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[Clinical use of growth hormone and clonidine in growth disorders].

The aim of this study was to investigate the effects of the recombinant human growth hormone and of the alpha-2 adrenergic agonist clonidine in three groups of prepuberal children with growth disorders. Three children with GH-deficiency were treated with 0.5 U kg/week i.m. of recombinant growth hormone; 13 children (7 with constitutional delay of growth and 6 with familiar short stature) were treated with 0.08 mg/m2/die per os of clonidine. The results confirmed the growth promoting effect of GH in GH-deficiency. Clonidine restored GH-secretion in children with constitutional delay, but had a very poor or no effect in familiar short children.

Adolescent↗
PubMed2001

The growth hormone and insulin-like growth factor axis: its manipulation for the benefit of growth disorders in renal failure.

Renal failure is associated with dramatic changes in the growth hormone/insulin-like growth factor (GH/IGF) axis. In children, this results in growth retardation, which is treated with injections of recombinant human GH (rhGH). Given the many recent advances in the knowledge of the components of the GH/IGF axis, it is timely to review the role of GH in renal failure and to discuss likely new treatments for growth failure. Renal failure is not a state of GH deficiency but a state of GH and IGF resistance, making other approaches to manipulating the GH axis more logical than treatment with rhGH alone. Although in children rhGH is safe, in critically ill adults it can be lethal. As the mechanisms of these lethal actions of rhGH are unknown, caution is advised when using rhGH outside approved indications. In renal failure, an optimal balance between safety and efficacy for growth may be achieved with the use of the combination of rhGH and rhIGF-I, as animal studies have shown synergistic growth responses. However, inhibition of the GH axis, with the use of GH antagonists, is likely to be tested clinically given the beneficial effects of GH antagonists on renal function in animal models of renal disease. Manipulating IGF-I by either administering rhIGF-1 or its binding proteins or increasing IGF-I bioavailability with the use of IGF displacers could prove to be a safer and more effective alternative to the use of rhGH in renal failure. In the future, both rhGH and rhIGF-1 likely will be included in growth-promoting hormone cocktails tailored to correct specific growth disorders.

Growth Disorders↗
PubMed2003

Double heterozygosity in bone growth disorders: four new observations and review.

Because matings between individuals of small stature is common, information regarding double heterozygosity for dominantly inherited bone growth disorders is of considerable importance. We summarize seven occurrences of four combinations of double heterozygosity (achondroplasia/spondyloepiphyseal dysplasia congenita, achondroplasia/pseudoachondroplasia, achondroplasia/osteogenesis imperfecta type I, achondroplasia/hypochondroplasia (non-FGFR3)), and review additional reports from the literature. Each of the eight different examples of double heterozygosity for bone growth disorders now reported results in distinct phenotypic features, differing severity, and disparate expectations. We document the natural history of each. The genetic processes underlying these disorders also are examined to assess whether knowledge of molecular mechanisms can be used to predict clinical severity.

Abnormalities, Multiple↗
PubMed1997

Urinary IGF and IGF binding protein-3 in children with disordered growth. The North West Paediatric Endocrine Group.

OBJECTIVE: Both IGF-I and IGFBP-3 reflect spontaneous GH secretion in healthy individuals. We have evaluated the clinical usefulness of urinary IGF-I and IGFBP-3 measurements in the diagnosis of children with disordered growth. DESIGN: Serum IGF-I and IGFBP-3 radioimmunoassays (RIA) were developed, and modified for quantitation in urine. The relationship between serum and urine levels, and the performance of these tests in the diagnosis of GH deficiency (GHD) were examined. PATIENTS: Sixty-nine children (age 9.5 +/- 3.6 years; 37 boys, 32 girls) provided a timed overnight urine collection and a serum sample collected on the same morning. Subjects were defined as GHD (n = 22) or short normal (SN; n = 47) on the basis of medical history, clinical examination, auxology and peak response to a GH stimulation test (< 20 mU/L in GHD patients). MEASUREMENTS: IGF-I and IGFBP-3 in serum and urine were measured by RIA, urinary GH (uGH) by immunoradiometric assay (IRMA) after dialysis and urinary creatinine by the alkaline picrate method. Urine results were expressed as total amount excreted (tulGFBP-3 (microgram), tulGF-1 (ng), tuGH (ng), tuCrt (mmol). RESULTS: Urine IGF-I and IGFBP-3 excretion correlated significantly to serum levels of IGF-I and IGFBP-3 and also to tuGH excretion. There was a strong positive relationship between both urinary peptides and tuCrt, which suggested that renal filtration was the source of these peptides in urine. In addition, there were significant correlations with age, bone age and height SD score, of similar magnitude to those for tuGH. In prepubertal children, serum IGF-I and IGFBP-3 were significantly lower in GHD compared with SN children, while in puberty only serum IGFBP-3 was significantly lower in GHD. There was no difference however, in tulGF-I or tulGFBP-3 between GHD and SN children either prepubertally or in puberty with near complete overlap of the values between groups. CONCLUSIONS: Measurements of tulGF-I and tulGFBP-3 have no place in the diagnosis of childhood GHD. Nonetheless, the significant correlations between serum and urinary IGF-I and IGFBP-3 levels and their correlation to uGH indicate that these peptides could be used as non-invasive physiological markers of the GH-IGF axis.

Adolescent↗
PubMed1991

Body water measurement in growth disorders: a comparison of bioelectrical impedance and skinfold thickness techniques with isotope dilution.

Total body water was estimated as part of the assessment of body composition in children with growth disorders, using the newly commercially available method of bioelectrical impedance. This was undertaken to compare the precision and accuracy of the results with those derived from skinfold thickness against measurement of stable isotopically labelled water (H2(18)O) dilution as a standard. The comparisons were carried out to see to what extent the impedance method could be applied with confidence to assessment of children with growth disorders. Total body water was derived from impedance (I) using an association with height (Ht2/I). Impedance and skinfold thickness estimates of total body water were equally precise when compared with values obtained from H2(18)O dilution (limits of agreement -1.9 to +1.3 and -1.7 to +2.0 kg respectively). The mean intraobserver coefficient of variation for repeat measurements of impedance was 0.9% compared with 4.6% for skinfold thickness with an interobserver coefficient of variation for impedance of 2.8%. Bioelectrical impedance estimation of body composition is likely to be of value in the growth clinic when expertise in measurement of skinfold thickness is limited or repeated measurements are to be undertaken by different observers.

Body Composition↗
PubMed1991

Serum concentrations of the type I and III procollagen propeptides as biochemical markers of growth velocity in healthy infants and children and in children with growth disorders.

The reproducibility and specificity of a new, rapid, simple RIA for measuring the concentration of the soluble carboxypropeptide of type I procollagen (PICP) in serum was confirmed. Serum PICP was determined in 442 healthy Caucasian subjects ranging in age from 3 wk to 18 y. Highest PICP values (mean +/- SD: 2200 +/- 350 micrograms/L) occurred in infants less than 3 mo of age, falling by 70% at 2 y and by an additional 10% at 4 y. There was no significant change in serum PICP between 4 and 16 y of age (330 +/- 130 micrograms/L), but a decrease to adult levels of less than 160 micrograms/L occurred by 18 y. In 76 children with growth disorders, serum PICP was related to linear growth velocity (p less than 0.001), although there were no significant differences in PICP among the 38 children with growth hormone insufficiency, the 21 short children with no endocrinologic abnormality, or the 17 tall children. All 15 prepubertal children treated with growth hormone for 3 mo showed significant increases in both growth velocity and serum PICP, with a significant relationship (p less than 0.01) between the degree of increases. The rise in serum PICP at 3 mo (but not baseline PICP values) predicted the increase in growth velocity after 1 y of treatment. Similar changes were observed in the concentration of the aminopropeptide of type III procollagen, except that serum aminopropeptide of type III procollagen showed a definite increase during puberty and a wider spread of values in growth disorders. We conclude that measuring serum PICP by the new, reproducible assay reflects height velocity in prepubertal children and may be a useful biochemical means of monitoring growth rates.

Adolescent↗
PubMed1992

The school nurse's role: early detection of growth disorders.

Many school-age children with short stature or apparent growth excess are growing normally; however, for the minority of children experiencing growth problems, treatment may be indicated. The school nurse is in an ideal position to perform a preliminary growth-screening program. For accurate identification of potential growth problems, children must be properly weighed and measured, and the numbers plotted on a growth chart. Growth disorders can be caused by numerous underlying pathologies and diseases. Knowledge of these conditions can raise the index of suspicion so that appropriate referral can be made.

Child↗
PubMed1980

[Contribution of the IGF (insulin-like growth factors or somatomedins) competitive binding assay in the study of growth disorders in children (results for 124 observations) (author's transl)].

A competitive binding assay for IGF (insulin-like growth factors) employing a specific carrier protein produced by rat liver in culture has been used in a study of a variety of growth disorders in children. In 34 subjects with a total somatotropic deficiency, serum IGF levels were significantly (p < 0.001) lower than those in normal children for whom the means were 0.57 +/- 0.05 (SEM) U/ml between the ages of 1 and 5, and 1.01 +/- 0.11 U/ml between the ages of 5 and 15. Within this group of patients, there was also a significant difference in IGF levels depending on whether the deficiency was idiopathic (0.16 +/- 0.03 U/ml) or caused by a tumour (0.49 +/- 0.06 U/ml). IGF levels were particularly low in 2 cases of Laron's syndrome (0.08 and 0.03 U/ml) and 6 cases of coeliac disease (0.19-0.27 U/ml). In the later group, a gluten-free diet resulted in a rise in IGF levels. However, the stunted growth observed in 10 cases of Cushing's syndrome was found to be independent of IGF levels which fell within the normal range (1.02 +/- 0.11 U/ml). For 34 children investigated because of idiopathic retarded growth varying from --2 to --4 SD, the mean IGF levels (0.68 +/- 0.04 U/ml) were significantly lower than controls (p < 0.001). By contrast, abnormally high IGF levels were found in children with tall stature (> 3 SD). In 7 children aged between 1 and 5, the mean was 0.94 +/- 0.05 U/ml and in 17 older patients, 1.47 +/- 0.11 U/ml, with some cases reaching levels similar to those of untreated acromegalics. In both age groups the means were significantly higher than control levels (p < 0.001). Oestrogen treatment led to a progressive drop in IGF levels accompanied by slower growth, and normal levels were reached by the time ossification was established.

Adolescent↗
PubMed1990

Serum growth hormone levels measured by radioimmunoassay and radioreceptor assay: a useful diagnostic tool in children with growth disorders?

Serum GH levels were measured by RIA and RRA in 133 subjects (19 healthy controls and 114 patients with various growth disturbances, aged 2.3-24.8 yr). Serum samples obtained from 147 stimulation tests representing a total of 1065 samples were analyzed by both methods, and the results compared. The data are expressed in absolute values and in RRA/RIA ratios. The area under the curve after a stimulation test (area GH) was calculated by planimetry. RIA was performed by the classical double antibody method using a polyclonal anti-serum. For the RRA, human cultured lymphocytes (IM-9 cells) were used, and 125I-labeled human GH was purified by high performance liquid chromatography. The same human GH standard was used in both assay systems. In control subjects a significant (P less than 0.0001) positive correlation was found at all ages between GH levels measured by RIA and RRA (r = 0.69 after insulin and r = 0.77 after glucagon). The RRA/RIA ratio (mean +/- SEM) for the peak GH level was 0.88 +/- 0.05, and the area under the GH curve was 0.85 +/- 0.05. The peak mean RRA/RIA ratios were significantly lower (P less than 0.05 and P = 0.03, respectively). No relationship was found with the absolute value of either peak or area GH. In patients with growth delay and Turner's syndrome, lower GH levels were found than in control subjects in both assay systems. The RRA/RIA ratios were also lower. In the other patients with some growth disorder, normal GH levels and ratios were found. In patients with renal failure, high levels of RIA-GH and RRA-GH were found, with a normal RRA/RIA ratio. In patients with documented pituitary GH deficiency, GH-releasing factor administration resulted in an increase in GH levels that was identical in both assays. The RRA/RIA ratio remained constant throughout the test. No correlation was found between the ratio and the absolute value of either RIA-GH or RRA-GH regardless of the stimulation test used. It is concluded that the presence of an abnormal GH molecule is extremely rare in patients with short stature. Thus, the presence of a bioinactive hormone is not a common cause of growth failure. During provocative testing some changes in the ratio may occur that do not appear after GH-releasing factor, further illustrating the different mechanisms involved in GH secretion.

Adolescent↗
PubMed1989

[Growth disorders. Recommendations for a practice-oriented classification].

Besides acute illnesses, including allergies, growth disturbances are among the most frequent reasons for parents to consult a physician about their children. The basis of diagnosis is a detailed family and personal history. Actual measurement of the parents is necessary for calculation of the patient's target height. The growth data obtained must be charted on percentile curves. Only in the second line of the diagnostic approach should the physician resort to hormone determinations and X-rays of the left hand and wrist for bone age determination. For practical purposes, growth aberrations may be subdivided into normal variants and pathologic processes. The latter may cause proportionate or disproportionate disturbances. For therapeutic reasons it is also important to know whether the deviation of growth started pre- or postnatally. Many growth disorders that develop postnatally are amenable to therapy. They include the following endocrinopathies associated with short stature: isolated growth hormone deficiency (treatment with hGH), congenital adrenal hyperplasia due to enzyme deficiencies (treatment by replacement of cortisol), idiopathic, iso-sexual precocious puberty (treatment with LHRH agonists), and hypothyroidism (treatment with thyroxine). Patients with Turner syndrome benefit from sex hormones only insofar as secondary sexual characteristics develop: these agents do not promote overall growth. The treatment of patients with tall stature by administration of estrogens/gestagens in high dosages is viewed with increasing scepticism. On the average, only a 4-cm reduction in length can be achieved if patients are treated from the onset of puberty through a bone age of 16 years. All secondary growth disturbances are improved by efficient treatment of the primary, underlying disease entity.

Body Height↗
PubMed1994

[Screening for a growth disorder using the Dr. Keller precision measuring instrument and system].

The regulation of growth is as complex process involving the interaction of a number of genetic, hormonal, psychosomal, and environmental factors. Abnormal growth is an alarming sign for the worsening of health. Therefore is it necessary to provide exact and quick information about the growth of the child. With the body length device "System Dr. Keller" is it possible to collect 1. exact data about the actual height of a child, 2. information about the normal range of height for the chronological age of a child, 3. information about abnormal height (< 3., > 97. percentile) of a child. These informations are visible exclusively by application of the "System Dr. Keller". With use of this unique system and the data of corresponding national growth studies it will be possible to screen the whole population by paediatricians, general practitioners, school doctors, health care centers, outpatient departments and hospitals. While normal growth usually represents health, growth disorders should stimulate doctors to exclude possibly underlying pathological processes.

Adolescent↗
PubMed2003

Evaluation of growth disorders in the paediatric clinic.

Growth is one of the most important indicators of child's well-being. The growth pattern is the result of the complex interaction between genetic and environment factors. The gold standard for the diagnosis of GH-deficient (GHD) children is not yet defined. In this review we focused on sensitivity and specificity of the commonly used test for GH secretion and neuroimaging evaluation. Initially, accurate determinations of height, weight, head circumferences and growth velocity should be performed and plotted on an appropriate growth chart. Once chronic non-endocrine diseases such as celiac disease, chronic inflammatory bowel diseases, liver disorders and renal failure have been excluded, children whose height is lower than the 2nd percentile or 2 SD below the mean associated with a decreased height velocity (less than 25th percentile), or height less than -2.4 SD alone, or height velocity less than 10th percentile alone, should be investigated for possible abnormalities in the GH-IGF-I axis. A single IGF-I determination will be the great diagnostic value in all patients with severe GHD or GH insensitivity. Stimulation tests and imaging studies will confirm the etiology. One of the major problems of the provocative tests lies in their poor reproducibility and in the great number of falsely abnormal responses observed also in normal children. Genetic tests are also indicated in all cases of genetic forms. Patients with growth failure and abnormal MRI findings have a very high probability of having GHD and can be identified easily by serum IGF-I or by GH testing. All patients with subnormal GH responses to pharmacological stimulation either with normal or low IGF-I concentration but normal MRI findings should be followed up before a diagnosis of GHD is firmly established.

Adolescent↗
PubMed1981

Growth of adipose tissue in infants, children and adolescents: variations in growth disorders.

In order to identify factors important in the growth of adipose tissue, four groups of children were studied. Infants of gestational diabetic mothers demonstrated increased fat cell numbers as early as age two months, a finding which accelerated with increasing age, and which was associated with persistent hyperinsulinemia and increasing obesity. Children with growth hormone deficiency increased their adipose cell number following treatment with exogenous hormone. Patients with the Prader-Willi syndrome, who developed obesity after the age of two, did so primarily via increases in fat cell size. Identical twins who were concordant for birthweight continued to have similar weights and total adipocyte numbers, while in those with discordant birthweights the smaller twin displays lower body weight and adipose cell number. The data indicate that growth hormone and insulin, as well as genetic factors, which may be modified by the in-utero environment, are important determinants of human adipose tissue mass.

Adipose Tissue↗
PubMed1990

Low prevalence of insulin-like growth factor-I gene mutations in human growth disorders.

In an attempt to identify genetic lesions contributing to human growth disorders, we evaluated a prospectively recruited group of children with growth failure for mutations in the insulin-like growth factor-I (IGF-I) gene. Two complementary approaches were used: Southern blot analysis to examine the large scale organization of the gene, and a solution hybridization, nuclease protection assay to identify small alterations, such as point mutations. From a total of 61 subjects studied, 52 had no organic basis for their short stature. Analysis of chromosomal DNA from these individuals failed to reveal any variation in the IGF-I gene except for a HindIII site polymorphism which maps near the 3' end of the last IGF-I exon. No single nucleotide substitutions were found within IGF-I-coding regions. Since the frequency of the length polymorphism was the same for both normal-sized and short individuals, it is unlikely to be associated with growth abnormalities. Our results suggest that there is minimal DNA sequence variability in the human IGF-I gene and that mutations in IGF-I exons are infrequent causes of growth failure.

Blotting, Southern↗