title: Cardiac changes associated with growth hormone therapy among children treated with anthracyclines.
abstract: OBJECTIVE
  The objective was to assess the cardiac effects of growth hormone (GH) therapy. Anthracycline-treated childhood cancer survivors frequently have reduced left ventricular (LV) wall thickness and contractility, and GH therapy may affect these factors.
  
  
  METHODS
  We examined serial cardiac findings for 34 anthracycline-treated childhood cancer survivors with several years of GH therapy and baseline cardiac z scores similar to those of a comparison group (86 similar cancer survivors without GH therapy).
  
  
  RESULTS
  LV contractility was decreased among GH-treated patients before, during, and after GH therapy (-1.08 SD below the age-adjusted population mean before therapy and -1.88 SD 4 years after therapy ceased, with each value depressed below normal). Contractility was higher in the control group than in the GH-treated group, with this difference being nearly significant. The GH-treated children had thinner LV walls before GH therapy (-1.38 SD). Wall thickness increased during GH therapy (from -1.38 SD to -1.09 SD after 3 years of GH therapy), but the effect was lost shortly after GH therapy ended and thickness diminished over time (-1.50 SD at 1 year after therapy and -1.96 SD at 4 years). During GH therapy, the wall thickness for the GH-treated group was greater than that for the control group; however, by 4 years after therapy, there was no difference between the GH-treated group and the control group.
  
  
  CONCLUSIONS
  GH therapy among anthracycline-treated survivors of childhood cancer increased LV wall thickness, but the effect was lost after therapy was discontinued. The therapy did not affect the progressive LV dysfunction.
authors.affiliation: Department of Pediatrics, Miller School of Medicine, University of Miami, Holtz Children's Hospital, Sylvester Comprehensive Cancer Center, Miami, Florida, USA. slipshultz@med.miami.edu
authors.forename: Steven E
authors.initials: SE
authors.lastname: Lipshultz
authors.forename: Sarah A
authors.initials: SA
authors.lastname: Vlach
authors.forename: Stuart R
authors.initials: SR
authors.lastname: Lipsitz
authors.forename: Stephen E
authors.initials: SE
authors.lastname: Sallan
authors.forename: Marcy L
authors.initials: ML
authors.lastname: Schwartz
authors.forename: Steven D
authors.initials: SD
authors.lastname: Colan
mesh_terms: D000293:Adolescent; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D018943:Anthracyclines / Q000008:administration & dosage / Q000009:adverse effects*; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000008:administration & dosage / Q000009:adverse effects*; D001827:Body Height; D002317:Cardiovascular Agents / Q000627:therapeutic use; D002648:Child; D002675:Child, Preschool; D004656:Enalapril / Q000627:therapeutic use; D005260:Female; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced; D007018:Hypopituitarism / Q000139:chemically induced / Q000188:drug therapy / Q000209:etiology; D007223:Infant; D008297:Male; D009200:Myocardial Contraction; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000150:complications / Q000188:drug therapy; D017741:Survivors; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced* / Q000000981:diagnostic imaging / Q000188:drug therapy
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D018943:Anthracyclines; D002317:Cardiovascular Agents; D019382:Human Growth Hormone; D004656:Enalapril