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Long-Term Response to GH Therapy in Short Children With a Delayed Infancy-Childhood Transition (DICT)
Göteborg Pediatric Growth Research Center (GP-GRC), The Sahlgrenska Academy at University of Gothenburg, Sweden.
Department of Clinical Science, Umeå University, Sweden.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa. (Barnendokrinologisk forskning/Gustafsson)
Department of Pediatric Endocrinology, Meyer Children's Hospital at Rambam Medical Center, Haifa, Israel.
2011 (engelsk)Inngår i: Pediatric Research, ISSN 0031-3998, E-ISSN 1530-0447, Vol. 69, nr 6, s. 504-510Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Transition of growth from infancy to childhood is associated with activation of the GH-IGF-I axis. Children with a delayed infancy-childhood transition (DICT) are short as adults. Thus, age at ICT may impact on growth response to GH. The objective was to investigate associations between growth response to GH treatment and ICT timing in children with idiopathic short stature (ISS) in a randomized, controlled, multicenter trial, TRN 88-080. A total of 147 prepubertal children (mean age, 11.5 +/- 1.4 y) were randomized to receive GH 33 mu g/kg/d (GH(33), n = 43), GH 67 mu g/kg/d (GH(67), n = 61), or no treatment (n = 43). Data on growth to final height (FH) were analyzed after categorization into those with normal (n = 76) or delayed ICT (n = 71). Within the GH(33) group, significant height gain at FH was only observed in children with a DICT (p < 0.001), with each month of delay corresponding to gain of 0.13 SD score (SDS). For the GH(67) group, the timing of the onset of the ICT had no impact on growth response. In conclusion, ISS children with a DICT responded to standard GH dose (better responsiveness), whereas those with a normal ICT required higher doses to attain a significant height gain to FH.

sted, utgiver, år, opplag, sider
2011. Vol. 69, nr 6, s. 504-510
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URN: urn:nbn:se:uu:diva-145702DOI: 10.1203/PDR.0b013e3182139243ISI: 000290831700007PubMedID: 21297523OAI: oai:DiVA.org:uu-145702DiVA, id: diva2:396618
Tilgjengelig fra: 2011-02-10 Laget: 2011-02-10 Sist oppdatert: 2017-12-11bibliografisk kontrollert

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