Although several theories have been suggested, the
exact pathogenesis of PM remains to be clarified. Autoantibodies
against thyroid antigens and reactive T lymphocytes
are thought to cross-react with connective tissue
and muscle antigens. TSH receptor antibodies binding to
the receptors in the connective tissue may stimulate fibroblasts
to produce a large amount of glycosaminoglycans
(5). It was speculated that pretibial fibroblast may
react with T cell lymphocytes on their thyrotrophin receptors
and then they may overproduce glycosaminoglycans
(6). The predilection of localization to the pretibial
area may result from trauma with the release of inflammatory
cytokines and inflammatory cells or local hypoxia
that results from arterial or venous insufficiency. Although
PM does not seem to be related to the levels of T3 and
T4, only three euthyroid cases with PM have been reported
in the literature
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Jeu 3 Fév 2011 - 23:04
et si on prend en compte cette deuxième constatation l'origine la plausible serait une hyperstimulations des recepteurs des recepteurs extra throidien(puisque dans l'hypothyroidie peripherique il y a une elevation de la TSH ) mais comme on dit c trop beau pour etre vrai 
