk. C3Nef is also associated with type II, dense-deposit membranoproliferative glomerulonephritis in which subendothelial deposits of immunoglobulin and C3 are probably due to a deregulated alternative complement pathway.
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