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Article: Growth hormone treatment of short chinese children with β-thalassaemia major without GH deficiency

TitleGrowth hormone treatment of short chinese children with β-thalassaemia major without GH deficiency
Authors
Issue Date1995
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0300-0664
Citation
Clinical Endocrinology, 1995, v. 42 n. 4, p. 359-363 How to Cite?
AbstractObjective. Despite regular transfusion and desferrioxamine treatment, growth failure is commonly seen in adolescent children with β-thalassaemia major. The growth failure has been thought to be due to GH resistance rather than GH deficiency. We investigated the effect of GH on short non-GH deficient children with β-thalassaemia. Design. Recombinant human GH was given in a dose of 0.14 IU/kg/day subcutaneously in an open study. Patients. Fifteen prepubertal Chinese children with β-thalassaemia major (ranging from 7.16 to 14.7 years in age) with height -1.5 SD or more below the population mean for age and a growth velocity of less than 5 cm/year were treated with growth hormone for one year. All children had peak GH response >15mIU/I to insulin induced hypoglycaemia and normal thyroid function and adrenal reserve. Measurements. Anthropometric measurements were performed every 3 months. Morning urine was tested twice weekly for glycosuria. Blood count, renal and liver function tests, fasting blood glucose, IGF-I and fructosamine levels were assessed at entry and every 3 months during treatment. Pasting insulin was measured before and after 3 and 12 months of GH treatment. Skeletal maturity was assessed before and after one year of treatment. Results. Treatment was stopped in two children after 6 months because of poor growth response and noncompliance with treatment and in one child at 9 months because of bone marrow transplantation. In the 13 children, the growth velocity increased from 3.6 ± 7 cm/year to 8 ± 1.2 cm/year after one year of GH treatment (P < 0.001). IGF-I was low before treatment (10.1 ± 2.7 nmol/l), rising significantly to 15.8 ± 4.8, 18.4 ± 4.6, 19.3 ± 6.4 and 21.9 ± 7.5 nmol/l at 3, 6, 9 and 12 months of treatment (P < 0.005). The mean pretreatment bone age in the 13 children was 9.58 ± 1.41 years and increased to 10.53 ± 1.43 years after one year of treatment (ΔBA/CA 0.95 ± 0.3 years). None of the patients developed glycosuria or hypertension. There was no significant change in blood count, renal and liver function, thyroid function, fasting blood glucose or insulin concentrations during treatment. Conclusion. Growth failure in these children with normal GH reserve and low serum IGF-I concentrations would suggest GH insensitivity. Supraphysiological doses of exogenous GH can cause a significant increase in serum IGF-I levels and a significant improvement in short-term growth of short children with β-thalassaemia major.
Persistent Identifierhttp://hdl.handle.net/10722/162080
ISSN
2015 Impact Factor: 3.487
2015 SCImago Journal Rankings: 1.314
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLow, LCKen_HK
dc.contributor.authorKwan, EYWen_HK
dc.contributor.authorLim, YJen_HK
dc.contributor.authorLee, ACWen_HK
dc.contributor.authorTam, CFen_HK
dc.contributor.authorLam, KSLen_HK
dc.date.accessioned2012-09-05T05:17:07Z-
dc.date.available2012-09-05T05:17:07Z-
dc.date.issued1995en_HK
dc.identifier.citationClinical Endocrinology, 1995, v. 42 n. 4, p. 359-363en_HK
dc.identifier.issn0300-0664en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162080-
dc.description.abstractObjective. Despite regular transfusion and desferrioxamine treatment, growth failure is commonly seen in adolescent children with β-thalassaemia major. The growth failure has been thought to be due to GH resistance rather than GH deficiency. We investigated the effect of GH on short non-GH deficient children with β-thalassaemia. Design. Recombinant human GH was given in a dose of 0.14 IU/kg/day subcutaneously in an open study. Patients. Fifteen prepubertal Chinese children with β-thalassaemia major (ranging from 7.16 to 14.7 years in age) with height -1.5 SD or more below the population mean for age and a growth velocity of less than 5 cm/year were treated with growth hormone for one year. All children had peak GH response >15mIU/I to insulin induced hypoglycaemia and normal thyroid function and adrenal reserve. Measurements. Anthropometric measurements were performed every 3 months. Morning urine was tested twice weekly for glycosuria. Blood count, renal and liver function tests, fasting blood glucose, IGF-I and fructosamine levels were assessed at entry and every 3 months during treatment. Pasting insulin was measured before and after 3 and 12 months of GH treatment. Skeletal maturity was assessed before and after one year of treatment. Results. Treatment was stopped in two children after 6 months because of poor growth response and noncompliance with treatment and in one child at 9 months because of bone marrow transplantation. In the 13 children, the growth velocity increased from 3.6 ± 7 cm/year to 8 ± 1.2 cm/year after one year of GH treatment (P < 0.001). IGF-I was low before treatment (10.1 ± 2.7 nmol/l), rising significantly to 15.8 ± 4.8, 18.4 ± 4.6, 19.3 ± 6.4 and 21.9 ± 7.5 nmol/l at 3, 6, 9 and 12 months of treatment (P < 0.005). The mean pretreatment bone age in the 13 children was 9.58 ± 1.41 years and increased to 10.53 ± 1.43 years after one year of treatment (ΔBA/CA 0.95 ± 0.3 years). None of the patients developed glycosuria or hypertension. There was no significant change in blood count, renal and liver function, thyroid function, fasting blood glucose or insulin concentrations during treatment. Conclusion. Growth failure in these children with normal GH reserve and low serum IGF-I concentrations would suggest GH insensitivity. Supraphysiological doses of exogenous GH can cause a significant increase in serum IGF-I levels and a significant improvement in short-term growth of short children with β-thalassaemia major.en_HK
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0300-0664en_HK
dc.relation.ispartofClinical Endocrinologyen_HK
dc.rightsClinical Endocrinology. Copyright © Blackwell Publishing Ltd.-
dc.subject.meshAdolescenten_US
dc.subject.meshBody Height - Drug Effectsen_US
dc.subject.meshChilden_US
dc.subject.meshFemaleen_US
dc.subject.meshGrowth Disorders - Blood - Drug Therapy - Etiologyen_US
dc.subject.meshGrowth Hormone - Blood - Therapeutic Useen_US
dc.subject.meshHumansen_US
dc.subject.meshInsulin-Like Growth Factor I - Analysisen_US
dc.subject.meshMaleen_US
dc.subject.meshRecombinant Proteins - Therapeutic Useen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshBeta-Thalassemia - Blood - Complicationsen_US
dc.titleGrowth hormone treatment of short chinese children with β-thalassaemia major without GH deficiencyen_HK
dc.typeArticleen_HK
dc.identifier.emailLow, LCK: lcklow@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.authorityLow, LCK=rp00337en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1365-2265.1995.tb02643.x-
dc.identifier.pmid7750189-
dc.identifier.scopuseid_2-s2.0-0028940585en_HK
dc.identifier.hkuros8437-
dc.identifier.volume42en_HK
dc.identifier.issue4en_HK
dc.identifier.spage359en_HK
dc.identifier.epage363en_HK
dc.identifier.isiWOS:A1995QR35900004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLow, LCK=7007049461en_HK
dc.identifier.scopusauthoridKwan, EYW=7006484387en_HK
dc.identifier.scopusauthoridLim, YJ=16413395300en_HK
dc.identifier.scopusauthoridLee, ACW=7405631431en_HK
dc.identifier.scopusauthoridTam, CF=18736693400en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK

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