title: Pathogenesis and treatment of pretibial myxedema.
abstract: Pretibial myxedema is considered an autoimmune complication or association of Graves' disease, Hashimoto's thyroiditis, and primary myxedema. The mechanism of lesion formation is unknown; the most plausible theory is that it arises as a result of a target cell in the skin, probably the fibroblast, being stimulated to produce abnormally high amounts of glycosoaminoglycans (especially hyaluronic acid) by autoantibodies directed against a thyroid antigen(s)--that is, by a cross reaction. One or more intermediary humoral agents may be involved in pathogenesis. The reason for the localization to the pretibial region is unknown; there is evidence that most patients with the disorder have similar abnormalities in the preradial skin. The condition may persist for months or years but often regresses spontaneously, accompanied by a parallel decline in, or disappearance of, serum anti-TSH-receptor autoantibody levels. Skin biopsies reveal evidence of increased amounts of hyaluronic acid and damage to collagen and elastic fibers. Local symptomatic treatment with corticosteroids is effective in most cases with slight to moderate severity of skin involvement. Repeated treatments are advised until such time that a spontaneous clinical remission occurs.
authors.affiliation: Division of Nuclear Medicine, Stanford University School of Medicine, California.
authors.forename: J P
authors.initials: JP
authors.lastname: Kriss
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D006111:Graves Disease / Q000150:complications; D006801:Humans; D007868:Leg Dermatoses / Q000150:complications / Q000209:etiology* / Q000628:therapy; D009230:Myxedema / Q000150:complications / Q000209:etiology* / Q000628:therapy; D013967:Thyroiditis, Autoimmune / Q000150:complications
chemical_list: D000305:Adrenal Cortex Hormones