FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2140740673> ?p ?o ?g. }

• W2140740673 endingPage "400" @default.
• W2140740673 startingPage "394" @default.
• W2140740673 abstract "The causes of growth retardation of children with thalassaemia major are multifactorial. We studied the GH response to provocation by clonidine and glucagon, measured the circulating concentrations of insulin, IGF-I, IGF-binding protein-3 (IGFBP-3) and ferritin, and evaluated IGF-I generation after a single dose of GH (0.1 mg/kg per dose) in 15 prepubertal patients with thalassaemia, 15 age-matched children with constitutional short stature (CSS) (height standard deviation score less than -2, with normal GH response to provocation) and 11 children with isolated GH deficiency (GHD). Children with thalassaemia had significantly lower peak GH response to provocation by clonidine and glucagon (6.2 +/- 2.3 and 6.8 +/- 2.1 microg/l respectively) than the CSS group (18.6 +/- 2.7 and 16.7 +/- 3.7 microg/l respectively). They had significantly decreased circulating concentrations of IGF-I and IGFBP-3 (47.5 +/- 19 ng/ml and 1.2 +/- 0.27 mg/l respectively) compared with those with CSS (153 +/- 42 ng/ml and 2.06 +/- 0.37 mg/l respectively), but the IGF-I and IGFBP-3 concentrations were not different from those with GHD (56 +/- 25 ng/ml and 1.1 +/- 0.32 mg/l respectively). These data demonstrate that the GH-IGF-I-IGFBP-3 axis in thalassaemic children is defective. Serum ferritin concentration correlated significantly with GH peak response to provocation (r = -0.36, P < 0.05) and circulating IGF-I (r = -0.47, P < 0.01) and IGFBP-3 (r = -0.42, P < 0.01) concentrations. In the IGF-I generation test, after GH injection, the thalassaemic children had significantly lower IGF-I and IGFBP-3 levels 86.7 +/- 11.2 ng/ml and 2.05 +/- 0.51 mg/l respectively) than those in the CSS group (226 +/- 45.4 ng/ml and 2.8 +/- 0.43 mg/l respectively). The IGF-I response was significantly higher in children with GHD (158 +/- 50 ng/ml) than in thalassaemic children. Six short (height standard deviation score less than -2) thalassaemic children who had defective GH response to provocation (< 10 microg/l), all the children with GHD and eight short normal children (CSS) were treated for 1 year with human GH (18 units/m2 per week divided into daily s.c. doses). After 1 year of GH therapy there was a marked acceleration of growth velocity in both thalassaemic children (from 3.8 +/- 0.6 cm/year to 7.2 +/- 0.8 cm/year) and controls. However, the linear acceleration of growth velocity on GH therapy was significantly slower in thalassaemic children (3.3 +/- 0.3 cm/year increment) compared with those with CSS (5.3 +/- 0.4 cm/year increment) and GHD (6.9 +/- 1.2 cm/year increment) (P < 0.05). Their circulating IGF-I concentration (105 +/- 36 ng/ml) was significantly lower than those for CSS (246 +/- 58 ng/ml) and GHD (189 +/- 52 ng/ml) after 1 year of GH therapy. These data prove that some children with beta-thalassaemia major have a defective GH-IGF-I-IGFBP-3 axis and suggest the presence of partial resistance to GH." @default.
• W2140740673 created "2016-06-24" @default.
• W2140740673 creator A5017025007 @default.
• W2140740673 creator A5048664693 @default.
• W2140740673 creator A5059708636 @default.
• W2140740673 date "1998-04-01" @default.
• W2140740673 modified "2023-10-12" @default.
• W2140740673 title "GH response to provocation and circulating IGF-I and IGF-binding protein-3 concentrations, the IGF-I generation test and clinical response to GH therapy in children with beta-thalassaemia" @default.
• W2140740673 cites W1510647987 @default.
• W2140740673 cites W1602203395 @default.
• W2140740673 cites W1964059575 @default.
• W2140740673 cites W1967664560 @default.
• W2140740673 cites W1975228316 @default.
• W2140740673 cites W1989831107 @default.
• W2140740673 cites W1992668278 @default.
• W2140740673 cites W2003016121 @default.
• W2140740673 cites W2007006137 @default.
• W2140740673 cites W2007210480 @default.
• W2140740673 cites W2011921105 @default.
• W2140740673 cites W2013564424 @default.
• W2140740673 cites W2014633710 @default.
• W2140740673 cites W2015003884 @default.
• W2140740673 cites W2016788433 @default.
• W2140740673 cites W2023205840 @default.
• W2140740673 cites W2023941312 @default.
• W2140740673 cites W2031414974 @default.
• W2140740673 cites W2032558447 @default.
• W2140740673 cites W2037632772 @default.
• W2140740673 cites W2053429397 @default.
• W2140740673 cites W2058462436 @default.
• W2140740673 cites W2058472505 @default.
• W2140740673 cites W2061188554 @default.
• W2140740673 cites W2071375355 @default.
• W2140740673 cites W2083744069 @default.
• W2140740673 cites W2087645454 @default.
• W2140740673 cites W2087949553 @default.
• W2140740673 cites W2089184786 @default.
• W2140740673 cites W2093099445 @default.
• W2140740673 cites W2107026509 @default.
• W2140740673 cites W210896705 @default.
• W2140740673 cites W2111851887 @default.
• W2140740673 cites W2120612509 @default.
• W2140740673 cites W2121975985 @default.
• W2140740673 cites W2127494214 @default.
• W2140740673 cites W2138451102 @default.
• W2140740673 cites W2139461594 @default.
• W2140740673 cites W2159209503 @default.
• W2140740673 cites W2161209070 @default.
• W2140740673 cites W2465855473 @default.
• W2140740673 doi "https://doi.org/10.1530/eje.0.1380394" @default.
• W2140740673 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9578506" @default.
• W2140740673 hasPublicationYear "1998" @default.
• W2140740673 type Work @default.
• W2140740673 sameAs 2140740673 @default.
• W2140740673 citedByCount "47" @default.
• W2140740673 countsByYear W21407406732012 @default.
• W2140740673 countsByYear W21407406732014 @default.
• W2140740673 countsByYear W21407406732015 @default.
• W2140740673 countsByYear W21407406732016 @default.
• W2140740673 countsByYear W21407406732017 @default.
• W2140740673 countsByYear W21407406732018 @default.
• W2140740673 countsByYear W21407406732019 @default.
• W2140740673 countsByYear W21407406732020 @default.
• W2140740673 countsByYear W21407406732022 @default.
• W2140740673 crossrefType "journal-article" @default.
• W2140740673 hasAuthorship W2140740673A5017025007 @default.
• W2140740673 hasAuthorship W2140740673A5048664693 @default.
• W2140740673 hasAuthorship W2140740673A5059708636 @default.
• W2140740673 hasBestOaLocation W21407406731 @default.
• W2140740673 hasConcept C110586980 @default.
• W2140740673 hasConcept C126322002 @default.
• W2140740673 hasConcept C134018914 @default.
• W2140740673 hasConcept C142724271 @default.
• W2140740673 hasConcept C204787440 @default.
• W2140740673 hasConcept C2778563252 @default.
• W2140740673 hasConcept C2778754045 @default.
• W2140740673 hasConcept C2779306644 @default.
• W2140740673 hasConcept C2984496839 @default.
• W2140740673 hasConcept C71315377 @default.
• W2140740673 hasConcept C71924100 @default.
• W2140740673 hasConceptScore W2140740673C110586980 @default.
• W2140740673 hasConceptScore W2140740673C126322002 @default.
• W2140740673 hasConceptScore W2140740673C134018914 @default.
• W2140740673 hasConceptScore W2140740673C142724271 @default.
• W2140740673 hasConceptScore W2140740673C204787440 @default.
• W2140740673 hasConceptScore W2140740673C2778563252 @default.
• W2140740673 hasConceptScore W2140740673C2778754045 @default.
• W2140740673 hasConceptScore W2140740673C2779306644 @default.
• W2140740673 hasConceptScore W2140740673C2984496839 @default.
• W2140740673 hasConceptScore W2140740673C71315377 @default.
• W2140740673 hasConceptScore W2140740673C71924100 @default.
• W2140740673 hasLocation W21407406731 @default.
• W2140740673 hasLocation W21407406732 @default.
• W2140740673 hasOpenAccess W2140740673 @default.
• W2140740673 hasPrimaryLocation W21407406731 @default.
• W2140740673 hasRelatedWork W1980943558 @default.
• W2140740673 hasRelatedWork W1989970750 @default.
• W2140740673 hasRelatedWork W2043934172 @default.

• next