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Familial partial lipodystrophy, also known as Köbberling–Dunnigan syndrome, [2] is a rare genetic metabolic condition characterized by the loss of subcutaneous fat. [ 3 ] : 495 FPL also refers to a rare metabolic condition in which there is a loss of subcutaneous fat in the arms, legs and lower torso.
Dunnigan-type familial partial lipodystrophy, also known as FPLD Type II and abbreviated as (FPLD2), is a rare monogenic form of insulin resistance characterized by loss of subcutaneous fat from the extremities, trunk, and gluteal region.
In general, treatment for acquired partial lipodystrophy is limited to cosmetic, dietary, or medical options. [9] Currently, no effective treatment exists to halt its progression. Diet therapy has been shown to be of some value in the control of metabolic problems.
Lipodystrophy can be divided into the following types: [5]: 495–7 Congenital lipodystrophy syndromes Congenital generalized lipodystrophy (Berardinelli-Seip syndrome) Familial partial lipodystrophy; Marfanoid–progeroid–lipodystrophy syndrome; Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature syndrome [6]
Acquired generalized lipodystrophy (AGL), also known as Lawrence syndrome [1] and Lawrence–Seip syndrome, [1] is a rare skin condition that appears during childhood or adolescence, characterized by fat loss affecting large areas of the body, particularly the face, arms, and legs.
Congenital generalized lipodystrophy (also known as Berardinelli–Seip lipodystrophy) is an extremely rare autosomal recessive condition, characterized by an extreme scarcity of fat in the subcutaneous tissues. [2] It is a type of lipodystrophy disorder where the magnitude of fat loss determines the severity of metabolic complications. [3]
Lipoprotein lipase deficiency is a genetic disorder in which a person has a defective gene for lipoprotein lipase, which leads to very high triglycerides, which in turn causes stomach pain and deposits of fat under the skin, and which can lead to problems with the pancreas and liver, which in turn can lead to diabetes.
Lipedema has been described in familial clusters, suggesting a genetic component. [9] It often appears around times of hormonal change such as puberty, pregnancy, and menopause, suggesting a potential hormonal component. [10] Having obesity doesn’t cause lipedema, but more than half of people with this condition have a BMI higher than 35. [11]