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PubMed2006

Growth hormone: historical notes.

A brief review of important contributions to our present knowledge of growth hormone is given. In 1887 it had been noted that a pituitary tumor was present in most patients with acromegaly. Even at the beginning of the 20. Century relationship between growth disorders and the pituitary was contested. From 1908 pituitary surgery became established treatment in GH hypersecretion. In 1922 it was demonstrated that injection of pituitary extract to animals caused excessive growth and soon after the opposite: removal of the pituitary caused growth retardation. A huge number of studies on the effects of GH were subsequently reported as were trials with GH treatment. They were impeded by failure to recognize the impact of species specificity of GH. After this issue was clarified in 1957, treatment with human growth hormone proved effective. In 1985 it was realized that Creutzfeldt-Jakob's disease might be transmitted through human growth hormone. At this time recombinant GH had become available. In 1971 the structure of human GH was established. In the same period both GH releasing and inhibiting hormones were identified and an analogue of somatostatin had evolved into the first effective pharmacological treatment for acromegaly.

Acromegaly↗
PubMed1986

The human erythrocyte insulin-like growth factor I receptor: characterization and demonstration of ligand-stimulated autophosphorylation.

To characterize the insulin-like growth factor I (IGF-I) receptor on human erythrocytes, cells were purified from peripheral blood by Ficoll-Hypaque gradient centrifugation and incubated with [125I]IGF-I. Specific binding was maximal at pH 8.0 after 24 h at 4 C and increased linearly with cell number to 3.9 +/- 0.2% (+/- SEM) for 3.0 X 10(9) cells/ml. The Scatchard plot of the binding data was linear, with 7 fmol [125I]IGF-I bound/10(9) cells and an affinity constant (K) of 1.8 X 10(9) M-1. Unlabeled IGF-I inhibited tracer binding half-maximally at 6 ng/ml. Multiplication-stimulating activity (or rat IGF-II) was 40% as potent (ED50, 15 ng/ml), whereas insulin and proinsulin were 30- to 500-fold less potent. A monoclonal antibody to the IGF-I receptor (alpha IR-3) inhibited IGF-I binding by 50% at a 1:1000 dilution and by 80% at a 1:250 dilution. Insulin binding was unaffected by the same dilutions. IGF-I receptor phosphorylation was studied in erythrocyte ghosts prepared by hypotonic lysis and solubilized in 1% Triton. The extract was preincubated with and without 100 ng/ml IGF-I or porcine insulin and incubated with [gamma-32P]ATP in the presence of Mn2+, and the receptor was identified by immunoprecipitation with alpha IR-3 antibody and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. IGF-I stimulated 4-fold the incorporation of 32P into a protein of 95,000 mol wt, which was immunoprecipitated by alpha IR-3; insulin produced a 2-fold stimulation of this protein. This protein corresponds to the beta-subunit of the IGF-I receptor. These data demonstrate that human erythrocytes have specific receptors for IGF-I, and that this IGF-I receptor, like the insulin receptor, undergoes ligand-stimulated autophosphorylation. Thus, analysis of erythrocyte IGF-I binding and receptor phosphorylation may be useful tools for the study of patients with a variety of growth disorders.

Adult↗
PubMed2000

Genomic imprinting, uniparental disomy and foetal growth.

Genomic imprinting is an epigenetic phenomenon identified in the past 15 years. Thus, maternally imprinted genes are only expressed from the paternal allele and vice versa. The mechanism of imprinting is still far from certain, but most probably it involves differential methylation of specific sites in or near imprinted genes. Disrupted imprinting can lead to phenotypic changes, and an increasing number of resultant clinical disorders are being identified. Many of these conditions involve disordered growth and/or development, particularly prenatal.

Animals↗
PubMed1997

Nerve growth factor levels in cerebrospinal fluid from patients neurologic disorders.

Nerve growth factor levels were measured in the cerebrospinal fluid from 73 patients with neurologic disorders and non-neurologic acute illnesses by a two-site enzyme immunoassay. Elevated nerve growth factor levels in cerebrospinal fluid were demonstrated in 2 of 7 patients with bacterial meningitis, 7 of 14 patients with viral meningitis or encephalitis, and 1 with multiple sclerosis. Follow-up examinations of the 3 patients (1 with bacterial meningitis, 1 with viral meningitis, and 1 with multiple sclerosis) at convalescent stage showed diminished nerve growth factor levels in cerebrospinal fluid. None of the other patients showed elevation of nerve growth factor levels in cerebrospinal fluid. Nerve growth factor levels in cerebrospinal fluid were not correlated with cell numbers in patients with meningitis or encephalitis. No relationship was observed between nerve growth factor levels and outcome in patients with viral meningitis or encephalitis and bacterial meningitis. Nerve growth factor in cerebrospinal fluid may play a role in neuronal recovery or function as an immunomodulator in children with inflammatory and immune-mediated neurologic disorders.

Adolescent↗
PubMed2000

Is routine growth monitoring effective? A systematic review of trials.

BACKGROUND: Growth monitoring consists of routine measurements to detect abnormal growth, combined with some action when this is detected. It aims to improve nutrition, reduce the risk of death or inadequate nutrition, help educate carers, and lead to early referral for conditions manifest by growth disorders. As primary care workers world wide invest time in this activity, evidence for its benefits and harms was sort. INCLUSION CRITERIA STUDIES: randomised or quasi-randomised controlled trials of growth monitoring. INTERVENTIONS: regular growth monitoring, combined with some intervention targeted at abnormal growth, compared with controls. OUTCOMES: anthropometric measures; referrals to primary and specialist care, or community services; maternal knowledge, anxiety, and satisfaction; child morbidity and mortality. COMPARISONS: Routine growth monitoring compared with no routine growth monitoring; routine growth monitoring by plotting onto a standard chart compared with monitoring with no chart. SEARCH STRATEGY: Cochrane controlled trials register; World Health Organisation and World Bank publications; contact with specialist community paediatricians working in the field. RESULTS: Two trials met the inclusion criteria. One compared growth monitoring with no growth monitoring, in a cluster randomised trial nested in a nutritional intervention programme, and detected no difference in nutritional outcomes between the two groups. Another trial compared growth monitoring with and without a standard chart, measuring maternal knowledge of women about nutrition. It showed small numerical differences in test scores. DISCUSSION AND IMPLICATIONS: Current policies appear to be based on the opinion that investment in the activity has worthwhile health benefits, and does no harm. No reliable evidence was found to support or refute this.

Child↗
PubMed2002

Prepubertal growth in congenital disorder of glycosylation type Ia (CDG-Ia).

AIMS: To delineate the pattern of growth in prepubertal children with congenital disorder of glycosylation type Ia (CDG-Ia) in order to identify critical period(s) and possible cause(s) of growth failure. METHODS: Longitudinal measurements of weight, length/height, and head circumference from birth to 10 years of age in 25 CDG-Ia patients with the R141H/F119L PMM2 genotype were analysed. The data and derived body mass indices (BMI) were compared with standards and expressed as standard deviation scores (SDS). A linear mixed effects model was fitted to each set of data, and mean curves were estimated. RESULTS: The mean weight SDS decreased from -0.3 at birth to -3.0 at 7 months of age and remained low or increased slightly. The mean length SDS decreased from zero at birth to -2.4 at 7 months of age followed by a slight increase to a maximum of -1.8 SDS at the end of the second year of life. After age 2 the mean length/height SDS decreased again. The mean BMI SDS at birth was -0.7 and declined to a minimum of -2.8 at the end of the second year of life followed by a gradual increase. The mean head circumference SDS declined gradually from 0 at 3 months of age to -1.9 at age 5. CONCLUSION: CDG-Ia patients with the R141H/F119L genotype have normal fetal growth and an immediate postnatal onset of severe growth failure. A notable decline in weight end length SDS takes place during the first seven months of life with no prepubertal catch up.

Adolescent↗
PubMed1986

Radioimmunoassay of growth hormone-dependent insulinlike growth factor binding protein in human plasma.

A specific radioimmunoassay has been established for a growth hormone-dependent insulinlike growth factor (IGF) binding protein (BP) from human plasma. Although the assay was directed against a 53-kD, acid-stable BP subunit, the main immunoreactive BP in the circulation had an apparent molecular mass of approximately 125 kD. Only higher primate species showed cross-reactivity, and IGF-I, IGF-II, and other peptides were without effect. Circulating BP levels in healthy subjects rose threefold from early childhood to puberty. In 65 adults aged 18 to 65, the mean level (+/- SD) was 6.12 +/- 1.43 micrograms/ml, and declined with age. Strong growth hormone-dependence of BP was also seen; there was a 2.2-fold increase in active acromegaly and a 50-80% reduction in growth hormone deficiency. Poorly controlled diabetic subjects had BP levels 40% below normal, whereas in renal failure and third-term pregnancy a mild elevation was seen. Measurement of BP may provide a useful adjunct to IGF assays in growth disorders.

Adolescent↗
PubMed2006

Matrix metalloproteinase-9 induces the formation of cartilage canals in the chondroepiphysis of the neonatal rabbit.

BACKGROUND: An investigation of matrix metalloproteinase-9 (MMP-9) and its influence on vascular invasion in the secondary ossification center at the chondroepiphysis of developing long bones was undertaken. The effect of MMP-9 was compared with that of basic fibroblast growth factor (b-FGF), a potent angiogenic factor, and we assessed the chorioallantoic membrane (CAM) culture as a model for angiogenesis in osteochondral tissue. METHODS: Seventy-two femoral and seventy-two humeral heads of thirty-six four-day postnatal rabbits were dissected immediately after each animal was killed. Solutions of MMP-9, b-FGF, and phosphate-buffered saline solution were applied, and the femoral and humeral chondroepiphyseal explants were incubated for ten days in CAM culture. This was used as an in vivo model to investigate the growth of blood vessels into the femoral and humeral heads of the neonatal rabbit. The explants were harvested from the CAM culture and analyzed histologically. A three-day incubation was also performed to look for early signs of vascular ingrowth into the cartilage matrix. RESULTS: One hundred and twenty epiphyses from thirty rabbits were placed onto CAM culture successfully; of these, two were harvested at three days to assess early changes and 118 were harvested at ten days. Forty of the 118 cultures were still viable when harvested after ten days, giving a 33% yield. Both MMP-9 and b-FGF caused an increased vascular invasion into the chondroepiphysis. New blood vessels derived from the chorioallantoic membrane within cartilage canals were more numerous in MMP-9 treated epiphyses, and larger canals were more commonly seen when compared with a control group. CONCLUSIONS: These findings confirmed that b-FGF is angiogenic at the chondroepiphysis. Matrix metalloproteinase-9 appears to be implicated in vascular invasion and induces the formation of new cartilage canals at the chondroepiphysis. The CAM culture model was a useful model for investigating angiogenesis in osteochondral tissue. CLINICAL RELEVANCE: This study adds to the understanding of the complex biochemical interaction that occurs in cartilage when the advancing vasculature begins growing into the chondroepiphysis. A better knowledge of this angiogenic process will enable a better understanding of the pathological failure or disturbance of vasculogenesis, which results in dysplastic growth disorders and osteonecrosis.

Animals↗
PubMed2001

Floating-Harbor syndrome in two unrelated girls: mild short stature in one patient and effective growth hormone therapy in the other.

We report two female patients, 11 and eight years old, with clinical findings consistent with the Floating-Harbor syndrome (FHS). The first patient presented with characteristic facial features, brachydactyly, broad thumbs, and delay of speech development, but less pronounced short stature (-2 standard deviation (SD) below mean) than previously reported. The second patient presented with short stature, characteristic facial features, brachydactyly, and delay of speech as well as mental development; she was successfully treated with growth hormone. Metacarpophalangeal pattern profiles (MCPP) were performed in both patients and compared to those of previously published patients.

Abnormalities, Multiple↗
PubMed1991

Growth hormone and insulin-like growth factor I: nutritional pathophysiology and therapeutic potential.

The growth hormone--insulin-like growth factor I axis has been appreciated for more than 30 years and the effects of malnutrition on this axis for more than 20 years. Over the last decade, advances in molecular biology have permitted enhanced understanding of feedback regulation between growth hormone and IGF-I at the gene level, including limited information on nutritional influences. Similarly, the availability of recombinant human growth hormone has allowed controlled clinical studies demonstrating its net anabolic actions at hypocaloric dietary energy intake levels and its ability to enhance height velocity in children with various causes of diminished growth. Although investigational use of recombinant IGF-I in humans has been limited, its actions are likely to complement those of growth hormone during periods of profound dietary energy deficit. From the information presented, two hypotheses are developed. First, recombinant IGF-I administration will enhance substrate anabolic events during the acutely malnourished state when dietary intake is severely limited. Second, administration of recombinant human growth hormone will accelerate protein anabolism and catch-up growth during the period of recovery from protein-energy malnutrition. Given current clinical investigational tools and the availability of both recombinantly-produced hormones, these are testable hypotheses.

Growth Disorders↗
PubMed2006

Growing up with idiopathic short stature: psychosocial development and hormone treatment; a critical review.

To facilitate decisions on interventions in medically referred children with idiopathic short stature, the research on psychosocial functioning of these children, possible risk and protective factors influencing adaptation, and effects of hormone treatment were reviewed. Parents ranked the behaviour of their children on average between normal and below normal. The magnitude of these deviations varied from small to large. Little is known about the children's self-perceived psychosocial functioning. Some risk factors were found: being teased, being juvenilised, being a boy, having a younger but taller sibling, low intelligence, and low socioeconomic status. There have been few studies on the impact of protective factors including temperament, coping strategies, and social support. On average, hormone treatment did not improve psychosocial functioning. The research shows the advantages and disadvantages of hormone treatment that must be considered when choosing a suitable intervention. It is suggested that psychosocial adjustment can be improved by focusing on factors other than height alone.

Adaptation, Psychological↗
PubMed1992

Malnutrition in Crohn's disease: substrate deficiency or misuse?

Growth failure is frequently associated with Crohn's disease. However, it does not seem to be fully accounted for by overt endocrinological abnormalities or nutrient deficiencies. It may be related to an abnormal utilization of available substrates, particularly proteins, due to an imbalance in protein metabolism kinetics. Its primary mechanism may be an increase in protein breakdown rates over synthesis, specifically related to the associated inflammatory syndrome, and progressively leading to a protein debt. Reduction in food intake would only exaggerate this trend by further reducing the synthesis to breakdown ratio, whereas nutrient supplementation merely compensates for the deficit by promoting protein synthesis.

Child↗
PubMed1983

Somatomedin activity and cartilage [35S]sulphate incorporation in the growth-retarded neonatal rat.

Plasma somatomedin activity, cartilage metabolism and the levels of insulin and growth hormone were studied during relative neonatal malnutrition in the rat, produced by the small and large litter method. In growth-retarded rats reduced somatomedin activity and raised growth hormone concentration were found. Neither basal cartilage activity nor cartilage responsiveness to somatomedin was altered in the growth-retarded animals.

Animals↗
PubMed1986

Efficacy of mathematical methods for ultrasound examinations in diabetic pregnancies.

The efficacy of a new principle for evaluation of fetal growth has been compared to standard methods in a population of pregnant diabetic women. Methods for projecting fetal weight at birth and determining the deviation of growth from an expected fetal weight increase based on our growth model provided significant information for the detection of fetal growth abnormalities 3 weeks (mean) before delivery. (Large for gestational age: sensitivity, 81%; specificity, 85%. Small for gestational age: sensitivity, 100%; specificity, 98%.) With the exception of two models for estimation of fetal weight based on ultrasound measurements of the fetal head and abdomen only, none of the standard methods gave results that were significantly better than the use of the biparietal diameter against a population standard. The new methods are expected to provide valuable information for the treatment of fetal growth disorders.

Anthropometry↗
PubMedDate not supplied

Expression of human growth hormone-releasing factor in transgenic mice results in increased somatic growth.

The neurohumoral regulation of growth hormone secretion is mediated in part by two hypothalamic peptides that reach the anterior pituitary via the hypothalamo-hypophysial portal blood system. Somatostatin inhibits the release of growth hormone, whereas growth hormone-releasing factor (GRF) positively regulates both growth hormone synthesis and secretion. Two forms of human GRF, 40 and 44 amino acids long, have been characterized from extra-hypothalamic tumours as well as from the hypothalamus. Analysis of human GRF complementary DNA and genomic clones indicates that the GRF peptides are first synthesized as a 107- or 108-amino-acid precursor protein. To examine the physiological consequences of GRF expression, we have established strains of transgenic mice containing a fusion gene including the promoter/regulatory region of the mouse metallothionein-I (MT-I) gene and the coding region of the human GRF gene. We report that expression of the human GRF precursor protein in these animals results in measurable levels of human GRF and increased levels of mouse growth hormone in plasma and accelerated growth rates relative to control littermates. These results demonstrate a direct role for GRF in the positive regulation of somatic growth. Unexpectedly, female transgenic mice carrying the MT-GRF fusion gene are fertile, in contrast to female transgenic mice expressing human or rat growth hormone, which are generally infertile. These transgenic mouse strains should provide useful animal models for the study of several types of human growth disorders.

Animals↗
PubMed1999

Cloning of breakpoints in and downstream the IGF2 gene that are associated with overexpression of IGF2 transcripts in colorectal tumours.

The human IGF2 gene belongs to a group of imprinted genes clustered on the short arm of chromosome 11, band p15.5. It contains 9 exons and spans over 30 kb. IGF2 mRNA overexpression has been reported in human tumours and in some inherited growth disorders. It was recently demonstrated that IGF2 mRNA overexpression contributes to tumour progression and that loss of parental imprinting as well as altered transcription factors are contributing to this overexpression. We have reported structural alterations in the 3' region of the IGF2 gene in two colorectal tumours that overexpressed the IGF2 transcript by 200- and 800-fold. We cloned by the vectorette-PCR strategy, genomic DNA fragments containing the breakpoints from these tumours. The sequencing of these fragments positioned the breakpoint 2 kb downstream the IGF2 gene in one tumour, and in exon 9 in the second. Both breakpoints occurred in regions containing repetitive elements: a TGGA repeat we have identified downstream the gene, and the (CA)n repetition in exon 9. We hypothesize that a negative regulatory element, located downstream the IGF2 gene, has been deleted following these structural alterations and leads to IGF2 gene overexpression.

Chromosome Aberrations↗