Peripheral parameters of oxidative stress in patients with infiltrative Graves' ophthalmopathy treated with corticosteroids.
Infiltrative ophthalmopathy, which may develop in patients with Graves' disease, is considered an inflammatory disorder of autoimmune background. There is growing evidence that changed reactive oxygen species (ROS) metabolism plays an important role in pathogenesis of autoimmune diseases. Corticotherapy is a principal method of ophthalmopathy treatment, and its therapeutic effect is partially connected with influence on ROS generation systems. This study was undertaken to investigate corticosteroids treatment influence on blood extracellular indices of ROS metabolism in Graves' ophthalmopathy patients. Plasma indices of free radical generation and scavenging were determined in 22 euthyroid patients with active infiltrative Graves' ophthalmopathy initially, after intensive corticotherapy and after completing of steroid treatment. Age- and sex-matched 24 healthy volunteers and 25 euthyroid Graves' patients without overt ophthalmopathy served as controls. In the ophthalmopathy patients hydrogen peroxide (H(2)O(2)), lipid hydroperoxides (ROOH), thiobarbituric acid-reacting substances (TBARS) and ceruloplasmin (CP) levels and superoxide dismutase (SOD) and catalase (CAT) activities were increased, whereas glutathione peroxidase (GPx) and glutathione reductase (GR) activities were reduced. Intensive corticotherapy resulted in normalization (partial for ROOH) of ROS metabolism peripheral markers. After the withdrawal of corticosteroids a reduction of ophthalmopathy clinical activity was present, yet a marked restoration of increased oxidative stress indices was observed, along with activation of antioxidant defence systems (not significant for CAT activity). These data demonstrate that corticosteroids are effective in reduction of peripheral oxidative stress present in infiltrative Graves' ophthalmopathy, but this effect tends to be transient.
Bednarek
Janusz
J
Department of Endocrinology, Metabolism and Internal Medicine, Poznań University of Medical Sciences, Przybyszewskiego 49, PL-60355, Poznan, Poland. bednarek@post.pl
Wysocki
Henryk
H
Sowiński
Jerzy
J
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D000328:Adult; D001323:Autoantibodies / Q000097:blood; D002374:Catalase / Q000097:blood; D002570:Ceruloplasmin / Q000032:analysis; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D006111:Graves Disease / Q000097:blood* / Q000145:classification / Q000188:drug therapy; D006801:Humans; D006861:Hydrogen Peroxide / Q000097:blood; D018828:Immunoglobulins, Thyroid-Stimulating; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000097:blood* / Q000378:metabolism; D011989:Receptors, Thyrotropin / Q000097:blood; D013482:Superoxide Dismutase / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D016896:Treatment Outcome; D014284:Triiodothyronine / Q000097:blood
D000305:Adrenal Cortex Hormones; D001323:Autoantibodies; D018828:Immunoglobulins, Thyroid-Stimulating; D008054:Lipid Peroxides; D017382:Reactive Oxygen Species; D011989:Receptors, Thyrotropin; D017392:Thiobarbituric Acid Reactive Substances; C094372:thyrotropin-binding inhibitory immunoglobulin; D014284:Triiodothyronine; D013972:Thyrotropin; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D002570:Ceruloplasmin; D005980:Glutathione Reductase; D013974:Thyroxine