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PubMedDate not supplied

Prospects for epidermal growth factor in the management of corneal disorders.

Epidermal growth factor (EGF) is a naturally occurring mitogen which, in its recombinant form, is under intensive investigation for therapeutic use. Receptor activation by EGF induces up-regulation of synthesis of specific proteins as well as proliferation and differentiation of the corneal epithelium, keratocytes, and endothelium both in vivo and in vitro. With topical application of EGF, corneal wounds could possibly heal within hours, and the strength of the stromal scars is also increased; this may lead to the prospect of sutureless surgery. It may be possible to treat degenerative and dystrophic disorders of the cornea, especially of the endothelium, and to enhance the density of endothelial cells in donor corneas prior to transplantation. Combination therapy with EGF, fibroblast growth factor, and corticosteroids may be advantageous in producing a synergistic effect. It is possible that, with increased knowledge of the pharmacokinetics and the development of appropriate delivery systems, EGF could become an integral part of the next generation of ophthalmic pharmaceuticals.

Adrenal Cortex Hormones↗
PubMed1991

Tumour progression and the nature of cancer.

The nature of neoplasia and its sometime end result, cancer, has been studied by exposition and explanation of the sequential lesions of tumour progression. Neoplastic lesions were divided into four classes on the basis of growth characteristics and whether lesional growth is confined to one or more tissue compartments. Class IA, the initial lesion, an orderly, probably clonal growth, usually differentiates and disappears. Class IB: Failure to differentiate accompanied by disorderly growth. Class IC: Randomly dispersed atypical cells, constituting a precursor state. Class II, intermediate lesions, apparently arising from the atypical cells, show temporally unrestricted growth within the tissue compartment of origin. Class III lesions, primary invasive cancers, show temporally unrestricted growth in two or more tissue compartments and metastasise along different paths, a property associated with extracellular matrix interaction. The metastatic pathways may result from different subsets of cells in the primary cancer. Class IV lesions are the metastases. It was concluded that, all neoplasms develop in the same way, have the same general behavioural characteristics, and, when malignant, all interact with the extracellular matrix of the primary and the secondary sites. The origins and development of cancer are considered to be pluralistic and not due to a discrete change in a cell, whose progeny, as a result of that discrete change, carries all of the information required to explain the almost limitless events of a neoplastic system.

Cell Division↗
PubMed1995

Conditional reference charts to assess weight gain in British infants.

Growth monitoring in infancy is a useful tool for detecting growth disorders and failure to thrive. However, current weight charts do not monitor growth as such, they only identify infants whose weight centile is low and/or falling. A reference of conditional weight gain is described which compares an infant's current weight with that predicted from their previous weight, allowing for the fact that on average, light infants tend to grow faster than heavier infants. The reference, which expresses conditional weight gain as an SD score of centile, is based on the UK 1990 weight reference supplemented with correlation data on 223 infants from the Cambridge Infant Growth Study measured regularly between 4 weeks and 2 years of age. The reference is validated with data on 727 infants from the Newcastle Regional Health Authority database. The conditional reference provides a valid assessment of the weight gain of British infants, over time periods of four or more weeks, throughout the first two years of life.

Female↗
PubMed2004

Somatropin and its variants: structural characterization and methods of analysis.

Human Growth hormone (hGH, somatotrophin) is a 22 kDa, 191 amino-acid single chain protein produced by somatroph cells of the anterior pituitary gland. It is the major physiological regulator of growth, and deficiencies in growth hormone levels have long been recognized as the underlying cause of growth disorders (dwarfism). The ability of exogenous hGH to restore normal rates of growth in both human and animal models of growth retardation has long been recognized and the use of hGH in therapy goes back several decades. Initial preparations were prepared by extraction and purification from cadaveric pituitary tissue, and since 1984, hGH has been prepared by recombinant Deoxyribosenucleic acid (rDNA) technology. As is usually the case with "biologicals", characterization of the drug substance depended on a combination of physico-chemical and biological methods, and the hGH molecule became well characterized fairly early in its life as a drug. Indeed, by 1980 the major degradation forms and structural variants of the hGH molecule had been described and reviewed. Little satisfactory progress had been made in refining biological assays for hGH, and, although in vitro assays were described, potency-defining assays remained dependant on the whole body growth response in rats, and were both invasive and imprecise. In the early 1990's a series of collaborative studies on analysis of recombinant hGH (somatropin) established that available bioassays were much less selective that physico-chemical methods in detecting and quantifying structural degradation, and 1994 saw an international consensus to replace the bioassays with physico-chemical analytical methods for the routine batch release of somatropin. During the last decade in most markets somatropin has, unusually for a protein, been subject to batch release and control dependent entirely on physico-chemical analysis, without the routine use of any form of bioassay. During that time there has been a continuous development and refinement of methods, and the identification of a range of structural variants and degradation products of the molecule. The present review sets out to summarise the current knowledge on physico-chemical analytical methods for somatropin, and the structural variants that have been identified and characterized. A survey of available biological analytical methods is beyond the scope of this review, as is consideration of the earlier pituitary preparations and the recombinant 192 amino-acid methionyl form of the molecule (somatrem), although it is likely that many of the methods and variants described would be equally applicable to somatrem.

Chromatography, High Pressure Liquid↗
PubMed2005

Intrauterine growth restriction--diagnosis and management.

BACKGROUND: Fetal growth disorders are an important cause of perinatal morbidity and mortality with long term health implications for the survivors of intrauterine growth restriction (IUGR). The accurate assessment of fetal growth during pregnancy is difficult, but recent advances have improved this important aspect of obstetric care with positive implications for antenatal patients and their babies. OBJECTIVE: This article provides an overview of the detection of fetal growth problems in pregnancy, the determination of the likely cause, and the antenatal and intrapartum care of women with pregnancies identified as being affected by IUGR. The role of customised fetal growth assessment in the detection of IUGR is considered and followed by an outline of the appropriate monitoring and management of these pregnancies based on the underlying pathophysiology. DISCUSSION: Accurate assessment of fetal growth is improved by early clarification of gestational age and the use of customised fetal growth charts. Once infections and anomalies have been excluded, it is imperative to distinguish the healthy small fetus from the growth restricted fetus. While treatment options are limited, the optimal management of the IUGR affected fetus aims to achieve the delivery of the newborn in the best possible condition, balancing the risks of prematurity against those of continued intrauterine existence.

Chromosome Disorders↗
PubMed2006

Pemphigoid gestationis: report of a case with umbilical artery Doppler assessment.

BACKGROUND: Pemphigoid gestationis is a rare autoimmune disorder of pregnancy characterized clinically by a pruritic, papular rash and in some cases intrauterine growth restriction and premature delivery. The growth disorder is secondary to antibody deposition in the placental bed, with resultant placental insufficiency. The appropriate fetal assessment required during these gestations remains uncertain. The use of serial Doppler velocimetry of the umbilical arteries has not been reported to date in this disorder. CASE: A woman had pemphigoid and progressively decreasing umbilical artery end-diastolic flow over a period of weeks without documented fetal growth restriction. Delivery was finally prompted by reversal of end-diastolic flow. CONCLUSION: We suggest that parturients with this condition undergo frequent umbilical artery Doppler studies to document end-diastolic velocity even without the ultrasound finding of intrauterine growth restriction.

Cesarean Section↗
PubMed1980

Prolactin and growth hormone responses in the amenorrhea-galactorrhea syndrome.

Fifteen patients with hyperprolactinemia, amenorrhea, and galactorrhea were studied; 10 of these patients had apparent tumors. Nine of 12 patients had a suppression of prolactin with oral L-dopa, and all of 4 patients undergoing dopamine infusion had suppression of prolactin. Eleven and 8 patients underwent chlorpromazine stimulation and insulin-induced hypoglycemia, respectively; none responded. Three of the 4 patients did not show a growth hormone response with dopamine infusion, and L-dopa testing failed to achieve a growth hormone response in 7 of 10 patients. The data suggest an intact dopaminergic inhibition of prolactin with exogenous agents. However, inhibition of endogenous dopamine by chlorpromazine failed to elicit a prolactin response. The disordered growth hormone response to dopaminergic agents suggests a central disorder of dopamine generation. The possible implication of these results with respect to the pathogenesis of hyperprolactinemia is discussed.

Amenorrhea↗
PubMed1985

Perturbation of differentiated functions during viral infection in vivo. II. Viral reassortants map growth hormone defect to the S RNA of the lymphocytic choriomeningitis virus genome.

Lymphocytic choriomeningitis virus (LCMV) Armstrong caused disordered growth and glucose metabolism secondary to growth hormone deficiency in infected C3H/St mice. In contrast, LCMV strain WE replicated in fewer growth hormone-producing cells, failed to disrupt growth hormone synthesis, and did not cause growth hormone-induced disease in infected, matched controls. The generation of genetic reassortant viruses between the virulent strain of LCMV:Armstrong and the avirulent strain, LCMV:WE, is reported. Using such reassortants and both parental strains of virus in C3H/St mice, the perturbation of growth hormone synthesis was clearly mapped to the S RNA segment of LCMV:ARM.

Animals↗
PubMed1992

Diagnosis of growth hormone deficiency.

Many ways of evaluating the physiological state of hGH secretion exist, some of which have been touched upon and none of which has as yet proven infallible. Apart from important clinical features like history, physical data and growth rate, the diagnosis of altered pituitary function is based on tests and their interpretation. The physician responsible has to be informed on their effectiveness and pitfalls. Results should be interpreted in relation to developmental age (bone age) rather than chronological age. Research is under way to try to facilitate the diagnosis of varying degrees of alterations of hGH secretion. Reliability in predicting the effect of therapy with hGH is the ultimate aim in order to prevent unnecessary cost and disappointment for the patients. With the help of doctors involved in child care, such as physicians at kindergarten or school, it should be possible to start the slow process of investigating growth disorders at an early age.

Deficiency Diseases↗
PubMed1989

Therapy with growth hormone--old and new indications.

Pituitary dwarfism with severe growth hormone deficiency (GHD) represents the classical indication for treatment by recombinant human growth hormone (hGH). With continuous GH replacement and early start of treatment, normal adult height can be achieved. During puberty the dosage of hGH administered should be increased. Numerous growth disorders do not coincide with major GHD as determined by provocative tests but only with diminished spontaneous hormone secretion. Typical examples are constitutional delay of growth and adolescence and growth retardation after irradiation of the skull. Also in these disorders treatment by recombinant hGH in replacement doses renders favorable results. The more normal the spontaneous GH secretion is, e.g. in familial short stature and in skeletal dysplasias, the higher doses of GH are needed to stimulate growth. For treatment of patients with Turner's syndrome a combined therapy with high doses of GH and with oxandrolone has proven rather effective. With endogenous and exogenous hypercortisolism the metabolic balance is shifted towards catabolism and spontaneous GH secretion is depressed. In such situations, e.g. after severe traumas, operations, infections and combustions, administration of GH can be rather helpful. Recent trials in children with stunted growth due to chronic renal insufficiency show that it is possible also in this condition to effectively stimulate growth by hGH.

Clinical Trials as Topic↗
PubMed1995

Effect of growth hormone on IGF-I levels in a patient with growth hormone deficiency and Wilson disease.

This is a case report of a boy with a combination of two rare disorders:growth hormone deficiency (GHD) and Wilson disease. To our knowledge, no comparable case has yet been published in the literature. GHD was diagnosed at the age of 4.5 years (height standard deviation score (SDS) -4.85). However, because of a difficult family background, growth hormone (GH) therapy could not be started. The boy was not seen again until the age of 7.7 years (height SDS -4.77), when GHD was reconfirmed and GH therapy could be initiated (dose 0.6 IU/kg/week). At that time, elevated liver enzymes (GPT 128 U/l, GOT 67 U/l, gamma-GT 28 U/l) confused diagnostic procedures. On GH, growth velocity SDS increased from -1.86 to +4.50 in the first year and +3.87 in the second year, and height SDS increased to -4.26 and -3.59. However, serum IGF-I levels did not normalize (max. 67 ng/ml), and liver enzymes were still elevated. At the age of 10 years, Wilson disease was diagnosed in view of low concentration of serum ceruloplasmin, elevated urinary copper excretion and high copper content in a liver biopsy sample. Under a combined therapy with D-penicillamine and GH, serum liver enzymes decreased, and IGF-I levels increased to normal. Height SDS for chronological age has improved constantly.

Ceruloplasmin↗
PubMed1994

Perspectives on craniofacial growth.

This article underscores the importance of the growth process in the production of normal and abnormal craniofacial morphology. Although much has been learned over the past century, we still have only a limited appreciation of the 3D changes that occur in the skull during postnatal growth. We have also stressed that the current cooperation between reconstructive surgeons and radiologists is producing a substantive amount of data that could be used to further our understanding of the postnatal growth process. At The Johns Hopkins University we are putting our efforts toward the collection and organization of a large data base of craniofacial images that will allow us to study questions about the role growth plays in mediating the results of reconstructive surgery. Our ultimate goal is to provide information about the future appearance of craniofacial patients based on empirically derived growth patterns. In a recent article Dufresne and Richtsmeier proposed that the results of surgical correction may be predicted based on the etiology of the craniofacial condition, and not necessarily the degree or character of the dysmorphology. The authors hypothesize that a categorization or classification of craniofacial dysmorphology can be proposed, based on the response of individuals to surgery, and that such a classification reflects real differences in etiology. Hence, a poor response to surgery reflects a condition that includes a growth disorder, whereas cases that respond positively to reconstructive surgery are those in which the growth process is not part of the dysmorphology. In the latter cases, a dysmorphic face is surgically transformed into an acceptable morphology, and normative growth vectors maintain or improve postoperative facial appearance. Thus, Dufresne and Richtsmeier13 suggest that this divergence in the response to surgery among patients relates directly to the role of the growth process in various types of dysmorphologies. Using our tools and the data base we are forming, we envision a markedly different preoperative consultation for future craniofacial patients. When a patient is evaluated, images from the data base with a similar diagnosis will be used to calculate a growth pattern for the proper age interval. The patient's scan is then "grown" according to the appropriate growth pattern. The parents and patient can evaluate this new image and see what their child's skull will look like 2, 3, or 4 years from the present, both with and without reconstructive surgery. In addition, our tools will statistically compare the simulated (or "grown") skull to samples of craniofacial images of normal and affected children of an age/sex/ethnic population that matches the patient. This testing will determine whether growth results in the patient becoming more normal, or more different from normal, with time.(ABSTRACT TRUNCATED AT 400 WORDS)

Child↗
PubMed1981

Effect on growth in pemoline-treated children with attention deficit disorder.

The growth of 22 children with attention deficit disorder (ADD) was monitored longitudinally for up to four years. Each child received at least one year of continuous, successful pemoline (Cylert) therapy, after which drug "vacations" were allowed. The effective dosage of pemoline ranged from 56 to 150 mg/day during the first year of treatment. Stature and weight measurements at six-month intervals were matched to those of paired "normal" children from the Fels Longitudinal Study. Significant deficits were observed for mean weight change at six and 12 months after baseline, and for mean stature change at 12 and 18 months after baseline. However, all subsequent six-month results up to four years did not differ significantly between the two groups. These results show a temporary retardation in the rate of growth in weight and stature with later catch-up growth in children treated wih pemoline.

Adolescent↗
PubMed1991

[Endocrine complications of treatment of brain tumors in children].

The recent treatment protocols used in the management of children with brain tumors have greatly improved the survival rate in these patients. The authors present a review of the endocrine dysfunctions associated with the different types of treatment. Cranial irradiation is the first cause of endocrine disorders, growth failure being the main risk. A simplified protocol for endocrine evaluation and treatment of the disorders is suggested.

Adolescent↗
PubMed1990

[Radiologic and clinical evaluation of the wrist in some movement disorders of children].

The wrist angle in X-ray pictures of the hand in 47 children, aged 6-16 years, treated for bone growth disorders, was evaluated. The obtained results were compared with the wrist angle in normal children. The increase of the wrist angle was observed in deformations: dwarfism, gargoylism and dysplasia multiplex, and the decrease of this angle in the Turner syndrome. The range of passive and active movements of the wrist was evaluated. Passive and active mobility of the wrist (especially the radial and the ulnar deviations) was smaller in the cases of increased wrist angle.

Adolescent↗
PubMed2001

Intrauterine growth retardation in experimental diabetes: possible role of the placenta.

Fetal growth disorders are common in pregnancy complicated by diabetes. Whereas macrosomia often occurs in infants of diabetic women, growth retardation is almost a rule in spontaneous and experimental diabetes in animals. However, it is not clear when during development growth inhibition starts and how placental pathology might affect fetal growth in maternal diabetes. In this study pregnant Wistar rats were injected (ip) with a single dose of 50 mg/kg of streptozotocin (STZ) on gestation day (GD) 2 and a blood glucose level of 200 mg/dl or more determined 24 hrs later indicated diabetes. The controls were non-treated, buffer treated or, following confirmation of diabetes, injected with a single dose of 2--6 IU of insulin (Novo Ultralente) once daily. Fetuses and placentae were collected from GD 14--20. Intrauterine growth retardation (IUGR) in STZ group was significant as early as GD 15 and persisted to GD 20. Insulin produced a significant recovery in fetal weight gain. The placentas of STZ-treated group were significantly heavier than those of the control groups. The reduction in cord length of the STZ group became apparent on GD 16 and remained so to term. The placenta of GD 14 STZ group had a thicker decidua basalis and dilated maternal sinusoids. By GD 16, the decidua basalis contained glycogen-containing decidual cells and scattered glycogen cells confirmed by Best's carmine with or without diastase. The glycogen cells of the basal zone were more abundant, and had degenerated in some sites leaving behind cysts with eosinophilic mass. The giant cells had proliferated enormously. The labyrinthine zone appeared spongy with persistent fetal mesenchyme, peri-vascular fibrosis, and enhanced placental barrier. The trophoblasts of the labyrinths also contained traces of glycogen unlike the controls. By GD 18, the decidua basalis of the STZ group was thinner than that of the controls and contained necrotic giant cells and lymphocytic aggregations. In the basal zone, the giant cells had proliferated further; more glycogen cells had degenerated. Perivascular fibrosis was still extensive in the labyrinthine zone. Bloodless maternal sinusoids, extensive vacuolization, degeneration of glycogen islands and formation of cysts characterized the labyrinthine zone. These changes varied in intensity from one area to another in the same placenta and between placentas of the same and of different litters. The development of the upper and lower jaws, elevation and fusion of palatal shelves, reduction of physiological umbilical hernia, descent of the testes, fusion of the urethral folds and separation of digits of the paws were significantly delayed in the STZ group. The consistent association of placental pathology with fetal growth retardation is suggestive of an alteration in placental function possibly contributing to IUGR in STZ-induced diabetes in rats.

Animals↗
PubMed2005

FGF upregulates osteopontin in epiphyseal growth plate chondrocytes: implications for endochondral ossification.

Fibroblast growth factor receptor 3 (FGFR3) signaling pathways are essential for normal longitudinal bone growth. Mutations in this receptor lead to various human growth disorders, including Achondroplasia, disproportionately short-limbed dwarfism, characterized by narrowing of the hypertrophic region of the epiphyseal growth plates. Here we find that FGF9, a preferred ligand for FGFR3 rapidly induces the upregulation and secretion of the matrix resident phosphoprotein, osteopontin (OPN) in cultured chicken chondrocytes. This effect was observed as early as two hours post stimulation and at FGF9 concentrations as low as 1.25 ng/ml at both mRNA and protein levels. OPN expression is known to be associated with chondrocyte and osteoblast differentiation and osteoclast activation. Unexpectedly, FGF9 induced OPN was accompanied by inhibition of differentiation and increased proliferation of the treated chondrocytes. Moreover, FGF9 stimulated OPN expression irrespective of the differentiation stage of the cells or culture conditions. In situ hybridization analysis of epiphyseal growth plates from chicken or mice homozygous for the Achondroplasia, G369C/mFGFR3 mutation demonstrated co-localization of OPN expression and osteoclast activity, as evidenced by tartarate resistant acid phosphatase positive cells in the osteochondral junction. We propose that FGF signaling directly activates OPN expression independent of chondrocytes differentiation. This may enhance the recruitment and activation of osteoclasts, and increase in cartilage resorption and remodeling in the chondro-osseus border.

Achondroplasia↗