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GH Treatment (gh + treatment)
Selected AbstractsGrowth hormone in short children: beyond medicine?ACTA PAEDIATRICA, Issue 1 2001LLE Bolt The indications for growth hormone (GH) treatment in non-GH-deficient short children are in debate, with some arguing that this treatment does not belong solely in the medical domain. We describe three different approaches to the issue, and argue that neither a disease-oriented nor client-oriented approach is sufficient. Both lead to withdrawal of medical interventions or to an undesirable application. Conclusion: An approach focusing on suffering as an indication for treatment of short stature is the most appropriate. The challenge is to develop proper tools by which to evaluate suffering and the efficacy of GH treatment in these children in order to relieve or prevent suffering. [source] Therapeutic aspects of growth hormone and insulin-like growth factor-I treatment on visceral fat and insulin sensitivity in adultsDIABETES OBESITY & METABOLISM, Issue 1 2007K. C. J. Yuen Growth hormone (GH) is generally considered to exert anti-insulin actions, whereas insulin-like growth factor I (IGF-I) has insulin-like properties. Paradoxically, GH deficient adults and those with acromegaly are both predisposed to insulin resistance, but one cannot extrapolate from these pathological conditions to determine the normal metabolic roles of GH and IGF-I on glucose homeostasis. High doses of GH treatment have major effects on lipolysis, which plays a crucial role in promoting its anti-insulin effects, whereas IGF-I acts as an insulin sensitizer that does not exert any direct effect on lipolysis or lipogenesis. Under physiological conditions, the insulin-sensitizing effect of IGF-I is only evident after feeding when the bioavailability of circulating IGF-I is increased. In contrast, many studies in GH deficient adults have consistently shown that GH replacement improves the body composition profile although these studies differ considerably in terms of age, the presence or absence of multiple pituitary hormone deficiency, and whether GH deficiency was childhood or adult-onset. However, the improvement in body composition does not necessarily translate into improvements in insulin sensitivity presumably due to the anti-insulin effects of high doses of GH therapy. More recently, we have found that a very low dose GH therapy (0.1 mg/day) improved insulin sensitivity without affecting body composition in GH-deficient adults and in subjects with metabolic syndrome, and we postulate that these effects are mediated by its ability to increase free ,bioavailable' IGF-I without the induction of lipolysis. These results raise the possibility that this low GH dose may play a role in preventing the decline of ,-cell function and the development of type 2 diabetes in these "high risk" subjects. [source] Growth-enhanced fish can be competitive in the wildFUNCTIONAL ECOLOGY, Issue 5 2001J. I. Johnsson Summary 1,The widespread commercial interest in producing growth-enhanced organisms has raised concerns about ecological consequences, emphasizing the need to understand the costs and benefits associated with accelerated growth in nature. Here, sustained-release growth hormone (GH) implants were used to estimate the competitive ability of growth-enhanced fish in the wild. Growth rate, movements and survival over winter were compared between GH-implanted and control Brown Trout in a natural stream. The study was repeated over two consecutive years. 2,GH treatment had no effect on recapture rates, indicating that mortality rates did not differ between GH-treated and control fish. More GH-treated trout (63%) than control fish (41%) were recaptured within their 10 m section of release. Thus, GH-treated fish were more stationary than control fish over winter. 3,GH-treated fish grew about 20% faster than control fish. This was mainly because of a three-fold growth rate increase in GH-treated fish in late summer, whereas growth rates over winter did not differ significantly between treatment groups. These results were consistent over both replicate years. 4,This first study of growth-enhanced fish in the wild shows that they can survive well and therefore may out-compete normal fish with lower growth rates. Although selection against rapid growth may be more intense at other life-history stages and/or during periods of extreme climate conditions, our findings raise concerns that released or escaped growth-enhanced salmonids may compete successfully with resident fish. It is clear that the potential ecological risks associated with growth-enhanced fish should not be ignored. [source] Adult-onset deficiency in growth hormone and insulin-like growth factor-I alters oligodendrocyte turnover in the corpus callosumGLIA, Issue 10 2009Kun Hua Abstract Growth hormone (GH) and insulin-like growth factor-I (IGF-I) provide trophic support during development and also appear to influence cell structure, function and replacement in the adult brain. Recent studies demonstrated effects of the GH/IGF-I axis on adult neurogenesis, but it is unclear whether the GH/IGF-I axis influences glial turnover in the normal adult brain. In the current study, we used a selective model of adult-onset GH and IGF-I deficiency to evaluate the role of GH and IGF-I in regulating glial proliferation and survival in the adult corpus callosum. GH/IGF-I-deficient dwarf rats of the Lewis strain were made GH/IGF-I replete via twice daily injections of GH starting at postnatal day 28 (P28), approximately the age at which GH pulse amplitude increases in developing rodents. GH/IGF-I deficiency was initiated in adulthood by removing animals from GH treatment. Quantitative analyses revealed that adult-onset GH/IGF-I deficiency decreased cell proliferation in the white matter and decreased the survival of newborn oligodendrocytes. These findings are consistent with the hypothesis that aging-related changes in the GH/IGF-I axis produce deficits in ongoing turnover of oligodendrocytes, which may contribute to aging-related cognitive changes and deficits in remyelination after injury. © 2008 Wiley-Liss, Inc. [source] Growth hormone stimulates proliferation of old-aged regenerating liver through forkhead box m1bHEPATOLOGY, Issue 6 2003Katherine Krupczak-Hollis The Forkhead Box (Fox) proteins are an extensive family of transcription factors that shares homology in the winged helix DNA-binding domain and the members of which play essential roles in cellular proliferation, differentiation, and longevity. Reduced cellular proliferation during aging is associated with a progressive decline in both growth hormone (GH) secretion and Foxm1b expression. Liver regeneration studies with 12-month-old (old-aged) transgenic mice indicated that increased hepatocyte expression of Foxm1b alone is sufficient to restore hepatocyte proliferation to levels found in 2-month-old (young) regenerating liver. GH therapy in older people has been shown to cause an increase in cellular proliferation, but the transcription factors that mediated this stimulation in proliferation remain uncharacterized. In this study, we showed that human GH administration to old-aged Balb/c mice dramatically increased both expression of Foxm1b and regenerating hepatocyte proliferation. This increase in old-aged regenerating hepatocyte proliferation was associated with elevated protein expression of Cdc25A, Cdc25B, and cyclin B1, with reduced protein levels of cyclin-dependent kinase inhibitor p27Kip1 (p27). GH treatment also was found to stimulate hepatocyte proliferation and expression of Foxm1b protein without partial hepatectomy (PHx). Furthermore, GH treatment of young Foxm1b ,/, mice failed to restore regenerating hepatocyte DNA replication and mitosis caused by Foxm1b deficiency. These genetic studies provided strong evidence that the presence of Foxm1b is essential for GH to stimulate regenerating hepatocyte proliferation. In conclusion, our old-aged liver regeneration studies show that increased Foxm1b levels are essential for GH to stimulate hepatocyte proliferation, thus providing a mechanism for GH action in the elderly. [source] Growth Hormone Increases Bone Mineral Content in Postmenopausal Osteoporosis: A Randomized Placebo-Controlled TrialJOURNAL OF BONE AND MINERAL RESEARCH, Issue 3 2003Kerstin Landin-Wilhelmsen Abstract Eighty osteoporotic, postmenopausal women, 50,70 years of age, with ongoing estrogen therapy (HRT), were randomized to recombinant human growth hormone (GH), 1.0 U or 2.5 U/day, subcutaneous, versus placebo. This study was double-blinded and lasted for 18 months. The placebo group then stopped the injections, but both GH groups continued for a total of 3 years with GH and followed for 5 years. Calcium (750 mg) and vitamin D (400 U) were given to all patients. Bone mineral density and bone mineral content were measured with DXA. At 18 months, when the double-blind phase was terminated, total body bone mineral content was highest in the GH 2.5 U group (p = 0.04 vs. placebo). At 3 years, when GH was discontinued, total body and femoral neck bone mineral content had increased in both GH-treated groups (NS between groups). At 4-year follow-up, total body and lumbar spine bone mineral content increased 5% and 14%, respectively, for GH 2.5 U (p = 0.01 and p = 0.0006 vs. placebo). Femoral neck bone mineral density increased 5% and bone mineral content 13% for GH 2.5 U (p = 0.01 vs. GH 1.0 U). At 5-year follow-up, no differences in bone mineral density or bone mineral content were seen between groups. Bone markers showed increased turnover. Three fractures occurred in the GH 1.0 U group. No subjects dropped out. Side effects were rare. In conclusion, bone mineral content increased to 14% with GH treatment on top of HRT and calcium/vitamin D in postmenopausal women with osteoporosis. There seems to be a delayed, extended, and dose-dependent effect of GH on bone. Thus, GH could be used as an anabolic agent in osteoporosis. [source] Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in ratsJOURNAL OF DIGESTIVE DISEASES, Issue 1 2001Wang Xingpeng OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or a placebo. Laparotomized animals without ANP induction (sham operation) served as controls. Twenty-four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of [125I]-labeled albumin from blood to the intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcription,polymerase chain reaction (RT-PCR). Morphological changes in the pancreas and ileum were also analyzed. RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in the pancreas and ileum was reduced by GH treatment. Ileal mucosal thickness, villus height and crypt depth in GH-treated rats were obviously increased as compared with those of ANP rats. The intestinal permeability was markedly decreased in the GH group as compared with the ANP group. GH treatment resulted in upregulation of IGF-1 mRNA expression in ileum, but not in liver. CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the upregulation of IGF-1 mRNA in the intestine by GH. [source] Pituitary mRNA Expression of the Growth Hormone Axis in the 1-Year-Old Intrauterine Growth Restricted RatJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2006T. Prins Intrauterine growth restriction (IUGR) is one of the major causes of short stature in childhood. Abnormalities in the growth hormone (GH) axis have frequently been observed in children who are born intrauterine growth restricted and GH treatment is effective to improve final height. However, the way that the GH axis is involved is not fully understood. Previously, when investigating the effect of IUGR on the central somatotrophic axis, a hypothalamic effect was discovered with elevated somatostatin and decreased neuropeptide Y mRNA expression levels, whereas serum GH and insulin-like growth factor I (IGFI) were unaltered. These findings were thought to indicate a hypothalamic alteration of the GH axis due to IUGR, probably to compensate pituitary output, thereby normalising peripheral values of GH and IGFI. Therefore, the present study aimed to evaluate the effect of IUGR on the pituitary GH axis in this rat model. Pups from rats that underwent bilateral uterine artery ligation at day 17 of pregnancy were studied. Pituitary glands were collected from 1-year-old offspring for quantitative measurements of GH, GH-receptor (GH-R), GH-releasing hormone receptor (GHRH-R), somatostatin receptor subtype 2 and 5, IGFI and IGFI receptor mRNA levels using a real-time reverse transcriptase-polymerase chain reaction. In addition, liver GH-R and IGFI mRNA expression levels were measured and a radioimmunoassay was performed to determine serum IGFI levels. In the IUGR rat, levels of pituitary GH, GH-R and GHRH-R relative gene expression (RGE) were increased. No differences were found in the RGE level of all other pituitary growth factors, liver GH-R and IGFI, and serum IGFI concentration between IUGR and control rats. The present data show that intrauterine growth failure leads to changes in the pituitary that might counterbalance the effects found previously in the hypothalamus. [source] Growth hormone regulates osteogenic marker mRNA expression in human periodontal fibroblasts and alveolar bone-derived cellsJOURNAL OF PERIODONTAL RESEARCH, Issue 4 2003H. R. Haase Background:, Growth hormone (GH) is a potent regulator of bone formation. The proposed mechanism of GH action is through the stimulation of osteogenic precursor cell proliferation and, following clonal expansion of these cells, promotion of differentiation along the osteogenic lineage. Objectives:, We tested this hypothesis by studying the effects of GH on primary cell populations of human periodontal ligament cells (PLC) and alveolar bone cells (ABC), which contain a spectrum of osteogenic precursors. Methods:, The cell populations were assessed for mineralization potential after long-term culture in media containing ,-glycerophosphate and ascorbic acid, by the demonstration of mineral deposition by Von Kossa staining. The proliferative response of the cells to GH was determined over a 48-h period using a crystal violet dye-binding assay. The profile of the cells in terms of osteogenic marker expression was established using quantitative reverse transcriptase polymerase chain reaction (RT-PCR) for alkaline phosphatase (ALP), osteopontin, osteocalcin, bone sialoprotein (BSP), as well as the bone morphogenetic proteins BMP-2, BMP-4 and BMP-7. Results:, As expected, a variety of responses were observed ranging from no mineralization in the PLC populations to dense mineralized deposition observed in one GH-treated ABC population. Over a 48-h period GH was found to be non-mitogenic for all cell populations. Quantitative reverse transcriptase polymerase chain reaction (RT-PCR) BSP mRNA expression correlated well with mineralizing potential of the cells. The change in the mRNA expression of the osteogenic markers was determined following GH treatment of the cells over a 48-h period. GH caused an increase in ALP in most cell populations, and also in BMP expression in some cell populations. However a decrease in BSP, osteocalcin and osteopontin expression in the more highly differentiated cell populations was observed in response to GH. Conclusion:, The response of the cells indicates that while long-term treatment with GH may promote mineralization, short-term treatment does not promote proliferation of osteoblast precursors nor induce expression of late osteogenic markers. [source] Pharmacodynamic interaction of captopril with garlic in isoproterenol-induced myocardial damage in ratPHYTOTHERAPY RESEARCH, Issue 5 2010Syed Mohammed Basheeruddin Asdaq Abstract It is known that various preparations of garlic and angiotensin-converting enzyme (ACE) inhibitor such as captopril (CAP) have beneficial effects on the left ventricular function and cardiovascular events after myocardial infarction (MI) when used individually. There is no reported interaction between garlic homogenate (GH) and CAP during and after acute MI. Thus the purpose of the current study was to evaluate the possible pharmacodynamic interaction of GH with CAP on isoproterenol (ISO)-induced myocardial damage in rat. Female Wistar albino rats were treated with GH at three different doses of 125; 250 and 500,mg/kg orally for 30 days and CAP (30,mg/kg, p.o.) was incorporated in the interactive groups during the last seven days of GH treatment. Myocardial damage was induced by administration of ISO (150,mg/kg, s.c.) for two consecutive days. Biochemical parameters were studied in serum and heart tissue homogenate of all animals. The GH 250,mg/kg was found to dislodge the effect of ISO on superoxide dismutase and catalase and retained the activities of LDH and CK-MB. Incorporation of CAP during GH treatment provided further protection to myocardium from injury. However, higher dose of GH alone or with CAP failed to prevent damaging effect of ISO. Histopathological determinations confirmed biochemical findings. Thus it is concluded that the combination needs to be used carefully when garlic is consumed at high doses. Copyright © 2009 John Wiley & Sons, Ltd. [source] Effects of Growth Hormone on Female Reproductive OrgansANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 5 2001G. G. Kaiser During the last decade many experiments have been performed to study the effects of growth hormone (GH, somatotropin) on reproductive functions. Most of the studies found only slight or no effects of GH treatment, both on the oestrous cycle and on gonadotropin, progesterone, or oestrogen serum levels. In GH-treated animals, elevated levels of insulin-like growth factor I and GH in the serum could be correlated with an increased number of small (<5 mm in diameter) ovarian follicles, possibly as a consequence of a reduction of apoptosis and follicular atresia. There is still controversy over the effects of GH on in vivo and in vitro embryo production and on the gestation period. Recent studies produced some evidence that GH-receptor is expressed in ovarian tissue, implying a direct role for GH in the ovary. [source] Late effects of early growth hormone treatment in Down syndromeACTA PAEDIATRICA, Issue 5 2010Å Myrelid Abstract Objective:, Down syndrome (DS) is associated with short stature and psychomotor delay. We have previously shown that growth hormone (GH) treatment during infancy and childhood normalizes growth velocity and improves fine motor skill performance in DS. The aim of this study was to investigate late effects of early GH treatment on growth and psychomotor development in the DS subjects from the previous trial. Design:, Twelve of 15 adolescents with DS (3 F) from the GH group and 10 of 15 controls (5 F) participated in this follow-up study. Fifteen other subjects with DS (6 F) were included as controls in anthropometric analyses. Cognitive function was assessed with the Leiter International Performance Scale-Revised (Leiter-R) and selected subtests of the Wechsler Intelligence Scale for Children, Third edition (WISC-III). The Bruininks-Oseretsky Test of Motor Proficiency, Second edition (BOT-2), was used to assess general motor ability. Results:, Although early GH treatment had no effect on final height, the treated subjects had a greater head circumference standard deviation score (SDS) than the controls (,1.6 SDS vs. ,2.2 SDS). The adolescents previously treated with GH had scores above those of the controls in all subtests of Leiter-R and WISC-III, but no difference in Brief IQ-score was seen between the groups. The age-adjusted motor performance of all subjects was below ,2 SD, but the GH-treated subjects performed better than the controls in all but one subtest. Conclusion:, The combined finding of a greater head circumference SDS and better psychomotor performance indicates that DS subjects may benefit from early GH treatment. [source] ORIGINAL ARTICLE: Metabolic outcome of GH treatment in prepubertal short children with and without classical GH deficiencyCLINICAL ENDOCRINOLOGY, Issue 3 2010Ralph Decker Summary Context, Few studies have evaluated the metabolic outcomes of growth hormone (GH) treatment in idiopathic short stature (ISS). Moreover, children with ISS appear to need higher GH doses than children with GH deficiency (GHD) to achieve the same amount of growth and may therefore be at increased risk of adverse events during treatment. The individualized approach using prediction models for estimation of GH responsiveness, on the other hand, has the advantage of narrowing the range of growth response, avoiding too low or high GH doses. Design, Short prepubertal children with either isolated GHD (39) or ISS (89) participated in a 2-year randomized trial of either individualized GH treatment with six different GH doses (range, 17,100 ,g/kg/day) or a standard dose (43 ,g/kg/day). Objective, To evaluate if individualized GH treatment reduced the variance of the metabolic measures as shown for growth response and to compare changes in metabolic variables in children with ISS and GHD. Hypothesis, Individualized GH dose reduces the range of metabolic outcomes, and metabolic outcomes are similar in children with ISS and GHD. Results, We observed a narrower variation for fasting insulin (,34·2%) and for homoeostasis model assessment (HOMA) (,38·9%) after 2 years of individualized GH treatment in comparison with standard GH dose treatment. Similar metabolic changes were seen in ISS and GHD. Delta (,) height SDS correlated with ,insulin-like growth factor I (IGF-I), ,leptin and ,body composition. Principal component analysis identified an anabolic and a lipolytic component. Anabolic variables [,lean body mass (LBM) SDS and ,IGF-I SDS] clustered together and correlated strongly with ,height SDS and GH dose, whereas lipolytic variables [,fat mass (FM) SDS and ,leptin] were clustered separately from anabolic variables. Regression analysis showed GH dose dependency in ISS, and to a lesser degree in GHD, for ,LBM SDS and ,height SDS, but not for changes in FM. Conclusions, Individualized GH dosing during catch-up growth reduces the variance in insulin and HOMA and results in equal metabolic responses irrespective of the diagnosis of GHD or ISS. [source] ORIGINAL ARTICLE: Should short children born small for gestational age with a distance to target height <1 standard deviation score be excluded from growth hormone treatment?CLINICAL ENDOCRINOLOGY, Issue 3 2010Annemieke J. Lem Summary Context, The criteria for starting growth hormone (GH), an approved treatment for short children born small for gestational age (SGA), differ between Europe and the USA. One European requirement for starting GH, a distance to target height (DTH) of ,1 standard deviation score (SDS), is controversial. Objective, To investigate the influence of DTH on growth during GH treatment in short SGA children and to ascertain whether it is correct to exclude children with a DTH <1 SDS from GH. Patients, A large group of short prepubertal SGA children (baseline n = 446; 4 years GH n = 215). Measurements, We analysed the prepubertal growth response during 4 years of GH. We investigated the influence of the continuous variable DTH SDS on growth response and a possible DTH SDS cut-off level below which point the growth response is insufficient. Results, Height gain SDS during 4 years of GH showed a wide variation at every DTH SDS level. Multiple regression analyses demonstrated that, after correction for other significant variables, an additional DTH of 1 SDS resulted in 0·13 SDS more height gain during 4 years of GH. We found no significant differences in height gain below and above certain DTH SDS cut-off levels. Conclusions, DTH SDS had a weak positive effect on height gain during 4 years of GH, while several other determinants had much larger effects. We found no support for using any DTH cut-off level. Based on our data, excluding children with a DTH <1 SDS from GH treatment is not justified. [source] Influence of parental origin of the X chromosome on physical phenotypes and GH responsiveness of patients with Turner syndromeCLINICAL ENDOCRINOLOGY, Issue 1 2010Jung Min Ko Summary Objective, Previous studies have reported the effects of parental origin of the X chromosome on specific phenotypic and cognitive profiles in Turner syndrome (TS). Here, we investigate the possible parent-of-origin effects on physical phenotypes and responsiveness to GH in Korean patients with TS. Design and patients, Thirty-three patients with TS with nonmosaic karyotype and their parents participated in this study. The parental origin of the normal X chromosome was determined by comparing parental DNA polymorphisms using nine highly polymorphic microsatellite markers on the X chromosome. For the evaluation of parent-of-origin effects, typical phenotypic traits, including congenital malformations, auxological and endocrinological profiles, were compared. Results, The retained X chromosome was of maternal (Xm) origin in 60·6% patients and paternal (Xp) origin in 39·4% patients. No significant parent-of-origin effects on stature, body mass index, cardiac, renal, skeletal, lymphatic, hearing or ocular systems were evident. We observed no differences in height gain after GH treatment. In patients with the 45,X karyotype, patient height was positively correlated with maternal height in the Xm group (r = 0·60, P = 0·04). Moreover, patient height was more significantly correlated with maternal than paternal height, irrespective of the parental origin of the retained X chromosome. Conclusion, While we observed no significant impact of parental origin of the X chromosome on several phenotypic traits in patients with TS, a maternal imprinting effect on stature was suggested at least in patients with 45,X. Further studies on a larger number of patients with TS are essential to define the potential imprinting effects of undetermined genes on the X chromosome. [source] Interactions between TCF7L2 genotype and growth hormone-induced changes in glucose homeostasis in small for gestational age childrenCLINICAL ENDOCRINOLOGY, Issue 1 2010Sandra W. K. De Kort Summary Context, The Transcription factor 7-like 2 (TCF7L2) rs7903146 gene polymorphism has been associated with risk of developing type 2 diabetes mellitus (DM), possibly by decreasing insulin secretion. Small for gestational age (SGA) birth has been associated with type 2 DM in later life. Growth hormone (GH) treatment reduces insulin sensitivity and increases insulin secretion. Therefore, GH-treated SGA children are an ideal group to investigate whether the TCF7L2 rs7903146 genotype is associated with changes in glucose homeostasis. Objective, To determine the impact of the TCF7L2 rs7903146 polymorphism on changes in insulin secretion and insulin sensitivity during 4 years of GH treatment in children born SGA. Subjects, A total of 246 Caucasian short children born SGA, with a median age of 7·8 years. Outcome measures, Insulin sensitivity and insulin secretion were measured by the frequently sampled intravenous glucose tolerance test (FSIGT) (n = 68) and homeostasis model assessment (HOMA) calculations (all). Results, There was no association between rs7903146 genotype and insulin sensitivity or insulin secretion at baseline but after adjustment for possible confounders, insulin secretion was higher in the CT/TT group than in the CC group. During GH treatment, carriers of the rs7903146 T allele had an increase in insulin secretion similar to that of carriers of the CC genotype. The decrease in insulin sensitivity was only significant in the CT/TT group, but the difference in decrease between genotype groups did not reach significance (P = 0·06). The disposition index (insulin secretion × insulin sensitivity), which is an estimate of beta cell function, was not associated with genotype and did not change during GH treatment. Conclusion, The TCF7L2 rs7903146 polymorphism is not associated with the change in insulin secretion during GH treatment in short SGA children. [source] The effect of growth hormone treatment on metabolic and cardiovascular risk factors is similar in preterm and term short, small for gestational age childrenCLINICAL ENDOCRINOLOGY, Issue 1 2009Sandra W. K. De Kort Summary Context, We previously reported that short, small for gestational age (SGA) children who were born preterm have a lower body fat percentage and a higher blood pressure, insulin secretion and disposition index than short SGA children born at term. Whether preterm birth also influences these parameters during GH treatment is unknown. Objective, To compare blood pressure, insulin sensitivity, beta-cell function and body composition during 4 years of GH treatment, between preterm and term short SGA children. Patients, A total of 404 prepubertal non-GH-deficient short SGA children were divided into 143 preterm (< 36 weeks) and 261 term children. Outcome measures, Height, blood pressure (n = 404), body composition measured by dual energy X-ray absorptiometry (DXA) (n = 138) and insulin sensitivity and beta-cell function calculated from a frequent sampling intravenous glucose tolerance test (FSIGT) with tolbutamide (n = 74) or from the homeostasis model assessment of insulin resistance (HOMA-IR) (n = 204). Results, In preterm and term children, GH treatment resulted in a similar decrease in systolic and diastolic blood pressure, body fat percentage, limb fat/total fat ratio and insulin sensitivity, and a similar increase in insulin secretion and disposition index. Lean body mass (LBM) corrected for gender and height increased in term children and did not change in preterm children. Multiple regression analysis revealed that this difference in GH effect on LBM was not associated with gestational age. Conclusion, The effect of GH treatment on metabolic and cardiovascular risk factors is similar in preterm and term short, SGA children. [source] Growth hormone (GH) replacement in hypopituitary adults with GH deficiency evaluated by a utility-weighted quality of life index: a precursor to cost,utility analysisCLINICAL ENDOCRINOLOGY, Issue 1 2008Maria Ko, towska-Häggström Summary Objectives To examine quality of life (QoL) measured by a utility-weighted index in GH-deficient adults on GH replacement and analyse the impact of demographic and clinical characteristics on changes in utilities during treatment. Design Utilities for items in the QoL-Assessment of Growth Hormone Deficiency in Adults (QoL-AGHDAutility) were estimated based on data obtained from the general population in England and Wales (E&W). These estimates were used to calculate QoL changes in GH-treated patients and compare these with normative population values. Patients A total of 894 KIMS patients (53% women) from E&W were followed for 1 to 6 years. Measurements QoL-AGHDAutility at baseline and at the last reported visit, total QoL-AGHDAutility gain and QoL-AGHDAutility gain per year of follow-up. Results QoL-AGHDAutility in patients before GH treatment differed from the expected population values [0·67 (SD 0·174) vs. 0·85 (SD 0·038), P < 0·0001], constituting a mean deficit of ,0·19 (SD 0·168). There was a difference in the mean QoL-AGHDAutility deficit for men [,0·16 (SD 0·170)] and women [,0·21 (SD 0·162)] (P < 0·001). The main improvement occurred during the first year of treatment [reduction of a deficit to ,0·07 (SD 0·163) (P < 0·001) in the total cohort]; however, patients' utilities remained lower than those recorded for the general population during subsequent follow-up (P < 0·001). Despite an observed impact of age, primary aetiology, disease onset and comorbidities on QoL-AGHDAutility, all patients showed a similar beneficial response to treatment. Conclusions QoL-AGHDAutility efficiently monitors treatment effects in patients with GHD. The study confirmed the QoL-AGHDAutility deficit before treatment and a similar QoL-AGHDAutility gain observed after commencement of GH replacement in all patients. [source] Long-term effects of growth hormone (GH) treatment on body composition and bone mineral density in short children born small-for-gestational-age: six-year follow-up of a randomized controlled GH trialCLINICAL ENDOCRINOLOGY, Issue 4 2007Ruben H. Willemsen Summary Context, Alterations in the GH-IGF-I axis in short small-for-gestational-age (SGA) children might be associated with abnormalities in bone mineral density (BMD) and body composition. In addition, birth weight has been inversely associated with diabetes and cardiovascular disease in adult life. Data on detailed body composition in short SGA children and long-term effects of GH treatment are very scarce. Objective, To investigate effects of long-term GH treatment on body composition and BMD by dual energy X-ray absorptiometry (DXA) in short SGA children. Design, Longitudinal 6-year GH study with a randomized controlled part for 3 years. Results, At baseline, fat percentage standard deviation score (SDS) and lumbar spine BMD SDS corrected for height (BMADLS SDS) were significantly lower than zero. Lean body mass (LBM) SDS adjusted for age was also reduced, but LBM adjusted for height (LBM SDSheight) was not decreased. GH treatment induced a decrease in fat percentage SDS and an increase in BMADLS SDS. LBM SDSheight remained similar in GH-treated children, but deteriorated in untreated controls. When these untreated controls subsequently started GH treatment, their LBM SDSheight rapidly normalized to values comparable with zero. Conclusion, During long-term GH treatment in short SGA children, fat percentage SDS decreased and BMADLS SDS increased. These effects of GH treatment were most prominent in children who started treatment at a younger age and in those with greater height gain during GH treatment. LBM SDSheight remained around 0 SDS in GH-treated children, but declined to low normal values in untreated controls. [source] Thyroid hormone levels in children with Prader,Willi syndrome before and during growth hormone treatmentCLINICAL ENDOCRINOLOGY, Issue 3 2007D. A. M. Festen Summary Background, Prader,Willi syndrome (PWS) is a neurogenetic disorder characterized by muscular hypotonia, psychomotor delay, obesity and short stature. Several endocrine abnormalities have been described, including GH deficiency and hypogonadotrophic hypogonadism. Published data on thyroid hormone levels in PWS children are very limited. Objective, To evaluate thyroid function in children with PWS, before and during GH treatment. Design/patients, At baseline, serum levels of T4, free T4 (fT4), T3, reverse T3 (rT3) and TSH were assessed in 75 PWS children. After 1 year, assessments were repeated in 57 of the them. These children participated in a randomized study with two groups: group A (n = 34) treated with 1 mg GH/m2/day and group B (n = 23) as controls. Results, Median age (interquartile range, IQR) of the total group at baseline was 4·7 (2·7,7·6) years. Median (IQR) TSH level was ,0·1 SDS (,0·5 to 0·5), T4 level ,0·6 SDS (,1·7 to 0·0) and fT4 level ,0·8 SDS (,1·3 to ,0·3), the latter two being significantly lower than 0 SDS. T3 level, at 0·3 SDS (,0·3 to 0·9), was significantly higher than 0 SDS. After 1 year of GH treatment, fT4 decreased significantly from ,0·8 SDS (,1·5 to ,0·2) to ,1·4 SDS (,1·6 to ,0·7), compared to no change in untreated PWS children. However, T3 did not change, at 0·3 SDS (,0·1 to 0·8). Conclusions We found normal fT4 levels in most PWS children. During GH treatment, fT4 decreased significantly to low-normal levels. TSH levels remained normal. T3 levels were relatively high or normal, both before and during GH treatment, indicating that PWS children have increased T4 to T3 conversion. [source] GH responsiveness in a large multinational cohort of SGA children with short stature (NESTEGG) is related to the exon 3 GHR polymorphismCLINICAL ENDOCRINOLOGY, Issue 3 2007M. Tauber Summary Objective, The polymorphic deletion of exon 3 of the GH receptor (d3-GHR) has recently been linked to the magnitude of growth response to recombinant human GH (rhGH) therapy in short children with or without GH deficiency. We investigated this association in a large multinational cohort from the Network of European Studies of Genes in Growth (NESTEGG), comprising short children born small for gestational age (SGA). Design, The study included short prepubertal SGA children treated with rhGH for 1 or 2 years. Population, Two hundred and forty white Caucasian SGA children (138 male, 102 female) aged 6·6 ± 2·3 years with a height at ,3·0 ± 0·7 SDS at start of rhGH treatment; 193 ethnically matched controls. Methods, The GHR polymorphism (fl/fl, fl/d3 or d3/d3) was genotyped by polymerase chain reaction (PCR) multiplex assay. Growth velocity (G/V) in cm/year and changes in GV during the first and second year of rhGH treatment were evaluated. Results, The change in GV was significantly greater in SGA children carrying one or two copies of the d3-GHR allele (P = 0·038 for the first year and P = 0·041 for the second year of GH treatment), but the change in height was not significantly different. Birthweight was significantly lower in SGA children with the d3/d3 genotype than in SGA children with the fl/fl genotype (P = 0·034) and in those with the fl/d3 genotype (P = 0·016). Conclusion, Our data, based on a large cohort, showed that the exon 3 GHR polymorphism is associated with responsiveness to rhGH treatment in SGA children with short stature. [source] Unmasking of central hypothyroidism following growth hormone replacement in adult hypopituitary patientsCLINICAL ENDOCRINOLOGY, Issue 1 2007Amar Agha Summary Background, The effect of GH replacement on thyroid function in hypopituitary patients has hitherto been studied in small groups of children and adults with conflicting results. Objective, We aimed to define the effect and clinical significance of adult GH replacement on thyroid status in a large cohort of GH-deficient patients. Patients and method, We studied 243 patients with severe GH deficiency due to various hypothalamo-pituitary disorders. Before GH treatment, 159 patients had treated central hypothyroidism (treated group) while 84 patients were considered euthyroid (untreated group). GH dose was titrated over 3 months to achieve serum IGF-1 concentration in the upper half of the age-adjusted normal range. Serial measurements of serum T4, T3, TSH and quality of life were made at baseline and at 3 and 6 months after commencing GH replacement. Results, In the untreated group, we observed a significant reduction in serum T4 concentration without a significant increase in serum T3 or TSH concentration; 30/84 patients (36%) became hypothyroid and needed initiation of T4 therapy. Similar but lesser changes were seen in the treated group, 25 of whom (16%) required an increase in T4 dose. Patients who became hypothyroid after GH replacement had lower baseline serum T4 concentration, were more likely to have multiple pituitary hormone deficiencies and showed less improvement in quality of life compared with patients who remained euthyroid. Conclusion, GH deficiency masks central hypothyroidism in a significant proportion of hypopituitary patients and this is exposed after GH replacement. We recommend that hypopituitary patients with GH deficiency and low normal serum T4 concentration should be considered for T4 replacement prior to commencement of GH in order to provide a robust baseline from which to judge the clinical effects of GH replacement. [source] Lower ability to oxidize lipids in adult patients with growth hormone (GH) deficiency: reversal under GH treatmentCLINICAL ENDOCRINOLOGY, Issue 4 2006F. Brandou Summary Background, The aim of the study was to characterize lipid oxidation at exercise in adults with growth hormone deficiency (GHD) and to evaluate the effect of 6 and 12 months of GH replacement therapy on substrate carbohydrate (CHO) and lipid utilization at exercise. Patients and measurements, Twenty-five patients with GHD and 40 matched controls participated in the study. Ten of the 25 GH-deficient patients were treated with recombinant GH for 12 months. Anthropometric measurements and exercise calorimetry were performed before and after treatment. Maximal fat oxidation and the crossover point [that is the percentage of the theoretical maximal power (Wmax th) where CHO become the predominant fuel used for oxidation] were determined. Results and conclusion, The GH-deficient patients exhibited a highly significant shift in the balance of substrate oxidation during exercise, towards a decrease in fat oxidation, and a shift towards lower intensities of the crossover (52 ± 5·5%vs. 72·6 ± 6·6% of Wmax th, P < 0·03) and maximal fat oxidation (131·04 ± 14 vs. 234·4 ± 30·1 mg/min, P < 0·03) in the GHD and control groups, respectively. However, GH treatment at 6 and 12 months partially reversed this defect, resulting in an increase (+83%, P < 0·001) in the maximal ability to oxidize fat during exercise. These findings are consistent with the hypothesis that a lack of GH reduces the ability to oxidize lipids during exercise and that GH treatment restores this muscular metabolic property. [source] Improved final height with long-term growth hormone treatment in Noonan syndromeACTA PAEDIATRICA, Issue 9 2005Deborah Osio Abstract Aim: To assess whether children with Noonan syndrome on long-term growth hormone (GH) therapy improve their final height to near mid-parental height. Methods: Twenty-five prepubertal children (13 girls) with Noonan syndrome (NS) were studied. A single clinician made the diagnosis based on clinical criteria. GH treatment started at an age ranging from 3.1 to 13.8 y and was continued for at least 2 y. Improvement or "gain" in final height (FH) was defined as either the difference between adult height SD scores (SDS) and pre-treatment height SDS (the childhood component of the Swedish reference) or height SDS compared to the Noonan reference. Results: Ten children received a GH dose of 33 ,g/kg/d (mean age at start 7.7±2.1 y, mean age at stop 17.6±1.7 y) and 15 received a dose of 66 ,g/kg/d (mean age at start 8.6±3.3 y, mean age at stop 18.4±2.1 y). Eighteen out of 25 patients reached FH. A substantial improvement in FH of 1.7 SDS, equivalent to 10.4 cm compared to pre-treatment height, was observed. No significant difference was seen between the two GH doses. Females gained a mean height of 9.8 cm and males 1,13 cm (FH 174.5±7.8 cm vs mean adult height of 162.5±5.4 cm for males with NS) at final height. Moreover, 60% reached a mid-parental height of±1 SD. Conclusion: GH treatment improves final height in patients with Noonan syndrome, with a mean gain of 1.7 SDS. The prepubertal height gain is maintained to final height and the children achieve a height close to their mid-parental height. [source] The impact of idiopathic childhood-onset growth hormone deficiency (GHD) on bone mass in subjects without adult GHDCLINICAL ENDOCRINOLOGY, Issue 1 2005Martin Lange Summary objective, Despite seemingly adequate growth hormone (GH) treatment during childhood, children with GH deficiency (GHD) have reduced bone mineral density (BMD) at final height. The aim was to evaluate BMD and bone mineral content (BMC) in adults treated for idiopathic childhood-onset (CO) GHD, 18 years after stopping GH treatment. subjects and methods, Twenty-six (11 females) patients with idiopathic CO GHD participated. All patients but two had been treated for isolated GHD in childhood. The childhood diagnosis was established by an insulin tolerance test (ITT) and reassessed in adulthood by an ITT (N = 21) or arginine test (n = 5), revealing that 10 patients had GHD according to adult criteria. Accordingly, the patient group was divided into (1) patients who did not have persistent GHD in adulthood and (2) patients who did have persistent adult GHD. Twenty-six healthy subjects acted as age-, gender- and body mass index (BMI)-matched controls. results, The patients who did not have persistent GHD had significantly lower IGF-I values and whole-body, femoral neck and lumbar spine BMD compared to controls [0·994 ± 0·10 vs. 1·114 ± 0·11 g/cm2 (P = 0·003), 0·842 ± 0·12 vs. 0·962 ± 0·11 g/cm2 (P = 0·006) and 1·026 ± 0·14 vs. 1·127 ± 0·13 g/cm2 (P = 0·004), respectively]. Femoral neck BMD was significantly reduced in the patients who had persistent GHD, compared to controls (0·842 ± 0·09 vs. 0·938 ± 0·11, P = 0·04). Significant correlations were observed between all bone variables and IGF-I in all subjects, whereas no correlations were observed between bone variables and GH peak levels in the 26 patients. conclusion, In conclusion, we found that (1) patients with idiopathic CO GHD, who at retest in adulthood did not have GHD according to adult criteria, had reduced serum IGF-I and BMD/BMC compared to controls. (2) This observation was also made in the patients who did have persistent GHD in adulthood. The findings may reflect the fact that the present diagnostic criteria for adult GHD (i.e. response to the ITT) do not reflect the clinical consequences of disordered GH,IGF axis in CO GHD young adults who were treated with GH in childhood. Alternatively, despite seemingly adequate GH treatment in childhood an optimal peak bone mass in adolescence may never have been reached in either of the groups. (3) IGF-I levels correlated with clinical signs of the adult GHD syndrome. We believe that further studies on the indications and diagnostic procedures for GH treatment after cessation of linear growth are necessary. [source] Insulin sensitivity in growth hormone-deficient children: influence of replacement treatmentCLINICAL ENDOCRINOLOGY, Issue 4 2004Giorgio Radetti Summary objective, In adults, excessive GH secretion may lead to secondary diabetes mellitus, while prolonged GH treatment may accelerate the onset of type 2 diabetes mellitus in predisposed children. The aim of the study was to evaluate insulin sensitivity (IS) and glucose tolerance (GT) in a group of GH-deficient children treated with GH for a period of 6 years. patients and design, One hundred and twenty-eight children (40 females, 88 males) were included in the study. At the beginning of treatment chronological age was 8·9 ± 3·2 years, height standard deviation score (SDS) ,2·43 ± 0·90 and body mass index (BMI) SDS 0·18 ± 1·60. At the end of the study chronological age was 13·0 ± 2·9 years, height SDS ,1·24 ± 1·27 and BMI SDS 0·23 ± 1·54. GH was administered at a mean weekly dosage of 0·3 mg/kg, injected subcutaneously over 6,7 days. GT was assessed according to the criteria of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. IS was evaluated with the quantitative insulin sensitivity check index (QUICKI). results, No cases of impaired GT or diabetes were recorded during the follow-up period. IS, already lower than in controls before starting treatment with GH, decreased significantly during the first year of therapy (QUICKI: 0·346 ± 0·033 vs. 0·355 ± 0·044, P < 0·05), with no further decrease in the following years. No correlation was found between QUICKI, BMI, years of treatment and onset of puberty. conclusions, GH treatment in GH-deficient children does not lead to an impaired GT or type 2 diabetes mellitus, although it does significantly decrease IS. [source] Recombinant hGH replacement therapy and the hypothalamus,pituitary,thyroid axis in children with GH deficiency: when should we be concerned about the occurrence of central hypothyroidism?CLINICAL ENDOCRINOLOGY, Issue 6 2003Claudia Giavoli Summary objective, Recombinant hGH treatment may alter thyroid hormone metabolism and we have recently reported that 50% of patients with GH deficiency (GHD) due to organic lesions, previously not treated with thyroxine, developed hypothyroidism during treatment with recombinant human GH (rhGH). These results prompted us to evaluate the impact of rhGH treatment on thyroid function in children with GHD. design, Open study of GH treatment up to 12 months. Investigations were performed at baseline, and after 6 and 12 months of GH therapy. measurement and study subjects, Serum TSH, FT4, FT3, AbTg and AbTPO, IGF-I, height and weight, were evaluated in 20 euthyroid children (group A) with idiopathic isolated GHD and in six children (group B) with multiple pituitary hormone deficiencies (MPHD) due to organic lesions. Among the latter, four already had central hypothyroidism and were on adequate LT4 replacement therapy, while two were euthyroid at the beginning of the study. results, Serum IGF-I levels normalized in all patients. In both groups, a significant reduction in FT4 levels (P < 0·01) occurred during rhGH therapy. No patient in group A had FT4 values into the hypothyroid range, while in four of six patients in group B, fell FT4 levels into the hypothyroid range during rhGH. In particular, the two euthyroid children developed central hypothyroidism during rhGH treatment, and their height velocities did not normalize until the achievement of euthyroidism through appropriate LT4 substitution. No variation in serum FT3 and TSH levels was recorded in either groups. conclusion, Contrary to that observed in patients with MPHD, rhGH replacement therapy does not induce central hypothyroidism in children with idiopathic isolated GHD, further supporting the view that in children with MPHD, as in adults, GHD masks the presence of central hypothyroidism. Slow growth (in spite of adequate rhGH substitution and normal IGF-I levels) is an important clinical marker of central hypothyroidism, therefore a strict monitoring of thyroid function is mandatory in treated children with MPHD. [source] Re-assessment of growth hormone secretion in young adult patients with childhood-onset growth hormone deficiencyCLINICAL ENDOCRINOLOGY, Issue 4 2003Juliane Donaubauer Summary objective Patients with childhood-onset GH deficiency (coGHD) need retesting in late adolescence or young adulthood to verify whether they need to continue GH treatment. For this purpose the Growth Hormone Research Society (GRS) recommends the insulin tolerance test (ITT), or as an alternative the arginine + growth hormone releasing hormone test (ARG + GHRH test) as a diagnostic tool in adolescents and adults. However, there are no standardized cut-off levels based on normal GH secretion for determining GHD vs. GH sufficiency in young adults for the ITT, the ARG + GHRH test or the pyridostigmine + GHRH (PD + GHRH) test, a further new GH stimulation test. patients and measurements We studied 43 patients (28 with organic coGHD, 15 with idiopathic coGHD; 30 males, 13 females; aged 20·4 years, range 16·2,25·4; body mass index 23·5, range 16·3,35·8) using the ARG [0·5 g/kg intravenously (i.v.)] + GHRH (1 µg/kg i.v.) test, the PD (120 mg orally) + GHRH (1 µg/kg i.v.) test and the ITT (0·1 IU/kg i.v.) and compared these data with the results of 40 healthy age- and weight-matched volunteers. results The GH response in patients was significantly lower than in healthy controls: ARG + GHRH test, 0·8 µg/l (interquartile range 0·3,2·6) vs. 51·8 µg/l (32·6,71·2) in controls (P < 0·0001); PD + GHRH test, 0·9 µg/l (0·3,1·9) vs. 40·4 µg/l (27·1,54·4) in controls (P < 0·0001); ITT, 0.1 µg/l (0·0,0·8) vs. 20·3 µg/l (14·7,31·7) in controls (P < 0·0001). In the ARG + GHRH test we found a diagnostic sensitivity of 100% and a specificity of 97·5% for a cut-off range from 15·1 to 20·3 µg/l, in the PD + GHRH test a sensitivity of 100% and a specificity of 97% (cut-off range 9·1,13·1 µg/l) and in the ITT a sensitivity and specificity of 100% each within a cut-off range from 2·7 to 8·8 µg/l. conclusion There were no marked differences in sensitivity and specificity in young adults among ARG + GHRH test, PD + GHRH test and the ITT in assessing GH secretion. Because of the lack of side-effects, the ARG + GHRH test is the recommended method for re-evaluation of coGHD in young adults when pituitary GHD is suspected. Furthermore, in adult patient groups where organic pituitary coGHD is common, the ITT may be completely replaced by the ARG + GHRH test. Because of the predominance of hypothalamic GHD in childhood, the ITT is commonly performed for the re-evaluation of patients with childhood-onset GHD because of its mechanism of GH stimulation. The present results confirm the high discriminatory capability of the ITT in young adults. [source] Confirmation of severe GH deficiency after final height in patients diagnosed as GH deficient during childhoodCLINICAL ENDOCRINOLOGY, Issue 4 2002Andrea F. Attanasio Summary objective Human GH treatment of patients with childhood-onset (CO) growth hormone deficiency (GHD) ceases when they reach final height; this provides an opportunity to retest GH status in all patients before determining whether GH therapy will be required in adult life. At present, the diagnostic approach to these patients is not fully standardized. This study aimed to characterize a large group of previously GH-treated CO GHD patients and establish their GH status. patients and methods The multinational study included 167 patients diagnosed as GH deficient and treated with hGH to final height during childhood. Mean age was 19·2 years and mean height standard deviation score (SDS) was ,1·08. Peak serum GH concentrations were determined in standard GH stimulation tests. IGF-I and IGFBP-3 concentrations were determined at a central laboratory and converted to SDS values by reference to a normal population. results Using only a peak GH value of less than 3 µg/l (1 mg = 3 U) in stimulation tests as the cut-off, 133 (79·6%) patients would be classed as GH deficient. Using only an IGF-I value less than ,2 SDS as the cut-off, 134 (80·2%) patients would be classed as GH deficient. However, by using both criteria there were 120 (71·9%) patients who were definitely severely GH deficient (group 1) and 20 (12·0%) who were not GH deficient (group 2), leaving 14 (8·4%) classed as GH deficient from IGF-I SDS only (group 3) and 13 (7·8%) classed as GH deficient from stimulation test only (group 4). There was no difference between the groups in height SDS or body mass index (BMI), but the GH-deficient patients tended to have been diagnosed at a younger age (group 1, 8·2 ± 3·9; group 2, 10·0 ± 4·0; P = 0·052). For patients classed as GH deficient compared with those not GH deficient, the percentage of males was lower (group 1, 64·2%; group 2, 90·0%; P = 0·022) and the percentage with multiple pituitary hormone deficiencies was higher (group 1, 81·7%; group 2, 20·0%; P < 0·001), with the other two groups being intermediate in each case. Only the group classed as GH deficient by both criteria had a mean IGFBP-3 less than ,2 SDS and both IGF-I SDS and IGFBP-3 SDS increased steadily across the four groups. conclusions A high percentage (71·9%) of these childhood-onset GH-deficient patients were still GH deficient in adult life and are likely to require further hGH treatment. While 12·0% could be classed as definitely no longer GH deficient, there are some patients who are intermediate (16·2%) and may be classed as GH deficient by one criterion but not the other. When GH stimulation test results and IGF-I concentration are discordant, the IGFBP-3 level does not establish diagnosis and the hGH treatment requirement of such patients remains a dilemma. [source] Improved final height in Turner's syndrome following growth-promoting treatment at a single centreACTA PAEDIATRICA, Issue 9 2003EJ Gault Aims: To examine the final height (FH) outcome of girls with Turner's syndrome (TS) treated at a single Scottish centre (Glasgow group), to compare it with an earlier national analysis (Scottish group) and to suggest reasons for any change. Methods: Retrospective growth and treatment data for 29 Glasgow patients were compared with those of 26 Scottish patients. Results: Age at GH start (mean ± SD) was 10.1 ± 2.6 vs 12.1 ± 1.7 y (p < 0.01) in the Glasgow versus Scottish groups, with overall duration of treatment 6.2 ± 2.4 vs 3.7 ± 1.1 y (p < 0.001) and years of GH treatment before pubertal induction 2.7 ± 2.8 vs 0.3 ± 0.8 y (p < 0.001), respectively. Pubertal induction was at a similar age: 12.7 ± 1.8 vs 12.8 ± 1.8 y (ns). FH was 151.1 ± 4.6 cm in the Glasgow group compared with 142.6 ± 5.6 cm in the Scottish group (p < 0.001), with FH -projected adult height (PAH) 5.7 ± 4.6 cm vs 0.6 ± 3.6 cm (p < 0.001), respectively. Univariate analysis of the Glasgow group's FH , PAH with a number of growth and treatment variables identified no statistically significant relationships. Conclusion: This group's improved FH and FH , PAH, relative to an earlier sample, are attributed to the introduction of GH treatment from a younger age and for longer, overall and before pubertal induction. In addition, the authors believe that compliance with treatment has been enhanced by this single centre's dedicated Turner clinic and the efforts of its established "growth team". These data demonstrate that a favourable FH can be achieved using a safe and financially viable dose of GH, while inducing puberty at a "normal" age. [source] | |||||||||||||