A cukorbetegséghez társuló idegrendszeri károsodás kialakulásának mechanizmusa ma sem teljes mértékben tisztázott, bár az utóbbi évtizedben számos, részben terápiás konzekvenciával járó adat vált ismertté. Az endoneuralis véráramlás csökkenése részben a primer haemostasis károsodásának, a koagulációs rendszer trombogén irányú elmozdulásának következménye. A hyperglykaemia a szuperoxid-anion fokozott képződése révén a glikolízisben kulcsszerepet játszó glicerin-aldehid-3-foszfát-dehidrogenáz aktivitásának csökkenéséhez, alternatív anyagcsereutak (poliol-, hexóz-amin-, diacil-glicerol-, proteinkináz-C anyagcsereút, fehérjeglikáció) aktiválódásához vezet. A végglikációs fehérjék fokozzák a nukleáris faktor κ-B aktivitását, vazoaktív tényezők és citokinek (interleukin-1, -6, tumornekrózis-faktor-α) termelődését. A patogenetikai alapon nyugvó oki kezelés célja a neuropathiás károsodás progressziójának lassítása, megállítása vagy visszafordítása. Az oki kezelés legfontosabb összetevői: a szénhidrátanyagcsere-helyzet optimális beállítása, a rizikófaktorok kezelése, valamint benfotiamin és alfa-liponsav adása. A transzketoláz-aktivátor benfotiamin egyrészt gátolja a hyperglykaemia következményeként előtérbe kerülő legfontosabb alternatív anyagcsereutak (fehérjeglikáció, diacil-glicerol-, proteinkináz-C-aktiváció, poliol- és hexóz-amin-anyagcsereút) aktivitását, másrészt fokozza a pentóz-foszfát-sönt aktivitását. A benfotiamin klinikai hatékonyságát számos hazai és nemzetközi tanulmány igazolta. Az antioxidáns hatású alfa-liponsav az oxidatív stressz csökkentése révén elősegíti a glicerin-aldehid-3-foszfát-dehidrogenáz aktivitásának fokozódását. Az alfa-liponsav mind infúzióban, mind per os adagolva csökkenti a neuropathiával összefüggő tüneteket és mérsékli a neuropathiás károsodást. Összességében a neuropathia diabetica jól illusztrálja, hogy a patomechanizmussal kapcsolatos ismereteink bővülése számottevően hozzájárulhat a terápia sikeréhez is.
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