title: N-terminal-pro-B-type natriuretic peptide (NT-pro-BNP) in different thyroid function states.
abstract: OBJECTIVE
  N-terminal B-type natriuretic peptide (NT-pro-BNP) is secreted from the cardiac ventricles in response to volume expansion and pressure overload, and serum levels are elevated in systolic heart failure. The aim of this study was to evaluate the influence of thyroid function on NT-pro-BNP.
  
  
  METHODS
  Patients with overt or subclinical thyroid disease were evaluated before and after treatment for their dysthyroid state.
  
  
  METHODS
  Seventeen overt and 21 subclinical hypothyroid patients together with six subclinical and 13 overt hyperthyroid patients without cardiac disease were included. Subclinical states had, by definition, free T4 and free T3 estimates within reference ranges.
  
  
  METHODS
  Serum levels of NT-pro-BNP and thyroid hormones were measured, and in 31 patients resting cardiac output was measured by impedance cardiography in the untreated state.
  
  
  RESULTS
  NT-pro-BNP levels were more than four times higher in hyperthyroid than hypothyroid patients, with mean values of 30 and 7 pmol/l, respectively (P < 0.001). Serum NT-pro-BNP levels correlated to the thyroid function (vs. free T4 estimate: r = 0.52, P < 0.0001, n = 57). Treatment resulted in significant increases in NT-pro-BNP in both hypothyroid groups, and decreases in both hyperthyroid groups. A multiple linear regression analysis demonstrated that free T4 and free T3 (P < 0.001) estimates were independently associated with a high serum NT-pro-BNP, whereas cardiac output and resting pulse rate were not.
  
  
  CONCLUSIONS
  Serum NT-pro-BNP levels are affected by thyroid function. This seems due to a direct stimulatory effect of thyroid hormones.
authors.affiliation: Department of Cardiology and Endocrinology E, Frederiksberg University Hospital, Frederiksberg, Denmark.
authors.forename: Marianne
authors.initials: M
authors.lastname: Schultz
authors.forename: Jens
authors.initials: J
authors.lastname: Faber
authors.forename: Caroline
authors.initials: C
authors.lastname: Kistorp
authors.forename: Anne
authors.initials: A
authors.lastname: Jarløv
authors.forename: Frants
authors.initials: F
authors.lastname: Pedersen
authors.forename: Niels
authors.initials: N
authors.lastname: Wiinberg
authors.forename: Per
authors.initials: P
authors.lastname: Hildebrandt
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D013956:Antithyroid Agents / Q000627:therapeutic use; D002302:Cardiac Output; D005260:Female; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood / Q000188:drug therapy; D007037:Hypothyroidism / Q000097:blood / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain; D009419:Nerve Tissue Proteins / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*; D012044:Regression Analysis; D013959:Thyroid Diseases / Q000097:blood* / Q000188:drug therapy; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood / Q000627:therapeutic use; D014284:Triiodothyronine / Q000097:blood
chemical_list: D013956:Antithyroid Agents; D009419:Nerve Tissue Proteins; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D014284:Triiodothyronine; D020097:Natriuretic Peptide, Brain; D013972:Thyrotropin; D013974:Thyroxine