title: Exogenous subclinical hyperthyroidism impairs endothelial function in nodular goiter patients.
abstract: BACKGROUND
  Exogenous subclinical hyperthyroidism is associated with cardiovascular and metabolic changes. The aim of this study was to evaluate the effect of levothyroxine (LT4) suppression on endothelial function and insulin sensitivity in euthyroid nodular goiter patients.
  
  
  METHODS
  Twenty-two euthyroid patients with multinodular goiter (MNG) and 22 matched healthy controls were studied. LT4 was administered in doses ranging from 50 to 150 microg/day to reach target serum thyroid-stimulating hormone (TSH) levels <0.5 mIU/L. Patients were studied before and after 8 weeks after the target TSH level <0.5 mIU/L. The control group was studied twice, 16 weeks apart. Flow mediated vasodilatation (FMD), insulin sensitivity index (ISI), lipid peroxidation, and high-sensitivity C-reactive protein (hsCRP) were the outcome measures.
  
  
  RESULTS
  LT4 treatment significantly suppressed TSH levels to 0.2 +/- 0.1 mIU/L (minimum and maximum range was 0.05-0.3 mIU/L). FMD decreased from 10.7 +/- 2.7% to 5.4 +/- 1.7% (p < 0.001) and mean ISI decreased from 2.56 +/- 1.10 to 1.41 +/- 0.50 (p < 0.001) with LT4 treatment in the MNG group. Lipid peroxidation measured as thiobarbituric acid reactive substances (Tbars) (p < 0.05), and hsCRP (p < 0.001) levels significantly increased compared to the baseline in the MNG group. FMD measurement inversely correlated with free T4 (p = 0.008) and Tbars (p = 0.004), and positively correlated with ISI (p = 0.004). Serum Tbars and hsCRP were independent predictors of FMD (p = 0.004) in multivariate analysis. All results expressed as mean +/- SD.
  
  
  CONCLUSIONS
  TSH suppression therapy with LT4 leading to subclinical hyperthyroidism may cause impaired endothelial function, increased oxidative stress, and decreased insulin sensitivity in euthyroid nodular goiter patients.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Internal Medicine, Marmara University Medical School, Istanbul, Turkey. dilekgogas@marmara.edu.tr
authors.forename: Dilek Gogas
authors.initials: DG
authors.lastname: Yavuz
authors.forename: Dilek
authors.initials: D
authors.lastname: Yazici
authors.forename: Ahmet
authors.initials: A
authors.lastname: Toprak
authors.forename: Oguzhan
authors.initials: O
authors.lastname: Deyneli
authors.forename: Hasan
authors.initials: H
authors.lastname: Aydin
authors.forename: Meral
authors.initials: M
authors.lastname: Yüksel
authors.forename: Sema
authors.initials: S
authors.lastname: Akalin
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D004727:Endothelium / Q000473:pathology*; D005260:Female; D006044:Goiter, Nodular / Q000150:complications* / Q000175:diagnosis*; D006801:Humans; D006980:Hyperthyroidism / Q000150:complications* / Q000175:diagnosis*; D007328:Insulin / Q000378:metabolism; D015227:Lipid Peroxidation; D008875:Middle Aged; D018384:Oxidative Stress; D013961:Thyroid Gland / Q000276:immunology / Q000378:metabolism; D013974:Thyroxine / Q000037:antagonists & inhibitors
chemical_list: D007328:Insulin; D002097:C-Reactive Protein; D013974:Thyroxine