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      Is the Response to Growth Hormone in Short Children Born Small for Gestational Age Dependent on Genetic or Maternal Factors?

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          Abstract

          Background/Aims: We investigated whether genetic or maternal/environmental risk factors for being born small for gestational age (SGA), e.g. Silver-Russell syndrome, congenital heart defects, infections of mothers or smoking during pregnancy, explain the variation in the first-year growth response to GH therapy. Methods: Secondary analysis was made of growth response in 135 short prepubertal German children (66% males) enrolled in a SGA phase III trial. Initial mean patient age was 6.8 ± 2.6 years; mean patient height SDS –3.8 ± 1.2, and GH treatment dose was 0.066 mg/kg body weight per day. Results: Growth velocity increased by 4.5 ± 2.0 cm/year and height SDS by 1.0 ± 0.5 SDS. Although patient number was limited and variation was high, both growth response (cm/year) and change in height SDS did not appear to differ between subgroups which also did not differ in terms of Studentized residuals set up in the KIGS growth prediction model for SGA. Likewise, in a step-forward multivariate analysis, the variables Silver-Russell syndrome, congenital heart defects, infections of mothers and smoking were not identified as independent factors influencing growth velocity. Conclusion: The retrospectively analyzed genetic and maternal/environmental risk factors for SGA do not appear to explain the observed patient variance in response to GH. Larger prospective studies are needed, however, to substantiate these preliminary findings.

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          International Small for Gestational Age Advisory Board consensus development conference statement: management of short children born small for gestational age, April 24-October 1, 2001.

          P. A. Lee, S Chernausek, A Hokken-Koelega … (2003)
          To provide pediatric endocrinologists, general pediatricians, neonatologists, and primary care physicians with recommendations for the management of short children born small for gestational age (SGA). A 13-member independent panel of pediatric endocrinologists was convened to discuss relevant issues with respect to definition, diagnosis, and clinical management of short children born SGA. Panel members convened over a series of 3 meetings to thoroughly review, discuss, and come to consensus on the identification and treatment of short children who are born SGA. SGA is defined as birth weight and/or length at least 2 standard deviations (SDs) below the mean for gestational age ( 2 SD below the mean; this catch-up process is usually completed by the time they are 2 years of age. A child who is SGA and older than 3 years and has persistent short stature (ie, remaining at least 2 SD below the mean for chronologic age) is not likely to catch up and should be referred to a pediatrician who has expertise in endocrinology. Bone age is not a reliable predictor of height potential in children who are SGA. Nevertheless, a standard evaluation for short stature should be performed. A diagnosis of SGA does not exclude growth hormone (GH) deficiency, and GH assessment should be performed if there is clinical suspicion or biochemical evidence of GH deficiency. At baseline, insulin-like growth factor-I, insulin-like growth factor binding protein-3, fasting insulin, glucose, and lipid levels as well as blood pressure should be measured, and all aspects of SGA-not just stature-should be addressed with parents. The objectives of GH therapy in short children who are SGA are catch-up growth in early childhood, maintenance of normal growth in childhood, and achievement of normal adult height. GH therapy is effective and safe in short children who are born SGA and should be considered in those older than 2 to 3 years. There is long-term experience of improved growth using a dosage range from 0.24 to 0.48 mg/kg/wk. Higher GH doses (0.48 mg/kg/wk [0.2 IU/kg/d]) are more effective for the short term. Whether the higher GH dose is more efficacious than the lower dose in terms of adult height results is not yet known. Only adult height results of randomized dose-response studies will give a definite answer. Monitoring is necessary to ensure safety of medication. Children should be monitored for changes in glucose homeostasis, lipids, and blood pressure during therapy. The frequency and intensity of monitoring will vary depending on risk factors such as family history, obesity, and puberty.
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            Inflammation in pregnancy: its roles in reproductive physiology, obstetrical complications, and fetal injury.

            Roberto Romero, Francesca Gotsch, Beth Pineles … (2007)
            Fetal development and growth occur in a sterile amniotic cavity while first exposure to microorganisms happens at birth. However, at least 25% of all preterm births, the leading cause of perinatal morbidity and mortality worldwide, occur in mothers with microbial invasion of the amniotic cavity. Microbial attack of the fetus takes place in approximately 10% of pregnancies with intra-amniotic infection, and the human fetus is capable of deploying an inflammatory response (cellular and humoral) in the mid-trimester of pregnancy. The onset of premature labor in the context of infection is mediated by pro-inflammatory cytokines, such as interleukin (IL)-1beta and tumor necrosis factor alpha (TNF-alpha), as these cytokines are produced by intrauterine tissues in response to microbial products, can stimulate prostaglandin production, and induce labor in animals. Moreover, knockout experiments suggest that infection is less likely to lead to premature labor when the IL-1 and TNF signaling pathways are disrupted. A fetal inflammatory systemic response occurs in a fraction of fetuses exposed to microorganisms in utero, and is associated with the impending onset of labor as well as multisystem organ involvement. Neonates born with funisitis, the histologic marker of such inflammation, are at increased risk for neurologic handicap and cerebral palsy. Evidence has begun to accumulate that gene-environment interactions determine the likelihood of preterm labor and delivery and, probably, the risk of fetal injury. Fetal inflammation has emerged as a major mechanism of disease responsible for complications in the perinatal period (in utero and in the first 28 days of life), as well as in infancy. Moreover, reprogramming of the fetal immune response may predispose to diseases in adulthood.
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              Adult height after long-term, continuous growth hormone (GH) treatment in short children born small for gestational age: results of a randomized, double-blind, dose-response GH trial.

              José Jansen, Yvonne van Duynhoven, Paul Mulder … (2003)
              The GH dose-response effect of long-term continuous GH treatment on adult height (AH) was evaluated in 54 short children born small for gestational age (SGA) who were participating in a randomized, double-blind, dose-response trial. Patients were randomly and blindly assigned to treatment with either 3 IU (group A) or 6 IU (group B) GH/m(2).d ( approximately 0.033 or 0.067 mg/kg.d, respectively). The mean (+/-SD) birth length was -3.6 (1.4), the age at the start of the study was 8.1 (1.9) yr, and the height SD score (SDS) at the start of the study -3.0 (0.7). Seventeen of the 54 children were partially GH deficient (stimulated GH peak, 10-20 mU/liter). Fifteen non-GH-treated, non-GH-deficient, short children born SGA, with similar inclusion criteria, served as controls [mean (+/-SD) birth length, -3.3 (1.2); age at start, 7.8 (1.7) yr; height SDS at start, -2.6 (0.5)]. GH treatment resulted in an AH above -2 SDS in 85% of the children after a mean (+/-SD) GH treatment period of 7.8 (1.7) yr. The mean (SD) AH SDS was -1.1 (0.7) for group A and -0.9 (0.8) for group B, resulting from a mean (+/-SD) gain in height SDS of 1.8 (0.7) for group A and 2.1 (0.8) for group B. No significant differences between groups A and B were found for AH SDS (mean difference, 0.3 SDS; 95% confidence interval, -0.2, 0.6; P > 0.2) and gain in height SDS (mean difference, 0.3 SDS; 95% confidence interval, -0.1, 0.7; P > 0.1). When corrected for target height, the mean corrected AH SDS was -0.2 (0.8) for group A and -0.4 (0.9) for group B. The mean (+/-SD) AH SDS of the control group [-2.3 (0.7)] was significantly lower than that of the GH-treated group (P < 0.001). Multiple regression analysis indicated the following predictive variables for AH SDS: target height SDS, height SDS, and chronological age minus bone age (years) at the start of the study. GH dose had no significant effect. In conclusion, long-term continuous GH treatment in short children born SGA without signs of persistent catch-up growth leads to a normalization of AH, even with a GH dose of 3 IU/m(2).d ( approximately 0.033 mg/kg.d).
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                Author and article information

                Journal
                Journal ID (publisher-id): HRE
                Journal ID (nlm-ta): Horm Res Paediatr
                Journal ID (doi): 10.1159/issn.1663-2818
                Title: Hormone Research in Paediatrics
                Publisher: S. Karger AG
                ISSN (Print): 1663-2818
                ISSN (Electronic): 1663-2826
                Publication date Subscription-year: 2009
                Publication date (Print): August 2009
                Publication date (Electronic): 18 August 2009
                Volume: 72
                Issue: 2
                Pages: 106-113
                Affiliations
                Divisions of aPaediatric Nephrology and bPaediatric Endocrinology, University Hospital for Children and Adolescents, Heidelberg, Germany; cPfizer Endocrine Care, KIGS/KIMS/ACROSTUDY Medical Outcomes, Stockholm, Sweden; dDivision of Paediatric Endocrinology, University Hospital for Children and Adolescents, Erlangen, eDepartment of Paediatric, Endocrinology and Diabetes, University Hospital for Children and Adolescents, University Duisburg-Essen, fPfizer Pharma GmbH, Medical Affairs, Karlsruhe, gPaediatric Diabetes Unit, Department of Paediatric and Adolescent Medicine, Saarland University Hospital, Homburg/Saar, hPaediatric Endocrinology, Endokrinologikum, Hamburg, and iDepartment of Paediatrics and Endocrinology, University Children’s Hospital, Tübingen, Germany
                Article
                Publisher ID: 232163 Other ID: Horm Res 2009;72:106–113
                DOI: 10.1159/000232163
                PubMed ID: 19690428
                SO-VID: d3b3f1b5-27c8-4f91-84e1-9f25fc1641b0
                Copyright © © 2009 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 30 June 2008
                Date accepted : 16 October 2008
                Page count
                Figures: 2, Tables: 2, References: 50, Pages: 8
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Endocrinology & Diabetes,Neurology,Nutrition & Dietetics,Sexual medicine,Internal medicine,Pharmacology & Pharmaceutical medicine
                Keywords: Infections,Small for gestational age,Smoking,Heart defects,Growth hormone treatment,Silver-Russell syndrome
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes, Neurology, Nutrition & Dietetics, Sexual medicine, Internal medicine, Pharmacology & Pharmaceutical medicine
                Keywords: Infections, Small for gestational age, Smoking, Heart defects, Growth hormone treatment, Silver-Russell syndrome

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