HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms

Kenneth Lichtenstein¹ , Ashok Balasubramanyam² , Rajagopal Sekhar² and Eric Freedland³

¹University of Colorado Infectious Disease Group Practice, Denver, CO, USA

²Division of Diabetes, Endocrinology & Metabolism, Baylor College of Medicine, Houston, TX, USA

³EMD Serono, Inc., Rockland, MA, USA

author email corresponding author email

AIDS Research and Therapy 2007, 4:14doi:10.1186/1742-6405-4-14


Published:	27 June 2007

Abstract

Human immunodeficiency virus (HIV)-associated adipose redistribution syndrome (HARS) is a fat accumulation disorder characterized by increases in visceral adipose tissue. Patients with HARS may also present with excess truncal fat and accumulation of dorsocervical fat ("buffalo hump"). The pathophysiology of HARS appears multifactorial and is not fully understood at present. Key pathophysiological influences include adipocyte dysfunction and an excessive free fatty acid release by adipocyte lipolysis. The contributory roles of free fatty acids, cytokines, hormones including cortisol, insulin and the growth hormone-adipocyte axis are significant. Other potential humoral, paracrine, endocrine, and neural influences are also discussed.