title: Post-ablative hypothyroidism.
abstract: OBJECTIVE
  To determine the incidence of hypothyroidism following radioactive iodine (RAI) treatment for hyperthyroidism and to study the relationship between pretreatment RAI uptake and treatment dose and the subsequent development of hypothyroidism.
  
  
  METHODS
  Retrospective chart review of patients treated with RAI for hyperthyroidism between 1995 and 2000. 180 charts were reviewed; 41 met the inclusion criteria. Data were collected regarding the cause of hyperthyroidism, initial RAI uptake, initial dose of RAI, number of RAI treatments, and post treatment thyroid status.
  
  
  RESULTS
  Patients in toxic nodular goiter group had significantly lower 24-hour RAI-123 uptake as compared to those with Graves' disease. However patients with Graves' disease received significantly lower RAI dose in comparison to those with toxic nodular goiters. Cure rates following RAI administration were similar in both groups. 70% of patients with Graves' disease developed post-ablative hypothyroidism as compared to 42% in toxic nodular goiter group (p = 0.086). There was no relationship between the dose of RAI or pretreatment RAI uptake and the likelihood of developing hypothyroidism.
  
  
  CONCLUSIONS
  We found that, within our study population, post-ablative hypothyroidism tended to be more prevalent in patients with Graves' disease as compared to those with toxic nodular goiter. However cure rates following RAI administration were similar in both groups. We also found that neither the magnitude of the administered RAI dose nor the pre-treatment RAI uptake predicted the development of subsequent hypothyroidism.
authors.affiliation: Joan C. Edwards School of Medicine, Marshall University, Huntington, USA.
authors.forename: Abid
authors.initials: A
authors.lastname: Yaqub
authors.forename: Muhammad I
authors.initials: MI
authors.lastname: Choudhry
authors.forename: Jennifer
authors.initials: J
authors.lastname: Wheaton
authors.forename: Todd
authors.initials: T
authors.lastname: Gress
mesh_terms: D000328:Adult; D000368:Aged; D013956:Antithyroid Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000493:pharmacokinetics; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D005260:Female; D006044:Goiter, Nodular / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006111:Graves Disease / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006980:Hyperthyroidism / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D007037:Hypothyroidism / Q000139:chemically induced / Q000453:epidemiology / Q000378:metabolism; D007049:Iatrogenic Disease; D015994:Incidence; D007457:Iodine Radioisotopes / Q000008:administration & dosage / Q000009:adverse effects / Q000493:pharmacokinetics; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D013963:Thyroid Hormones / Q000097:blood*; D014018:Tissue Distribution; D016896:Treatment Outcome
chemical_list: D013956:Antithyroid Agents; D007457:Iodine Radioisotopes; D013963:Thyroid Hormones