title: Qualitative and quantitative impact of protective glucocorticoid therapy on the effective 131I half-life in radioiodine therapy for Graves disease.
abstract: This aim of this retrospective study was to determine the impact of glucocorticoid therapy on the effective (131)I half-life in radioiodine therapy for Graves disease.
  
  
  METHODS
  Three hundred fifteen consecutive Graves disease patients undergoing radioiodine therapy at our institution between August 2004 and January 2009 were enrolled. We investigated the influences of thyroid state (hypothyroidism, euthyroidism, hyperthyroidism), antithyroid drug dose before (131)I therapy, thyroid-stimulating hormone receptor antibody (TRAb) level, and qualitative and quantitative factors of prednisolone therapy on the effective (131)I half-life, applying univariate (paired t test) and multivariate (multiple-regression) analyses.
  
  
  RESULTS
  Multivariate analyses revealed independent significant effects of the thyroid metabolic state (P = 0.004), antithyroid drugs (P < 0.001), presence of TRAb (P = 0.004), and glucocorticoids (P = 0.046) on thyroidal radioiodine half-life. Compared with euthyroidism, thyrotoxicosis and hypothyroidism reduced the effective half-life; high doses of antithyroid drugs and high TRAb levels had the same effect. Also, glucocorticoid therapy shortened the effective thyroidal radioiodine half-life in a dose-dependent manner. Pharmacologically, this effect is attributable to the prednisolone-induced increase of renal plasma (131)I clearance and the resulting reduction of plasma (131)I available for reuptake into the thyroid during radioiodine therapy.
  
  
  CONCLUSIONS
  Oral treatment with prednisolone results in a reduction of effective thyroidal (131)I half-life in Graves disease, especially at higher doses.
authors.affiliation: Department of Nuclear Medicine, University of Düsseldorf, Düsseldorf, Germany. h.hautzel@fz-juelich.de
authors.forename: Hubertus
authors.initials: H
authors.lastname: Hautzel
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Pisar
authors.forename: Nahid
authors.initials: N
authors.lastname: Yazdan-Doust
authors.forename: Matthias
authors.initials: M
authors.lastname: Schott
authors.forename: Markus
authors.initials: M
authors.lastname: Beu
authors.forename: Hans-Wilhelm
authors.initials: HW
authors.lastname: Müller
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000906:Antibodies / Q000032:analysis; D013956:Antithyroid Agents / Q000627:therapeutic use; D004347:Drug Interactions; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006111:Graves Disease / Q000188:drug therapy* / Q000532:radiotherapy*; D006207:Half-Life; D006801:Humans; D007457:Iodine Radioisotopes / Q000493:pharmacokinetics* / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use*; D011989:Receptors, Thyrotropin / Q000276:immunology; D012044:Regression Analysis; D013961:Thyroid Gland / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D000906:Antibodies; D013956:Antithyroid Agents; D005938:Glucocorticoids; D007457:Iodine Radioisotopes; D011989:Receptors, Thyrotropin; D011239:Prednisolone