title: The insulin-like growth axis in patients with autoimmune thyrotoxicosis: effect of antithyroid drug treatment.
abstract: OBJECTIVE
  Hyperthyroidism is associated with altered growth hormone (GH) secretion. Many patients with thyroid dysfunction experience several poorly described complications such as symptoms and signs also seen in patients with growth hormone deficiency (GHD). We have therefore prospectively evaluated a possible relationship between the thyroid function, body composition, leptin levels and insulin-like growth factor (IGF) related peptides in patients with Graves' disease. DESIGN, PATIENTS, AND MEASUREMENTS: In a prospective group of 24 fasting female patients with Graves' disease (mean age (CI 95%): 40 years (33-47)), we measured serum thyroxine, triiodothyronine, thyrotropine (TSH), TSH receptor antibodies, anti-thyroid peroxidase, leptin, body composition, body mass index (BMI) and IGF-related peptides at diagnosis and after 12 months of treatment with thiamazol (ATD).
  
  
  RESULTS
  In thyrotoxic patients IGF-I plus IGF-II correlated positively with IGFBP-3 at baseline (r = 0.90, p < 0.1 x 10(16)) and after 12 months follow-up (r = 0.87, p < 0.1 x 10(-16)). In the thyrotoxic state total IGF-I, IGF-II, IGF binding protein 3 (IGFBP-3) and acid-labile subunit (ALS) but not free IGF-I decreased significantly from 223 microg/L (189-260) (mean (CI 95%), 877 microg/L (801-953), 4165 microg/L (3772-4577) and 22 mg/L (18-26)) to 198 microg/L (172-226), 788 microg/L (711-865), 3431 microg/L (3135-3741) and 19 mg/L (16-26) (p <0.006), respectively, after 12 months of ATD despite an increase in BMI from 22 (21-23) to 23 kg/m(2) (22-25) (p < 0.0004) but no significant changes in leptin.
  
  
  CONCLUSIONS
  The complex IGF systems seemed intact in thyrotoxic patients but change in body composition and the regulation of leptin and insulin secretion during treatment of autoimmune thyroid disease influence IGF-related peptides leaving the patient in a state somewhat similar to partial GHD, but the mechanism behind these alterations remains unclear.
authors.affiliation: Department of Endocrinology, PE-2131, University Hospital, Rigshospitalet, Blegdamsvej 9, Copenhagen DK-2100, Denmark. tzb@dadlnet.dk
authors.forename: T
authors.initials: T
authors.lastname: Zimmermann-Belsing
authors.forename: A
authors.initials: A
authors.lastname: Juul
authors.forename: J
authors.initials: J
authors.lastname: Juul Holst
authors.forename: U
authors.initials: U
authors.lastname: Feldt-Rasmussen
mesh_terms: D000328:Adult; D001823:Body Composition; D005260:Female; D006111:Graves Disease / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D018828:Immunoglobulins, Thyroid-Stimulating / Q000097:blood; D007328:Insulin / Q000097:blood / Q000378:metabolism; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000378:metabolism; D007335:Insulin-Like Growth Factor II / Q000032:analysis / Q000378:metabolism; D007453:Iodide Peroxidase / Q000097:blood / Q000378:metabolism; D020738:Leptin / Q000097:blood / Q000378:metabolism; D008297:Male; D008713:Methimazole / Q000627:therapeutic use; D008875:Middle Aged; D013002:Somatomedins / Q000032:analysis*; D013963:Thyroid Hormones / Q000097:blood / Q000378:metabolism; D013971:Thyrotoxicosis / Q000188:drug therapy* / Q000378:metabolism
chemical_list: D018828:Immunoglobulins, Thyroid-Stimulating; D007328:Insulin; D018972:Insulin-Like Growth Factor Binding Protein 3; D020738:Leptin; D013002:Somatomedins; D013963:Thyroid Hormones; D008713:Methimazole; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; D007453:Iodide Peroxidase