PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Growth Disorders”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMedDate not supplied

Adjustment in conditions with short stature: a conceptual framework.

A major justification of extended indications for GH therapy in conditions with short stature is based on the objective of preventing or alleviating suspected psychosocial maladjustment. Despite more sophisticated research, results are still controversial concerning the actual seriousness of adjustment difficulties in various conditions with short stature, thus making it difficult to determine a patient's need for treatment. This paper discusses different concepts and assessment strategies of "adjustment" as a major source of the apparent heterogeneity among study findings, conclusions and treatment recommendations. A concise framework is developed that identifies and differentiates three hierarchical levels of research on adjustment in conditions with growth retardation: (1) stress exposure due to short stature, (2) quality of coping responses, and (3) occurrence of psychopathology. Choosing a particular research level and its corresponding measures may imply whether a high, medium or very low impact of short stature on adjustment is found, and the need for treatment that is inferred. The integration of these different research approaches within an integrative model may help to resolve apparent inconsistencies among empirical studies and reveal sources of confoundation due to other, short stature independent risk factors associated with the particular underlying growth disorder. The key terms of the suggested model are transformed into a clinical guideline for psychological assessment in patients with growth retardation and into three key criteria for the decision making process on extended indications for GH treatment with respect to the improvement of psychosocial adjustment.

Adaptation, Psychological↗
PubMed1993

[Fibroblast growth factors (FGFs) in neurodegenerative disorders].

Fibroblast growth factors (FGFs) are a family consisting of at least seven members, and the FGF family will continue to expand. The best studied members of this family are acidic and basic FGF (aFGF and bFGF). They are richly concentrated in brain, and have potent trophic effects for neurons and glia. I now report that expressions of aFGF and bFGF are altered in several neurodegenerative disorders such as Alzheimer disease (AD), Huntington disease (HD) and Parkinson disease (PD). In AD aFGF was upregulated in reactive astrocytes in severely affected areas. The bFGF-positive astrocytes were also increased. In addition, bFGF was detected in senile plaques, neurofibrillary tangles and neuropil threads. In AD, aFGF and bFGF showed a similar alteration pattern. A large number of aFGF- or bFGF-positive astrocytes were observed in the striatum. Some remaining neurons were strongly stained for aFGF or bFGF. In PD, marked loss of bFGF was observed on midbrain dopaminergic neurons, The depletion of bFGF preceded the loss of tyrosine hydroxylase. Since bFGF has a potent trophic effect on midbrain dopaminergic neurons, this depletion may be related to the disease process.

Alzheimer Disease↗
PubMed1996

The changes in serum type I and III procollagen, insulin-like growth factor-I and insulin-like growth factor binding protein-3 levels in children with chronic renal failure.

Serum levels of carboxyterminal propeptide of type I procollagen (PICP) and aminoterminal propeptide of type III procollagen (PIIINP) can be used as markers of bone formation and the evaluation of children with growth disorders. We measured the serum levels of these collagens by radioimmunoassay (RIA), insulin-like growth factor I (IGF-I) (by immunoradiometric assay) and insulin-like growth factor binding protein-3 (IGFBP-3) (by RIA) levels in 24 children aged between 4 and 14 years with chronic renal failure (CRF) (n = 12 dialysis, n = 12 non-dialysis) and 12 age-matched healthy controls, to find out whether these parameters have a prognostic or therapeutic value on monitoring of growth retardation in CRF. Mean serum IGFBP-3 and PIIINP levels in the dialysis patients were higher than the control group, the difference between the groups was statistically significant (P < 0.05). It seemed that the pubertal stage of the patients did not affect the levels of PICP, PIIINP, and IGFBP-3 while serum IGF-I levels in pubertal patients were significantly higher than those in prepubertal patients (P < 0.001). There was no significant correlation between PICP and PIIINP in any patients. Neither PICP nor PIIINP correlated with height z-score, bone age, IGF-I, or IGFBP-3. It was concluded that the increased serum IGFBP-3 and PIIINP levels in chronic renal disease are poor prognostic indicators leading to progressive renal failure and end-stage renal disease (ESRD). Further investigations into the effects of these collagens on growth failure associated with CRF are needed.

Adolescent↗
PubMed1997

Computation of time-specified tolerance intervals for hybrid time series with nonequidistant sampling, illustrated for plasma growth hormone.

The ideal reference interval for a variable of clinical interest would be specific for all deterministic factors affecting that variable, including the time of sampling in relation to biological rhythms. In particular, growth hormone is characterized in children by circadian and ultradian variability, with high peaks of secretion occurring mainly during sleep. For clinical applications, the use of tolerance intervals has been recommended, and they should substitute, whenever possible, for prediction limits. In the case of hybrid data (time series of data collected from a group of subjects), such a tolerance interval could be very difficult to determine following a parametric approach similar to the procedure used for the computation of prediction intervals, especially when consideration of both within-subjects and among-subjects variances is wanted. Accordingly, we have developed a nonparametric method for the computation of such tolerance intervals. Because the method is based on bootstrap techniques, it does not require the assumption of normality or symmetry in the data and is also more appropriate when dealing with small samples. The method was used to establish time-qualified reference limits for a series of growth hormone sampled around the clock in groups of prepubertal children differentiated according to stature. The use of these tolerance intervals may eliminate many false-positive and false-negative diagnoses that might be obtained when relying on time-unspecified single samples. The provision of such tolerance limits introduces time-specification and time-structure evaluation into prevention, diagnosis, and treatment of growth disorders.

Activity Cycles↗
PubMed1999

STAT5 signaling in sexually dimorphic gene expression and growth patterns.

The past 10 years have seen enormous advances in our understanding of how cytokine signals are mediated intracellularly. Of particular significance was the discovery of a family of seven Signal Transducer and Activators of Transcription (STAT) proteins. Each of these has now been studied in detail, and appropriate gene-disrupted mouse models are available for all except STAT2 (Leonard and O'Shea 1998). Fetal lethality is observed in Stat3-deficient mice, and various immunodeficiencies characterize mice with disrupted Stat1, Stat4, and Stat6 genes, which is consistent with impaired signaling from the specific cytokines that activate each of these proteins. The recent characterization of Stat5-deficient mice has led to several unanticipated findings that point to diverse biological functions for the two STAT5 forms, STAT5a and STAT5b. These include roles for one or both STAT5 forms in the immune system, hematopoiesis, sexually dimorphic growth, mammary development, hair growth, deposition of adipose tissue, and pregnancy. Here we review the hormone- and cytokine-activated signaling pathways in which STAT5 participates and the extensive evidence, from laboratory animals, that these factors are required for sex-specific aspects of development, including control of body size. Finally, we consider human growth disorders that may involve defects in STAT5-dependent signal transduction.

Animals↗
PubMed2004

Growth hormone treatment in children: review of safety and efficacy.

Since the advent of growth hormone (GH), the pediatric applications of GH therapy have expanded. Children with a wide variety of growth disorders have received GH treatment. The therapeutic effects and safety profile of GH in a number of pediatric conditions are reviewed, including GH deficiency (GHD), Turner syndrome, chronic renal failure, children born small for gestational age, Prader-Willi syndrome, juvenile chronic arthritis, and cystic fibrosis. GH therapy has been clearly shown to improve height velocity during childhood in a variety of pediatric conditions in which growth is compromised. There is now data that confirms GH treatment also improves final height in a number of diagnostic subgroups. Early initiation and individualization of GH treatment has the potential to normalize childhood growth in children with idiopathic GHD and enable them to achieve their genetic target height in a cost-effective manner. In children in whom GHD is not the main factor compromising growth, supra-physiological doses of GH have been shown to increase height velocity during childhood and final height. The development of predictive models for these conditions may allow further improvements in height outcome while maintaining an acceptable safety profile. Survivors of childhood malignancy, particularly those who have had craniospinal irradiation, represent a particularly challenging group. They appear to be less responsive to GH than children with idiopathic GHD and have a tendency to enter puberty at an earlier age. Both of these factors have a negative impact on their final height. Strategies that combine GH treatment with suppression of puberty using a gonadotropin releasing hormone analog may result in improved height outcomes. When children with GHD are treated with standard doses of GH there is a strong safety record. Adverse events during GH therapy are uncommon and often not drug related. Continued surveillance into adult life is crucial however, particularly in children receiving supra-physiological doses of GH or whose underlying condition increases their risk of adverse effects.

Child↗
PubMed1995

Interaction of craniofacial dysmorphology, growth, and prediction of surgical outcome.

Craniofacial surgery is a multidisciplinary specialty that often uses the expertise of many specialists including surgeons, orthodontists, geneticists, and anthropologists. The clinical experience gained by their collaboration enables predictions to be made of the ultimate success of the reconstructive surgery. Various patterns among surgical outcomes are noted as greater experience is gained. These observations prompted the following questions: Is there a way to classify patients according to surgical results? What factors underlie a successful response to surgery? In a clinical setting, we are faced with a spectrum of presentations of craniofacial dysmorphology. We propose that the results of surgical correction may be based on the cause of the condition and not necessarily on the degree or character of the dysmorphology. Craniofacial dysmorphologies are often grouped under the terms deformation, malformation, disruption, dysplasia, or syndrome. Our hypothesis is that a categorization of craniofacial dysmorphology can be proposed on the basis of the response of the individual to surgery. We propose that such a classification reflects real differences in cause. A poor response to surgery reflects a condition that includes a growth disorder. Alternatively, cases that respond best to surgery are those in which the growth process is not affected. In the latter cases, a dysmorphic face is surgically transformed into an acceptable morphology, and normative growth vectors maintain or improve postoperative facial appearance. It is our belief that the physiological differences underlying our categorization scheme have to do with embryological timing of insults or specific components of the ontogenic process. The divergence in the response to surgery among patients relates directly to the role of the growth process in the various types of dysmorphologies.

Child↗
PubMed2004

Genetics of growth retardation.

Genetic disorders of growth are numerous and include defects of the central nervous system, hypothalamus, pituitary, thyroid, skeleton and other glands, tissues or organs. These disorders are caused by genetic variations that interrupt different points of the hypothalamic-pituitary axis and other synthetic pathways that are required for growth. The resulting growth disorders can be classified by their 1) etiology (Mendelian, mode of inheritance or chromosomal basis), 2) phenotype (isolated or multiple hormone deficiencies), 3) genetic variations of different loci or alleles involved, and/or 4) the associated biochemical findings. The growth disorders selected for inclusion here are examples and are by no means a comprehensive list of all known genetic diseases that have some effect on growth. Information on each disorder is summarized and, for most, more detailed information can be obtained through the electronic database Online Mendelian Inheritance in Man (OMIM) which is available at http://www.ncbi.nlm.nih.gov/Omim.

Databases, Genetic↗
PubMed2001

[Measurements in child health services. Also experienced nurses obtain different results].

Growth reflects general health but also the nutritional and environmental health of a child. Disordered growth may be an early manifestation of disease or deficiency. In Sweden, the newly updated growth charts are highly valued at the child health services, yet measurements of height, weight and head circumference of four infants showed that even experienced nurses achieved noticeably large differences in their individual results. In several cases the plotted data also deviated concerning the exact age of the child or the registered value. Awareness of methodological problems should lead to more accurate advice and referral.

Anthropometry↗
PubMed2004

Pediatric Crohn's disease and growth retardation: the role of genotype, phenotype, and disease severity.

BACKGROUND: Delayed growth is a well-established feature of pediatric Crohn's disease. Several factors have been shown to affect growth, including disease location, severity, and treatment. The recently discovered NOD2 gene has been correlated to ileal location of Crohn's disease and subsequently could affect growth through the resulting phenotype or as an independent risk factor. The aim of our study was to determine if growth retardation is affected by genotype independently of disease location or severity. METHODS: Genotyping for 3 NOD2 single-nucleotide polymorphisms was performed in 93 patients with detailed growth records. Parameters including disease location, disease severity, and NOD 2 genotype and their effect on z scores for height and weight at disease onset and during follow-up were analyzed. RESULTS: NOD2 mutations were correlated with ileal location but not with disease severity or growth retardation. Ileal involvement was significantly associated with height retardation at disease onset and the lowest z score during follow-up. Use of steroids affected weight but not height. Regression models for growth variables revealed that the strongest association with impaired growth is with disease severity (weight- and height-failure odds ratios: 6.17 and 4.52, respectively). CONCLUSIONS: Severity of disease is correlated with growth failure for both height and weight. Location of disease is a weaker predictor of disordered growth and is correlated with growth retardation but not growth failure. The NOD2 genotype was not correlated with growth retardation or growth failure.

Child↗
PubMed2003

Comparative biology of the IGF system in endometrium, decidua, and placenta, and clinical implications for foetal growth and implantation disorders.

The insulin like growth factors and their binding proteins appear to play a central role during implantation and establishment of pregnancy in all species studied. Although there are similarities among species in the cell types that express IGFs and IGFBPs and their regulation during implantation and pregnancy, there are also significant differences. Understanding of the role of the IGF system in placental function in the human is of immense clinical importance, because serious complications of pregnancy such as intrauterine growth restriction and pre-eclampsia are thought to be associated with alterations in IGF system during early pregnancy and later in gestation. Research in laboratory and domestic animals, including transgenic and gene targeting studies in mice, has significantly improved our understanding of the role of IGF system in placental and foetal development. This paper reviews the diversity in the expression and regulation of IGF system in the decidua and placenta at the foetal-maternal interface in the human and different animal species, which may benefit in directing future studies in understanding of various complications of human pregnancy.

Animals↗
PubMed1997

Clinical usefulness of bone age determination in the management of tall stature.

Measurements of skeletal maturation are used in the study and management of growth and growth disorders because of the correlation between the degree of skeletal maturation and the potential for further growth. In a study of 147 tall girls, final height was overpredicted by 0.7 +/- 2.5 cm (mean +/- SD) when based on the Bayley-Pinneau method. The radius-ulna-short bones (Tanner-Whitehouse 2) mark II method of assessment produced an underprediction of final height by 0.8 +/- 2.9 cm and 1.0 +/- 2.8 cm when the rating was performed by a skilled human or by a computer-aided system, respectively. These errors in prediction were considered acceptable, although when predictions were made on five girls below 11 years of age, they were less accurate.

Adolescent↗
PubMed1987

Impaired synergism between somatomedin C/insulin-like growth factor I and dexamethasone in the growth of fibroblasts from a patient with insulin resistance.

To explore a possible mechanism for the diminished growth potential in a patient with an unusual form of insulin resistance, somatomedin C/insulin-like growth factor I (SM-C/IGF-I) and insulin stimulation of [3H]thymidine incorporation and cell replication were compared in skin fibroblasts from the patient (DF) and normal controls. There appeared to be no generalized abnormality in cellular responsiveness to growth factors. In both DF and control cells, SM-C/IGF-I (50 ng/ml), insulin (100 ng/ml), and epidermal growth factor (5 ng/ml) stimulated [3H]thymidine incorporation 5-, 2-, and 6-fold, respectively. Low concentrations of human hypopituitary serum (0.25%) enhanced the effectiveness of SM-C/IGF-I and insulin to a similar extent in both DF and control cells. On the other hand, 10% calf serum stimulated [3H]thymidine incorporation 37-fold in control cells, while DF cells were only 50% as responsive. Preincubation of control cells with dexamethasone (10(-7) M) caused a marked synergistic increase in SM-C/IGF-I stimulated [3H]thymidine incorporation (15- to 20-fold in serum-free medium; 50- to 80-fold in 0.25% human hypopituitary serum). In contrast, preexposure to dexamethasone did not augment SM-C/IGF-I stimulation of thymidine incorporation into DNA of DF cells. Furthermore, the stimulation of cell replication by SM-C/IGF-I and insulin was potentiated by dexamethasone in control but not DF cultures. These data suggest that impairment of the synergistic action of glucocorticoids with SM-C/IGF-I and insulin regulation of fibroblast growth may be involved in the pathology of this insulin-resistant growth disorder.

Cell Division↗
PubMed2002

Puberty in chronically diseased patients.

Delayed onset of puberty and a reduced pubertal growth spurt are often reported in patients suffering from chronic diseases. The basis of abnormal puberty in these patients is multifactorial. Nutritional deficiency may contribute to growth disorders and delayed puberty. Insufficient food supply and/or eating disorders and/or malabsorption of nutrients can be observed in these patients. Moreover, increased energy supplies are often needed in patients with chronic lung disease, infection or inflammation. More specific factors due to the disease itself may be involved in growth and puberty disorders. Abnormalities of the growth hormone (GH)-insulin-like growth factor (IGF)1 axis and gonadotrophin secretion have been described in patients with chronic renal failure, cystic fibrosis and Crohn's disease. More recently, it has been shown that cytokines produced during chronic diseases such as juvenile idiopathic arthritis may affect the GH-IGF1 axis. Finally, concomitant medication, namely corticosteroids, which are often given to these patients, may contribute to delayed puberty and poor pubertal growth.

Adolescent↗
PubMed1992

[New findings and the potential use of the growth hormone].

Use and potential use of human growth hormone (GH). The benefit of GH in classical growth hormone deficiency is well known. For the past six years, the availability of biosynthetic human growth hormone has permitted the investigation of the effect of GH in a variety of growth disorders. GH has been shown to be helpful in children with idiopathic short stature, Turner's syndrome, neuroendocrine deficiency, and chronic renal insufficiency. Although the experience is limited, GH would appear helpful in short children with intrauterine growth retardation and Noonan's and Prader-Willi syndromes. GH increases muscle mass and strength and decreases fat mass in young adults with GHD and treatment is under consideration. One of the areas of present interest and potentially of great benefit is the use of growth hormone in catabolic conditions (burns, surgical operations, patients with a prolonged stay in intensive care units, malnourished patients and patients with chronic obstructive pulmonary disease). In catabolic conditions, GH is effective in decreasing nitrogen loss, in maintaining nitrogen balance, even with hypocaloric diets, and in increasing protein synthesis and skeletal muscle mass when combined with adequate nutrition. GH has proven helpful in inducing ovulation and improving fertility in patients with GHD and in patients with ovarian resistance to gonadotropins. The field of growth hormone therapy is expanding and potentially GH could be of benefit to many children and adults with a variety of disorders.

Adolescent↗
PubMedDate not supplied

Psychosocial aspects of short stature.

Normal growth in childhood requires, amongst other factors, an emotionally supportive environment. Psychosocial deprivation results in poor growth, and also growth disorders themselves can cause psychosocial problems /1/.

Adaptation, Psychological↗
PubMed1985

Craniofacial dysmorphology in syndromes associated with abnormal physical growth.

Nine syndromes associated with varying patterns of abnormal physical growth were selected to study quantitative craniofacial dysmorphology with cephalometric analysis. A schematic diagram was developed in which a hexagon measures the neurocranium and facial skeletal size and form. This hexagon offers the possibility of quantitative dysmorphic roentgencephalometry to study the effects of various growth disorders on the craniofacial complex.

Cephalometry↗