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PubMed1998

'Short stature in children--a questionnaire for parents': a new instrument for growth disorder-specific psychosocial adaptation in children.

Recent studies report comparable psychosocial adaptation in children with or without a growth disorder. These findings may be due to a general lack of sensitive and specific techniques for analysing and comparing their respective qualities of life. In this study we present a new questionnaire for parents of short-statured children. We suggest both a qualitative and quantitative approach providing specific information about the relative extent of individual stress factors and sources of help. The parents of 442 children with growth retardation resulting from different aetiologies completed the questionnaire. A principal component analysis of the scaled items revealed four dimensions of psychosocial adaptation; suffering, future anxieties, behavioural problems and coping efforts. The index of internal consistency reliability was sufficient for all scales. The comparison of two selected growth disorder groups (achondroplasia versus growth hormone deficiency) demonstrated growth disorder-specific but not very different profiles of psychosocial adaptation. The qualitative analysis revealed a shift in the stress factor patterns (achondroplasia, more physical restrictions). These findings give evidence for both the specificity and construct validity of the new instrument. Therefore, we may conclude that this questionnaire is a helpful method in attaining growth disorder-specific information about individual stress factors, resources and psychosocial adaptation.

Adaptation, Psychological↗
PubMed1993

Urinary growth hormone excretion in the assessment of children with disorders of growth.

OBJECTIVE: We wished to evaluate the use of urinary GH measurements when compared to conventional GH provocation tests in the assessment of short children. DESIGN: Children presenting for the first time to a regional growth clinic were assessed clinically by one observer. Investigations comprising standard GH provocation tests and measurement of urinary GH were undertaken to exclude GH deficiency. PATIENTS: Fifty-eight children aged 5.8-16 years were enrolled. Ten were diagnosed on clinical assessment as GH deficient, 43 had delayed growth and/or familial short stature, and five had idiopathic short stature; the 48 children in the last two groups were defined as short normal. MEASUREMENTS: GH secretion was evaluated by two standard provocation tests and by the measurement of GH in five overnight urine collections. A normal peak GH concentration was defined as > 16 mU/l. The values for urinary GH excretion were compared to normal ranges (+/- 2 standard deviations from the mean), established in healthy schoolchildren of normal stature. RESULTS: All children considered GH deficient on clinical grounds had low peak GH concentrations on provocation tests, while 8/10 had low values of urinary GH excretion. All short normal children with normal peak GH concentrations (n = 36) on provocation tests and 11/12 children with low peak GH concentrations had urinary GH excretion within the normal range. There was therefore a significant difference in the classification of 'normal' GH secretion in the two tests. If the clinical diagnosis was used as the standard by which GH tests were judged, the predictive value of a positive urinary GH test in the diagnosis of GH deficiency was 89% compared with 45% for GH provocation tests.

Adolescent↗
PubMed1992

Essential hypertension: a disorder of growth with origins in childhood?

PURPOSE: To review evidence that essential hypertension is a growth-related disorder with origins in childhood and manifestations in adult life. PRINCIPAL EVIDENCE: Blood pressure rises with age in children and adults. In children, the rise closely relates to growth and to skeletal and sexual maturation. Adolescents with highest pressure are heavier and had as children grown fastest; as adults, they show the greatest increase of pressure with age and are more likely to develop hypertension and coronary heart disease. In adults, the rate of increase of pressure relates to earlier pressure. One interpretation of this is that a self-perpetuating mechanism is at work. Genetic and environmental factors influence these events. HYPOTHETICAL MECHANISMS: Most forms of secondary hypertension have two pressor mechanisms; a primary cause, e.g. renal clip, and a second process, which is slow to develop, capable of maintaining hypertension after removal of the primary cause, and probably self-perpetuating in nature. We suggest that essential hypertension also has two mechanisms, both based upon cardiovascular hypertrophy: (1) a growth-promoting process in children (equivalent to the primary cause in secondary hypertension); and (2) a self-perpetuating mechanism in adults.

Adult↗
PubMed1985

Perturbation of differentiated functions during viral infection in vivo. I. Relationship of lymphocytic choriomeningitis virus and host strains to growth hormone deficiency.

Disordered growth and glucose metabolism secondary to growth hormone deficiency is associated with persistent lymphocytic choriomeningitis virus (LCMV) infection. C3H/St, BALB/WEHI, and SWR/J mice infected at birth with LCMV:ARM carried virus in their blood and organs throughout life but only C3H/St mice developed growth hormone insufficiency. BALB/WEHI and SWR/J infected mice contained normal amounts of growth hormone in their pituitaries and a relatively small proportion of the cells containing growth hormone replicated the virus. In susceptible C3H/St mice, the disease-causing viral strains (LCMV:ARM, E-350, and Pasteur) replicated to higher titers and infected the vast majority of cells producing growth hormone in the anterior lobe of the pituitary. In contrast, LCMV strains Traub and WE replicated in far fewer growth hormone-producing cells and failed to disorder growth hormone synthesis. In another paper (Y. Riviere, R. Ahmed, P. Southern, and M. B. A. Oldstone (1985), Virology 142, 175-182) these findings are used to make reassortants between LCMV:ARM (disease positive) and LCMV:WE (disease nil) and the pathogenic effect is mapped to the small RNA segment of LCMV:ARM. Peptides cleaved by trypsin and chymotrypsin from growth hormone molecules isolated from infected cells or control cells were equivalent when examined by two-dimensional electrophoresis. Further, transfer of antibody to interferon failed to alter the growth hormone insufficiency in these mice, although it corrected LCMV-induced liver disease of BALB mice, suggesting that interferon did not play a dominant role in this disease. The selective tropism of LCMV:ARM for cells containing growth hormone over cells that contain prolactin was observed in both infected animals and in cultured GH-3 cells.

Animals↗
PubMed1996

Genomic imprinting in disorders of growth.

This review has briefly considered some of the vast amount of information that has been gathered on genomic imprinting and its role in PWS, AS, BWS and Russell-Silver syndrome. The pace of investigation into the phenomenon of imprinting will undoubtedly continue, because our understanding remains far from complete. Newer approaches to identifying imprinted genes based on their expression rather than their location are likely to uncover currently unknown genes. We can also look forward to more insight into the fascinating complexities of the imprinting process.

Angelman Syndrome↗
PubMed2002

Coronary heart disease: a disorder of growth.

The search for the causes of CHD has been guided by a 'destructive' model, which proposes that influences acting in adult life, such as smoking, obesity or high saturated fat intakes, lead to an acceleration of age-related destructive processes, including a rise in blood pressure and the formation of atheroma. One explanation for the failure of the model to account for, or indeed to prevent rising epidemics of CHD, is that individuals are heterogeneous in their responses to such influences. This heterogeneity in response is linked to different paths of early growth. The recent discovery that individuals who develop CHD grew differently from other individuals during fetal life and in childhood has led to a new 'developmental' model for the disease. Reduced fetal growth followed by poor growth in infancy leads to an increased risk of development of CHD, and its associated conditions, stroke, hypertension and impaired glucose tolerance. These effects are compounded by accelerated weight gain, which may represent 'compensatory growth' in childhood.

Aging↗
PubMed1998

Cellular expression of growth hormone and prolactin receptors in human breast disorders.

Growth hormone (GH) and prolactin (PRL) exert their regulatory functions in the mammary gland by acting on specific receptors. Using isotopic in situ hybridization and immunohistochemistry, we have localized the expression of hGH receptor (hGHR) and hPRL receptor (hPRLR) in a panel of human breast disorders. Surgical specimens from adult females included normal breast, inflammatory lesions (mastitis) benign proliferative breast disease (fibroadenoma, papilloma, adenosis, epitheliosis), intraductal carcinoma or lobular carcinoma in situ, and invasive ductal, lobular or medullary carcinoma. Cases of male breast enlargement (gynecomastia) were also studied. In situ hybridization analysis demonstrated the co-expression of hGHR and hPRLR mRNA in all samples tested. Epithelial cells of both normal and tumor tissues were labelled. Quantitative estimation of receptor mRNA levels was regionally measured in areas corresponding to tumor cells and adipose cells from the same section. It demonstrated large individual variation and no correlation emerged according to the histological type of lesion. Receptor immunoreactivity was detected both in the cytoplasm and nuclei or in the cytoplasm alone. Scattered stromal cells were found positive in some cases, but the labeling intensity was always weaker than for neoplastic epithelial cells. Our results demonstrate the expression of the hGHR and hPRLR genes and their translation in epithelial cells of normal, proliferative and neoplastic lesions of the breast. They also demonstrate that stromal components express GHR and PRLR genes. Thus the putative role of hGH or hPRL in the progression of proliferative mammary disorders is not due to grossly altered levels of receptor expression.

Adult↗
PubMed1987

Growth hormone-releasing hormone: studies in normal subjects and patients with disorders of growth hormone secretion.

Growth hormone-releasing hormone (GHRH) has been characterised as a 40-44 residue peptide with full biological activity residing in the first 29 residues. In normal subjects GHRH selectively promotes the release of growth hormone (GH) with little change in responsiveness throughout childhood and young adult life. The majority of 'GH-deficient patients' show a GH response to GHRH, suggesting that they have a hypothalamic defect in GH release. GHRH given subcutaneously promotes growth in 50% of GH-deficient children, and it is likely that depot-preparations of GHRH will provide a practical alternative treatment for GH deficiency. GHRH has provided an important method to evaluate pituitary GH reserve and has greatly improved our understanding of both normal and abnormal GH secretion.

Cushing Syndrome↗
PubMed1997

Growth hormone response to the GABAB agonist baclofen in major depressive disorder.

Growth hormone (GH) response to the gamma-aminobutyric acid B receptor agonist, baclofen, was measured in 16 male patients with major depressive disorder and in 16 age-matched healthy male controls. No significant differences were found in the GH response to baclofen between the depressed patients and controls. On repeat testing, the GH response to baclofen showed significant retest reliability in both groups. There was no significant correlation between serum baclofen levels and the GH response to baclofen. Age significantly correlated with GH response, with older subjects having lower GH response to baclofen. These data do not suggest that a blunted GH response to baclofen. represents a specific neuroendocrine feature of major depression.

Adult↗
PubMed2003

The acrophysis: a unifying concept for enchondral bone growth and its disorders. I. Normal growth.

In order to discuss and illustrate the common effects on normal and abnormal enchondral bone at the physes and at all other growth plates of the developing child, the term "acrophysis" is proposed. Acrophyses include the growth plates of secondary growth centers including carpals and tarsals and apophyses, and the growth plates at the non-physeal ends of small tubular bones. The last layer of development of both physes and acrophysis is the cartilaginous zone of provisional calcification (ZPC). The enchondral bone abutting the ZPC shares similar properties at physes and acrophyses, including the relatively lucent metaphyseal bands of many normal infants at several weeks of age. The bone-in-bone pattern of the normal vertebral bodies and bands of demineralization of the tarsal bones just under the ZPC are the equivalent of those bands. The growth arrest/recovery lines of metaphyses similarly have equivalent lines in growth centers and other acrophyseal sites. Nearly the same effects can also be anticipated from the relatively similar growth plate at the cartilaginous cap of benign exostoses ("paraphysis"). The companion article will explore abnormalities at acrophyseal sites, including metabolic bone disease and dysplasias.

Bone Development↗
PubMed2003

The acrophysis: a unifying concept for understanding enchondral bone growth and its disorders. II. Abnormal growth.

In order to discuss and illustrate the effects common to normal and abnormal enchondral bone at the physes and at all other growth plates of the developing child, the term "acrophysis" was proposed. Acrophyses include the growth plates of secondary growth centers including carpals and tarsals and apophyses, and the growth plates at the nonphyseal ends of small tubular bones. Abnormalities at acrophyseal sites are analogous to those at the physeal growth plates and their metaphyses. For example, changes relating to the zone of provisional calcification (ZPC) are often important to the demonstration of such similarities. Lead lines were an early example of the concept of analogy from abnormality due to physeal and to acrophyseal disturbance. The ZPC is a key factor in understanding patterns of rickets and its healing. Examples (including hypothyroidism, scurvy and other osteoporosis, Ollier disease, achondroplasia, and osteopetrosis, as well as the family of frostbite, Kashin-Beck disease, and rat bite fever) illustrate the acrophysis principle and in turn their manifestations are explained by that principle.

Bone Development↗
PubMed2004

Growth in disorders of adrenal hyperfunction.

This article reviews how growth is affected in disorders of adrenal hyperfunction. Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Adrenal androgens, when in excess, lead to advanced linear growth and skeletal maturation, and prolonged hypercortisolemia leads to the suppression of growth hormone (GH) secretion and inhibition of somatomedin C and other growth factor effects on their target tissues. In virilizing adrenal tumors height is increased at diagnosis, but after surgical cure the final height is usually in the normal range. In congenital adrenal hyperplasia height is usually compromised by advanced skeletal maturation or by suppressed growth, particularly in the first years of life, due to excess glucocorticoid treatment. The final height is reduced in both clinical forms (salt wasting and simple virilizing) and sexes in patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Growth impairment is also the hallmark of Cushing syndrome of whatever etiology when it occurs in children and growing adolescents, and the final height of these patients, even after surgical cure, remains compromised. This is apparently due to direct or indirect growth impairment by the hypercortisolism during the disease, followed by inadequate catch-up growth. Although it seems that GH treatment might be beneficial for improving final height both in patients with congenital adrenal hyperplasia who have poor height predictions and in patients with Cushing disease and GH deficiency, a larger number of studies is needed to confirm this suggestion.

Adrenal Cortex Hormones↗