title: Are women at an increased risk of gestational thyrotoxicosis?
abstract: OBJECTIVE
  To evaluate the relative importance of thyroid hormones and human chorionic gonadotropin in relation to the risk of gestational thyrotoxicosis in Saudi women living in Jeddah, Kingdom of Saudi Arabia.
  
  
  METHODS
  A prospective study was conducted on Saudi healthy pregnant women (N=406) at 12-15 weeks of gestation and compared with healthy non-pregnant controls (N=200). Maternal serum levels of free thyroxine free triiodothyronine, thyrotropin, human chorionic gonadotropin and free b-human chorionic gonadotropin together with urinary iodine excretion were determined. Analysis of variance was used to examine differences among the groups for different variables and the Bonferroni criterion was used when significance tests were made.
  
  
  RESULTS
  Pregnant women were classified into 2 groups according to the lower limit of serum thyrotropin levels in non-pregnant euthyroid controls at >= 0.3 mIU/L (Group one) or < 0.30 mIU/L (Group 2). Suppressed levels of serum thyrotropin (< 0.30 mIU/L) were found in 11.1% of pregnant women which was accompanied by significant increases in free thyroxine (P<0.001), free triiodothyronine (P < 0.05), human chorionic gonadotropin (P<0.001) and b-human chorionic gonadotropin (P<0.001). A significant negative correlation between serum levels of thyrotropin and that of human chorionic gonadotropin (r=-0.381, P<0.001) was observed. The relative risk of having a serum thyrotropin level of < 0.30 mIU/L was 4.89 (P<0.001) for the pregnant women examined as compared with non-pregnant controls. Approximately 5.6% of the women examined exhibited biochemical evidence of thyrotoxicosis.
  
  
  CONCLUSIONS
  The results of the present study show that Saudi pregnant women are at risk of developing biochemical evidence of thyrotoxicosis during early gestation, and thus, are likely to be at greater risk of clinically evident gestational thyrotoxicosis and hyperemesis gravidarum. Genetically determined differences in the synthesis or metabolism of human chorionic gonadotropin isoforms, or both may contribute to this increased risk.
authors.affiliation: Department of Clinical Biochemistry and Laboratory of Medicine, New Jeddah Clinic Hospital, Kingdom of Saudi Arabia. ardawims@yahoo.com
authors.forename: Mohammed Salleh M
authors.initials: MS
authors.lastname: Ardawi
authors.forename: Hassan A
authors.initials: HA
authors.lastname: Nasrat
authors.forename: Abdulrahim A
authors.initials: AA
authors.lastname: Rouzi
authors.forename: Bader E
authors.initials: BE
authors.lastname: Mustafa
mesh_terms: D000328:Adult; D006063:Chorionic Gonadotropin / Q000097:blood; D018997:Chorionic Gonadotropin, beta Subunit, Human / Q000097:blood; D005260:Female; D006801:Humans; D007455:Iodine / Q000652:urine; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood*; D012529:Saudi Arabia / Q000453:epidemiology; D013960:Thyroid Function Tests; D013963:Thyroid Hormones / Q000097:blood; D013971:Thyrotoxicosis / Q000097:blood / Q000150:complications* / Q000453:epidemiology
chemical_list: D006063:Chorionic Gonadotropin; D018997:Chorionic Gonadotropin, beta Subunit, Human; D013963:Thyroid Hormones; D007455:Iodine