title: The effect of L-thyroxine substitution on lipid profile, glucose homeostasis, inflammation and coagulation in patients with subclinical hypothyroidism.
abstract: OBJECTIVE
  Subclinical hypothyroidism (SH) is associated with increased risk for atherosclerosis, mainly attributable to dyslipidaemia and hypercoagulability. However, conflicting data exist regarding the effect of L-thyroxine substitution on these parameters. The purpose of this study was to assess the effect of L-thyroxine therapy on lipidaemic profile, coagulation markers, high-sensitivity C-reactive protein (hsCRP) and glucose homoeostasis in SH patients.
  
  
  METHODS
  It was a prospective open-label study. The following parameters were measured before and 6 months after intervention: anthropometric data, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), apolipoproteins B (apoB) and A1 (apoA1), lipoprotein (a) [Lp(a)], fasting plasma glucose and insulin, homoeostasis model assessment-insulin resistance (HOMA-IR), hsCRP, antithrombin III (AT-III), protein C (PC), protein S (PS), fibrinogen and homocysteine.
  
  
  RESULTS
  Thirty-two patients (30 women) aged 52.1 ± 13.9 years with SH completed the study. Baseline mean TSH levels were 6.79 ± 2.58 mIU/ml. Achievement of euthyroidism significantly reduced systolic blood pressure (BP) in patients with SH (from 135.2 ± 18.5 to 129.7 ± 15.8 mmHg, p = 0.03) and diastolic BP only in those with baseline TSH levels > 7 mIU/ml (from 79.5 ± 9.8 to 72.1 ± 7.3 mmHg, p = 0.03). No significant changes in body weight, TC, LDL-C, HDL-C, TG, apoB, glucose, insulin, HOMA-IR, hsCRP, AT-III, PC, PS, fibrinogen or homocysteine levels were noticed after restoration of euthyroidism, except for a decrease in apoA1 (p = 0.04) and an increase in Lp(a) levels (p = 0.02).
  
  
  CONCLUSIONS
  Except for a reduction in systolic and diastolic BP, thyroid substitution therapy does not affect lipidaemic profile, systematic inflammation, glucose homoeostasis or coagulation in patients with SH.
authors.affiliation: Department of Endocrinology, Hippokration Hospital of Thessaloniki, Thessaloniki, Greece.
authors.forename: P
authors.initials: P
authors.lastname: Anagnostis
authors.forename: Z A
authors.initials: ZA
authors.lastname: Efstathiadou
authors.forename: A
authors.initials: A
authors.lastname: Slavakis
authors.forename: D
authors.initials: D
authors.lastname: Selalmatzidou
authors.forename: M
authors.initials: M
authors.lastname: Poulasouchidou
authors.forename: S
authors.initials: S
authors.lastname: Katergari
authors.forename: E
authors.initials: E
authors.lastname: Karathanasi
authors.forename: F
authors.initials: F
authors.lastname: Dogramatzi
authors.forename: M
authors.initials: M
authors.lastname: Kita
mesh_terms: D000328:Adult; D000368:Aged; D001777:Blood Coagulation / Q000187:drug effects*; D001786:Blood Glucose / Q000187:drug effects*; D002784:Cholesterol / Q000097:blood; D057915:Drug Substitution; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000150:complications / Q000188:drug therapy*; D007249:Inflammation / Q000188:drug therapy*; D008055:Lipids / Q000097:blood; D008875:Middle Aged; D011446:Prospective Studies; D013974:Thyroxine / Q000187:drug effects* / Q000494:pharmacology; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D008055:Lipids; D014280:Triglycerides; D002784:Cholesterol; D013974:Thyroxine