Lipodystrophy is a rare, heterogeneous group of syndromes characterized by the complete or partial loss or absence of subcutaneous adipose tissue (1,2). Lipodystrophy is often, though not always, accompanied by metabolic derangements, including insulin resistance, diabetes mellitus, hepatic steatosis or steatohepatitis, and dyslipidemia (1,2). The metabolic derangements associ-ated with lipodystrophy can be severe and lead to sub-stantial comorbidities, including acute pancreatitis (due to severe hypertriglyceridemia), hepatic cirrhosis, and premature cardiovascular disease (1,2). Other manifesta-tions of metabolic derangements can include polycystic ovarian syndrome (PCOS), acanthosis nigricans (due to severe insulin resistance), and eruptive xanthomas (due to severe hypertriglyceridemia) (1,2). Since the key charac-teristic of lipodystrophy is the selective absence of adipose tissue (primarily subcutaneous), the levels of adipocyte hormones can be altered (3). The best characterized of these hormones is leptin, with low leptin levels typically observed in patients with lipodystrophy (4); however, lev-els of other adipocytokines, such as adiponectin, are also lower in lipodystrophy (5).
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The Clinical Approach to the Detection of Lipodystrophy - An AACE Consensus Statement © 2013