Document Detail


Comparison between weight-based and IGF-I-based growth hormone (GH) dosing in the treatment of children with GH deficiency and influence of exon 3 deleted GH receptor variant.
MedLine Citation:
PMID:  19036620     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Compare the most frequently used weight-based GH dosing with an IGF-I level-based strategy in the treatment of children with severe GH deficiency. Additionally, analyse the influence of the GH receptor exon 3 polymorphism on IGF-I levels during GH therapy. DESIGN: Thirty children with GH deficiency on treatment with GH for 4.3+/-3.2 yr in a single University Hospital were divided in group W (weight-based GH dosing) and group I (IGF-I-based dosing). In group I, GH doses were changed by 8.3 microg/kg d to maintain IGF-I levels between 0 and +2 SDS, whereas in group W the dose was fixed at 30 microg/kg d in prepubertal and 50 microg/kg d in pubertal patients. Growth velocity was measured after 1 yr, IGF-I and IGFBP3 levels quarterly. GH receptor exon 3 was genotyped by PCR. RESULTS: Most patients in Group I reached target IGF-I levels after 6 months with a GH dose ranging between 25 and 66 microg/kg d (mean+/-SD, 38+/-8). Each change of 8.3 microg/kg d of GH dose, resulted in change of 1.17+/-0.6 SDS of IGF-I levels. Mean IGF-I levels were higher in Group I 0.8+/-0.5 SDS than in Group W -0.3+/-1.9 SDS (p<0.05), but growth velocities were similar, 6.8+/-2.6 cm/yr and 6.9+/-2.6 cm/yr (p=NS), respectively. Serum IGFBP3 levels were similar in both groups and were less useful to individualize GH therapy. Even treated with a similar mean GH dose, patients carrying at least one GH receptor d3-allele reached higher IGF-I levels (0.7+/-1.2 SDS) than those homozygous for the full-length allele (-0.3+/-1.2 SDS; p<0.05), however, growth velocities were not different. CONCLUSIONS: By adjusting the GH dose, it was feasible to maintain IGF-I in the desired range (0-+2 SDS). Patients carrying at least one GH receptor d3-allele reached higher circulating IGF-I levels than those homozygous for the full-length allele. A multiple regression analysis failed to demonstrate an independent influence of IGF-I levels on GV during the 12 months of observation.
Authors:
Frederico Guimarães Marchisotti; Alexander Augusto Lima Jorge; Luciana Ribeiro Montenegro; Karina Berger; Luciani Renata Silveira de Carvalho; Berenice Bilharinho Mendonca; Ivo Jorge Prado Arnhold
Publication Detail:
Type:  Comparative Study; Journal Article     Date:  2008-11-25
Journal Detail:
Title:  Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society     Volume:  19     ISSN:  1532-2238     ISO Abbreviation:  Growth Horm. IGF Res.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-16     Completed Date:  2009-07-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9814320     Medline TA:  Growth Horm IGF Res     Country:  Scotland    
Other Details:
Languages:  eng     Pagination:  179-86     Citation Subset:  IM    
Affiliation:
Unidade de Endocrinologia do Desenvolvimento, Laboratorio de Hormonios e Genetica Molecular LIM/42, Disciplina de Endocrinologia, Hospital das Clinicas, Avenida Dr. Enéas de Carvalho Aguiar 155, São Paulo, CEP 05403-900, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Body Weight*
Child
Exons
Female
Human Growth Hormone / administration & dosage*,  deficiency*,  therapeutic use
Humans
Insulin-Like Growth Factor Binding Proteins / blood*
Insulin-Like Growth Factor I / metabolism*
Male
Mutation
Receptors, Somatotropin / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/IGFBP3 protein, human; 0/Insulin-Like Growth Factor Binding Proteins; 0/Receptors, Somatotropin; 12629-01-5/Human Growth Hormone; 67763-96-6/Insulin-Like Growth Factor I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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