title: Lifetime, untreated isolated GH deficiency due to a GH-releasing hormone receptor mutation has beneficial consequences on bone status in older individuals, and does not influence their abdominal aorta calcification.
abstract: The GH/IGF-I axis has essential roles in regulating bone and vascular status. The age-related decrease in GH secretion ("somatopause") may contribute to osteoporosis and atherosclerosis, commonly observed in the elderly. Adult-onset GH deficiency (GHD) has been reported to be associated with reduced bone mineral density (BMD), increased risk of fractures, and premature atherosclerosis. We have shown the young adult individuals with isolated GHD (IGHD) due to a homozygous for the c.57+1G>A GHRH receptor gene mutation have normal volumetric BMD (vBMD), and not develop premature atherosclerosis, despite adverse risk factor profile. However, the bone and vascular impact of lifetime GHD on the aging process remains unknown. We studied a group of ten older IGHD subjects (≥60 years) homozygous for the mutation, comparing them with 20 age- and gender-matched controls (CO). Areal BMD was measured, and vBMD was calculated at the lumbar spine and total hip. Vertebral fractures and abdominal aortic calcifications (expressed as calcium score) were also assessed. Areal BMD was lower in IGHD, but vBMD was similar in the two groups. The percent of fractured individuals was similar, but the mean number of fractures per individual was lower in IGHD than CO. Calcium score was similar in the two groups. A positive correlation was found between calcium score and number of fractures. Untreated lifetime IGHD has beneficial consequences on bone status and does not have a deleterious effect on abdominal aorta calcification.
authors.affiliation: Division of Endocrinology, Department of Medicine, School of Medicine, Federal University of Sergipe, Aracaju, Brazil.
authors.forename: Anita H O
authors.initials: AH
authors.lastname: Souza
authors.forename: Maria I T
authors.initials: MI
authors.lastname: Farias
authors.forename: Roberto
authors.initials: R
authors.lastname: Salvatori
authors.forename: Gabriella M F
authors.initials: GM
authors.lastname: Silva
authors.forename: João A M
authors.initials: JA
authors.lastname: Santana
authors.forename: Francisco A
authors.initials: FA
authors.lastname: Pereira
authors.forename: Francisco J A
authors.initials: FJ
authors.lastname: de Paula
authors.forename: Eugenia H O
authors.initials: EH
authors.lastname: Valença
authors.forename: Enaldo V
authors.initials: EV
authors.lastname: Melo
authors.forename: Rita A A
authors.initials: RA
authors.lastname: Barbosa
authors.forename: Rossana M C
authors.initials: RM
authors.lastname: Pereira
authors.forename: Miburge B
authors.initials: MB
authors.lastname: Gois-Junior
authors.forename: Manuel H
authors.initials: MH
authors.lastname: Aguiar-Oliveira
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000502:physiology*; D001012:Aorta, Abdominal / Q000473:pathology; D001018:Aortic Diseases / Q000453:epidemiology*; D015519:Bone Density; D016022:Case-Control Studies; D004393:Dwarfism, Pituitary / Q000453:epidemiology* / Q000235:genetics; D005260:Female; D006304:Health Status; D019382:Human Growth Hormone / Q000172:deficiency; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D018013:Receptors, Neuropeptide / Q000235:genetics; D018017:Receptors, Pituitary Hormone-Regulating Hormone / Q000235:genetics; D016103:Spinal Fractures / Q000453:epidemiology; D013131:Spine; D061205:Vascular Calcification / Q000453:epidemiology*
chemical_list: D018013:Receptors, Neuropeptide; D018017:Receptors, Pituitary Hormone-Regulating Hormone; D019382:Human Growth Hormone; C048250:somatotropin releasing hormone receptor