title: Lack of evidence of premature atherosclerosis in untreated severe isolated growth hormone (GH) deficiency due to a GH-releasing hormone receptor mutation.
abstract: BACKGROUND
  GH deficiency (GHD) acquired at adult age as a result of pathological processes of the pituitary gland or the hypothalamus causes changes that are associated with worsening cardiovascular risk. They include increase in abdominal obesity, total and low- density lipoprotein cholesterol, and C-reactive protein. GHD adults also have thickening of the carotid arteries. It has been postulated that GHD is the link between hypopituitarism and the increase in cardiovascular and cerebrovascular mortality observed in hypopituitarism. However, several confounding factors exist, such as associated pituitary deficits and replacement of other hormones or surgical or radiological therapies used to treat the underlying pituitary of hypothalamic pathologies.
  
  
  OBJECTIVE
  The aim of this study was to determine the consequences of lifetime isolated GHD (IGHD) on the metabolic and cardiovascular status of adult members of a large Brazilian cohort with severe IGHD due to a homozygous mutation in the GHRH receptor gene.
  
  
  METHODS
  Twenty-two GH naive adult dwarfs (10 men and 12 women; aged 44 +/- 12 yr) were compared with 22 healthy volunteers (10 men and 12 women; aged 45 +/- 12 yr) living in the same area.
  
  
  RESULTS
  GHD subjects had increased abdominal obesity, higher total and low-density lipoprotein cholesterol, and higher C-reactive protein than controls. They did not have an increase in carotid wall thickness, and there was no evidence of premature atherosclerosis as evaluated by exercise echocardiography.
  
  
  CONCLUSIONS
  In this homogeneous cohort residing in a rural area of Brazil, lifetime, untreated severe IGHD is not associated with evidence of premature atherosclerosis despite unfavorable cardiovascular risk profile.
authors.affiliation: Division of Endocrinology, Johns Hopkins University, 1830 East Monument Street, #333, Baltimore, Maryland 21287, USA.
authors.forename: Joselina Luzia
authors.initials: JL
authors.lastname: Menezes Oliveira
authors.forename: Celi
authors.initials: C
authors.lastname: Marques-Santos
authors.forename: José Augusto
authors.initials: JA
authors.lastname: Barreto-Filho
authors.forename: Roberto
authors.initials: R
authors.lastname: Ximenes Filho
authors.forename: Allan Valadão
authors.initials: AV
authors.lastname: de Oliveira Britto
authors.forename: Anita Hermínia
authors.initials: AH
authors.lastname: Oliveira Souza
authors.forename: Clarisse Miranda
authors.initials: CM
authors.lastname: Prado
authors.forename: Carla Raquel
authors.initials: CR
authors.lastname: Pereira Oliveira
authors.forename: Rossana Maria C
authors.initials: RM
authors.lastname: Pereira
authors.forename: Tábita de Almeida
authors.initials: Tde A
authors.lastname: Ribeiro Vicente
authors.forename: Catarine Teles
authors.initials: CT
authors.lastname: Farias
authors.forename: Manuel Hermínio
authors.initials: MH
authors.lastname: Aguiar-Oliveira
authors.forename: Roberto
authors.initials: R
authors.lastname: Salvatori
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000209:etiology*; D002097:C-Reactive Protein / Q000032:analysis; D008078:Cholesterol, LDL / Q000097:blood; D004452:Echocardiography; D005260:Female; D019382:Human Growth Hormone / Q000172:deficiency*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009154:Mutation; D018013:Receptors, Neuropeptide / Q000235:genetics*; D018017:Receptors, Pituitary Hormone-Regulating Hormone / Q000235:genetics*
chemical_list: D008078:Cholesterol, LDL; D018013:Receptors, Neuropeptide; D018017:Receptors, Pituitary Hormone-Regulating Hormone; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D002097:C-Reactive Protein; C048250:somatotropin releasing hormone receptor