Table 2.

Classification, clinical features, and pathogenetic basis of acquired lipodystrophies

Type	Subtype	Clinical features	Pathogenetic basis/other comments
Lipodystrophy in HIV-infected patients	PI-induced NRTI-induced	Loss of sc fat from the face and extremities and excess fat deposition in the neck and abdomen	PI may inhibit ZMPSTE24 and/or cause dysregulation of transcription factors involved in adipogenesis.
			NRTI may inhibit mitochondrial polymerase-γ and cause mitochondrial toxicity.
Acquired partial lipodystrophy	Autoimmune MPGN-associated Idiopathic	Loss of sc fat from the face, neck, upper limbs, and trunk, sparing the lower abdomen and lower limbs	Low serum complement 3 levels and presence of an autoantibody, complement 3 nephritic factor, in most of the patients suggest autoimmune-mediated loss of adipose tissue.
Acquired generalized lipodystrophy	Autoimmune Panniculitis-associated Idiopathic	Generalized loss of fat associated with tender sc nodules, autoimmune or other diseases	Panniculitis preceding the loss of sc fat and association of autoimmune diseases suggest immune-mediated loss of adipose tissue. Other mechanisms may also be involved.
Localized lipodystrophy	Drug-induced Panniculitis-induced Pressure-induced Centrifugal Idiopathic	Loss of sc fat from small areas of the body	Multiple mechanisms including local drug-induced, immune-mediated, or pressure-induced atrophy of adipose tissue. Other unknown mechanisms may also be involved.

MPGN, Membranoproliferative glomerulonephritis.