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New challenges in the growth field.

When unlimited supplies of biosynthetic human growth hormone (hGH) became available in the late 1980s, the envisaged potential of its therapeutic applications was enormous in that it was hoped that perhaps most short children would be able to be made taller. However, this seems to have been far too simplistic a view and certainly in those children with various growth disorders treated with pharmacological doses of growth hormone (GH), the potential for increased final height does not appear to be fulfilled, with the exception of girls with Turner's syndrome. Further challenges in the growth field involve the manipulation of pubertal development during concomitant GH therapy.

Body Height↗

Hair growth modulation by topical immunophilin ligands: induction of anagen, inhibition of massive catagen development, and relative protection from chemotherapy-induced alopecia.

Selected immunophilin ligands (IPLs) are not only potent immunosuppressants but also modulate hair growth. Their considerable side effects, however, justify at best topical applications of these drugs for the management of clinical hair growth disorders. Therefore, we have explored hair growth manipulation by topical cyclosporin A (CsA) and FK 506 in previously established murine models that mimic premature hair follicle regression (catagen) or chemotherapy-induced alopecia, two major pathomechanisms underlying human hair loss. We confirm that topical CsA and FK 506 induce active hair growth (anagen) in the back skin of C57BL/6 mice with all follicles in the resting stage (telogen) and show that both IPLs also inhibit massive, dexamethasone-induced, premature catagen development in these mice. Furthermore, we demonstrate that CsA and FK 506 provide relative protection from alopecia and follicle dystrophy induced by cyclophosphamide, possibly by favoring the dystrophic anagen pathway of follicle response to chemical damage. Although it remains to be established whether these IPLs exert the same effects on human hair follicles, our study provides proof of the principle that topical IPLs can act as potent manipulators of clinically relevant hair-cycling pathomechanisms. This strongly encourages one to explore the use of topical IPLs in the management of human hair growth disorders.

Administration, Topical↗

The effects of long-term normalization of sodium balance on linear growth in disorders with aldosterone deficiency.

The effect of normalization of sodium balance was evaluated in children with aldosterone deficiency of several etiologies. In salt-losing congenital adrenal hyperplasia (CAH), treatment with a mineralocorticoid in doses that normalized plasma renin activity (PRA) induced a marked increase in linear growth. Serum 17-hydroxyprogesterone (17-OHP) and androgens fell further when adequate sodium balance was achieved, allowing in some cases a reduction in glucocorticoid replacement dose. Together with PRA measurement they were the most sensitive indicators of adequate mineralocorticoid and glucocorticoid replacement therapy. In 2 teenage children with aldosterone deficiency due to Addison's and autoimmune polyglandular disease similar improvement in growth as well as onset of puberty occurred when sodium balance was normalized by increased mineralocorticoid therapy. These studies show that adequate sodium balance is essential for normal growth and pubertal development.

17-alpha-Hydroxyprogesterone↗

Growth factors and cytokines in hair follicle development and cycling: recent insights from animal models and the potentials for clinical therapy.

Hair growth disorders, particularly those that lead to hair loss (alopecia), are common and frequently cause significant mental anguish in affected individuals. The mechanisms underlying the majority of these disorders are unknown. However, insights into the specific molecular mechanisms of hair follicle development and cycling have recently been made using animal models, particularly mice that over- or underexpress a specific gene for a growth factor or cytokine. Other animal models have demonstrated that certain growth factors and cytokines can prevent much of the alopecia caused by cancer chemotherapeutic agents. These animal models have confirmed the importance of growth factors and cytokines in hair follicle development and cycling, and have formed the foundation for potential clinical therapy of hair growth disorders, particularly alopecia. Nevertheless, important questions concerning their efficacy, safety and delivery will need to be answered before successful clinical therapy of any hair growth disorder becomes a reality.

Alopecia↗

The short child. A matter of time or cause for concern?

Short stature is less likely to have an endocrine basis than is commonly thought. Any of a number of chronic systemic diseases can slow growth, short stature may result from a genetic tendency or disorder, growth may be constitutionally delayed, or it may be retarded by intrauterine influences. True endocrine causes include thyroid or adrenal disorder, growth hormone deficiency, and psychosocial dwarfism. Although growth hormone deficiency is quite rare, it has received increased attention recently. The capability to produce human growth hormone by recombinant DNA techniques presents the prospect that replacement therapy will be more readily available to those patients who might benefit from it. Caution is called for, however, in making use of this agent for patients other than those with proven growth hormone deficiency.

Body Height↗

[A syndrome of congenital diabetes with disordered epiphyseal growth with autosomal recessive inheritance (author's transl)].

A child is described with insulin dependent diabetes of neonatal onset and a disorder of endochondral growth. Radiological and histological bone appearances differ from those observed in other types of chondrodysplasia. The association of diabetes and chondrodysplasia is not likely to occur by chance but is probably a genuine clinical entity. The condition is probably inherited as a autosomal recessive and its possible pathogenesis is discussed.

Child↗

Long-term effects of extended-release mixed amphetamine salts treatment of attention- deficit/hyperactivity disorder on growth.

OBJECTIVE: The aim of this study was to examine the long-term effects of extended-release mixed amphetamine salts (MAS-XR) with 10-30-mg doses on the growth of children being treated for attention-deficit/hyperactivity disorder (ADHD). METHODS: Long-term growth data were collected from 568 children, 6-12 years of age, enrolled in a multicenter, open-label study of the safety of MAS-XR for the treatment of ADHD symptoms over the course of 6-30 months. RESULTS: Children taking MAS-XR grew less than expected, based on the norms provided by the Centers for Disease Control (CDC). The losses in expected weight and body mass index (BMI) were greatest for the heaviest children, and the losses in expected height were greatest for the tallest children. For weight, height, and BMI, we found that nearly all of the growth deficits occurred in year one. For each of these growth parameters, the loss in expected growth was not significant in the second year of treatment. CONCLUSIONS: Our results suggest that treatment with MAS-XR can lead to reductions in expected height and weight that are not fully rectified over the course of treatment, although they did show attenuation with treatment over time. Although this does not eliminate the need for clinicians to monitor growth, as they should for all stimulant formulations, it suggests that deficits in growth are not likely to be a clinical concern for most children treated with MAS-XR.

Amphetamine↗

Insulin-like growth factor 2 and overgrowth: molecular biology and clinical implications.

The insulin-like growth factors, IGF1 and IGF2, play a fundamental role in human fetal growth. Of the growth disorders that involve excessive growth, many could be attributable to overexpression of IGF2. Because one copy of the IGF2 gene is silenced by genomic imprinting, several different molecular errors can double the number of active copies of the IGF2 gene. Although not formally demonstrated, each of these errors is expected to double the level of IGF2 expression. The nature and severity of the overgrowth might be dependent on the number and location of cells that carry the molecular defect.

Animals↗

LPS-induced lung injury in neonatal rats: changes in gelatinase activities and consequences on lung growth.

Postnatal lung growth disorders may involve imbalance between metalloproteinases and their inhibitors. Inflammatory cell 92-kDa gelatinase overactivity has been reported in adults with lung injury but has not been looked for in neonates. We compared gelatinase activity in neonatal and adult rats and evaluated postnatal lung growth after lipopolysaccharide (LPS)-induced lung injury. Significant intra-alveolar inflammatory cell recruitment occurred in adults and neonates; cell counts increased 16-fold in adults and 2.7-fold in neonates. Total 92-kDa gelatinase activity was increased in neonates and adults and was significantly correlated to inflammatory cell counts. For a given cell count, 92-kDa gelatinase increased more in neonates than in adults. Morphometric neonatal lung analysis showed that LPS-injured lungs had decreases in absolute values of lung volume (P < 0.03), alveolar surface (P < 0.004), and air space volume (P < 0.03). Doxycycline, a nonspecific metalloproteinase inhibitor, partly inhibited LPS-induced 92-kDa gelatinase overactivity but did not improve LPS-induced alveolar growth disorders. LPS-mediated lung injury in neonatal rats induced both gelatinase B overactivity and alveolar growth disorders, although no causal link between these two effects was demonstrated.

Animals↗

Genetic disorders of human growth.

Growth in humans is a complex process, controlled at numerous levels and by a myriad of factors. These factors may act centrally or peripherally and may be hormones, receptors, or transcription factors. Many of these probably are still unknown. The factors that are discussed here include those that act on the developing pituitary gland (transcription factors including LHX3, HESX1, PROP1, and PIT-1); those that regulate the normal activity of the pituitary (hypothalamic hormones such as GHRH, Ghrelin [growth hormone secretagoguel and somatostatin); those factors coming from the pituitary (essentially growth hormone [GH]); and the downstream modulators, transducers, and effectors of GH (including the GH receptor/GH binding protein, insulin-like growth factor-I and -II, their receptors, and their binding factors). What is becoming increasingly clear is the role of genetics in determining stature. This review discusses the most clinically relevant factors, with an emphasis on ontogeny, genetic inheritance, and clinical presentation.

Growth Disorders↗

Pediatric feeding disorder and growth decline following mandibular distraction osteogenesis.

BACKGROUND: Mandibular distraction osteogenesis has proven to be an effective treatment for upper airway obstruction related to micrognathia. Changes in the aerodigestive space can help facilitate tracheostomy removal in children and prevent tracheostomy in newborns. However, this may also precipitate changes in the ability to orally feed. There are few data on early postoperative feeding and growth rate following mandibular lengthening. The authors found evidence of growth rate decline and feeding difficulty in pediatric patients following mandibular distraction osteogenesis. METHODS: Ten pediatric patients underwent mandibular distraction osteogenesis for treatment of upper airway obstruction. Outcomes in resolution of upper airway obstruction, oral feeding success, and growth rate were analyzed. Follow-up ranged from 12 to 28 months. RESULTS: All 10 patients had complete resolution of upper airway obstruction. The length of distraction ranged from 10 to 17 mm. Three patients demonstrated a feeding disorder after mandibular distraction osteogenesis, defined as requiring a long-term (>1 month) alternate feeding method (gastric tube in two patients and gastric gavage in one). Seven of 10 patients exhibited an early decline in growth rate following distraction. Data used to determine growth rate changes were weight measurements at the time of distraction, at the time of distractor removal (6 to 8 weeks after distraction), and at 6 and 12 months after the date of distraction initiation. CONCLUSION: These results suggest that infants and children undergoing mandibular lengthening by distraction osteogenesis should be carefully monitored for postdistraction feeding disorder and growth rate disturbance.

Airway Obstruction↗

IMAGe syndrome: a complex disorder affecting growth, adrenal and gonadal function, and skeletal development.

IMAGe syndrome (intrauterine growth restriction, metaphyseal dysplasia, adrenal hypoplasia congenita, genital abnormalities; MIM 300290) is a multisystem disorder with a broad phenotype, which, if unrecognized, may result in major and possibly life-threatening complications. Initial clinical features overlap with those of Russell-Silver syndrome (RSS) and isolated growth hormone (GH) deficiency, conditions from which it must be distinguished. We report an Australian male with adrenal hypoplasia congenita (AHC) in association with IMAGe syndrome. The patient had intrauterine growth restriction (IUGR) and dysmorphic features comprising small, low-set ears, micrognathia, bilateral cryptorchidism, micropenis, and skeletal abnormalities. Signs of adrenal insufficiency occurred at aged 4.6 years. Our patient differs from those previously described by the late onset of adrenal insufficiency and the presence of GH deficiency. IMAGe is a complex syndrome involving dysmorphic features; disorders of growth, gonadal, and adrenal function; and skeletal abnormalities.

Adrenal Insufficiency↗

Noradrenergic receptor sensitivity in obsessive-compulsive disorders: I. Growth hormone response to clonidine stimulation.

In 15 patients with obsessive-compulsive disorder (OCD) and in 15 healthy controls postsynaptic alpha-2-adrenoceptor sensitivity was examined by measuring the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) and to clonidine stimulation. Basal values of GH and somatomedin-C (SMD-C) and mean GH responses to GHRH were the same in patients and controls, thus suggesting that a peripheral pathology of the somatotropic axis should not be present. GH responses to clonidine stimulation were blunted in patients suggesting that post-synaptic alpha-2-adrenoceptors are subsensitive, possibly due to higher than normal noradrenergic secretion.

Adolescent↗

German pediatric reference data for quantitative transverse transmission ultrasound of finger phalanges.

Quantitative ultrasound (QUS) of the finger phalanges is a useful tool in the assessment of disease- or age-related deterioration of bone. For studying the impact of juvenile diseases or growth disorders affecting the skeleton, a reference database for QUS parameters is needed. The aim of this study was to establish a calibrated reference database of parameters of transverse ultrasound transmission through juvenile finger phalanges. A total of 1328 children (650 females, 678 males; ages 3-17 years) were measured in Heidelberg and Kiel in order to establish a German reference database. Highly significant gender-specific correlations (p<0.0001) were found between the QUS parameters amplitude-dependent speed of sound (AD-SoS) and bone transmission time (BTT) versus age, body height and body mass index (BMI). For AD-SoS the correlation coefficients were R2 = 0.64 against age in males and R2 = 0.73 in females, R2 = 0.60 against body height in males and R2 = 0.68 in females, and R2 = 0.19 against BMI in males and R2 = 0.23 in females. For BTT the correlation coefficients were R2 = 0.74 against age in males and R2 = 0.79 in females, R2 = 0.75 against body height in males and R2 = 0.77 in females, and R2 = 0.32 against BMI in males and R2 = 0.35 in females. Age and height were the strongest determinants of QUS results. Gender-specific differences were observed in AD-SoS (significant for ages 11-14 years and for 150-170 cm body height) and in BTT (significant for ages 7 and 11-17 years and for 160-170 cm body height). Tables of QUS parameters versus age and height can serve as a basis for the evaluation of the impact of skeletal diseases or growth disorders on phalangeal QUS. Depending on the type of disease or growth disorder, measurement results can be compared with age- or height- specific reference data. In this way a simple and radiation-free assessment of juvenile skeletal disorders using quantitative ultrasound might be possible in the future.

Adolescent↗

Gonadotropin-releasing hormone analog therapy for central precocious puberty and other childhood disorders affecting growth and puberty.

Gonadotropin-releasing hormone (GnRH) analog therapy relies primarily on the ability of these compounds to bind to and modulate GnRH-receptor activity. GnRH analogs have been used in pediatric patients where endogenous gonadotropin release is undesirable or potentially harmful, such as in: (i) patients with central precocious puberty (CPP); (ii) healthy short children where pubertal delay would provide an opportunity to supplement pre-pubertal linear growth; and (iii) children with malignancies and other disorders where treatment requires the use of gonadotoxic compounds. In the first two groups of patients, GnRH agonists may be used alone or in conjunction with somatropin (growth hormone [GH]) to prevent early skeletal maturation and increase the subsequent adult height, while in the latter case, GnRH agonists are used alone or in conjunction with GnRH antagonists in an attempt to preserve gonadal function.In children and adolescents with CPP, timely use of GnRH agonists alone can result in an adult height within the genetic potential of the individual (target height); however, minimal height is gained when GnRH agonist therapy is commenced after a marked advancement of skeletal age. This provides the rationale for combined therapy with GnRH agonists and somatropin in such patients, and studies have shown improved growth with this approach compared with GnRH agonists alone. Combination therapy with GnRH agonists and somatropin has also been shown to increase adult heights to a greater extent than GnRH agonists alone in pediatric patients with concomitant CPP and GH deficiency, those with idiopathic short stature, and those born small for gestational age; however, such combination therapy has shown no increased benefit over somatropin alone in pediatric patients with GH deficiency. Limited results in children and adolescents with congenital adrenal hyperplasia and chronic primary hypothyroidism have also shown increased growth rates, while no growth benefit was seen in pediatric renal transplant recipients.GnRH analogs also have potential as gonadoprotective agents; studies of GnRH agonists used alone and in combination with GnRH antagonists in women undergoing cytotoxic therapy have shown increased preservation of reproductive potential in patients who were receiving GnRH analog therapy versus those who were not.The adverse effects of GnRH analogs mainly consist of menopausal-like complaints. Increases in bodyweight and body mass index in children receiving GnRH agonist therapy have been shown; however, these increases do not persist after discontinuation of therapy. Adult bone mineral density and fertility are also not adversely affected by childhood GnRH agonist therapy.GnRH analog therapy appears to be both well tolerated and effective in pediatric patients, as it allows the preservation or improvement of adult height, and shows no longstanding negative effects on body composition, bone density, reproductive function, or endocrine physiology. These agents may also be useful for preservation of gonadal function in children and adolescents undergoing cytotoxic therapy.

Body Height↗

Growth and disorder of macromolecular crystals: insights from atomic force microscopy and X-ray diffraction studies.

The growth processes and defect structures of protein and virus crystals have been studied in situ by atomic force microscopy (AFM), X-ray diffraction topography, and high-resolution reciprocal space scanning. Molecular mechanisms of macromolecular crystallization were visualized and fundamental kinetic and thermodynamic parameters, which govern the crystallization process of a number of macromolecular crystals, have been determined. High-resolution AFM imaging of crystal surfaces provides information on the packing of macromolecules within the unit cell and on the structure of large macromolecular assemblies. X-ray diffraction techniques provide a bulk probe with poorer spatial resolution but excellent sensitivity to mosaicity and strain. Defect structures and disorder created in macromolecular crystals during growth, seeding, and post-growth treatments including flash cooling were characterized and their impacts on the diffraction properties of macromolecular crystals have been analyzed. The diverse and dramatic effects of impurities on growth and defect formation have also been studied. Practical implications of these fundamental insights into the improvement of macromolecular crystallization protocols are discussed.

Chemistry Techniques, Analytical↗

The pathophysiology of the growth plate in juvenile idiopathic arthritis.

Children with chronic inflammatory diseases, such as juvenile idiopathic arthritis (JIA), suffer from a variety of growth disorders. These range from general growth retardation to local acceleration of growth in the affected limb. These disorders are associated with the increased production of proinflammatory cytokines, which may influence growth through a local effect in the growth plates of long bones and/or systemic effects throughout the whole body. In this article we review these aspects and also discuss the evidence for interaction between the inflammatory cytokine and growth-signalling pathways.

Arthritis, Juvenile↗