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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.
Familial Partial Lipodystrophy, Dunnigan Type Autosomal dominant is the manner of inheritance of this condition 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 ...
Lipodystrophy syndromes are a group of genetic or acquired disorders in which the body is unable to produce and maintain healthy fat tissue. [ 1 ] [ 2 ] The medical condition is characterized by abnormal or degenerative conditions of the body's adipose tissue .
Other entities which are accompanied by multiple lipomas include Proteus syndrome, Cowden syndrome and related disorders due to PTEN gene mutations, benign symmetric lipomatosis (Madelung disease), Dercum's Disease, familial lipodystrophy, hibernomas, epidural steroid injections with epidural lipomatosis, [6] and familial angiolipomatosis.
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.
Barraquer–Simons syndrome is a rare form of lipodystrophy, which usually first affects the head, and then spreads to the thorax. [2] [3] It is named for Luis Barraquer Roviralta (1855–1928), a Spanish physician, and Arthur Simons (1879–1942), a German physician.
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]
Werner syndrome patients exhibit growth retardation, short stature, premature graying of hair, alopecia (hair loss), wrinkling, prematurely aged faces with beaked noses, skin atrophy (wasting away) with scleroderma-like lesions, lipodystrophy (loss of fat tissues), abnormal fat deposition leading to thin legs and arms, and severe ulcerations around the Achilles tendon and malleoli (around ankles).
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