L Tomisti1, C Urbani1, G Rossi2, F Latrofa1, C Sardella1, L Manetti1, I Lupi1, C Marcocci1, L Bartalena3, O Curzio2, E Martino1, F Bogazzi4. 1. Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Ospedale Cisanello, Via Paradisa, 2, 56124, Pisa, Italy. 2. Unit of Epidemiology and Biostatistics, Institute of Clinical Physiology, National Research Council, 56184, Pisa, Italy. 3. Endocrine Unit, Department of Clinical and Experimental Medicine, University of Insubria, 21100, Varese, Italy. 4. Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Ospedale Cisanello, Via Paradisa, 2, 56124, Pisa, Italy. fbogazzi@hotmail.com.
Abstract
PURPOSE: It is widely accepted that type 2 amiodarone-induced thyrotoxicosis (AIT) generally occurs in patients with a normal thyroid gland without signs of thyroid autoimmunity. However, it is currently unknown if the presence of anti-thyroglobulin (TgAb) and/or anti-thyroperoxidase antibodies (TPOAb) in AIT patients without other signs of an underlying thyroid disease may impair the response to glucocorticoid therapy. METHODS: We performed a pilot retrospective cohort study with matched-subject design and an equivalence hypothesis, comparing the response to glucocorticoid therapy between 20 AIT patients with a normal thyroid gland, low radioiodine uptake, undetectable TSH receptor antibodies and positive TgAb and/or TPOAb (Ab+ group), and 40 patients with the same features and absent thyroid antibodies (Ab- group). RESULTS: The mean cure time was 54 ± 68 days in the Ab+ group and 55 ± 49 days in the Ab- group (p = 0.63). The equivalence test revealed an equivalent cure rate after 60, 90 and 180 days (p = 0.67, 0.88 and 0.278, respectively). The occurrence of permanent hypothyroidism was higher in the Ab+ group than in the Ab- group (26.3 vs 5.13 %, p = 0.032). CONCLUSIONS: The presence of TgAb and/or TPOAb does not affect the response to glucocorticoid therapy, suggesting that the patients with features of destructive form of AIT should be considered as having a type 2 AIT irrespective of the presence of TGAb or TPOAb. These patients have a higher risk of developing hypothyroidism after the resolution of thyrotoxicosis and should be monitored accordingly.
PURPOSE: It is widely accepted that type 2 amiodarone-induced thyrotoxicosis (AIT) generally occurs in patients with a normal thyroid gland without signs of thyroid autoimmunity. However, it is currently unknown if the presence of anti-thyroglobulin (TgAb) and/or anti-thyroperoxidase antibodies (TPOAb) in AIT patients without other signs of an underlying thyroid disease may impair the response to glucocorticoid therapy. METHODS: We performed a pilot retrospective cohort study with matched-subject design and an equivalence hypothesis, comparing the response to glucocorticoid therapy between 20 AIT patients with a normal thyroid gland, low radioiodine uptake, undetectable TSH receptor antibodies and positive TgAb and/or TPOAb (Ab+ group), and 40 patients with the same features and absent thyroid antibodies (Ab- group). RESULTS: The mean cure time was 54 ± 68 days in the Ab+ group and 55 ± 49 days in the Ab- group (p = 0.63). The equivalence test revealed an equivalent cure rate after 60, 90 and 180 days (p = 0.67, 0.88 and 0.278, respectively). The occurrence of permanent hypothyroidism was higher in the Ab+ group than in the Ab- group (26.3 vs 5.13 %, p = 0.032). CONCLUSIONS: The presence of TgAb and/or TPOAb does not affect the response to glucocorticoid therapy, suggesting that the patients with features of destructive form of AIT should be considered as having a type 2 AIT irrespective of the presence of TGAb or TPOAb. These patients have a higher risk of developing hypothyroidism after the resolution of thyrotoxicosis and should be monitored accordingly.
Authors: Georgios K Markantes; Marina A Michalaki; George A Vagenakis; Fotini N Lamari; Efthymia Pitsi; Maria Eliopoulou; Nicholas G Beratis; Kostas B Markou Journal: Eur Thyroid J Date: 2019-07-15
Authors: E A Troshina; E A Panfilova; M S Mikhina; I V Kim; E S Senyushkina; A A Glibka; B M Shifman; A A Larina; M S Sheremeta; M V Degtyarev; P O Rumyanstsev; N S Kuznetzov; G A Melnichenko; I I Dedov Journal: Probl Endokrinol (Mosk) Date: 2021-04-12