title: [The specific features of thyrotoxicosis and euthyroid hyperthyroxinemia developed due to the use of cordarone].
abstract: Thyrotoxicosis (TT) is one of the thyroid (T) dysfunctions occurring with the use of cordarone. The clinical features of TT were studied in cordarone-treated patients living in Moscow and its regions (mild and moderate iodine deficiency regions). The patients were examined by using currently available procedures for measuring thyroid-stimulating hormone, free thyroxine, free triiodothyronine, antibodies to TH, TPO, interleukin-6 (IL-6), and C-reactive protein (CRP), and by employing T ultrasound study, Holter ECG monitoring. TT was ascertained to develop in the presence of both the pathologically altered (16/23, 69%) and intact T (7/23, 31%). Examining the course of cardiac arrhythmias (CA) in developed TT has established that this condition gives rise to their recurrence. As compared with the control group, the patients with TT were not found to have higher levels of IL-6 and CRP (p > 0.05; Mann-Whitney test). Therapy with thyrostatic agents alone or in combination with glucocorticosteroids normalizes the levels of thyroid hormonesfollowing, on the average, 2-3 months. Euthyroid hyperthyxinemia (EHT) is frequently recorded with the use of cordarone. Examination of 20 patients with EHT has revealed organic pathology in 13 (65%) patients and its absence in 7 (35%). Recurrences of prior CA have not been found in EHT (p < 0.05; McNemar test). The confidence interval for the difference of relative frequencies of signs did not include 0). Thus, TT is a condition that leads to the fact that cordarone loses its antiarrhythmic effects and TT requires compulsory treatment. If required, therapy should be performed during the continued administration of the drug. EHT is not thyrotoxicosis, which is to be followed up.
authors.forename: N V
authors.initials: NV
authors.lastname: Molashenko
authors.forename: N Iu
authors.initials: NIu
authors.lastname: Sviridenko
authors.forename: N M
authors.initials: NM
authors.lastname: Platonova
authors.forename: G S
authors.initials: GS
authors.lastname: Kolesnikova
authors.forename: S P
authors.initials: SP
authors.lastname: Golitsyn
authors.forename: S A
authors.initials: SA
authors.lastname: Bakalov
authors.forename: S E
authors.initials: SE
authors.lastname: Serdiuk
authors.forename: V P
authors.initials: VP
authors.lastname: Masenko
authors.forename: S P
authors.initials: SP
authors.lastname: Domogadskiĭ
mesh_terms: D000638:Amiodarone / Q000009:adverse effects* / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects* / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000503:physiopathology; D001323:Autoantibodies / Q000097:blood; D001783:Blood Flow Velocity; D004562:Electrocardiography; D005260:Female; D006801:Humans; D006981:Hyperthyroxinemia / Q000097:blood / Q000139:chemically induced* / Q000503:physiopathology; D007453:Iodide Peroxidase / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013954:Thyroglobulin / Q000276:immunology; D013961:Thyroid Gland / Q000098:blood supply / Q000000981:diagnostic imaging / Q000378:metabolism; D013971:Thyrotoxicosis / Q000097:blood / Q000139:chemically induced* / Q000503:physiopathology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D018615:Ultrasonography, Doppler, Color
chemical_list: D000889:Anti-Arrhythmia Agents; D001323:Autoantibodies; D014284:Triiodothyronine; D013972:Thyrotropin; D013954:Thyroglobulin; D007453:Iodide Peroxidase; D000638:Amiodarone; D013974:Thyroxine