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 631 records · Page 35Linked to original sources
PubMed1996

Disease-specific standards in congenital syndromes.

A number of congenital diseases are associated with growth disorders. Over the past decade, efforts have been made to define disease-specific growth standards for these diseases. Such standards allow patients to be counselled, and it is useful to take the predicted growth of an individual into account before initiating any treatment regimen. In addition, knowledge of the growth pattern associated with a particular disorder may facilitate a greater understanding of the pathology of the disease, and deviations from the predicted pattern of growth may be indicative of additional disease processes. However, although growth standards are extremely useful, it is important to note that they are subject to a number of biases, which result from the way in which the study on which data used to calculate the standards was conducted. Until these biases are addressed, the standards that are currently available will not be entirely suitable for routine use.

Adolescent↗
PubMed2003

MAP kinases in chondrocyte differentiation.

The majority of the vertebrate skeleton develops through the process of endochondral ossification and involves successive steps of chondrogenesis, chondrocyte proliferation, and hypertrophic chondrocyte differentiation. Interruption of this program through gene mutations and hormonal or environmental factors contributes to numerous diseases, including growth disorders and chondrodysplasias. While a large number of growth factors and hormones have been implicated in the regulation of chondrocyte biology, relatively little is known about the intracellular signaling pathways involved. Recent data provide novel insights into the mechanisms governing acquisition of new phenotypes within the chondrogenic program and suggest multiple pivotal roles for members of the mitogen-activated protein kinase family and their downstream targets in cartilage development. These data are summarized and discussed here.

Animals↗
PubMed1983

Skeletal growth in normal and pathological conditions.

The authors describe the morphological and functional differences between the various systems of enchondral ossification of the metaphysis and epiphysis of the long bones, the short bones and the zones of insertion of tendons and ligaments. They discuss the relationships between the various types of enchondral ossification, the rates of skeletal growth and a number of orthopaedic growth disorders. In deformity of the lower limb, skeletal growth produces spontaneous correction in the majority of cases. Spinal abnormalities, on the other hand, tend to deteriorate during the period of rapid growth of the trunk.

Adolescent↗
PubMed1996

Infradian rhythms in urinary growth hormone excretion.

All studies of urinary GH excretion in normal and disordered growth have revealed marked day to day (infradian) variation. We used serial overnight urinary GH estimations as an indirect measure of endogenous GH secretion in eight normal prepubertal children (aged 3.6-7.3 yr) over 90-365 days to determine whether longer term rhythms in GH output could exist. This study constitutes a first step in examining the potential relationship between GH excretion and growth. Urinary GH was measured by immunoradiometric assay after dialysis, expressed as the total amount excreted (nanograms per night) or as the GH/creatinine ratio (nanograms per mmol), and assessed by pulse counting techniques and time-series analysis. Variability in urinary GH excretion (median coefficient of variation, 46%) was significantly greater than creatinine (median coefficient of variation, 25%; P = 0.003). Additionally, there was marked month by month variation in baseline urinary GH in all children. High frequency pulses of urinary GH were defined in all children, with periods between 3-5 days. In the two children followed for 7 months or more, time-series analysis was also undertaken on urinary GH data divided into weekly series. This revealed significant rhythms present at 2.6 and 4.1 weeks. There were, therefore, three components to urinary GH excretion: long term basal fluctuation (over months), short term pulses (over days), and intermediate rhythms (over weeks). Further work is required to establish the relationship between these patterns of GH excretion and short term growth.

Child↗
PubMed1990

Growth and endocrine disorders in optic glioma.

Hypothalamo-pituitary function in children with optic glioma may be impaired by the tumour itself and by the high cranial radiation doses used in treatment. This study evaluates the effect of optic glioma and its treatment on patient growth and pubertal development. Twenty-one patients (13 boys, 8 girls), treated for optic glioma by cranial irradiation (45-55 Grays) at a mean age of 5.4 years, were evaluated before (n = 10) and/or after (n = 21) irradiation. Growth hormone (GH) deficiency was present in only 1 patient tested before irradiation and in all patients after irradiation. Precocious puberty occurred in 7/21 cases, before irradiation in 5 patients and after irradiation in 2 patients. The cumulative height loss during the 2 years after irradiation was 0.2 +/- 0.2 SD (m +/- SEM) in 7 patients with precocious puberty and 1.1 +/- 0.2 SD in 14 prepubertal patients (P less than 0.01). The corresponding bone age advance over chronological age, evaluated 1-3 years after irradiation, was 1.1 +/- 0.5 and -0.7 +/- 0.3 year in the two groups (P less than 0.01). The mean height loss between time of irradiation and the final height was 2.3 +/- 0.6 SD (n = 6). Primary amenorrhoea, associated with low oestradiol levels, occurred in two of the three girls of pubertal age. These data indicate that the high dose of cranial radiation used to treat optic glioma invariably results in GH deficiency within 2 years and that hGH therapy is required when GH deficiency is documented.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Determination by Skeleton↗
PubMed2000

Data and hypotheses on the role of nerve growth factor and other neurotrophins in psychiatric disorders.

Nerve growth factor (NGF) was discovered and characterized for its role on the growth, differentiation and maintenance of specific neurons of the peripheral nervous system. Subsequent studies revealed that NGF is synthesized and released within the central nervous system and exerts a trophic and functional role on basal forebrain cholinergic neurons; it is involved in a protective role following brain insults induced by an epileptic status, seizure, as well as surgical and chemical lesions.More recently our collaborative studies provided evidence that NGF is implicated in neurobehavioral response including cerebral alterations associated with psychiatric disorders. In this brief review, ongoing and emerging data are presented and discussed.

Animals↗
PubMed2002

[Transient cognitive disorder from sub clinical paroxysmal EEG activity].

INTRODUCTION: Transient cognitive disorder (TCD) defines the existence of a decrease in reaction time that coincides with an epileptiform EEG discharge, without any simultaneous manifestation of a classical epileptic seizure. Aims. To analyse the relation between episodes of TCD and the neurolopsychological manifestations in infancy that condition a high percentage of neuropaediatric visits to the surgery. At the same time we analyse the relation between the interictal paroxysmal disorders of patients with childhood benign partial idiopathic epilepsy with centrotemporal spikes (BIE CS) and the neurolopsychological manifestations that are frequently detected in such patients. PATIENTS AND METHODS: Two groups of patients were studied. Group A: 23 children who sought medical attention because of different neurolopsychological disorders (language retardation, hyperactivity, lack of attention, retarded academic achievement, behavioural disorders, bad social interaction); gender: 16 males and 7 females; age interval: from 2 years and 10 months to 11 years and 1 month (average age: 6 years and 8 months). Group B: 10 patients who were BIE CS carriers, two of which evolved toward atypical BIE; gender: 5 males and 5 females; age interval: from 3 years and 3 months to 9 years and 9 months (average age: 7 years and 4 months). Both groups were submitted to a clinical examination protocol involving neurological, EEG, child psychiatric and psychological aspects. RESULTS: In group A, sub clinical paroxysmal EEG discharges were seen in three cases, two of which corresponded to a lack of attention disorder with hyperactivity, and the third had a generalised growth disorder. In group B we detected a high percentage of perceptive and psychomotor disorders, without the existence of differences between those who displayed an irritative focus in the right or in the left hemisphere, although the alteration in the level of language was greater in the latter. Likewise, in a large percentage of cases (80%) the evaluation of the level of personality revealed obvious anxiety traits, which were related with suffering from seizures. CONCLUSIONS: Sufficient evidence has been found to demonstrate the existence of the possible relation between different neuropsychological disorders and epileptic EEG discharges, although revealing it in daily clinical practice requires a thorough diagnostic protocol and an accurate neuropsychological examination under video EEG monitoring, the positive results of which are considered to be decisive in evaluating the possibility of pharmacological treatment.

Child↗
PubMed2005

[Molecular diagnostics in endocrine diseases].

Molecular diagnostic techniques provide an unsurpassed opportunity to understand the pathophysiological basis of endocrine disorders. Diseases have been associated with mutations in almost every gene known to have a role in either the production or secretion of a hormone or the mediators of hormone signalling. Even though most of these mutations are rare and account for only a small fraction of endocrine diseases, molecular diagnostics offers a valuable tool for the clinician in these cases. The most common endocrine disorders such as autoimmune thyroiditis, type 2 diabetes mellitus, osteoporosis, growth disorders, and obesity have all major genetic components, but these are mostly unknown. In this review the clinical implications of molecular diagnostics are illustrated for some endocrine diseases: congenital adrenal hyperplasia, congenital hypothyroidism, thyroid hormone resistance, familial hypocalciuric hypercalcaemia, growth hormone deficiency and resistance, and monogenic obesity. Improved diagnostic specificity has direct implications for treatment and follow up in these syndromes. Molecular diagnostics in endocrine tumours and diabetes are presented in two other articles in this series.

Adrenogenital Syndrome↗
PubMed1990

Growth hormone dysregulation in children with major depressive disorder.

The growth hormone response to stimulation with oral clonidine and L-dopa was measured in 14 boys with major depressive disorder (MDD) and 15 normal boys. The six MDD boys who were prepubertal or in early puberty were significantly lower than the 10 normal subjects of this age in peak growth hormone response following clonidine administration (p = 0.029) and area under the curve for clonidine (p = 0.030) and L-dopa (p = 0.028). The eight later puberty MDD boys did not differ from the five later puberty normal boys on any measures.

Brain↗
PubMed2006

Endocrine assessment, molecular characterization and treatment of growth hormone insensitivity disorders.

Advances in the diagnosis and treatment of growth hormone insensitivity disorders have occurred in the past 15 years. We discuss the current status of endocrine and molecular evaluation, focusing on the pediatric age range. All the identified mutations of the growth hormone receptor are included. Treatment with recombinant human insulin-like growth factor (rhIGF) 1 in classical cases is summarized and new targets for treatment are discussed, together with therapy using the complex formed between rhIGF1 and rhIGF-binding protein 3.

Endocrine System↗
PubMed2005

Transforming growth factor-beta signalling in brain disorders.

Transforming growth factor-beta (TGF-beta) has been characterized as an injury-related factor, based on the observation that it is strongly up-regulated in many acute or chronic central nervous system disorders. TGF-beta is generally thought to be neuroprotective and several mechanisms have been proposed to explain this beneficial action. For instance, TGF-beta protects neurons against the potentiating effect of tissue-type plasminogen activator on NMDA receptor-mediated excitotoxicity, by up-regulating type-1 plasminogen activator inhibitor expression in astrocytes. TGF-beta has also anti-apoptotic properties, through a recruitment of a mitogen-activated protein kinase pathway and a concomitant activation of anti-apoptotic members of the Bcl-2 family. These multiple mechanisms might reflect the pleiotropic nature of TGF-beta, reinforcing the potential therapeutic value of this cytokine in several central nervous system disorders.

Animals↗
PubMedDate not supplied

[Various aspects of the influence of infection on growth and development].

It is pointed out how infections can delay growth and development through an aggressive and long-standing action, through direct action of an infecting agent (virus, bacteria, parasites). or through sequelae in main organs (brain, kidney, growth cartilage, muscular system, etc.). how infections impair nutrients' absortion, metabolism and excretion. The role of the leukocytes is evidenced in the liberation of two factors: MEL and pyrogen factor. Metabolic responses are classified in an anabolic anda catabolic phase. The second mechanism that interfers on growth and development is a specific action of various agents, particularly viruses on different tissues. Intrauterine infection is pointed out as determinant of growth disorders with increased IgM levels in cord blood; confirmed fetal infection on the 6th up to 8th week of gestation interferes with organogenesis. The action of CMV and rubella virus is mentioned as example. The action of viral infections on growth during the first three months of gestation, is mentioned. TBK and typhoid fever are mentioned as causative agents of corporal and urinary nitrogen loss. Negative action of infection on growth and development, particularly in malnourished patients, is discussed. Diarrhea, under certain condition, is pointed out as determinant of the kwashiorkor syndrome. The role of various parasite diseases on growth is mentioned with range according to the action of each agent on nutrients' absortion. A third mechanism which causes fail to thrive through sequelae lesions is considered. This disorders are ruled by the age of the patient with the onset of disease by the causative agent, by the inflammatory process involved, by the early diagnosis and appropriate treatment. The need of enhancing the actions to prevent communicable diseases and to diminish malnutrition rates is pointed out and the significance of taking into account calorie and protein intake in patients with severe and/or long-standing infectious disease.

Bacterial Infections↗
PubMed2001

[Mandibular growth, its environmental interactions].

A thorough knowledge of mandibular growth is necessary for proper comprehension of growth disorders and malformations affecting the lateral cranio-facial region. The growth mechanisms are complex and multifactorial, the mandible itself is subdivided into two heterogeneous and interdependent segments, as far as growth is concerned. These are the ramus and the corpus. The ramus is interacting with the middle cranial base through the TMJ and the temporo-pterygoid muscle belt. The mandibular body is interacting with the maxilla and the anterior cranial base. Its occlusal role is a function of the adaptive capacity of the alveolodental region.

Alveolar Process↗
PubMed1991

Research involving fetal drug therapy: ethical, legal, and practical considerations.

Fetal drug therapies have emerged as a promising avenue for the prevention or correction of disease during fetal or immediate postnatal life. Despite slow progress, several medications have been developed for in utero therapy of disorders which relate to fetal and neonatal pulmonary, cardiac, neurologic, and growth disorders. However, ethical and regulatory constraints require protection of the mother and fetus while causing no more than necessary additional risk. Appreciating these constraints will lead to the identification of pragmatic questions which should be answered before evaluating the efficacy and safety of a particular treatment or research proposal.

Aborted Fetus↗
PubMed2005

Endocrine regulation of the growth plate.

Longitudinal bone growth occurs at the growth plate by endochondral ossification. Within the growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in chondrogenesis. The newly formed cartilage is invaded by blood vessels and bone cells that remodel the newly formed cartilage into bone tissue. This process of longitudinal bone growth is governed by a complex network of endocrine signals, including growth hormone, insulin-like growth factor I, glucocorticoid, thyroid hormone, estrogen, androgen, vitamin D, and leptin. Many of these signals regulate growth plate function, both by acting locally on growth plate chondrocytes and also indirectly by modulating other endocrine signals in the network. Some of the local effects of hormones are mediated by changes in paracrine factors that control chondrocyte proliferation and differentiation. Many human skeletal growth disorders are caused by abnormalities in the endocrine regulation of the growth plate. This review provides an overview of the endocrine signals that regulate longitudinal bone growth, their interactions, and the mechanisms by which they affect growth plate chondrogenesis.

Androgens↗
PubMed2004

Novel mutations in the TRIM37 gene in Mulibrey Nanism.

Mulibrey nanism is an autosomal recessive prenatal-onset growth disorder of unknown pathogenesis. The main clinical features are pre- and postnatal growth failure, characteristic dysmorphic craniofacial features, heart disease, and hepatomegaly. Five truncating mutations in the TRIM37 gene have previously been reported in Mulibrey nanism patients. The TRIM37 protein encodes a novel protein of unknown function. It contains a tripartite motif (TRIM, also denoted the RING-B-box-Coiled-coil or RBCC domain) and a TRAF (tumor necrosis factor-receptor associated factor) domain. TRIM37 localizes to peroxisomes classifying Mulibrey nanism as a peroxisomal disorder. Here we have characterized the genomic structure of the TRIM37 gene, which has 24 exons spanning approximately 109 kb of genomic DNA. Further, we report six novel disease-associated mutations, five of which predict a truncated protein: c.745C>T (p.Gln249X), c.1411C>T (p.Arg471X), c.2056C>T (p.Arg686X), and an 8.6 kb genomic deletion (c.1314+507_1668-207del resulting in p.Arg439fsX4). The sixth mutation (c.965G>T) is the first missense mutation (p.Gly322Val) associated with Mulibrey nanism. It affects the TRAF domain of TRIM37 and results in altered subcellular localization of the mutant TRIM37 protein, further suggesting that it is pathogenic.

Animals↗