DOCSLIB.ORG

Total and Acylated Ghrelin Levels in Children with Poor Growth

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Total and Acylated Ghrelin Levels in Children with Poor Growth 0031-3998/11/6906-0517 Vol. 69, No. 6, 2011 PEDIATRIC RESEARCH Printed in U.S.A. Copyright © 2011 International Pediatric Research Foundation, Inc. Total and Acylated Ghrelin Levels in Children With Poor Growth JORDAN E. PINSKER, DEBORAH ONDRASIK, DEBORA CHAN, GREGORY J. FREDERICKS, ELUDRIZZA TABISOLA-NUESCA, MINELA FERNANDEZ-APONTE, DEAN R. FOCHT, AND MERRILY POTH Departments of Pediatrics [J.E.P., D.O., D.C., E.T.-N., M.F.-A.] and Clinical Investigation [G.J.F.], Tripler Army Medical Center, Honolulu, Hawaii 96859; Department of Pediatric Gastroenterology [D.R.F.], Geisinger Medical Center, Danville, Pennsylvania 17822; Department of Pediatrics [M.P.], Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814 ABSTRACT: Ghrelin, an enteric hormone with potent appetite Ghrelin is an enteric hormone with potent orexigenic and stimulating effects, also stimulates growth hormone release. We adipogenic effects, and it is also a potent stimulator of growth hypothesized that altered levels of total ghrelin (TG) or acylated hormone release, mediated by the growth hormone secreta- ghrelin (AG) could affect growth by altering growth hormone secre- gogue receptor (GHSR) type 1A (2). Ghrelin is produced tion, subsequently affecting insulin-like growth factor-1 (IGF-1) predominately by the stomach and serves to stimulate appetite generation or by altering appetite and food intake. After institutional and regulate positive energy balance (2,3). In addition to review board approval, 52 children presenting for evaluation of chronic gastrointestinal symptoms (group 1), poor weight gain (group serving as a potent stimulator of growth hormone release in 2), or poor linear growth (group 3) were evaluated for fasting TG and synergy with growth hormone releasing hormone, ghrelin AG levels in addition to their regular evaluation. Serum ghrelin, stimulates prolactin and adrenocorticotropic hormone IGF-1, and prealbumin were compared between groups. No differ- (ACTH) secretion, modulates insulin secretion and sensitivity, ence was observed for mean fasting TG between groups. However, and stimulates gastrointestinal tract motility (3). mean fasting AG was highest in patients in group 2 (465 Ϯ 128 Studies have reported a potential role for ghrelin in children pg/mL) versus group 1 (176 Ϯ 37 pg/mL) and group 3 (190 Ϯ 34 with Helicobacter pylori infection, a gastrointestinal disease pg/mL). IGF-1 was lowest in patients in group 2 despite similar that has been associated with poor growth (4). Some studies prealbumin levels among the three groups. We conclude that serum have shown that tissue concentrations of ghrelin are decreased AG levels are highest in children with isolated poor weight gain in the stomach in the presence of H. pylori infection, whereas compared with children with short stature or chronic gastrointestinal symptoms, suggesting the possibility of resistance to AG in under- others have shown that serum levels of acylated ghrelin (AG), weight children. Additional studies are needed to further clarify the active form of the peptide, are decreased (5–7). Other ghrelin’s role in growth and appetite. (Pediatr Res 69: 517–521, studies dispute these findings (8). Of particular interest, there 2011) are several other gastrointestinal diseases in children that may present with poor growth as a presenting symptom, including any children are referred to pediatric endocrinologists celiac disease and inflammatory bowel disease. Many patients M and gastroenterologists for evaluation of poor growth. with these disorders have nonspecific symptoms such as ab- There is often considerable overlap in the clinical presentation dominal pain, dyspepsia, or poor appetite (9). It is still un- of patients given the diagnosis of “failure-to-thrive,” or known how ghrelin levels are altered in these disease states. “growth failure” with some patients presenting with poor Thus, the potential relationships between gastrointestinal dis- linear growth, others with poor weight gain, and some with ease, ghrelin, growth, and appetite are still unclear. both. In addition, children with poor linear growth are often Underweight children have been found to have elevated poor eaters and have gastrointestinal symptoms (1). ghrelin levels, but only one study has shown low height SD Extensive workup, including a broad panel of screening score (SDS) as an independent determinant of elevated AG laboratories looking for the causes of poor growth, often fails levels in children with idiopathic short stature (10,11). Re- to reveal an underlying diagnosis. Therefore, there has been cently, in several patients, however, a missense mutation considerable interest in finding a definable link between poor resulting in a complete loss of GHSR constitutive activity has weight gain and poor linear growth. Ghrelin, a hormone that is been implicated in short stature with dominant transmission not routinely measured in this clinical setting, could theoret- (12). A syndrome of recessive isolated growth hormone defi- ically have a role in both poor growth and gastrointestinal ciency caused by mutations in the ghrelin receptor has also disease. been reported (13). We hypothesized that ghrelin could affect growth by two separate mechanisms: 1) by altering growth hormone secre- Received October 21, 2010; accepted December 29, 2010. Correspondence: Jordan E. Pinsker, M.D., Pediatric Endocrinology, Department of tion and subsequently affecting insulin-like growth factor Pediatrics, Mail Code: MCHK-PE, Tripler Army Medical Center, 1 Jarrett White Road, (IGF)-1 generation or 2) by stimulating appetite and food Honolulu, HI 96859; e-mail: [email protected] intake. The goal of this study was to test the first part of this Supported by the Tripler Army Medical Center Department of Clinical Investigation. The views expressed in this manuscript are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the U.S. Government. Abbreviations: AG, acylated ghrelin; GHSR, growth hormone secretagogue This study is registered at ClinicalTrials.gov, study number NCT01070173. receptor; SDS, SD score; TG, total ghrelin 517 518 PINSKER ET AL. hypothesis by determining how total ghrelin (TG), AG, and Kruskal–Wallis nonparametric, one-way ANOVA, comparing all three IGF-1 levels are altered in children with short stature and/or groups as a whole. Comparison between individual groups to determine specific differences between groups 1 and 2, 1 and 3, and 2 and 3 was poor weight gain. Therefore, we measured serum TG, AG, and completed using a t test. IGF-1 levels to determine whether they are altered in children In addition, age-, race-, and gender-adjusted height, weight, and BMI with these conditions. Currently, it is thought that AG is more z-scores were calculated for each patient in the study using the formula from the National Health and Nutrition Examination Survey. Comparison of height, important than TG as a marker of ghrelin activity (14). weight, and BMI SDS to ghrelin levels was performed to determine whether they were independently associated with ghrelin levels. METHODS Additional analysis was performed to determine whether there was a difference in IGF-1 and prealbumin levels among the three groups. Finally, Patients and measurements. All children who presented over a 6-mo subgroup analysis of ghrelin levels was performed to compare patients who period for their initial evaluation of isolated gastrointestinal symptoms, poor were eventually given an underlying diagnosis. All data are reported as the linear growth, or poor weight gain to the Tripler Army Medical Center mean Ϯ SEM. pediatric endocrinology and pediatric gastroenterology clinics and who sub- sequently required additional fasting laboratory workup were evaluated for RESULTS fasting serum TG and AG levels in addition to their standard of care workup. All ghrelin levels were drawn fasting at 0800 h. Children who presented for Fifty-two patients were recruited into the study. Eleven had similar symptoms but who did not require additional laboratory workup or who did not require fasting laboratories were excluded. chronic gastrointestinal symptoms without growth issues Patients were divided into three groups according to their presenting (group 1). Eight patients had poor weight gain (failure-to- symptoms: 1) isolated gastrointestinal symptoms without affects on growth or thrive), with weight significantly more affected than height weight gain, 2) failure-to-thrive (predominantly poor weight gain), and 3) short stature (or proportionally small height and weight). Patients with chronic (group 2). Thirty-three patients had short stature, with height gastrointestinal symptoms, defined as symptoms of gastrointestinal disease for being more affected than weight or were proportionally small, greater than 6 wk or recurrent symptoms but normal stature and growth, were with height and weight at similar percentiles (group 3). Except included in group 1. To be included in the failure-to-thrive group (group 2), subjects must have for two patients in group 1 and one in group 3, all patients had poor weight gain, defined as weight less than Ϫ2 SD for gender and age were prepubertal. Demographic data for all patients, including or less than expected rate of weight gain for gender and age. To be included mean height and weight SDS scores for each group, is sum- in the short stature group (group 3), subjects must have had short stature, defined as height less than Ϫ2 SD for gender and age or an abnormal growth marized in Table 1. velocity for gender and age. No difference was observed for mean fasting TG levels Patients who were affected in both weight and height were stratified by between groups 1, 2, and 3 (1157 Ϯ 105 pg/mL, 1264 Ϯ 245 which measurement was more severely affected, with poor weight gain being Ϯ ϭ the primary problem in the failure-to-thrive grouping (group 2) and poor pg/mL and 1063 77 pg/mL, respectively, p 0.217). These linear growth being the primary problem in the short stature group (group 3). values are similar to those reported by Soriano-Guille´n et al.
Load more

Recommended publications
  • Abstracts from the 9Th Biennial Scientific Meeting of The
    International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):15 DOI 10.1186/s13633-017-0054-x MEETING ABSTRACTS Open Access Abstracts from the 9th Biennial Scientific Meeting of the Asia Pacific Paediatric Endocrine Society (APPES) and the 50th Annual Meeting of the Japanese Society for Pediatric Endocrinology (JSPE) Tokyo, Japan. 17-20 November 2016 Published: 28 Dec 2017 PS1 Heritable forms of primary bone fragility in children typically lead to Fat fate and disease - from science to global policy a clinical diagnosis of either osteogenesis imperfecta (OI) or juvenile Peter Gluckman osteoporosis (JO). OI is usually caused by dominant mutations affect- Office of Chief Science Advsor to the Prime Minister ing one of the two genes that code for two collagen type I, but a re- International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):PS1 cessive form of OI is present in 5-10% of individuals with a clinical diagnosis of OI. Most of the involved genes code for proteins that Attempts to deal with the obesity epidemic based solely on adult be- play a role in the processing of collagen type I protein (BMP1, havioural change have been rather disappointing. Indeed the evidence CREB3L1, CRTAP, LEPRE1, P4HB, PPIB, FKBP10, PLOD2, SERPINF1, that biological, developmental and contextual factors are operating SERPINH1, SEC24D, SPARC, from the earliest stages in development and indeed across generations TMEM38B), or interfere with osteoblast function (SP7, WNT1). Specific is compelling. The marked individual differences in the sensitivity to the phenotypes are caused by mutations in SERPINF1 (recessive OI type obesogenic environment need to be understood at both the individual VI), P4HB (Cole-Carpenter syndrome) and SEC24D (‘Cole-Carpenter and population level.
    [Show full text]
  • Program Nr: 1 from the 2004 ASHG Annual Meeting Mutations in A
    Program Nr: 1 from the 2004 ASHG Annual Meeting Mutations in a novel member of the chromodomain gene family cause CHARGE syndrome. L.E.L.M. Vissers1, C.M.A. van Ravenswaaij1, R. Admiraal2, J.A. Hurst3, B.B.A. de Vries1, I.M. Janssen1, W.A. van der Vliet1, E.H.L.P.G. Huys1, P.J. de Jong4, B.C.J. Hamel1, E.F.P.M. Schoenmakers1, H.G. Brunner1, A. Geurts van Kessel1, J.A. Veltman1. 1) Dept Human Genetics, UMC Nijmegen, Nijmegen, Netherlands; 2) Dept Otorhinolaryngology, UMC Nijmegen, Nijmegen, Netherlands; 3) Dept Clinical Genetics, The Churchill Hospital, Oxford, United Kingdom; 4) Children's Hospital Oakland Research Institute, BACPAC Resources, Oakland, CA. CHARGE association denotes the non-random occurrence of ocular coloboma, heart defects, choanal atresia, retarded growth and development, genital hypoplasia, ear anomalies and deafness (OMIM #214800). Almost all patients with CHARGE association are sporadic and its cause was unknown. We and others hypothesized that CHARGE association is due to a genomic microdeletion or to a mutation in a gene affecting early embryonic development. In this study array- based comparative genomic hybridization (array CGH) was used to screen patients with CHARGE association for submicroscopic DNA copy number alterations. De novo overlapping microdeletions in 8q12 were identified in two patients on a genome-wide 1 Mb resolution BAC array. A 2.3 Mb region of deletion overlap was defined using a tiling resolution chromosome 8 microarray. Sequence analysis of genes residing within this critical region revealed mutations in the CHD7 gene in 10 of the 17 CHARGE patients without microdeletions, including 7 heterozygous stop-codon mutations.
    [Show full text]
  • Blueprint of Pediatric Endocrinology Book
    See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/317428263 blueprint of pediatric endocrinology book Book · January 2014 CITATIONS READS 0 27 1 author: Abdulmoein Eid Al - Agha King Abdulaziz University 148 PUBLICATIONS 123 CITATIONS SEE PROFILE Some of the authors of this publication are also working on these related projects: HYPOPHOSPHATEMIC RICKETS, EPIDERMAL NEVUS SYNDROME WITH... View project HYPERTRIGLYCERIDAEMIA-INDUCED ACUTE PANCREATITIS IN AN INFANT: A CASE REPORT View project All content following this page was uploaded by Abdulmoein Eid Al - Agha on 09 June 2017. The user has requested enhancement of the downloaded file. IN THE NAME OF ALLAH, THE MERCIFUL, THE MERCY-GIVING iii Blueprint in Pediatric Endocrinology Abdulmoein Eid Al-Agha, MBBS, DCH, FRCPCH Pediatric Endocrinologist King AbdulAziz University Faculty of Medicine Jeddah, Saudi Arabia © King Abdulaziz University: 1435 A.H. (2014 AD.) All rights reserved. 1st Edition: 1435 A.H. (2014 A.D.) Table of Contents Chapter 1: Basic Endocrinology Introduction…………………………………………………………………….. 3 Effects of hormones…………………………………………………………….. 3 Types of hormones……………………………………………………………… 4 Types of Hormone Receptors………………...………………………………... 5 Loss – of – function mutations………………………………………………….. 7 Gain – of – function mutations……………………………...………………….. 9 Fetal Brain Programming ………………………………………………………. 10 The endocrine system ……………………………...…………………………... 10 Hypothalamic-Pituitary Relationships………………………………………….. 10 Hypothalamic Controls………………………………………………………….
    [Show full text]
  • Childhood Growth and Puberty Delay Disorders
    Childhood Growth and Puberty Delay Disorders MAJ Craig Barstow, MD ACTIVITY DISCLAIMER The material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations. The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP. 1 DISCLOSURE It is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of participation. Only those participants who had no conflict of interest or who agreed to an identified resolution process prior to their participation were involved in this CME activity.
    [Show full text]
  • Incorrect Unit of Measure
    We agree with Berman that there may often be honest dif- (2) make the rationale public, and (3) provide opportunities for ferences of opinion among informed experts about the value of clinicians and members to appeal policies and specific deci- new treatments. As stated in our article, our study cannot sions.1 However, even in the outstanding programs we were establish whether current practices are right or wrong. How- privileged to study in our research on policymaking, we and ever, the wide gap between the recommendations of physi- the program leaders agreed there was room for significant cians and the approvals of insurers in the cases under study improvement. underscores a potentially far-reaching problem in the US Ms Tesch’s letter on behalf of the Turner’s Syndrome Soci- health care system. We believe that insurers often make very ety provides an example of well-conceived advocacy. The fact careful and fair analyses of information in arriving at coverage that GH has been recognized by the Food and Drug Admin- decisions.1 Nevertheless, greater dialogue between insurers istration as effective in the treatment of Turner syndrome and physicians is needed to minimize discrepancies in cover- puts a burden of explanation onto an insurer who chooses not age and to provide optimal patient care. to cover it. In asking whether decisions to deny coverage re- Dr Yaes asks about consensus among physicians for the flect “reasonable cost-benefit analysis or an inappropriate de- cases studied and about the value of a treatment such as GH, nial of care,” Tesch raises the key policy question in useful which is used for a non–life-threatening condition.
    [Show full text]
  • Guideline for the Diagnosis and Treatment of Celiac
    JOBNAME: gas 40#1 2005 PAGE: 1 OUTPUT: Wed December 15 18:39:15 2004 lww/gas/84141/MPG157309 Prod #: MPG157309 MS #xxx Journal of Pediatric Gastroenterology and Nutrition 40:1–19 Ó January 2005 Lippincott Williams & Wilkins, Philadelphia Clinical Guideline Guideline for the Diagnosis and Treatment of Celiac Disease in Children: Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition ABSTRACT The Committee examined the indications for testing, the value Celiac disease is an immune-mediated enteropathy caused by of serological tests, human leukocyte antigen (HLA) typing and a permanent sensitivity to gluten in genetically susceptible in- histopathology and the treatment and monitoring of children dividuals. It occurs in children and adolescents with gastroin- with celiac disease. It is recommended that children and ado- testinal symptoms, dermatitis herpetiformis, dental enamel lescents with symptoms of celiac disease or an increased risk defects, osteoporosis, short stature, delayed puberty and persis- for celiac disease have a blood test for antibody to tissue tent iron deficiency anemia and in asymptomatic individuals transglutaminase (TTG), that those with an elevated TTG be with type 1 diabetes, Down syndrome, Turner syndrome, Williams referred to a pediatric gastroenterologist for an intestinal biopsy syndrome, selective immunoglobulin (Ig)A deficiency and first and that those with the characteristics of celiac disease on degree relatives of individuals with celiac disease. The Celiac intestinal histopathology be treated with a strict gluten-free Disease Guideline Committee of the North American Society diet. This document represents the official recommendations of for Pediatric Gastroenterology, Hepatology and Nutrition has the North American Society for Pediatric Gastroenterology, formulated a clinical practice guideline for the diagnosis and Hepatology and Nutrition on the diagnosis and treatment of treatment of pediatric celiac disease based on an integration of celiac disease in children and adolescents.
    [Show full text]
  • Children with Idiopathic Short Stature Are Poor Eaters and Have Decreased Body Mass Index
    Children With Idiopathic Short Stature Are Poor Eaters and Have Decreased Body Mass Index Stefan A. Wudy*; Sandra Hagemann, MD*; Astrid Dempfle, PhD‡; Gundula Ringler, MSC‡; Werner F. Blum*§; Lars D. Berthold, MD࿣; Gerhard Alzen࿣; Ludwig Gortner¶; and Johannes Hebebrand# ABSTRACT. Objective. In children with idiopathic s.org/cgi/doi/10.1542/peds.2004-1684; eating behavior, short stature (ISS), studies investigating body mass index short stature, body mass index, leptin, ghrelin. (BMI) or parameters of satiety regulation are scarce, and studies analyzing eating behavior are lacking. Methods. We recruited 214 children (123 index cases ABBREVIATIONS. CDGP, constitutional delay of growth and and 91 siblings) with ISS from 123 families. Affected puberty; FSS, familial short stature; ISS, idiopathic short stature; IGF-I, insulin-like growth factor I; IGFBP-3, insulin-like growth children had to have a body height <5th percentile, or, in factor–binding protein 3; CEBQ, Child Eating Behavior Question- the case of siblings, the body height of 1 child had to be naire; SDS, standard deviation score; LFFQ, Leeds Food Fre- <5th percentile and the other <15th percentile. Medical quency Questionnaire. histories were recorded by using structured and stan- dardized interviews. Eating behavior was assessed by using the Child Eating Behavior Questionnaire. Percent hort stature is the most common cause for re- energy intake as fat was assessed by using the Leeds ferrals to pediatric endocrinologists. Many of Food Frequency Questionnaire. Endocrine markers of these patients have no identifiable medical ab- body weight regulation (leptin, ghrelin) were determined S normality and are classified with diagnoses such as in serum.
    [Show full text]
  • Short Stature in Childhood — Challenges and Choices
    T h e new england journal o f medicine clinical practice Short Stature in Childhood — Challenges and Choices David B. Allen, M.D., and Leona Cuttler, M.D. This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the authors’ clinical recommendations. From the Division of Pediatric Endocri- A family seeks evaluation and treatment of short stature in their 11.5-year-old son. He nology and Diabetes, American Family previously was in the 3rd percentile for height, but his growth rate has slowed during Children’s Hospital, University of Wis- consin School of Medicine and Public the past 2 years, and his height is now just below the 1st percentile (Fig. 1). His moth- Health, Madison (D.B.A.); and the Center er is 5 ft 0 in. (152 cm), and his father is 5 ft 6 in. (167 cm). The child’s size at birth was for Child Health and Policy and the Divi- normal. His medical history and a review of systems are unremarkable. His physical sion of Endocrinology and Diabetes, Rainbow Babies and Children’s Hospital, examination is normal and shows prepubertal development. The complete blood count, Case Western Reserve School of Medi- erythrocyte sedimentation rate, thyrotropin, tissue transglutaminase antibody, and cine, Cleveland (L.C.). Address reprint insulin-like growth factor I (IGF-I) levels and growth hormone levels after provoca- requests to Dr. Allen at the University of Wisconsin School of Medicine and Public tive testing are normal.
    [Show full text]
  • Prevalence of Short Stature and Malnutrition Among Egyptian Primary School Children and Their Coexistence with Anemia Ali M
    El-Shafie et al. Italian Journal of Pediatrics (2020) 46:91 https://doi.org/10.1186/s13052-020-00855-y RESEARCH Open Access Prevalence of short stature and malnutrition among Egyptian primary school children and their coexistence with Anemia Ali M. El-Shafie1 , Zeinab A. Kasemy2 , Zein A. Omar1 , Safa H. Alkalash3, Amal A. Salama3, Kerollos S. Mahrous1,4* , Shaimaa M. Hewedy5, Nessreen M. Kotb5, Heba S. Abd El-Hady5, Eman S. Eladawy5, Mohamed A. Zeid5, Manar E. Abd El Hamid5, Emad H. Hemeda5, Mohamed A. El-shafie5, Esraa A. El-Meligy5 and Wael A. Bahbah1 Abstract Background: Under nutrition and overweight typically occur during nutritional transition periods in developing countries including Egypt. Short stature and anemia are public health concern due to its strong link with malnutrition which is a preventable risk factor. Objectives: to estimate the prevalence of overweight, obesity, underweight and short stature and its concurrence with anemia, also to determine the etiological profile of short stature among primary school children in Egypt. Methods: A cross-sectional study was carried out on 33,150 Egyptian children aged 6–11 years old from January 2018 to January 2020, allocated in 59 primary schools from diverse geographical districts in Egypt. Complete anthropometric measurements were conducted and applied according to WHO growth charts. Hemoglobin level was measured. Systematic approach to detect the etiology of short stature was applied randomly to a sample of 380 stunted children. Results: The prevalence of underweight was 8.2%, while obesity and overweight represented 21.8% (9.6 and 12.2% respectively). Overall short stature constituted 17%.
    [Show full text]
  • Causes of Short Stature Author: Alan D Rogol, MD, Phd Section Editors
    Causes of short stature Author: Alan D Rogol, MD, PhD Section Editors Peter J Snyder, MD Mitchell Geffner, MD Deputy Editor Alison G Hoppin, MD Contributor disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Mar 2016. | This topic last updated: Aug 13, 2015. INTRODUCTION — Short stature is a term applied to a child whose height is 2 standard deviations (SD) or more below the mean for children of that sex and chronologic age (and ideally of the same racial-ethnic group). This corresponds to a height that is below the 2.3rd percentile. Short stature may be either a variant of normal growth or caused by a disease. The most common causes of short stature beyond the first year or two of life are familial (genetic) short stature and delayed (constitutional) growth, which are normal non-pathologic variants of growth. The goal of the evaluation of a child with short stature is to identify the subset of children with pathologic causes (such as Turner syndrome, inflammatory bowel disease or other underlying systemic disease, or growth hormone deficiency). The evaluation also assesses the severity of the short stature and likely growth trajectory, to facilitate decisions about intervention, if appropriate. This topic will review the main causes of short stature. The diagnostic approach to children with short stature is discussed separately. (See "Diagnostic approach to children and adolescents with short stature".) NORMAL VARIANTS OF GROWTH Familial short stature — Familial or genetic short stature is most often a normal variant, termed familial or genetic short stature (figure 1).
    [Show full text]
  • Nutrition and Growth
    J Clin Res Ped Endo 2009;1(4):157–163 ISSN: 1308-5727 DOI: 10.4274/jcrpe.v1i4.39 Online ISSN: 1308-5735 Nutrition and Growth Fima Lifshitz President, Pediatric Sunshine Academics, Inc; Director of Pediatrics & Senior Nutrition Scientist, Sansum Medical Research Institute, Santa Barbara, CA, USA and Professor of Pediatrics, Emeritus, Downstate Medical Center, State University of New York, Brooklyn, NY, USA; Former Professor of Pediatrics, Cornell University Medical College, New York, NY & University of Miami, Miami, FL, USA Keywords: ABSTRACT Nutritional growth retardation (NGR), nutrient intake, short stature, growth retardation, Nutrition plays a fundamental role in determining the growth of individuals. An appropri- metabolic rates, erythrocyte ate growth progression is considered a harbinger of adequate nutrient intake and good Na+,K+- ATPase activity. health. On the other hand growth deceleration with or without short stature may indicate inadequate nutrition, even when there is no body weight deficit for height. Nutritional growth Received: 11 November, 2008 Accepted: 04 December, 2008 retardation (NGR) is most prevalent in populations at risk of poverty. However in affluent com- munities patients with NGR are often referred to the specialist because of short stature and Corresponding Author: delayed sexual development. The diagnosis may be overlooked and/or be established after Fima Lifshitz exhaustive evaluations, if the pattern of weight progression over time is not considered. Pediatric Sunshine Academics, Inc. Director of Pediatrics & Patients with so-called idiopathic short stature may present diminished nutrient intake and Senior Nutrition Scientist decreased IGF-I levels, however their nutritional status and body weight progression patterns Sansum Medical Research are usually not addressed by pediatric endocrinologists.
    [Show full text]
  • Growth Hormone [Somatropin]
    Cigna National Formulary Coverage Policy Prior Authorization Growth Disorders - Growth hormone [somatropin] Table of Contents Product Identifer(s) National Formulary Medical Necessity ................ 1 12988 Conditions Not Covered....................................... 8 Background ........................................................ 10 References ........................................................ 14 Revision History ................................................. 16 INSTRUCTIONS FOR USE The following Coverage Policy applies to health benefit plans administered by Cigna Companies. Certain Cigna Companies and/or lines of business only provide utilization review services to clients and do not make coverage determinations. References to standard benefit plan language and coverage determinations do not apply to those clients. Coverage Policies are intended to provide guidance in interpreting certain standard benefit plans administered by Cigna Companies. Please note, the terms of a customer’s particular benefit plan document [Group Service Agreement, Evidence of Coverage, Certificate of Coverage, Summary Plan Description (SPD) or similar plan document] may differ significantly from the standard benefit plans upon which these Coverage Policies are based. For example, a customer’s benefit plan document may contain a specific exclusion related to a topic addressed in a Coverage Policy. In the event of a conflict, a customer’s benefit plan document always supersedes the information in the Coverage Policies. In the absence of a controlling federal or state coverage mandate, benefits are ultimately determined by the terms of the applicable benefit plan document. Coverage determinations in each specific instance require consideration of 1) the terms of the applicable benefit plan document in effect on the date of service; 2) any applicable laws/regulations; 3) any relevant collateral source materials including Coverage Policies and; 4) the specific facts of the particular situation.
    [Show full text]