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PubMed1986

High resolution CT scanning of the pituitary gland in growth disorders.

We have performed 217 GEC 8800 CT scans of the hypothalamus and pituitary glands of 202 children with disorders of growth and development. Pituitary morphological abnormalities were common. Intrapituitary low density lesions were found in 17% of the whole series and in 58% of children with tall stature. Seventy-seven children with idiopathic growth hormone deficiency could be divided on the basis of pituitary morphology seen on CT scan into pituitary aplasia (n = 11) and pituitary hypoplasia (n = 53). Patients with pituitary aplasia had an absent adenohypophysis which probably dated from early intrauterine life and therefore could not be related to birth trauma. We have found a high incidence of evolving endocrinopathy in children with pituitary insufficiency: thus, if a short child is investigated the initial endocrine findings need to be repeated as the pattern of pituitary insufficiency changes with time. An evolving endocrinopathy starting in later childhood is suggestive of the presence of a cerebral tumour. Children with subnormal growth velocities and a normal growth hormone response to pharmacological tests have a wide spectrum of pituitary morphological abnormalities which may be associated with growth hormone neurosecretory dysfunction.

Adolescent↗
PubMed2002

[Growth disorders in Down's syndrome: growth hormone treatment].

BACKGROUND: The aim of the study was evaluate the short and long-term effects of growth hormone therapy in subjects affected by Trisomy 21. METHODS: The growth curves of 10 Down's syndrome patients (3 males and 7 females) aged between 21 and 35 years old were analysed. During pre- or peripuberty these subjects had received growth hormone (GH) therapy lasting an average of 3.02 years. At distance of between 10 to 15 years after the end of GH therapy, routine laboratory tests (thyroid hormones, glycemia, glycosylated hemoglobin, transaminase) were carried out together with a full hematological assay (hemochrome using leukocyte formula, morphological study of blood components). RESULTS: GH therapy resulted in an increased rate of growth among these subjects and a improvement in final stature of 5.16 cm in males and 7.35 cm in females. The long-term controls did not reveal any hematological changes or changes in HbA1c concentrations, thyroid function and hepatic function, thus confirming the absence of collateral effects of GH therapy in subjects with Down's Syndrome. CONCLUSIONS: In view of these results, we are convinced that GH therapy is extremely positive in trisomy 21, given the marked improvements in terms of growth, the absence of collateral effects and the possible psychological benefits of increased stature, in particular a better insertion in society.

Adult↗
PubMed2002

School nurses' experiences, concerns, and knowledge of growth disorders in children: development of a monograph.

Growth disorders may be associated with difficult psychosocial adjustment, learning problems, and specific health risks. Appropriate school health programming relies on school nurses who are skilled in growth assessment, management of psychosocial and behavioral problems, and effective communication with school personnel, children, families, and health care resources. A monograph and model individualized healthcare plans were developed for growth disorders in school-age children as an educational resource for school nurses. Knowledge of growth disorders among nurses receiving the monograph was evaluated in a random sample of 336 school nurses, members of the National Association of School Nurses. Knowledge of growth assessment and individualized health care plans for children with specific growth disorders was significantly higher in the group of school nurses who received the monograph. Specific obstacles to implementing school-based health care for children with growth disorders are discussed.

Adult↗
PubMed1995

Normal growth and growth disorders in children.

Growth in children is influenced by innumerable factors, and to achieve optimal final height, the child has to be healthy, its nutrition sufficient, and the psychosocial environment stimulating and positive. During the 1st year of life nutritional factors and thyroid hormone seem to be the most important regulators of growth; during the following years growth hormone increases in importance. Puberty and its timing are factors of greatest importance during the 2nd decade of life; disturbances in puberty will compromise final height. Increased understanding of factors influencing growth and increased access to growth hormone and analogs of hormone that influence the timing of puberty have made it possible to increase final height in some groups of patients predisposed to short stature.

Adolescent↗
PubMedDate not supplied

Short-term growth in children with growth disorders.

OBJECTIVE: We have previously demonstrated that normal prepubertal growth over 1 year is composed of growth spurts lasting an average of 8 weeks, separated by periods of very slow growth or stasis. We have now analysed short-term growth patterns in eight children with different growth disorders: Turner syndrome (n = 2), intrauterine growth retardation (IUGR, n = 1) and growth hormone (GH) deficiency (GHD, n = 5). METHODOLGY: Height was measured daily in the morning by parents over 4-12 months. Regression and time series analysis were used to characterize short-term growth. In two boys (GHD and IUGR) their normal twin brother was measured in parallel. RESULTS: All height velocity curves, based on regression analysis, showed a biphasic pattern, characterized by growth spurts of varying amplitudes and periods of very slow growth or growth stasis. When compared to growth curves in normal children, the principal qualitative differences in GHD and Turner syndrome were increased stasis time and reduced growth spurt amplitude. In IUGR reduced amplitude and length of growth spurts were seen, but the time spent in stasis was similar to normal children. Two naive patients with GHD increased the amplitude of their growth spurts by a mean 0.013 cm day(-1) on GH treatment, with the mean length of their growth spurts increasing by 10 days. Their time spent in stasis decreased from 19% to 6% on GH. In two subjects with GHD the growth pattern during maintenance GH treatment was similar to that seen in normal children. Using time series analysis significant periodicities in height measurements were seen in the majority of children with growth disorders, which disappeared in patients with GHD in the catch-up phase after commencing GH therapy. CONCLUSIONS: (1) The growth spurts and stases seen in normal children are also observed in those with growth disorders, (2) different growth disorders have variable effects on the spurt stasis model of childhood growth, (3) catch-up growth on GH in children with GHD was achieved by increasing the amplitude of the growth spurts and reducing the time spent in stasis.

Body Height↗
PubMed1987

Evaluation of growth disorders in children.

Both pediatricians and pediatric endocrinologists are frequently required to evaluate children for possible disorders of linear growth. This article reviews the factors which influence growth as well as the etiologies of short and tall stature, and discusses the clinical and laboratory evaluation of abnormal growth. Recent developments in the evaluation of children with growth disorders are highlighted.

Adolescent↗
PubMed2001

Computer-guided, population-based screening system for growth disorders (CrescNet) and on-line generation of normative data for growth and development.

The mean age at which the diagnosis of growth disorders such as Turner's syndrome, growth hormone (GH) deficiency or true GH-dependent gigantism is established is still rather late in many countries around the world. In addition, the question of secular trends in a given population and the rate at which childhood obesity is increasing in industrialized countries make it mandatory to establish a time-adapted system to develop percentiles for body height, weight and body mass index (BMI) and also to develop a screening system for growth disorders. In 1998 we established a network, now involving more than 160 paediatric practices in Germany and seven paediatric endocrinology departments. Paediatricians record heights, weights and growth velocities of all children in their care and systematically feed the data into the database at our centre usually by mailing formatted, structured data tickets. Data are then continuously analysed at the centre and the paediatricians in the network are informed immediately about their individual patients' growth situations via phone or E-mail (feedback system). Regular annual conferences including structured reports, scientific presentations and discussion groups are organized for all participants at our centre. By May 2001, the data of 83,721 children and adolescents had been analysed. The mean values for height were 1-1.5 cm higher than the mean values in the German Synthetic Growth Curve, which serves as an internal standard. However, and most importantly, in comparison with the internal standard and historical normative data from Germany and Switzerland, there is a continuous increase in the 97th percentile for weight and BMI, while the third percentile remains unchanged. In addition, many children with short stature and tall stature due to a variety of endocrine disorders and genetic diseases which had not been diagnosed previously are now being identified. In conclusion, the databank allows for a continuous adaptation of normative curves based on a large number of children in a given population, i.e. eastern Germany. Secondly, the system allows for detection of pathological growth curves and is already serving to diagnose growth disorders in a defined population in a systematic way.

Adolescent↗
PubMed1999

Relationship between serum and urinary insulin-like growth factor-I through childhood and adolescence: their use in the assessment of disordered growth.

OBJECTIVE: Serum insulin-like growth factor-I (sIGF-I) measurement as an index of growth hormone status has become a common test in the investigation of disordered growth. IGF-I may also be measured in the urine. The aims of this study were to investigate the correlation between serum and urinary IGF-I in normal children and compare their use in the evaluation of growth disorders. DESIGN: Normal ranges for serum and urinary IGF-I were devised from a cross-sectional study of normal schoolchildren. These were then used to assess the sensitivity and specificity of serum and urinary IGF-I in the diagnosis of childhood GH deficiency. PATIENTS: A cohort of 333 (M = 156, F = 177) healthy schoolchildren aged 5-19 years were recruited and data previously collected from 22 growth hormone deficient (GHD) and 47 short normal (SN) children were compared with those of the normal children. MEASUREMENTS: Height, weight and pubertal status were assessed in all children. Serum IGF-I (sIGF-I) (n = 305) and total amount of urinary IGF-I excreted overnight (TuIGF-I) (n = 205) were measured by RIA using excess IGF-II to block the interference of IGFBPs. RESULTS: Serum IGF-I was loge transformed and overall levels (geometric mean +/- 1 tolerance factor) were higher in females than males (F: 569 (329, 985) micrograms/l; M: 398 (227, 696) micrograms/l). LogeIGF-I correlated with age (F: r = +0.76, P < 0.001, M: r = +0.71, P < 0.001) and was significantly affected by both sex and Tanner stage of puberty (TS) (both P < 0.001). The distribution of TuIGF-I was normalized by performing a square root transformation (square root of TuIGF-I). square root of TuIGF-I was correlated with age (F: r = +0.36, P < 0.001; M: r = +0.5, P < 0.001) and was significantly affected by TS (P < 0.001). In both sexes there was a highly significant correlation between logeIGF-I and square root of TuIGF-I (F: r = +0.39, P < 0.001; M: r = +0.41, P < 0.001). Using the third centile of our normal ranges as a cut off to identify GHD, sIGF-I had a sensitivity of 82% and specificity of 62%, whereas TuIGF-I had a sensitivity of 18% and specificity of 79%. CONCLUSIONS: This study demonstrates that although urinary IGF-I has no place in the diagnosis of growth disorders, in normal children there is a highly significant relationship between serum and urinary IGF-I with levels of each changing in a similar manner through childhood and adolescence. Thus, TuIGF-I could be used as a valid surrogate for sIGF-I in the physiological assessment of the relationship between IGF-I status and the normal growth process.

Adolescent↗
PubMed2000

Growth hormone use in pediatric growth hormone deficiency and other pediatric growth disorders.

The diagnosis and management of growth disorders in children, particularly disorders that respond to therapy with growth hormone (GH), raise challenging clinical and economic issues. Several such issues are presented in the following article in which Dr. Ron Rosenfeld examines the evaluation and diagnosis of the child with short stature; Dr. David B. Allen discusses the anabolic and metabolic indications for GH treatment in children; Dr. Margaret H. MacGillivray reviews GH dosing, height outcomes, and follow up; and Dr. Craig Alter presents the payer's perspective on the diagnosis and treatment of pediatric GH deficiency. In addressing the use of GH in other pediatric populations, Dr. Paul Saenger focuses on Turner syndrome, Dr. Henry Anhalt on chronic renal insufficiency of childhood, and Dr. Ray Hintz on idiopathic short stature. Dr. Harvey P. Katz presents one managed care organization's policy and implementation plan that is used to guide decisions regarding coverage for GH treatment.

Body Height↗
PubMed1988

[Genetic diagnosis of growth disorders].

The capability of examining genetic material with DNA probes and restriction endonucleases has opened up a new approach to clinical problems. Genetic disorders involving growth hormone can now be studied because the growth hormone gene (hGH-N) can be examined directly. Several distinct Mendelian disorders are associated with hGH deficiency. Some are caused by deletion of the hGH-N structural gene. In other instances, linkage analysis confirm that genetic disorders with hGH deficiency may be due to undetectable alterations in the hGH gene, or establish that the genetic abnormality does not involve the GH gene as such but rather affects some other gene essential for the production or release of factors involved in the regulation of growth hormone action.

Growth Disorders↗
PubMed2005

Child and adolescent growth disorders--an overview.

BACKGROUND: While many children presenting with apparent disorders of growth will be short or tall children growing normally, it is important to identify those children who have an underlying pathological cause. Parental expectation and anxiety will often accompany growth issues and this needs to be addressed. OBJECTIVE: The article aims to assist the clinician in distinguishing pathological short stature from normal variants, and to guide in the management of normal variants and common pathologies. DISCUSSION: Pathological short stature can be distinguished from normal variants by careful history and examination followed by accurate assessment of the growth parameters of height, weight, body proportions and growth velocity, and judicious use of investigations. Growth is a dynamic process that requires multiple measurements over time. If the patient has a nonpathological cause of short stature, explanation and reassurance are critical--for both the parents and child--to feel supported and comfortable with their height outcome.

Adolescent↗
PubMed1986

Sleep EEG in growth disorders.

The sleep of 30 children with disorders of growth and development was studied because of the known association between sleep and the secretion of hormones. Thirty three normal children were studied for comparison. The sleep of two consecutive nights was monitored at home using a small portable electroencephalogram and electro-oculogram recorder. Within the normal group there were no significant differences between sexes nor between the first and second nights of recording. There was a significant decrease in total sleep time with increasing age due to reduction in the amounts of rapid eye movement sleep and stage IV sleep. There was no change in rapid eye movement latency or overall rapid eye movement activity between the three age groups. Children with genetic short stature and those with poor growth as a result of poor eating habits had an increased percentage of rapid eye movement sleep. A significant decrease in the percentage of stage IV sleep, increased amount of rapid eye movement sleep (especially active rapid eye movement sleep), and decreased rapid eye movement cycling time was found in five children with severe psychosocial deprivation. Children with constitutional delay of growth and puberty had an increased rapid eye movement cycling time and thus less rapid eye movement sleep over the whole night.

Adolescent↗
PubMedDate not supplied

The association between prenatal and or post natal growth disorder and lipid profile in adolescents aged 12 - 15 years old in Tanjungsari Subdistrict, Sumedang, West Java.

AIM: to investigate association between growth disorders in pre and post natal period and abnormal lipid profile in adolescents aged 12 -15 years old in Tanjungsari population. METHODS: a cohort study was conducted in 3350 children who were born in 1988-1990 in Tanjungsari Subdistrict, Sumedang, West Java. A complete anthropometric data since their birth were collected from October 2002-February 2003. INCLUSION CRITERIA: Children who had birth weight in the range of +/- 3 of standard deviation (SD). Post natal growth disorder based on Z score of height according to age group and height changes at the age of 0-12 months and 12-36 months. SGA criteria were determined based on cross tabulation between weight and birth length at birth. Study subjects were divided into control group, groups of pre natal, post natal and pre-postnatal growth disorder. All subjects were checked for lipid profiles. Statistical calculation used analysis of variance, t test and logistic regression. 312 subjects were included in this study, 73 were in control group, 90 subjects in postnatal, 96 subjects were in pre natal and 53 subjects were in pre-post natal growth disorder group. RESULTS: this study has not shown significant difference in risk factor of having abnormal lipid profile between normal control group and growth disorder group except for those in prenatal growth disorder group with RR = 2.375 (p = 0.014). CONCLUSION: the post natal growth disorder had not influenced lipid profile in adolescents with SGA. Recent BMI was an additional risk factor for pre-post natal growth disorder group.

Adolescent↗