Circulating immunoreactive somatostatin in man. Effect of age, pregnancy, growth hormone deficiency and achlorhydria

1985 ◽  
Vol 110 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Susan M. Webb ◽  
John A. H. Wass ◽  
Erica Penman ◽  
M. Murphy ◽  
José Serrano ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Pernicious Anaemia ◽  
Hormone Deficiency ◽  
Control Group ◽  
Normal Children ◽  
The Third ◽  
Group 12 ◽  
The Mean ◽  
Effect Of Age

Abstract. Plasma immunoreactive somatostatin (IRS) levels were measured fasting at 09.00 h in groups of adult individuals and children of different ages, as well as in pregnant women, in patients with pernicious anaemia documented to be achlorhydric, and in children with growth hormone deficiency. There was a gradual rise in the mean level of IRS from the third decade (mean 35.8 ± 3.8 pg/ml), which reached significance at the seventh (61.1 ± 8.4 pg/ml), eighth (66.7 ± 5 pg/ml) and ninth decade (82.6 ± 13.8 pg/ml). No change was observed in the second 28.3 ± 3.8 pg/ml) and third (31.1 ± 3.2 pg/ml) trimester of pregnancy when compared with matched, non-pregnant controls (29.7 ± 2.2 pg/ml); however, the children aged under 2 years (69.6 ± 11.2 pg/ml) had significantly higher values than the eldest group (12 to 16 years old) (46.3 ± 7.2 pg/ml) (P < 0.05). In achlorhydric patients, basal (27.2 ± 3.7 pg/ml; P < 0.01) and postprandial IRS (42.8 ± 7.7 pg/ml; P < 0.001) was significantly lower than in a matched, normal control group (basal 59.4 ± 7.2; postprandial 132.1 ± 26.3 pg/ml). Growth hormone deficiency was not associated with any differences in circulating IRS, basally or after insulin hypoglycaemia, when compared with values in normal children. These results would suggest, 1) that age has a significant effect on plasma IRS, and should be considered in the interpretation of fasting plasma levels of IRS; 2) that pregnancy and growth hormone deficiency is not accompanied by any changes in circulating IRS and presumably, somatostatin binding proteins; 3) that gastric acid is necessary for a normal release of IRS from the gastrointestinal tract to the circulation.

scholarly journals Effects of human recombinant growth hormone on exercise capacity, cardiac structure, and cardiac function in patients with adult-onset growth hormone deficiency

2017 ◽  
Vol 45 (6) ◽  
pp. 1708-1719 ◽  
Author(s):  
S Gonzalez ◽  
JD Windram ◽  
T Sathyapalan ◽  
Z Javed ◽  
AL Clark ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cardiac Function ◽  
Growth Hormone Deficiency ◽  
Exercise Capacity ◽  
Left Ventricular ◽  
Hormone Deficiency ◽  
Control Group ◽  
Cardiac Structure ◽  
Adult Onset ◽  
Risk Of Death

Objective Epidemiological studies suggest that adult-onset growth hormone deficiency (AGHD) might increase the risk of death from cardiovascular causes. Methods This was a 6-month double-blind, placebo-controlled, randomised, cross-over trial followed by a 6-month open-label phase. Seventeen patients with AGHD received either recombinant human growth hormone (rGH) (0.4 mg injection daily) or placebo for 12 weeks, underwent washout for 2 weeks, and were then crossed over to the alternative treatment for a further 12 weeks. Cardiac magnetic resonance imaging, echocardiography, and cardiopulmonary exercise testing were performed at baseline, 12 weeks, 26 weeks, and the end of the open phase (12 months). The results were compared with those of 16 age- and sex-matched control subjects. Results At baseline, patients with AGHD had a significantly higher systolic blood pressure, ejection fraction, and left ventricular mass than the control group, even when corrected for body surface area. Treatment with rGH normalised the insulin-like growth factor 1 concentration without an effect on exercise capacity, cardiac structure, or cardiac function. Conclusion Administration of rGH therapy for 6 to 9 months failed to normalise the functional and structural cardiac differences observed in patients with AGHD when compared with a control group.

scholarly journals Síndrome de Klinefelter con deficiencia parcial de hormona de crecimiento.

2015 ◽  
Vol 10 (1) ◽  
pp. 38
Author(s):  
Carlos TORI TORI ◽  
Carlos ROE B.
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Short Stature ◽  
Klinefelter Syndrome ◽  
Bone Age ◽  
Hormone Deficiency ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
The Third ◽  
Rare Association

We present a case of Klinefelter’s syndrome and short stature due to partial growth hormone deficiency. His height was below the third percentile for age and his bone age lagged behind four years. Cases like this are generally due to the presence of a an isochromosome Xq or to an isolated partial or total deficiency of growth hormone, or to partial or panhypopituitarism. We wish de emphasize the rare association between Klinefelter syndrome and growth hormone deficiency.

A Review of Growth Hormone Stimulation Tests in Children

PEDIATRICS ◽  
1974 ◽  
Vol 53 (6) ◽  
pp. 929-937
Author(s):  
S. Douglas Frasier
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Hormone Deficiency ◽  
Current Evidence ◽  
Oral Glucose ◽  
Normal Children ◽  
Small Magnitude ◽  
Arginine Infusion ◽  
Sequential Administration ◽  
Stimulation Tests

No suggested screening test meets all of the criteria set for such a procedure. The minimum incidence of a positive response in normal children detected in a single blood sample after diethylstilbestrol, sleep or exercise is approximately 70%. This is higher than that observed when a single sample is obtained following oral glucose. While both sleep and exercise are physiologic stimuli, the former may be quite inconvenient unless an outpatient facility staffed with appropriate personnel is available. An exercise test employed in the office may well be the best screening procedure for the practicing physician. The optimal criteria for a definitive test of growth hormone function are also not met by any single stimulus. Insulin-induced hypoglycemia, arginine infusion, intramuscular glucagon and oral 1-DOPA are all useful procedures. None alone discriminate completely between the normal and the growth hormone-deficient child. Despite potential hazards, insulin-induced hypoglycemia remains the standard against which other stimuli are judged. Arginine and 1-DOPA appear to be equally effective. The literature contains insufficient data to allow adequate evaluation of intramuscular glucagon alone, and the results of combined propranolol-glucagon stimulation, while promising, require confirmation. Because of an inconstant and/or small magnitude of response leading to results which are difficult to interpret, the use of glucose, pyrogen, vasopressin and ACTH are not adequate tests of growth hormone function. Bovril® is a satisfactory stimulus for those children who will take it. Those factors which modify the growth hormone response must be considered in evaluating the results of stimulation tests. Blunted responses should be interpreted with extreme caution in the obese child. A fasting growth hormone concentration ≥ 7 ng/ml is presumptive evidence of intact growth hormone function regardless of the subsequent response to stimulation. It is essential that patients be euthyroid in order to interpret the results of growth hormone function tests. Physiologic glucocorticoid replacement therapy should not confuse the interpretation of results. Whether or not pretreatment with sex steroids is worthwhile in the routine evaluation of children for suspected growth hormone deficiency is an open question. Although it is agreed that the definitive diagnosis of growth hormone deficiency depends on the demonstration of failure to respond to two stimuli, which two are most satisfactory is not settled. The sequential administration of arginine and insulin on the same day appears to limit significantly the incidence of false-positive laboratory diagnoses of growth hormone deficiency. The significance of intermediate values in response to stimulation remains unclear. Caution should be exercised in assigning a child to the category of partial growth hormone deficiency. This question must be answered ultimately by the response to HGH therapy in the individual patient. Finally, several points should be kept in mind. All of the tests described depend on the detection and quantitation of immunologically active HGH and biological activity is not necessarily associated with the material(s) being measured. Since many of the stimuli used in the evaluation of growth hormone function are clearly pharmacologic, the physiological significance of the response to such stimuli must be interpreted with caution. The best current evidence suggests that all of the stimuli described act through an intact hypothalamus and pituitary. Differentiation between hypothalamic and pituitary sites of defective growth hormone function awaits the availability of growth hormone-releasing factor(s).

Erythrocytes from patients with low serum concentrations of IGF-I have an increase in receptor sites for IGF-I

1991 ◽  
Vol 125 (4) ◽  
pp. 354-358 ◽  
Author(s):  
R. Eshet ◽  
Z. Dux ◽  
A. Silbergeld ◽  
R. Koren ◽  
B. Klinger ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Specific Binding ◽  
Hormone Deficiency ◽  
Scatchard Analysis ◽  
Isolated Growth Hormone Deficiency ◽  
Receptor Sites ◽  
Igf I ◽  
The Mean ◽  
Low Serum

Abstract. The binding characteristics of insulin-like growth factor I on erythrocytes were studied in 11 patients with long-term IGF-I deprivation and low serum IGF-I levels. Six patients had Laron type dwarfism and 5 idiopathic isolated growth hormone deficiency, with a mean (± sem) serum IGF-I level of 6.01±1.01 nmol/l as compared with that in 25 normal controls of 26.35±2.73 nmol/l (p=0.00001). The mean (± sem) [125I]IGF-I specific binding at a concentration of 4×1012 cell/l was 12.11±1.29% for the patient group compared with 8.75±0.62% for the controls (p=0.005). Scatchard analysis showed a curvilinear plot. Using a non-linear curve fit, the mean (± sem) number of high-affinity receptor sites per cell was found to be 7.34±1.80 in the IGF-I-deprived patients and 2.84±0.29 in the controls (p=0.0005). The mean ± sem dissociation constant was found to be 0.33±0.10 nmol/l for the patients and 0.26±0.08 nmol/l for the controls (NS). This study has demonstrated that the low serum concentration of IGF-I in Laron type dwarfism and isolated growth hormone deficiency is associated with an increase in receptor sites for IGF-I on the erythrocytes. The application of this property as a diagnostic aid remains to be established.

scholarly journals Adult height prediction by bone age determination in children with isolated growth hormone deficiency

2020 ◽  
Vol 9 (5) ◽  
pp. 370-378
Author(s):  
Thomas Reinehr ◽  
Martin Carlsson ◽  
Dionisios Chrysis ◽  
Cecilia Camacho-Hübner
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Adult Height ◽  
Age Determination ◽  
Bone Age ◽  
Hormone Deficiency ◽  
Gh Treatment ◽  
Height Prediction ◽  
The Mean ◽  
Tw2 Method

Background The precision of adult height prediction by bone age determination in children with idiopathic growth hormone deficiency (IGHD) is unknown. Methods The near adult height (NAH) of patients with IGHD in the KIGS database was compared retrospectively to adult height prediction calculated by the Bayley–Pinneau (BP) prediction based on bone age by Greulich–Pyle (GP) in 315 children and based on the Tanner-Whitehouse 2 (TW2) method in 121 children. Multiple linear regression analyses adjusted for age at GH start, age at puberty, mean dose and years of of GH treatment, and maximum GH peak in stimulation test were calculated. Results The mean underestimation of adult height based on the BP method was at baseline 4.1 ± 0.7 cm in girls and 6.1 ± 0.6 cm in boys, at 1 year of GH treatment 2.5 ± 0.5 cm in girls and 0.9 ± 0.4 cm in boys, while at last bone age determination adult height was overestimated in mean by 0.4 ± 0.6 cm in girls and 3.8 ± 0.5 cm in boys. The mean underestimation of adult height based on the TW2 method was at baseline 5.3 ± 2.0 cm in girls and 7.9 ± 0.8 cm in boys, at 1 year of GH treatment adult height was overestimated in girls 0.1 ± 0.6 cm in girls and underestimated 4.1 ± 0.4 cm in boys, while at last bone age determination adult height was overestimated in mean by 3.1 ± 1.5 cm in girls and 3.6 ± 0.8 cm in boys. Conclusions Height prediction by BP and TW2 at onset of GH treatment underestimates adult height in prepubertal IGHD children, while in mean 6 years after onset of GH treatment these prediction methods overestimated adult height.

scholarly journals Growth hormone deficiency in adults. Introduction to the problem

1994 ◽  
Vol 40 (4) ◽  
pp. 65-81
Author(s):  
М. Bengt-Ake Bengtsson
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Replacement Therapy ◽  
Gh Deficiency ◽  
Hormone Deficiency ◽  
Control Group ◽  
Objective Criterion ◽  
Double Blind ◽  
Gh Replacement ◽  
Severe Degree

Growth hormone deficiency (GH) for a long time was recognized only in childhood. Compelling evidence has been obtained showing that HR replacement therapy effectively stimulates growth and, in many cases, achieves normal end-points of physical development. More recently, it was shown that the most effective in this regard was the appointment of regular evening injections of the drug, which mimic the physiological secretion of GH during sleep. Despite the fact that the acceleration of linear growth is the most objective criterion for the effectiveness of therapy for GH, it is known that GH has a significant effect on body structure, causing a decrease in fat mass and an increase in muscle mass. Until recently, GH was not considered an important hormonal regulator in adults, and therefore, there was no study of GH deficiency and treatment of children with GH deficiency when they reached adulthood, as well as patients with hypopituitarism who became ill in adulthood. However, in 1989, as a result of two double-blind trials using placebo in the control group, the effectiveness of GH replacement therapy in adults with an abnormally low level of GH, up to a severe degree of GH deficiency, was revealed. Further studies showed the presence of violations of both physical and mental status in adults in whom GH deficiency develops as a result of the tumor process in the pituitary gland or its therapy. Most of these disorders, but not all, can be corrected as a result of GH replacement therapy, which confirms the significant effect of GH throughout life.

scholarly journals Changes in ghrelin and nesfatin-1 in children with growth hormone deficiency treated by recombinant human growth hormone

2019 ◽  
Vol 17 ◽  
pp. 205873921882423
Author(s):  
Yu Wang ◽  
Meng Sun ◽  
Xin Wang ◽  
Ya-Ying Cheng
Keyword(s):  
Growth Hormone ◽  
Growth Rate ◽  
Growth Hormone Deficiency ◽  
Human Growth Hormone ◽  
Recombinant Human Growth Hormone ◽  
Human Growth ◽  
Hormone Deficiency ◽  
Control Group ◽  
Annual Growth Rate ◽  
Observation Group

This study aims to investigate the effects of recombinant human growth hormone (rhGH) on serum nesfatin-1 and ghrelin in children with growth hormone deficiency (GHD), in order to provide a reliable basis for the effectiveness and safety of applying rhGH in treating GHD children in the clinic. A total of 30 GHD pediatric patients were selected as the observation group. According to the peak of GH, these patients were divided into two subgroups: complete absence of growth hormone (CGHD) group and partial absence of growth hormone (PGHD) group. At the same time, 20 healthy children of normal height with matching age and gender were randomly selected as a normal control group. Serum ghrelin and nesfatin-1 levels were detected in children in the control group and observation group before rhGH treatment, and at 3 and 6 months after treatment. After 3 and 6 months of treatment, the height and growth rate of children in the PGHD and CGHD groups significantly increased ( P < 0.05), but their body weights did not significantly change ( P > 0.05), compared with those before treatment. Before treatment, ghrelin was higher in the PGHD group than in the control group, while ghrelin was lower in the CGHD group than in the control group. In addition, nesfatin-1 was higher in these two subgroups, compared with that in the control group. At pretreatment, and after 3  and 6 months of treatment, ghrelin and nesfatin-1 both decreased in the PGHD group, while ghrelin increased and nesfatin-1 decreased in the CGHD group. It was confirmed that ghrelin and nesfatin-1 were closely correlated with GHD. Furthermore, rhGH has a significant effect on children with GHD, and can significantly accelerate the annual growth rate.

Do Short Children Secrete Insufficient Growth Hormone?

PEDIATRICS ◽  
1985 ◽  
Vol 76 (3) ◽  
pp. 355-360
Author(s):  
Zvi Zadik ◽  
Stuart A. Chalew ◽  
Salvatore Raiti ◽  
A. Avinoam Kowarski
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Normal Growth ◽  
Mean Value ◽  
Hormone Deficiency ◽  
Short Children ◽  
Stimulation Tests ◽  
Normal Stature ◽  
Hormone Responses ◽  
The Mean

The 24-hour integrated concentration of growth hormone from 46 children of normal stature was compared with that of 90 short children. Nineteen of the short children had classic growth hormone deficiency by standard pharmacologic growth hormone stimulation tests. Seventy-one children had normal growth hormone responses to stimulation. The mean integrated concentration of growth hormone for children with normal stature (6.6 ± 1.9 ng/mL) was greater than the mean value for those with normal stimulated growth hormone (3.8 ± 2.3 ng/mL) and greater than the mean value for those with growth hormone deficiency (1.6 ± 0.6 ng/mL); differences between groups were all statistically significant (P &lt; .0001). Forty-five percent of children with normal stimulated growth hormone responses had integrated concentration of growth hormone within the range of values for the group with growth hormone deficiency; this finding may provide the explanation for their poor growth. Thus, patients with normal growth hormone responses have a spectrum of spontaneous growth hormone secretion ranging from normal to impaired. Recent reports indicate that children with normal growth hormone responses who have very low integrated concentration of growth hormone may have the potential to improve their growth with growth hormone therapy. Therefore, use of the integrated concentration of growth hormone may be a more effective method than standard pharmacologic stimulation tests for determining which short children are potentially able to respond to growth hormone therapy.

scholarly journals The Efficacy of Anastrozole and Growth Hormone Therapy on Adult Height in Six Adolescent Males with Growth Hormone Deficiency or Idiopathic Short Stature

2017 ◽  
Vol 2017 ◽  
pp. 1-6
Author(s):  
Serife Uysal ◽  
Juanita K. Hodax ◽  
Lisa Swartz Topor ◽  
Jose Bernardo Quintos
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Short Stature ◽  
Adult Height ◽  
Bone Age ◽  
Idiopathic Short Stature ◽  
Hormone Deficiency ◽  
Chronological Age ◽  
Gh Therapy ◽  
The Mean

Background. Data on adult height outcomes of the use of Anastrozole and Growth Hormone (GH) in pubertal males with Growth hormone deficiency (GHD) and Idiopathic short stature (ISS) are limited. Objective. We examined the effect of Anastrozole and GH therapy on near adult height (NAH) with pubertal males with GHD or ISS. Methods. Retrospective review of 419 charts from 2008 to 2015. The primary outcomes are NAH compared to mid-parental target height (MPTH) and predicted adult height (PAH). Results. We identified 23 patients (5 SGA/IUGR, 1 Noonan syndrome, 6 GHD, and 11 ISS). Six patients (4 GHD; 2 ISS) achieved NAH. Prior to Anastrozole treatment, the mean chronological age was 13.9±0.2 years (range 13.7–14.4), bone age was 13.6±0.6 years (range 12.5–14), mean height SDS was -1.5±0.5 (range −0.8 to −2.3), and mean PAH was 162.6±5.9 cm (range 153.5–168.6). MPTH was 173.6 cm ± 7 (range 161.8–181.6). Patients received Anastrozole for an average of 30.5 months (range 19–36 months). At NAH, the mean chronological age was 16.7±0.8 years (range 15.9–18.1 years) and height was 170±1.8 cm (range 168.5–173.4 cm). The mean height SDS improved to +0.81±0.6 (range +0.08 to +1.92, p=0.002). Net height gain was 7.3 cm compared to pretreatment PAH (p<0.01) and overall the mean adult height remained 3.5 cm below MPTH. Conclusion. Anastrozole and GH therapy can be effective in augmenting adult height without significant side effects. However, the long-term safety and efficacy of aromatase inhibitor use in pediatrics remain limited.

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