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Influence of methimazole treatment on parameters of oxidative stress in patients with Graves’ disease

Influence of methimazole treatment on parameters of oxidative stress in patients with Graves’... It is known that hyperthyroidism is associated with oxidative stress. Graves’ disease (GD) is an autoimmune thyroid disorder responsible for 70–80% of all cases of hyperthyroidism. The aim of this study was to examine the change of oxidative stress and antioxidant enzyme activities in 23 patients with Graves’ disease before and after treatment with methimazole and in 31 healthy controls. The level of malondialdehyde (MDA) in the plasma, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities in erythrocytes were measured. Serum levels of TSH and free thyroxin (FT4) were also estimated. We observed increased concentrations of FT4 and suppressed TSH levels before treatment. The concentrations of thyroid hormones and of TSH normalized after the methimazole treatment. Significantly higher MDA concentrations were found in hyperthyroid GD patients in comparison to controls (1.96±0.10 vs 1.71±0.05 μmol/l, p<0.05). After a long-term drug treatment, the plasma levels of MDA decreased and reached values close to the controls (mean 1.73 μmol/l). Activity of GPX in erythrocytes in hyperthyroidism was higher compared to controls (9.3±1.2 vs 6.6±0.5 U/gHb, p<0.05). After thyrostatic treatment in euthyroidism, the activity of GPX was found to decrease in euthyroid GD patients in comparison to hyperthyroid patients, compared to controls (3.9±0.5 vs 9.3±1.2 U/gHb and 3.9±0.5 vs 6.6±0.5 U/gHb; p<0.001, p<0.001, respectively). Our data confirm the presence of increase in lipid peroxidation in hyperthyroid patients, which is corrected in euthyroidism. We hypothesize that in hyperthyroidism, the enhanced activity of GPX was induced by oxidative stress and was connected with TSH receptor hyperstimulation. After treatment with methimazole, GPX activity was lowered. Observed alterations of GPX activity after Graves’ disease treatment may be related to the deficiency of cellular antioxidative defense that persists during the course of disease. The disturbed antioxidative defense in patients with Graves’ disease indicates the possible usefulness of supplementation with antioxidants in particular with selenium as an important component of selenoenzymes such as GPX. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Comparative Clinical Pathology Springer Journals

Influence of methimazole treatment on parameters of oxidative stress in patients with Graves’ disease

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Publisher
Springer Journals
Copyright
Copyright © 2006 by Springer-Verlag London Limited
Subject
Medicine & Public Health; Oncology ; Hematology; Pathology
eISSN
1618-565X
DOI
10.1007/s00580-006-0604-8
Publisher site
See Article on Publisher Site

Abstract

It is known that hyperthyroidism is associated with oxidative stress. Graves’ disease (GD) is an autoimmune thyroid disorder responsible for 70–80% of all cases of hyperthyroidism. The aim of this study was to examine the change of oxidative stress and antioxidant enzyme activities in 23 patients with Graves’ disease before and after treatment with methimazole and in 31 healthy controls. The level of malondialdehyde (MDA) in the plasma, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities in erythrocytes were measured. Serum levels of TSH and free thyroxin (FT4) were also estimated. We observed increased concentrations of FT4 and suppressed TSH levels before treatment. The concentrations of thyroid hormones and of TSH normalized after the methimazole treatment. Significantly higher MDA concentrations were found in hyperthyroid GD patients in comparison to controls (1.96±0.10 vs 1.71±0.05 μmol/l, p<0.05). After a long-term drug treatment, the plasma levels of MDA decreased and reached values close to the controls (mean 1.73 μmol/l). Activity of GPX in erythrocytes in hyperthyroidism was higher compared to controls (9.3±1.2 vs 6.6±0.5 U/gHb, p<0.05). After thyrostatic treatment in euthyroidism, the activity of GPX was found to decrease in euthyroid GD patients in comparison to hyperthyroid patients, compared to controls (3.9±0.5 vs 9.3±1.2 U/gHb and 3.9±0.5 vs 6.6±0.5 U/gHb; p<0.001, p<0.001, respectively). Our data confirm the presence of increase in lipid peroxidation in hyperthyroid patients, which is corrected in euthyroidism. We hypothesize that in hyperthyroidism, the enhanced activity of GPX was induced by oxidative stress and was connected with TSH receptor hyperstimulation. After treatment with methimazole, GPX activity was lowered. Observed alterations of GPX activity after Graves’ disease treatment may be related to the deficiency of cellular antioxidative defense that persists during the course of disease. The disturbed antioxidative defense in patients with Graves’ disease indicates the possible usefulness of supplementation with antioxidants in particular with selenium as an important component of selenoenzymes such as GPX.

Journal

Comparative Clinical Pathology – Springer Journals

Published: Apr 26, 2006

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