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At least 433 records · Page 24Linked to original sources
PubMed1996

Growth deficits in ADHD children revisited: evidence for disorder-associated growth delays?

OBJECTIVE: To reevaluate the hypothesis that stimulants cause growth deficits in children with attention-deficit hyperactivity disorder (ADHD). METHOD: Growth deficits in height and weight were examined in 124 children and adolescents with ADHD and 109 controls, using appropriate correction by age and parental height measures and attending to issues of pubertal stage, treatment, and psychiatric comorbidity. RESULTS: Small but significant differences in height were identified between ADHD children and controls. However, height deficits were evident in early but not late adolescent ADHD children and were unrelated to use of psychotropic medications. There was no evidence of weight deficits in ADHD children relative to controls, and no relationship between measures of malnutrition and short stature was identified. CONCLUSIONS: ADHD may be associated with temporary deficits in growth in height through mid-adolescence that may normalize by late adolescence. This effect appears to be mediated by ADHD and not its treatment.

Adolescent↗
PubMed1986

[Significance of radiologic skeletal age determination in clinical practice].

Skeletal development is an important maturity indicator during childhood. In clinical practice determination of skeletal age is helpful for the diagnosis of disorders of growth and development. Most hormones have specific effects on skeletal maturation. Thus, different disease states (growth disorders, disorders of pubertal development, chronic disorders of the bowels, kidneys, heart etc.) are characterized by retardation or acceleration of skeletal maturation. Therapeutic effects as well as side effects of hormones can be monitored by skeletal age determination. Typical disharmonic patterns in the appearance of bone centres of hand and wrist have been found in certain disorders of development.

Age Determination by Skeleton↗
PubMed1994

Short stature: a psychosocial burden requiring growth hormone therapy?

BACKGROUND: Changes in the diagnosis of endocrine-based growth disorders and the advent of biosynthetic growth hormone have altered the long-standing policy of treating only those individuals with "classic" growth hormone deficiency. One justification for treating short children is to improve their psychosocial adaptation. The present investigation assessed the positive and negative behavioral adaptation, self-perceptions of domain-specific competencies, and global self-worth of a large, diagnostically heterogeneous sample of children and adolescents referred to pediatric endocrinologists for a growth evaluation. METHODS: All patients seen in a pediatric endocrine clinic (180 boys and 78 girls; 4 to 18 years) with a height at the fifth percentile or lower were included. Parents of all participating children completed the Child Behavior Checklist. Patients 8 years and older completed the Self-Perception Profile and those 11 years and older, in addition, completed the Youth Self Report. Short-stature (SS) subjects were compared with normative and psychiatric samples. RESULTS: The SS boys were described by parents as being significantly less socially competent and showing more behavioral and emotional problems than a normative sample selected for mental health. However, they were significantly more socially competent and showed fewer psychopathologic symptoms than a psychiatric referred sample of comparable age. The SS boys described themselves as less socially active but did not report more behavior disturbance than the normative sample. The SS boys' self-perceptions of domain-specific competencies and global self-worth were comparable to a normative comparison group with the exception that older subjects (13 years or older) described their athletic abilities more positively and their work competence more negatively. The SS girls were, with few exceptions, indistinguishable from the normal comparison groups on both parent- and self-report measures of social competency and behavior disturbance. Younger SS girls (ages 8 to 12 years) described their athletic competence and behavioral conduct more positively than the comparison group on the self-esteem questionnaire. Patient height deficit was unrelated to scores on the three questionnaires. Finally, no statistically significant differences in psychosocial functioning were detected between children with "normal-variant" SS and those with pathologic growth disorders. SS and those with pathologic growth disorders. CONCLUSIONS: Short-stature girls show more adaptive psychosocial functioning than SS boys. In either sex, SS does not appear to be associated with clinically significant psychosocial morbidity. Severity of the height deficit does not correlate with the level of behavioral adaptation. These observations challenge the justification of providing growth hormone therapy for all short children to improve their psychosocial functioning.

Adolescent↗
PubMed1984

Comparative study of serum human growth hormone measurement with NB2 lymphoma cell bioassay, IM-9 receptor modulation assay, and radioimmunoassay in children with disorders of growth.

The biological activity of GH in serum from 10 adult volunteers, 6 children with normal stature, and 26 children with growth retardation was assessed using the Nb2 rat lymphoma cell bioassay and the IM-9 human lymphocyte receptor modulation assay. The bioassay/RIA ratios for both bioassays varied widely but the range of ratios found in the normal stature adults and children was not different than that found in the group of children with growth retardation, which included 4 children with a presumptive diagnosis of bioinactive GH. We conclude that the use of these two bioassays is a valid approach to the assessment of the bioactivity of the circulating molecular forms of GH and that a large number of children with disorders of growth can be screened to identify patients with bioinactive GH.

Adolescent↗
PubMed1985

Disorders of prolactin and growth hormone secretion.

A large range of tests is now available to help us understand, diagnose and manage GH-related growth disorders. The traditional provocative tests of GH secretion will identify short children with severe GH deficiency. However, evidence is emerging that these pharmacological tests may not be sufficiently sensitive to identify some subjects with GH deficiency arising from neurosecretory disturbance of GH release. There is a need for a simple sensitive test that will detect subtle GH secretion of this type. hGRF administration is a reliable test of GH reserve and, when used in combination with conventional tests, may help to identify GH-deficient children with hypothalamic GRF deficiency. Whether the GH responses following GRF administration reflects physiological GH secretory activity needs to be established. The diagnosis of acromegaly is made on clinical grounds. The abnormal GH responses to glucose and TRH support the diagnosis, but by themselves should not be considered to be diagnostic of acromegaly. An elevated Sm C level also helps to establish the diagnosis, although Sm C concentrations may be elevated to the same degree in pregnancy and during puberty. The use of Sm C to monitor disease activity remains to be established. Circulating GRF levels should be measured in patients with acromegaly so that ectopic production of GRF can be identified.

Acromegaly↗
PubMed1981

The use of a commercially available somatomedin-C radioimmunoassay in patients with disorders of growth.

Somatomedin-C concentrations were measured by a newly available commercial radioimmunoassay in plasma samples from 41 children undergoing clinical evaluation of hypothalamic-pituitary function because of varied disorders of growth. Sequential Sm-C levels were stable; the coefficient of variation remained below 10% over a three-hour period. The Sm-C values of 27% of the children were discordant with the GH responses; of 25 patients with normal provoked-GH levels, seven had low Sm-C values, whereas four of 16 patients with inadequate GH responses had normal Sm-C concentrations. All of the discordant data occurred in 31 patients with diminished linear growth velocity. More patients with decreased growth velocity had diminished Sm-C levels than did short children with normal linear growth velocity. These data suggest that many variables, in addition to adequacy of GH production and plasma Sm-C levels, may affect net Sm-C activity. This possibly reduces the usefulness of the Sm-C radioimmunoassay as a single screening test for abnormalities of GH secretion.

Adolescent↗
PubMed2001

Assessment of the effects of intensive training of community based staff in the screening of children for disorders of growth and puberty.

INTRODUCTION: The effects of an intensive training programme involving screening of children for disorders of growth and puberty for community based nursing and medical staff employed by Cardiff Community Healthcare NHS Trust were audited to assess the impact of this training on referrals to the local hospital based growth clinic. METHOD: Referrals from community based staff to the growth clinic of patients living in the geographical area in which staff underwent training were compared with those from general practitioners in the 18 months prior to and following the training programme. Hospital notes were available for 209 of 254 (82.2%) patients identified. We excluded 112 referrals as they did not have a problem relating to growth or puberty or were inter-hospital referrals. Hence 97 referrals were included in the final audit. RESULTS: Forty referrals occurred prior to compared with 57 following the training programme. The number of referrals from community based staff increased threefold during the six months immediately following the training programme but then returned to the previous level. There were no differences in age or height standard deviation scores at referral between groups at any time. The proportion of children referred from the community with significant abnormalities of growth or puberty (for example, hypothyroidism or precocious puberty) increased from two of 15 referrals to six of 30 referrals following the training programme. CONCLUSIONS: Intensive training in screening for disorders of growth and puberty can increase the number of referrals of children with significant pathology but at the cost of increased total number of referrals. The increase in referrals is not sustained with time, suggesting continued training is necessary.

Adolescent↗
PubMed1990

Deprivation of growth hormone-releasing hormone early in the rat's neonatal life permanently affects somatotropic function.

This work investigated in rats whether passive immunization against the endogenous GHRF in the early postnatal period led to permanent alterations of somatotropic function, similar to those observed in several human growth disorders, e.g. constitutional growth delay (CGD). On postnatal days 1, 2, 4, 6, 8, and 10, rats were given an anti-GHRF-serum (GHRH-Ab, 100 microliters/rat, sc) and were tested 1, 30, and 60 days after this treatment for basal and GHRH-stimulated GH secretion both in vivo and in vitro. GHRH-Ab reduced both basal and GHRF-stimulated GH secretion at all intervals and induced marked and chronic impairment of growth rate. The following differences were observed in the GHRH-Ab treated rats compared to normal rabbit serum-treated controls: 1) GH biosynthesis (incorporation of L-[3H]leucine into the electrophoretic band of GH): reduction of about 70%, 1 day but not 30 days after treatment; 2) Pituitary weight: significant reduction in absolute weight (30-40%) at all posttreatment intervals, and relative weight, 1 and 30 days after treatment. 3) Pituitary GH concentration: significant reduction in GH content (about 40%) but not concentration, at all posttreatment intervals; 4) Percentage of somatotrophs (immunocytochemistry): about 40% reduction 1 day, but not 30 and 60 days after treatment; 5) Hypothalamic somatostatin messenger RNA (mRNA) levels in situ hybridization): selective reduction (40%) in the periventricular nucleus 1 day but not 30 days after treatment; 6) Hypothalamic somatostatin cell number (immunocytochemistry): no significant changes in any hypothalamic area at any interval; 7) Pituitary somatostatin binding (in situ autoradiography): significant reduction, 1 day and 30 days after treatment; 8) Somatostatin inhibition of GH release "in vitro": somatostatin effect on GH release was reduced 30 days after treatment. These and previous data indicate that: 1) Transient deprivation of GHRF in the immediate postnatal period of the rat leads to permanent impairment of growth rate and somatotropic function; 2) GHRF deficiency itself or through reduction of GH secretion impairs somatostatin functions temporarily in the hypothalamus and permanently in the pituitary; 3) This rat model may mimic some forms of growth disorders in humans and holds promise as useful tools for investigating the underlying pathophysiological mechanisms.

Animals↗
PubMed1996

Utility of the National Cooperative Growth Study database for safety reporting.

The National Cooperative Growth Study (NCGS) maintains the largest database in the world, collecting information on patients with growth disorders treated with growth hormone (GH). More than 24,000 children have been monitored during its first decade (1985 through 1995). The database provides unique opportunities to learn about effectiveness of GH therapy in a real-world context. Its size also makes it possible to investigate rare adverse reactions, which is not reasonable in a randomized controlled trial (RCT). The frequency of adverse experiences reported in an observational study like the NCGS is lower than in an RCT, because the investigators in an observational study typically do not report events that they believe are clearly unrelated to the study drug. Nevertheless the NCGS has greatly facilitated collecting adverse-event data; approximately 75% of all adverse-event reports for GH received by the manufacturer are through NCGS data-collection forms. The NCGS has thus amassed a repository of GH safety data that is unparalleled. Furthermore, in contrast to an RCT, the NCGS database reflects real-world experience with long-term GH therapy in North America. Although the advantages of an observational study such as the NCGS must be recognized, such a study does differ from an RCT in important ways. For example, because the NCGS protocol allows customized patient treatment and individualization of GH therapy, it may be difficult to use the database to address questions (e. g., estimation of dose-response relationships, true incidence of adverse events) that require RCT designs.

Adverse Drug Reaction Reporting Systems↗
PubMed2002

Short-term growth response to GH treatment and considerations upon the limits of short-term growth predictions.

OBJECTIVES: To investigate the impact of short-term growth measurements on predicting the individual growth response to GH treatment, and to elucidate the possible reasons for the limited accuracy of current growth prediction models for GH-treated children. METHODS: Short-term growth measurements by knemometry and stadiometer in 99 short, GH-treated children (27 girls, 72 boys), aged 10.3 +/- 2.3 years, from the Children's University Hospital, Leipzig, Germany. RESULTS: GH treatment significantly accelerated the mean height velocity (HV) from 4.3 +/- 1.0 to 8.1 +/- 1.8 cm/year during the first year of treatment, the average height standard deviation score (SDS) shifted by +0.52 SD. The variation in HV also increased, from S(2) = 1.0 before to S(2) = 3.4 cm(2)/year(2) during treatment. Lower leg length (LLL) velocity accelerated from 1.6 +/- 0.7 before treatment to 3.4 +/- 1.0 cm/year during the first 8 weeks of treatment. Four coefficients of correlation appeared clinically meaningful: (1) LLL velocity vs. body HV during the first year of GH treatment (r = 0.87), indicating that GH acts simultaneously on leg and rump growth; (2) early (first 8 weeks) LLL velocity vs. 1-year body HV during treatment, with r = 0.61 (R(2) = 0.38), indicating that 38% of the variation in HV during the first year of treatment is already predictable by an initial 8-week period of knemometry; (3) early (first 8 weeks) LLL velocity vs. 1-year LLL velocity during treatment, with r = 0.63 (R(2) = 0.39), and (4) early (first 8 weeks) LLL velocity vs. later LLL velocity, up to the end of the first year, with r = 0.53 (R(2) = 0.28) indicating that the early response on lower leg growth persists for at least 1 year of GH treatment. CONCLUSIONS: (1) Thirty-eight percent of the variation in HV during the first year of GH treatment is predictable by an initial 8-week period of knemometry. This parallels early changes in biochemical markers of bone turnover after GH treatment. (2) There is evidence for a baseline variability in HV both in healthy children and in children with growth disorders that make growth prediction difficult.

Anthropometry↗
PubMed1987

Human growth hormone therapy of non-growth hormone deficient children.

With biosynthetically derived human growth hormone (hGH) available in large quantities, attempts will be made to promote growth in short children who do not fulfill the 'classical' criteria for growth hormone deficiency (GHD). By these criteria, GHD is excluded if hGH levels to pharmacological stimuli exceed a definite level. Several studies have shown that a variety of short children, who are not growth hormone deficient by these criteria, will demonstrate an increased growth rate with hGH treatment. A subpopulation of children with clinical features of GHD, delayed bone age and low somatomedin levels, have low levels of spontaneously secreted growth hormone or 'bioinactive' growth hormone. These children increase their growth rates to substitution doses of hGH. In other children whose growth disorder is not likely to be caused by a disorder in the growth hormone-somatomedin axis, growth increments are occasionally seen on higher hGH doses. Future long-term studies--carefully considering the ethics of such approaches--will have to evaluate the relationships between hGH dose and both metabolic and growth responses and side effects in children with short stature in order to define more specifically further target groups of short children who will benefit from hGH therapy.

Body Height↗
PubMed1996

Carbohydrate metabolism in children receiving growth hormone for 5 years. Chronic renal insufficiency compared with growth hormone deficiency, Turner syndrome, and idiopathic short stature. Genentech Collaborative Group.

Carbohydrate metabolism was evaluated by fasting and postprandial glucose, insulin, and hemoglobin (Hb)Alc levels in children with chronic renal insufficiency and various other growth disorders treated with growth hormone. Mean fasting and postprandial glucose remained unchanged throughout the 5-year study period in all four study groups. Median fasting insulin levels rose from low-normal levels into the normal range after 5 years of growth hormone. Average fasting insulin level after 5 years was 10 mU/l. Median postprandial insulin values also rose, yet remained within the normal range at the 5-year mark. Mean Hb Alc levels remained within low to middle end of the normal range in the patients with growth hormone deficiency, Turner syndrome, and idiopathic short stature. Mean Hb Alc levels at the 5 years were slightly elevated to 6.3% for the patients with chronic renal insufficiency.

Blood Glucose↗
PubMed1991

Multiple epiphyseal dysplasia misdiagnosed as bioinactive growth hormone disorder.

We have reported a case of multiple epiphyseal dysplasia (MED) that was misdiagnosed for many years as bioinactive growth hormone disorder. The condition was misdiagnosed because of its rarity and the physicians' lack of familiarity with it. MED should be considered in the differential diagnosis of a child with short stature and delayed growth. Close follow-up of a patient receiving growth hormone is necessary.

Child↗
PubMed2003

Coronary heart disease: a disorder of growth.

A new 'developmental' model for the origins of coronary heart disease and the related disorders of type 2 diabetes, hypertension and stroke is emerging. The finding that people who develop these disorders have altered growth in utero, during infancy and childhood provides a new starting point for research. The immediate prospect for prevention is through protecting infant growth and preventing accelerated weight gain in children made vulnerable to later disease by small size at birth and during infancy. Ultimately we need to optimize maternal diet and composition before and during pregnancy. Despite current levels of nutrition in Western countries the nutrition of many fetuses and infants remains suboptimal because the nutrients available are unbalanced or because their delivery is constrained by the long and vulnerable fetal supply line.

Birth Weight↗
PubMed2001

Disorders of growth and puberty in children with non-tumoral hydrocephalus.

Hydrocephalus may cause disorders of growth and puberty. 31 patients (25 girls) with non-tumoral hydrocephalus were seen at 8.5 +/- 3.1 (SD) years for short stature (8 patients), overweight (8 patients), central early puberty (onset before 9 years, 21 patients), premature pubarche (1 patient) and/or delayed puberty (2 patients). Among the patients with short stature, 4 had meningomyelocele and one had untreated early puberty. Only 1/11 patients evaluated had growth hormone deficiency. Among the overweight patients, 5 had early puberty. The plasma leptin concentrations were positively correlated with the body mass index (r = 0.65, p < 0.01, n = 14). Free thyroxin, cortisol, prolactin and concomitant plasma and urinary osmolalities were normal in all cases evaluated, except one who had low free thyroxin. The 7 patients with early puberty and who were given gonadotropin releasing hormone analog for over 2 years had mean predicted adult height of -2.45 +/- 1.9 SD before treatment and -2.46 +/- 1.4 SD afterwards. Ventriculocisternostomy performed on 2 girls seen for delayed puberty was followed by breast development and menarche. In conclusion, in children with hydrocephalus, short stature is frequently due to meningomyelocele and rarely to GH deficiency. Central early puberty is the most frequent endocrine disorder.

Body Height↗
PubMed2005

Quantitative measurement of IGF-I and its use in diagnosing and monitoring treatment of disorders of growth hormone secretion.

Quantitative measurements of serum IGF-I concentrations are extremely useful in the diagnosis of growth hormone deficiency in children and young adults and in the diagnosis of acromegaly. Similarly, IGF-I measurements have been of great use to clinical investigators who are monitoring the effect of either growth hormone or IGF-I in various disorders. Several guidelines have proven very useful for assaying IGF-I and defining high-quality assays. Since IGF-I circulates associated with IGF binding proteins it is essential that a high-quality assay remove binding protein interference. Similarly, it is essential that the antibodies that are utilized in the assay have both high specificity and high affinity for IGF-I. Assay reproducibility is effected by such factors as quality of sample collection, utilization of proper internal and external standards and published validation using not only normal samples but samples from a variety of pathophysiologic conditions. Interlaboratory variability often is due to differences in one of more of these characteristics. When assessing the validity of abnormal assay results it is important to be able to compare the value to a normative dataset that has been developed on a large number of subjects. Recently a normative dataset was published on 2,812 subjects and this provides an important reference standard by which other assays should be judged. Careful attention to these characteristics is likely to result in valid and useful IGF-I assay results.

Biomarkers↗