Growth Hormone Neurosecretory Dysfunction Research Articles

BÜYÜME HORMONU TEDAVİSİ ALAN ÇOCUKLARIN KLİNİK ÖZELLİKLERİ: TEK MERKEZ DENEYİMİ

Objective: In this study, we aimed to investigate the clinical features of children who received growth hormone (GH) treatment with a diagnosis of GH deficiency (GHD). Material and Methods: The clinical features of children treated with GH treatment between 01.06.2013-31.12.2018 in a tertiary healthcare service were retrospectively analyzed. Children with isolated GHD and children with panhipopituitarism were compared. Results: In total, 70 boys 118 children were included in the study. 78 (66.3%) of patients were treated with GH due to isoleted GHD, 14 (11.9%) due to bio-inactive GH syndrome, 9 (7.6%) due to panhypopituitarism, 6 (5.1%) due to GH neurosecretory dysfunction, 6 (5.1%) due to Turner syndrome and 5 (4.2%) due to off-label reasons.There were no significant diffrence between groups of isoleted GHD and panhipopituitarism regarding gender, age of diagnosis and oxological features at diagnosis. Serum IGF-1 SDS, IGFBP-3 SDS, TSH and pik GH response to klonidine test were lower in panhipopituitarism group (p=0.026, p=0.002, p=0.009 ve p=0.005, respectively). Significantly higher growth rates in the first 2 years in the patient with panhypopituitarism were determined (p<0.001 and p=0.005, respectively). A correlation was found between the growth rate in the first year and age of diagnosis, GH stimulation test responses, serum IGFBP-3 SDS and difference between chronologic age and bone age. Conclusion: Patients with panhypopituitarism had more significant laboratory findings for GHD at admission and better GH treatment responses in follow-up compared to patients with isolated GHD.

Growth hormone neurosecretory dysfunction as part of the spectrum of growth hormone deficiency disorders which benefit from growth hormone treatment

Growth hormone neurosecretory dysfunction as part of the spectrum of growth hormone deficiency disorders which benefit from growth hormone treatment

GENETIC FORMS OF GROWTH HORMONE INSUFFICIENCY, PECULIARITIES OF CLINIC AND DIAGNOSTIC

The article considers genetic forms of growth hormone insufficiency in children. Analysis of genes, defects of which can lead to severe growth retardation due to somatotropic insufficiency or syndromal disorders, is important not only to improve the diagnosis, but also for choosing of adequate therapy and prediction of final height. Choice of analyzed gene is determined by a combination of clinical data and features of hormone secretion.Are discussed primary IGF-1 deficiency (disturbance of synthesis and secretion of growth hormone (neurosecretory dysfunction), biologically inactive growth hormone (GH1 gene mutation), and partial insensitivity to growth hormone as a result of its receptor defects (GHR gene mutations).The article details the principles of diagnostic search in the genetic forms of growth hormone insufficiency, was analyzed molecular-genetic defects in genes of the growth axis system: growth hormone - insulin-like growth factor 1.

Growth hormone deficiency after childhood bone marrow transplantation with total body irradiation: interaction with adiposity and age

Bone marrow transplantation with total body irradiation (BMT/TBI) has adverse effects on growth, growth hormone status and adiposity. We investigated the GH-IGF-I axis in relation to adiposity. Cross-sectional case control study. BMT/TBI survivors (n = 22) and short stature control participants (n = 19), all GH-naïve or off GH treatment >3 months. Auxology, DEXA scans and GH-IGF-I axis investigation: (i) 12-h overnight GH profiles; (ii) insulin tolerance test (ITT); and (iii) IGF-I generation test. auto-deconvolution of GH profile data and comparison of quantitative parameters using ANOVA. Eighty-two percent of BMT/TBI survivors had growth hormone deficiency (GHD) using ITT. GH profile area-under-the-curve (GH-AUC) was reduced in BMT/TBI survivors vs short stature control participants [geometric mean (range) 209 (21-825) vs 428 (64-1400) mcg/l/12 h, respectively, P = 0·007]. GHD was more marked in those who had additional cranial irradiation (CRT) [ITT peak 1·4 (0·2-3·0) vs TBI only 4·1 (1·1-14·8) mcg/l, P = 0·036]. GHD was more marked at the end of growth in BMT/TBI survivors vs short stature control participants (GH-AUC 551 (64-2474) vs 1369 (192-4197) mcg/l/12 h, respectively, P = 0·011) and more prevalent (9/11 vs 1/9, respectively, P = 0·005). GH profile data were consistent with ITT results in 80% of participants. IGF-I generation tests were normal. BMT/TBI survivors still demonstrated lower GH levels after adjustment for adiposity (fat-adjusted mean difference for GH-AUC 90·9 mcg/l/12 h, P = 0·025). GHD was more prevalent in BMT/TBI survivors than expected for the CRT dose in TBI, worsened with time and persisted into adulthood. GHD could not be explained by adiposity. There was no evidence of GH neurosecretory dysfunction or resistance after BMT/TBI.

Long-term auxological and endocrinological evaluation of patients with 9p trisomy: a focus on the growth hormone-insulin-like growth factor-I axis

BackgroundTrisomy 9p is an uncommon anomaly characterised by mental retardation, head and facial abnormalities, congenital heart defects, kidney abnormalities, and skeletal malformations. Affected children may also show growth and puberty retardation with delayed bone age. Auxological and endocrinological data are lacking for this syndrome.MethodsWe describe three girls and one boy with 9p trisomy showing substantial growth failure, and we evaluate the main causes of their short stature.ResultsThe target height was normal in all families, ranging from 0.1 and -1.2 standard deviation scores (SDS). The patients had a low birth-weight (from -1.2 to -2.4 SDS), birth length (from -1.1 to -3.2 SDS), and head circumference (from -0.5 to -1.6 SDS). All patients presented with substantial growth (height) retardation at the time of 9p trisomy diagnosis (from -3.0 to -3.8 SDS).The growth hormone stimulation test revealed a classic growth hormone (GH) deficiency (GHD) in patients 1, 3, and 4. In contrast, patient 2 was determined to have a GH neurosecretory dysfunction (GHNSD). The plasma concentrations of IGF-I and IGFBP-3 were low in all patients for their ages and sexes (from -2.0 to -3.4 SDS, and from -1.9 to -2.8 SDS, respectively).The auxological follow-up showed that those patients who underwent rhGH treatment exhibited a very good response to the GH therapy, whereas patients 3 and 4, whose families chose not to use rhGH treatment, did not experience any significant catch-up growth.ConclusionsGH deficiency appears to be a possible feature of patients with 9p trisomy syndrome. These patients, particularly those with growth delays, should be evaluated for GH secretion.

The endocrine spectrum of intracranial cysts in childhood and review of the literature

Intracranial cysts (ICC) may cause a wide spectrum of endocrinological disorders. We evaluated 27 patients who were diagnosed with ICC during investigation for neuroendocrine dysfunctions and reviewed the relevant literature. The types of ICC in the patients were arachnoid cysts (n = 13); Rathke cleft cysts (n = 7); pineal cysts (n = 5); an ependymal cyst (n = 1) and a cavum septum pellucidum cyst (n = 1). The neuroendocrine dysfunctions of the patients were obesity (n = 7), isolated growth hormone deficiency (n = 6), central precocious puberty (n = 6), multiple pituitary hormone deficiency (n = 3), central diabetes insipidus (n = 1), growth hormone deficiency and central precocious puberty (n = 1), obesity and galactorrhea (n = 1), obesity and hypogonadotropic hypogonadism (n = 1) and growth hormone neurosecretory dysfunction (n = 1). Only three patients, who had arachnoid cysts, showed neurologic symptomatology. Although three patients underwent surgery, no improvements in endocrinological dysfunctions were observed. ICC should be considered when evaluating patients with endocrinological problems and patients with coincidental ICC should be recommended for follow-up.

Irradiation-Induced Growth Hormone Neurosecretory Disfunction In ALL Patients

AbstractAbstract 4329With the recent developments in the treatment of ALL life expectancy is prolonged and complications due to therapy are increased. Combined chemotherapy may be applied in combination with distinct doses and schema of cranial radiotherapy according to the risk groups of patients. CRT damages the hypothalamus-hypophysis axis and affects the secretion of growth hormone (GH) at first and the other anterior hypophysis hormones also. At high doses of CRT, GH deficiency might occur in the long term follow-up, at lower doses the secretion pattern of GH may change. In this study, GH axis of the ALL patients treated with prophylactic CRT were evaluated.Thirty-two children (14 girls and 18 boys), diagnosed as ALL and applied prophylactic cranial therapy were enrolled to the study. Physical findings, weight and height measurements, Tanner stagings and bone age evaluations were performed to all patients. In order to interpret the functions of anterior and posterior hypophysis morning basal IGF-1, IGFBP-3, thyroid hormones, cortisol, prolactin and dansity of urine were measured. Gonodotrophins were not tested because none of our patients had the signs of early or late puberty. In order to evaluate the growth rate, weights and heights of the patients were measured after the first year. Even though the growth rate of some patients were normal, GH stimulation tests with clonidine were done to all cases, due to the fact that GH deficiency and neurosecretory dysfunction might be present pharmacologically. Second GH stimulation test with L-dopa were applied to patients with peak GH levels of <10 ng/ml. If the level was low in the second test, patients were accepted as GH deficient. For patients with low growth rate, low IGF-1/IGFBP-3 according to age and sex, but normal GH levels, night GH secretion pattern were tested. Patients with inadequate response to night secretion test were accepted as neurosecretory dysfunction.In our study, 25% of the patients were found to have complete and 21,7% incomplete GH deficiency. In 9.3% of cases there was GH-neurosecretory dysfunction (GH_NSD). There was no statistically significant relationship between the time passed after radiotherapy and GH axis dysfunction degree. IGF-BP3 was found to be more reliable than IGF-1 in estimating GH deficiency/GH-NSD.As a result, it is clear that prophylactic CRT affects the GH axis negatively in ALL patients, so their close follow-up is precious and mandatory. Disclosures:No relevant conflicts of interest to declare.

Spontanes Wachstumshormonsekretionsprofil

Growth hormone neurosecretory dysfunction (NSD) can only be diagnosed by the analysis of a spontaneous growth hormone (GH) secretion profile over a defined period of time. Since the procedure is not regulated uniformly, examination periods of 2-24 h with blood withdrawal intervals of 10-30 min can be encountered. To answer the question of whether the analysis of spontaneous GH secretion over 2.6 h after falling asleep is comparable to that over 10 h, we recalculated the datasets of 60 children with a diagnosis of GH deficiency (GHD, n=20), NSD (n=20) and idiopathic short stature (ISS, n=20). We analysed GH values in blood specimens taken every 20 min from 8 pm to 6 am. All calculations were made using PULSAR program. All children with GHD had a pathological GH secretion values, whereas children with NSD had significantly higher GH values after 2.6 h than after 10 h. The analysis of spontaneous GH secretion over a period of 2.6 h after falling asleep seems to be insufficient for the diagnosis of NSD. This complex diagnostic procedure should be left to hospitals which have the prerequisites to perform a GH secretion profile over at least 10 h.

Growth Hormone Neurosecretory Dysfunction in a Boy with Hypohidrotic/Anhidrotic Ectodermal Dysplasie: Definition of Short Stature, Molecular Characterization and Long-term hGH Replacement Treatment to Final Height

Anhidrotic/hypohidrotic ectodermal dysplasia is a rare disorder, genetically heterogeneous, commonly X-linked recessive inherited, characterized by hypoplasia up to the absence of the eccrine glands with hypo-anhidrosis and secondary hyperpyrexia, hypodontia and some typical craniofacial features. Some papers have described how these patients may show poor growth, while other recent research shows normal growth. We report a boy with anhidrotic/hypohidrotic ectodermal dysplasia and growth hormone neurosecretory dysfunction, an association not previously reported, and we discuss the possible causes as well as the patient's response to growth hormone treatment until he reached final height.

Combined Growth Hormone-Releasing Hormone and Growth Hormone-Releasing Peptide-6 Test for the Evaluation of Growth Hormone Secretion in Children with Growth Hormone Deficiency and Growth Hormone Neurosecretory Dysfunction

Background: The combined growth hormone-releasing hormone and growth hormone-releasing peptide-6 (GHRH + GHRP-6) test is most potent in evaluating GH secretion. Aims: To assess its capability in children with GH deficiency and low spontaneous GH secretion (GH neurosecretory dysfunction). Methods: 35 children with GH <10 µg/l after levo-dopa/clonidine (GHD), 15 with normal provocative tests but abnormal 24-hour spontaneous GH secretion (GHND), and 20 controls (C) were given 1 µg/kg of GHRH and GHRP-6 i.v. and GH (µg/l) was measured at –15, 0, 5, 10, 15, 30, 45 and 60 min. Results: Six were nonresponders to the combined test, with significantly lower peak GH 20.7 (7.8–31.8) than C and the rest of the patients (responders). Peak GH was similar between prepubertal (PP) controls 167 ± 88, GHD 202 ± 110 and GHND 155 ± 83. Pubertal (P) controls had higher peak GH 328 ± 149 than P-GHD 203 ± 105 and P-GHND 186 ± 105. While P-C had higher peak GH than PP-C, PP and P children had similar responses within the GHD and GHND groups. Conclusions: The GHRH + GHRP-6 test detects children with severe GH insufficiency. Patients with GHD respond similarly to those with GHND, indicating a possible hypothalamic GH neuroregulatory dysfunction in GHD. Responders to the combined test may be eligible for treatment with a synthetic GH secretagogue.

Pituitary hypoplasia and growth hormone deficiency in a woman with glycogen storage disease type Ia: a case report

IntroductionGrowth retardation is one of the cardinal manifestations of glycogen storage disease type Ia. It is unclear which component of the growth hormone and/or insulin-like growth factor axis is primarily disrupted, and management of growth impairment in these patients remains controversial. Here we report the first case in the literature where glycogen storage disease type Ia is associated with pituitary hypoplasia and growth hormone deficiency.Case presentationA 20-year-old woman with glycogen storage disease type Ia was admitted to our endocrinology department because of growth retardation. Basal and overnight growth hormone sampling at 2-hour intervals demonstrated low levels; however, provocative testing revealed a relatively normal growth hormone response. A hypoplastic anterior pituitary with preserved growth hormone response to provocative testing suggested the possibility of growth hormone neurosecretory dysfunction and/or primary pituitary involvement.ConclusionPituitary hypoplasia may result from growth hormone-releasing hormone deficiency, a condition generally known as growth hormone neurosecretory dysfunction. It is an abnormality with a spontaneous and pulsatile secretion pattern, characterized by short stature, growth retardation and normal serum growth hormone response to provocative testing. However, in the case described in this report, a normal although relatively low growth hormone response during insulin tolerance testing and pituitary hypoplasia suggested that primary pituitary involvement or growth hormone neurosecretory dysfunction may occur in glycogen storage disease type Ia. This is a potential cause of growth failure associated with a lower somatotroph mass, and may explain the variable responsiveness to growth hormone replacement therapy in people with glycogen storage disease.

Hypopituitarism following radiotherapy

Deficiencies in anterior pituitary hormones secretion ranging from subtle to complete occur following radiation damage to the hypothalamic-pituitary (h-p) axis, the severity and frequency of which correlate with the total radiation dose delivered to the h-p axis and the length of follow up. Selective radiosensitivity of the neuroendocrine axes, with the GH axis being the most vulnerable, accounts for the high frequency of GH deficiency, which usually occurs in isolation following irradiation of the h-p axis with doses less than 30 Gy. With higher radiation doses (30-50 Gy), however, the frequency of GH insufficiency substantially increases and can be as high as 50-100%. Compensatory hyperstimulation of a partially damaged h-p axis may restore normality of spontaneous GH secretion in the context of reduced but normal stimulated responses; at its extreme, endogenous hyperstimulation may limit further stimulation by insulin-induced hypoglycaemia resulting in subnormal GH responses despite normality of spontaneous GH secretion in adults. In children, failure of the hyperstimulated partially damaged h-p axis to meet the increased demands for GH during growth and puberty may explain what has previously been described as radiation-induced GH neurosecretory dysfunction and, unlike in adults, the ITT remains the gold standard for assessing h-p functional reserve. Thyroid-stimulating hormone (TSH) and ACTH deficiency occur after intensive irradiation only (>50 Gy) with a long-term cumulative frequency of 3-6%. Abnormalities in gonadotrophin secretion are dose-dependent; precocious puberty can occur after radiation dose less than 30 Gy in girls only, and in both sexes equally with a radiation dose of 30-50 Gy. Gonadotrophin deficiency occurs infrequently and is usually a long-term complication following a minimum radiation dose of 30 Gy. Hyperprolactinemia, due to hypothalamic damage leading to reduced dopamine release, has been described in both sexes and all ages but is mostly seen in young women after intensive irradiation and is usually subclinical. A much higher incidence of gonadotrophin, ACTH and TSH deficiencies (30-60% after 10 years) occur after more intensive irradiation (>60 Gy) used for nasopharyngeal carcinomas and tumors of the skull base, and following conventional irradiation (30-50 Gy) for pituitary tumors. The frequency of hypopituitarism following stereotactic radiotherapy for pituitary tumors is mostly seen after long-term follow up and is similar to that following conventional irradiation. Radiation-induced anterior pituitary hormone deficiencies are irreversible and progressive. Regular testing is mandatory to ensure timely diagnosis and early hormone replacement therapy.

Radiation-induced GH neurosecretory dysfunction might not be a real entity

Radiation-induced GH neurosecretory dysfunction might not be a real entity

Combined effect of mutations of the GH1 gene and its proximal promoter region in a child with growth hormone neurosecretory dysfunction (GHND)

Mutational analysis of the growth hormone 1 (GH1) gene and its promoter in a patient with GH neurosecretory dysfunction (GHND) revealed a heterozygous new deletion of one base 7-bp downstream from the 3'-splice site of exon 4 (IVS4'del+7) of the GH1 gene and two new heterozygous mutations at sites -135 and -138 of the GH1 promoter. In addition, two polymorphisms at sites -301 and -308 of the GH1 promoter were observed. All other family members had either the -301/-308 polymorphisms or the IVS4'del+7 mutation, but none had both. The IVS4'del+7 mutation located close to the splice donor site possibly interferes with the success of the splicing process, or the mutant transcripts are highly unstable because of nonsense-mediated mRNA decay. The -135/-138 mutations, albeit in close proximity to a putative Pit-1 recognition site, do not seem to affect binding of this transcription factor. The combination of the two polymorphisms, -301/-308, results in significantly reduced DNA-binding activity as monitored by electrophoretic mobility-shift assay. Transcription factor recognition site analysis of the GH1 promoter (MatInspector) revealed that HES1, one of the effectors of the Notch signalling system, is the only transcription factor whose binding is expected to be disrupted by each haplotype or by their combination. We provide evidence that the combination of -301/-308 polymorphisms with the IVS4'del+7 mutation in a GHND patient probably accounts for the reduced amount of growth hormone spontaneously secreted from his pituitary gland and for the severe growth delay.

Cranial Irradiation and Growth Hormone Neurosecretory Dysfunction: A Critical Appraisal

It has been suggested that radiation-induced GH neurosecretory dysfunction exists in children; however, the pathophysiology is poorly understood, and it is unknown if such a phenomenon exists in adult life. Twenty-four-hour spontaneous GH secretion was studied by 20-min sampling both in the fed state (n = 16; six women) and the last 24 h of 33-h fast (n = 10; three women) in adult cancer survivors of normal GH status defined by two GH provocative tests, 13.1 +/- 1.6 (range, 3-28) yr after cranial irradiation (18-40 Gy) for nonpituitary brain tumors (n = 12) or leukemia (n = 4) in comparison with 30 (nine women) age- and body mass index-matched normal controls (fasting, 11 men and three women). Using previously published diagnostic thresholds, all patients had stimulated peak GH responses in the normal range to both the insulin tolerance test and the combined GHRH plus arginine stimulation test, as well as normal individual mean profile GH levels during the fed and fasting states. However, gender-specific comparisons revealed marked reduction (by 40%) in the overall peak GH responses to both provocative tests but similar GH secretory profiles; no differences were seen in the pulsatile attributes of GH secretion (cluster analysis) or the profile absolute and mean GH levels in the fed state or when the hypothalamic-pituitary axis was stimulated by fasting. Radiation-induced GH neurosecretory dysfunction either does not exist or is a very rare phenomenon in irradiated adult cancer survivors. The normality of physiological GH secretion in the context of reduced maximum somatotroph reserve suggests compensatory overdrive of the partially damaged somatotroph axis and constitutes a relative argument against somatotroph dysfunction being explained purely by hypothalamic damage with secondary atrophy due to GHRH deficiency. It is therefore possible that radiation in doses less than 40 Gy causes dual damage to both the pituitary and the hypothalamus.

Growth of children with β-thalassemia major

Hypertransfusion and regular chelation therapy have allowed improved survival in patients with thalassemia major (TM). Despite medical advances, growth failure and hypogonadism remain significant clinical problems in these patients in adolescence. Disproportionate truncal shortening which is common especially among adolescents with thalassemia, is due to platyspondyly resulting from a combination of factors like hemosiderosis, desferrioxamine toxicity or deficiency of trace elements. Although growth hormone (GH) deficiency and GH neurosecretory dysfunction have been described in TM patients, most short TM patients have normal GH reserve. The low serum IGF-1 and IGFBP-3 concentrations in TM patients despite having normal GH reserve and serum GH binding protein levels suggest that a state of secondary GH insensitivity exists. The pubertal growth spurt may be impaired in TM patients going through spontaneous or induced puberty and may have a negative effect on final adult height. GH therapy in dosages ranging from 0.5-1.0 IU/kg/wk has resulted in a significant improvement in growth velocity in short TM children without any adverse effects on skeletal maturation, blood pressure, glucose tolerance and serum lipids. There is limited evidence that GH treatment can result in an improved final adult height in short TM children. Careful and regular clinical and biochemical monitoring should be preformed on these patients while they are treated with GH.

Physiological and Pathological Growth Hormone Secretion

Growth hormone (GH) secretion is normally episodic, with discrete bursts of GH super-imposed on a minimal basal level of production. This pattern of GH production yields a dynamic state between a low baseline and intervening peaks, posing a challenge for the clinician attempting to understand the 'true GH status' in a specific patient. This pulsatile pattern is maintained throughout the day, but there are clear differences between different segments of the day, with approximately two-thirds of the total daily secretion produced at night. The dynamic nature of GH production has led many investigators to suggest that when evaluating short stature, parameters of spontaneous GH production be applied rather than the GH response to artificial stimulation. GH secretory patterns in healthy control populations are compared to those in patients with several conditions seen by the pediatric endocrinologist (classical GH deficiency, GH neurosecretory dysfunction, acute lymphoblastic leukemia, hypothyroidism, small for gestational age, Russell-Silver syndrome, constitutional delay of growth and puberty and Fanconi's anemia) and variables used for analysis of these patterns are described. Inferences made from comprehensive evaluations of the GH axis in Fanconi's anemia provide unique insight into general GH pathophysiology.

Spontaneous Growth Hormone (GH) Secretion Is Not Directly Affected by Ghrelin in Either Short Normal Prepubertal Children or Children with GH Neurosecretory Dysfunction

Ghrelin, a specific endogenous ligand for the GH secretagogue receptor, stimulates GH secretion in humans when given in pharmacological amounts. Under physiological conditions, however, it is controversial whether ghrelin affects GH secretion and vice versa. No studies have reported on the relationship between daily ghrelin and GH secretion in children. Therefore, plasma ghrelin and GH concentrations over a 24-h period were studied in 10 prepubertal short normal children (five females and five males) to determine the potential relationship between the secretion of these two hormones. Furthermore, five prepubertal patients (two females and three males) with GH neurosecretory dysfunction (GHNSD) were studied in the same way to assess potential alterations in ghrelin secretion in a condition associated with distinct GH changes. No gender difference in ghrelin spontaneous secretion was detected in either short normal children or GHNSD patients, and in both male and female subjects, ghrelin was secreted in a pulsatile and circadian fashion, with a nocturnal surge. Twenty-four-hour secretion and daytime ghrelin secretion of short normal children were similar to those in GHNSD patients, whereas nighttime hormone secretion in the latter group was significantly greater than that in short normal children. The cross-correlation of 24-h ghrelin and GH levels revealed significant positive and negative correlations, which were similar in the two groups examined. The positive one, with GH leading ghrelin, might reflect a somatostatin (SMS)-mediated inhibitory effect on both GH and ghrelin secretion (low SMS levels are followed by high GH and ghrelin levels, and vice versa). The negative correlation, with ghrelin leading GH, might again reflect the positive effect of ghrelin on SMS, as shown in both animal and human studies. In conclusion, the results of the present study indicate that ghrelin secretion in prepubertal children is pulsatile and is not sexually dimorphic. Although the parallelism of ghrelin and GH dynamics hints at the potential relevance of endogenous ghrelin as a promoter of GH release, our data do not support this hypothesis. We suggest that the interactions of ghrelin and GH are the result of SMS action. SMS inhibits GH secretion not only by a direct effect on the pituitary and by inhibiting hypothalamic GHRH, but also through the suppression of ghrelin release.

A visual motor psychological test as a predictor to treatment in nocturnal enuresis

Background and Aims: The neurological control of bladder function and the ability to be dry at night involves not only the acquisition of normal daytime control, but also the establishment...

Behavioral evaluation of GH treatment in short statured children and adolescents: findings from a pilot study.

A cohort of 93 short-statured children and adolescents undergoing GH treatment were evaluated with respect to behavior, emotions, and attitudes. The sample consisted of patients suffering from either idiopathic GH deficiency or neurosecretory dysfunction (no.=47), Turner syndrome (no.=20), organic GH deficiency due to brain tumors (no.=10), or other etiologies (no.=16). The Child Behavior Checklist (CBCL) together with a brief Evaluation of Treatment Questionnaire (ETQ) were filled out by the patient's parents. These evaluations were performed at onset and after 12 and 24 months of GH treatment, respectively. There was a highly significant but clinically small decline of behavioral abnormalities over time and parents saw major benefits of GH treatment in the total group of patients. The behavioral changes over time were independent of diagnostic category, gender, height velocity, puberty and age.