C R de Farias1, B R Cardoso2, G M B de Oliveira3, I C de Mello Guazzelli4, R M Catarino5, M C Chammas6, S M F Cozzolino7, M Knobel8. 1. Thyroid Unit and Laboratory of Cellular and Molecular Biology (LIM-25), Division of Endocrinology and Metabolism, University of São Paulo Medical School, Hospital das Clínicas, Av. Dr. Enéas de Carvalho Aguiar, 155, 8th floor, bl 3, PAMB, São Paulo, SP, 05403-900, Brazil. cleyrocha@uol.com.br. 2. Department of Food and Experimental Nutrition, Faculty of Pharmaceutical Science, University of São Paulo, Av. Prof. Lineu Prestes 580, bl 14, Cidade Universitária, São Paulo, SP, 05508-000, Brazil. baritacardoso@gmail.com. 3. Ultrasound Unit, Department of Radiology, University of São Paulo Medical School, Hospital das Clínicas, Av Dr Enéas de Carvalho Aguiar, 255, 3rd floor, Unit 013, São Paulo, SP, 05403-900, Brazil. giovannambo@hotmail.com. 4. Laboratory of Cellular and Molecular Endocrinology, LIM-25, Division of Endocrinology and Metabolism, University of São Paulo Medical School, Av. Dr. Arnaldo 455, 4th floor, Units 4305/4307, São Paulo, SP, 01246-903, Brazil. belmello@usp.br. 5. Hematology and Biochemistry, Center of Pathology, Adolpho Lutz Institute, Av. Dr. Arnaldo 351, 7th floor, São Paulo, SP, 01246-000, Brazil. rmcatarino@yahoo.com.br. 6. Ultrasound Unit, Department of Radiology, University of São Paulo Medical School, Hospital das Clínicas, Av. Dr. Enéas de Carvalho Aguiar, 255, 3rd floor, Unit 013, São Paulo, SP, 05403-010, Brazil. mcchammas@hotmail.com. 7. Department of Food and Experimental Nutrition, Faculty of Pharmaceutical Science, University of São Paulo, Av. Prof. Lineu Prestes 580, bl 14, Cidade Universitária, São Paulo, SP, 05508-000, Brazil. smfcozzo@usp.br. 8. Thyroid Unit and Laboratory of Cellular and Molecular Biology (LIM-25), Division of Endocrinology and Metabolism, University of São Paulo Medical School, Hospital das Clínicas, Av. Dr. Enéas de Carvalho Aguiar, 155, 8th floor, bl 3, PAMB, São Paulo, SP, 05403-900, Brazil. meyer.knobel@hc.fm.usp.br.
Abstract
PURPOSE: To analyze the impact of selenium supplementation on serum antiTPO levels and thyroid echogenicity in patients with CAT, evaluating the response in subgroups with different GPx1 genotypes. METHODS:CAT patients (n = 55) with positive antiTPO were randomized to selenomethionine (SeMet) 200 μg daily (n = 28) or placebo (n = 27) for 3 months. Assessments included GPx1 genotyping at baseline and serum levels of plasma selenium, erythrocyte GPx1 activity, antiTPO and thyroid echogenicity at baseline, and 3 and 6 months. RESULTS: In the SeMet group, the increase in plasma levels of selenium and erythrocyte GPx1 activity was similar among patients with different GPx1 genotypes. In the overall cohort, patients randomized to SeMet showed a 5 % decrease in antiTPO levels at 3 months (p = non-significant) and 20 % at 6 months (p < 0.001 versus 3 months). In contrast, patients in the placebo group did not show significant changes in antiTPO levels at any time point. Subgroup analysis showed that patients with different GPx1 genotypes presented comparable responses in antiTPO levels and echogenicity index to SeMet. CONCLUSIONS:Selenium supplementation decreased serum antiTPO levels in CAT patients, with similar response among patients with different GPx1 genotypes.
RCT Entities:
PURPOSE: To analyze the impact of selenium supplementation on serum antiTPO levels and thyroid echogenicity in patients with CAT, evaluating the response in subgroups with different GPx1 genotypes. METHODS: CAT patients (n = 55) with positive antiTPO were randomized to selenomethionine (SeMet) 200 μg daily (n = 28) or placebo (n = 27) for 3 months. Assessments included GPx1 genotyping at baseline and serum levels of plasma selenium, erythrocyte GPx1 activity, antiTPO and thyroid echogenicity at baseline, and 3 and 6 months. RESULTS: In the SeMet group, the increase in plasma levels of selenium and erythrocyte GPx1 activity was similar among patients with different GPx1 genotypes. In the overall cohort, patients randomized to SeMet showed a 5 % decrease in antiTPO levels at 3 months (p = non-significant) and 20 % at 6 months (p < 0.001 versus 3 months). In contrast, patients in the placebo group did not show significant changes in antiTPO levels at any time point. Subgroup analysis showed that patients with different GPx1 genotypes presented comparable responses in antiTPO levels and echogenicity index to SeMet. CONCLUSIONS:Selenium supplementation decreased serum antiTPO levels in CAT patients, with similar response among patients with different GPx1 genotypes.
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