[Inflammation theory for etiopathogenesis of algodystrophy].
Algodystrophy (reflex sympathetic dystrophy, Sudeckłs atrophy) is the condition of still unclear pathogenesis. Paul Sudeck, who described the syndrome was convinced of its inflammatory nature; later research established the inducing role of the sympathetic nervous system for many years. This view has been questioned in the last decade. This paper presents some evidence of inflammatory explanation of the disorder: increased uptake of the immunoglobulin IgM labeled In111 in affected area, followed by increased vascular permeability for macromolecules, and impaired metabolism of the high energy phosphates following the impaired oxygen extraction in the affected extremity. Free oxygen and hydroxyl radicals injurious role in the course of algodystrophy is also established by beneficial treatment with the use of free radicals scavengers (mannitol, dimethyl sulfoxide, N-acetylcysteine) and by pathologic ultrastructural changes in muscle cells due to oxidative stress. The view of the inflammatory nature of acute stage of algodystrophy does not preclude a role of sympathetic nervous system but it better explains some clinical aspects of this phase of the condition and increases recognition of its complicated nature.
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Kliniki Chirurgii Ogólnej i Chirurgii Reki Pomorskiej Akademii Medycznej w Szczecinie.
D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007075:Immunoglobulin M / Q000502:physiology; D007249:Inflammation / Q000503:physiopathology; D012019:Reflex Sympathetic Dystrophy / Q000209:etiology* / Q000503:physiopathology
D005609:Free Radicals; D007075:Immunoglobulin M