BACKGROUND: The effect of radioiodine (131I) in Graves' disease (GD) is probably due to the direct physical destruction of thyrocytes by beta radiation, and by the indirect action through stimulation of apoptosis in these cells. The aim of our study was to investigate the changes in serum concentrations of sFas and sFasL as stimulators of apoptosis, and Bcl-2 as an inhibitor of apoptosis in patients with GD following 131I administration. MATERIAL AND METHODS: The study was performed on 30 patients with GD (29 female and 1 male aged 25-45). All patients were euthyroid (biochemical and clinical) prior to radioiodine therapy. The target absorbed dose ranged between 90 and 160 Gy. We assessed markers of apoptosis and hormone concentrations (fT3, fT4 and TSH) in the following manner: before 131I administration, then two weeks, one month, two, three, four, and five months after 131I administration. RESULTS: After four months, the concentrations of sFas and sFasL rose by 50% and decreased during the next month. Pretherapeutic concentrations of Bcl-2 were elevated, and peaked two weeks after ingestion, showing a gradual decrease with time. We found a significant increase in serum TSH, and a decrease of fT3 and fT4 concentrations by the end of the third month of radioiodine therapy. CONCLUSIONS: Decreases in serum levels of sFas and sFasL and increases of Bcl-2 are regarded as characteristic for GD patients before radioiodine therapy. Radioiodine therapy reverses the ratio of estimated markers after four months. The concentrations of hormones reflect actual thyroid function, whereas concentrations of markers of apoptosis may suggest morphological changes.
BACKGROUND: The effect of radioiodine (131I) in Graves' disease (GD) is probably due to the direct physical destruction of thyrocytes by beta radiation, and by the indirect action through stimulation of apoptosis in these cells. The aim of our study was to investigate the changes in serum concentrations of sFas and sFasL as stimulators of apoptosis, and Bcl-2 as an inhibitor of apoptosis in patients with GD following 131I administration. MATERIAL AND METHODS: The study was performed on 30 patients with GD (29 female and 1 male aged 25-45). All patients were euthyroid (biochemical and clinical) prior to radioiodine therapy. The target absorbed dose ranged between 90 and 160 Gy. We assessed markers of apoptosis and hormone concentrations (fT3, fT4 and TSH) in the following manner: before 131I administration, then two weeks, one month, two, three, four, and five months after 131I administration. RESULTS: After four months, the concentrations of sFas and sFasL rose by 50% and decreased during the next month. Pretherapeutic concentrations of Bcl-2 were elevated, and peaked two weeks after ingestion, showing a gradual decrease with time. We found a significant increase in serum TSH, and a decrease of fT3 and fT4 concentrations by the end of the third month of radioiodine therapy. CONCLUSIONS: Decreases in serum levels of sFas and sFasL and increases of Bcl-2 are regarded as characteristic for GDpatients before radioiodine therapy. Radioiodine therapy reverses the ratio of estimated markers after four months. The concentrations of hormones reflect actual thyroid function, whereas concentrations of markers of apoptosis may suggest morphological changes.