title: Iodine treatment in children with subclinical hypothyroidism due to chronic iodine deficiency decreases thyrotropin and C-peptide concentrations and improves the lipid profile.
abstract: BACKGROUND
  Chronic iodine deficiency (ID) increases thyrotropin (TSH) concentrations and produces a thyroid hormone pattern consistent with subclinical hypothyroidism (ScH). ScH may be associated with cardiovascular disease risk factors. Thus, the study aim was to determine if iodine treatment of children with elevated TSH concentrations due to ID would affect their lipid profile, insulin (C-peptide) levels, and/or subclinical inflammation.
  
  
  METHODS
  In controlled intervention trials of oral iodized oil or iodized salt, 5-14-year-old children from Morocco, Albania, and South Africa with TSH concentrations > or = 2.5 mU/L (n = 262) received 400 mg iodine as oral iodized oil or household distribution of iodized salt containing 25 microg iodine/g salt. At baseline and after 5 or 6 months, urinary iodine (UI) and blood concentrations of total thyroxine, TSH, C-reactive protein (CRP), C-peptide, and lipids were measured.
  
  
  RESULTS
  Median (range) UI at baseline was 46 (2-601) microg/L. Compared to the control group, iodine treatment significantly increased UI and total thyroxine and decreased TSH, C-peptide, and total and low-density lipoprotein cholesterol. The mean low-density lipoprotein/high-density lipoprotein cholesterol ratio fell from 3.3 to 2.4 after iodine treatment (p < 0.001). Iodine treatment had no significant effect on concentrations of high-density lipoprotein cholesterol, triglycerides, or C-reactive protein.
  
  
  CONCLUSIONS
  Correction of ID-associated ScH improves the insulin and lipid profile and may thereby reduce risk for cardiovascular disease. This previously unrecognized benefit of iodine prophylaxis may be important because ID remains common in rapidly developing countries with increasing rates of obesity and cardiovascular disease.
authors.affiliation: Laboratory for Human Nutrition, Swiss Federal Institute of Technology, CH-8092 Zürich, Switzerland. michael.zimmermann@ilw.agrl.ethz.ch
authors.forename: Michael B
authors.initials: MB
authors.lastname: Zimmermann
authors.forename: Isabelle
authors.initials: I
authors.lastname: Aeberli
authors.forename: Alida
authors.initials: A
authors.lastname: Melse-Boonstra
authors.forename: Lindita
authors.initials: L
authors.lastname: Grimci
authors.forename: John
authors.initials: J
authors.lastname: Bridson
authors.forename: Noureddine
authors.initials: N
authors.lastname: Chaouki
authors.forename: Xikombiso
authors.initials: X
authors.lastname: Mbhenyane
authors.forename: Pieter L
authors.initials: PL
authors.lastname: Jooste
mesh_terms: D000293:Adolescent; D002096:C-Peptide / Q000097:blood*; D002318:Cardiovascular Diseases / Q000097:blood / Q000453:epidemiology; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000097:blood / Q000188:drug therapy*; D007249:Inflammation / Q000453:epidemiology; D007328:Insulin / Q000097:blood; D007455:Iodine / Q000172:deficiency* / Q000627:therapeutic use* / Q000652:urine; D008055:Lipids / Q000097:blood*; D008297:Male; D012307:Risk Factors; D013972:Thyrotropin / Q000097:blood*; D013974:Thyroxine / Q000097:blood
chemical_list: D002096:C-Peptide; D007328:Insulin; D008055:Lipids; D013972:Thyrotropin; D007455:Iodine; D013974:Thyroxine