Growth hormone (GH) replacement therapy in GH deficient adults: Predictors of one-year metabolic and clinical response

2007 ◽  
Vol 17 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Johan Svensson ◽  
Nick Finer ◽  
Pierre Bouloux ◽  
John Bevan ◽  
Björn Jonsson ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Clinical Response ◽  
Replacement Therapy ◽  
Gh Replacement ◽  
One Year

Changes In Prothrombin And Activated Partial Thromboplastin Time During Replacement Therapy With Human Recombinant Growth Hormone In Growth Hormone Deficient Adults

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S102-S103
Author(s):  
Y S Kamel
Keyword(s):  
Growth Hormone ◽  
Replacement Therapy ◽  
Healthy Subjects ◽  
Recombinant Growth Hormone ◽  
Gh Replacement ◽  
Coagulation Tests ◽  
Before And After ◽  
Human Recombinant Growth Hormone ◽  
Male Patients ◽  
One Year

Abstract Introduction/Objective The aim of this study was to investigate the effects of GH administration on basic coagulation parameters: PT, aPTT and fibrinogen concentrations in adult GHD patients before and during one year of GH replacement. Methods Twenty-one adult patients with severe GHD (mean age +/- SE: 38.6 +/- 2.8 years) were included in this hospital based, prospective, interventional study. All patients were treated with rhGH for 12 months (GH dose: 0.4 mg/day for male and 0.6 mg/day for female patients). IGF-1 concentrations were determined using RIA-INEP kits. Basic coagulation tests, i.e. aPTT and fibrinogen concentrations, were measured before and after 3, 6 and 12 months of treatment with rhGH. Control values were obtained from fourteen “healthy” subjects matched by age, sex and body mass index (BMI). Results At baseline, we observed no significant differences in PT, aPTT and fibrinogen values between GHD and healthy subjects. IGF-1 concentrations increased significantly within 3 months of GH therapy (8.2 +/- 1.5 vs. 24.2 +/- 2.9 nmol/l, p <0.05) and remained stable thereafter. A significant increase in PT values, which was more pronounced in female subjects, was noted after 6 and 12 months of treatment with GH. aPTT values increased significantly after 12 months of treatment only in male patients (28.8 +/- 4.6 vs. 39.7 +/- 2.1 s.; p <0.05). No significant changes in fibrinogen concentrations were found during the study. Conclusion Twelve months of GH replacement therapy led to a significant increase in PT and aPTT values in adult GHD patients, while fibrinogen concentrations did not change. Changes in PT were more pronounced in female GHD patients, while an increase in aPTT values was observed only in male patients with GHD. The clinical significance of these changes needs further evaluation.

scholarly journals Systemic ghrelin levels in subjects with growth hormone deficiency are not modified by one year of growth hormone replacement therapy

2001 ◽  
pp. 711-716 ◽  
Author(s):  
JA Janssen ◽  
FM van der Toorn ◽  
LJ Hofland ◽  
P van Koetsveld ◽  
F Broglio ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Replacement Therapy ◽  
Body Fat ◽  
Arcuate Nucleus ◽  
Gh Therapy ◽  
Percentage Body Fat ◽  
Gh Secretion ◽  
Gh Replacement ◽  
Igf I ◽  
One Year

OBJECTIVE: Ghrelin stimulates growth hormone (GH) secretion both in vivo and in vitro. Ghrelin is mainly produced in and released from the stomach but it is probably also produced in the hypothalamic arcuate nucleus. Whether pituitary GH release is under the control of ghrelin from the stomach and/or from the arcuate nucleus is not known. Moreover, no data on the feedback of GH on systemic ghrelin concentrations are available. It has recently been suggested that ghrelin may induce obesity. DESIGN: In this study, we addressed the following two questions: a) are circulating ghrelin levels increased in human GH deficiency (GHD), and b) does GH treatment modify ghrelin levels in human GHD? METHODS: The study group consisted of 23 patients with GHD. Eighteen had developed adult-onset GHD and five had developed GHD in their childhood (childhood-onset GHD). Ghrelin was measured with a commercially available radioimmunoassay. All measurements were performed twice, first at baseline, before the start of GH replacement therapy, and then again after one year of therapy. GH doses were adjusted every 3 months, targeting serum total IGF-I levels within the normal gender- and age-related reference values for the healthy population. Maintenance doses were continued once the target serum total IGF-I levels were reached. RESULTS: The sum of skinfolds and body water increased significantly, body fat mass and percentage body fat decreased significantly and body mass index and waist-hip ratio were not significantly changed by one year of GH replacement therapy.Before the start of GH replacement therapy, mean value and range for fasting ghrelin in the studied GHD subjects tended to be lower in comparison with healthy subjects in the control group although the difference did not reach significance (GHD ghrelin mean 67.8 pmol/l, range 37.6-116.3 pmol/l; control mean 83.8 pmol/l, range 35.4-132 pmol/l; P=0.11).One year of GH replacement therapy did not modify circulating ghrelin levels (ghrelin before GH therapy: 67.8 pmol/l, range 37.6-116.3 pmol/l; after GH therapy: 65.3 pmol/l, range 35.8-112.6; P=0.56). CONCLUSIONS: We did not observe elevated ghrelin levels in adult GHD subjects and GH replacement therapy did not modify circulating ghrelin levels, despite significant decreases in body fat mass and percentage body fat. It is conceivable that the lack of ghrelin modifications after long-term GH therapy was due to the reduction of adiposity and insulin on one hand, and increased GH secretion on the other. However, it is still possible that systemic ghrelin is involved in the development of obesity, both in normal and GHD subjects.

scholarly journals Pregnancy outcomes in women receiving growth hormone replacement therapy enrolled in the NordiNet® International Outcome Study (IOS) and the American Norditropin® Studies: Web-Enabled Research (ANSWER) Program

Pituitary ◽  
2021 ◽  
Author(s):  
Beverly M. K. Biller ◽  
Charlotte Höybye ◽  
Paul Carroll ◽  
Murray B. Gordon ◽  
Anna Camilla Birkegård ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Outcome Study ◽  
Real World Data ◽  
Multicenter Studies ◽  
Clinical Trial Registration ◽  
Normal Delivery ◽  
Growth Hormone Replacement Therapy ◽  
Gh Replacement

Abstract Purpose Data on the safety of growth hormone (GH) replacement therapy during pregnancy are limited. We report a combined analysis of data from pregnant women treated with GH while enrolled in two non-interventional, multicenter studies: NordiNet® International Outcome Study (IOS) and the American Norditropin® Studies: Web-Enabled Research (ANSWER) Program. Methods Pregnancy data were pooled from NordiNet® IOS and the ANSWER Program. Data were collected during routine clinic visits by participating physicians using a web-based system. Patients exposed to GH replacement therapy during pregnancy were included in the analysis. Results The study population included 40 female patients with typical causes of adult GH deficiency (GHD). Overall, there were 54 pregnancies. Of these, 47 were exposed to GH between conception and delivery. In 48.9% of pregnancies exposed to GH, the dose was > 0.6 mg/day. GH was continued past conception and then stopped during the first, second, and third trimester, in 27.7%, 17.0%, and 2.1% of pregnancies, respectively. In 29.8%, GH was continued throughout pregnancy, with an unchanged dose in most cases. Of the 47 GH-exposed pregnancies, 37 (78.7%) progressed to normal delivery. There were three adverse events reported in two pregnancies. Conclusion These real-world data suggest that there were no new safety signals related to GH exposure in women with GHD during pregnancy. These results are consistent with findings from previous studies reporting data in pregnancies exposed to GH at conception or throughout pregnancy. This observational study in additional pregnancies provides further evidence that GH exposure does not adversely affect pregnancy outcome. Clinical trial registration: ClinicalTrials.gov NCT00960128 (date of registration: August 13, 2009) and NCT01009905 (date of registration: November 5, 2009).

scholarly journals Utility of P300 auditory event related potential latency in detecting cognitive dysfunction in growth hormone (GH) deficient patients with Sheehan's syndrome and effects of GH replacement therapy

2004 ◽  
pp. 153-159 ◽  
Author(s):  
A Golgeli ◽  
F Tanriverdi ◽  
C Suer ◽  
C Gokce ◽  
C Ozesmi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cognitive Function ◽  
Replacement Therapy ◽  
Patient Group ◽  
Gh Deficiency ◽  
Event Related Potential ◽  
Sheehan’S Syndrome ◽  
Gh Replacement ◽  
Igf I ◽  
Sheehan's Syndrome

OBJECTIVE: Impaired cognitive function has been demonstrated in adults with growth hormone (GH) deficiency (GHD) by using different neuropsychological tests. Despite several studies, present knowledge about the impact of GHD and GH replacement therapy (GHRT) on cognitive function is limited. P300 event-related potential (ERP) application is a well-established neurophysiological approach in the assessment of cognitive functions including the updating of working memory content and the speed of stimulus evaluation. GHD is a well-known feature of Sheehan's syndrome and cognitive changes due to GHD and the effects of GHRT remain to be clarified. The present study was designed to investigate the effects of GHD and 6 months of GHRT on cognitive function in patients with Sheehan's syndrome by using P300 latency. DESIGN AND METHODS: The study comprised 14 patients with Sheehan's syndrome (mean age, 49.5+/-7.8 years) and 10 age-, education- and sex-matched healthy controls. With hormone replacement therapy, basal hormone levels other than GH were stable before enrollment and throughout the GHRT. The diagnosis of GH deficiency was established by insulin-tolerance test (ITT), and mean peak level of GH in response to insulin hypoglycemia was 0.77+/-0.35 mIU/l. Treatment with GH was started at a dose of 0.45 IU (0.15 mg)/day in month 1, was increased to 0.9 IU (0.30 mg)/day in month 2 and was maintained at 2 IU (0.66 mg)/day. Initially baseline auditory ERPs in patients and controls were recorded at frontal (Fz), central (Cz), and parietal (P3 and P4) electrode sites. In the patient group, ERPs were re-evaluated after 6 months of GH replacement therapy. During each session P300 amplitude and latency were measured. RESULTS: Mean serum insulin-like growth factor-I (IGF-I) concentration in the patient group before GHRT was 23+/-13 ng/ml. After 6 months of GH therapy mean IGF-I significantly increased to an acceptable level, 234+/-71 ng/ml (P<0.05). The mean latencies (at all electrode sites) of the patients before GHRT were found to be significantly prolonged when compared with those of normal controls (P<0.05). After 6 months of GHRT mean P300 latencies (at all electrode sites) were decreased significantly when compared with latencies before treatment (P<0.05). CONCLUSIONS: The present study, using P300 ERP latencies, therefore suggests an impairment of cognitive abilities due to severe GHD in patients with Sheehan's syndrome and an improvement of cognitive function after 6 months of physiological GHRT. Moreover, this was a novel application of P300 ERP latencies in cognitive function detection in patients with GHD. Further studies with different patient groups need to be done to assess the clinical use of this electrophysiological method in the diagnosis of cognitive dysfunction due to GHD.

Issues in the Transition From Childhood to Adult Growth Hormone Therapy

PEDIATRICS ◽  
1999 ◽  
Vol 104 (Supplement_5) ◽  
pp. 1004-1010
Author(s):  
David B. Allen
Keyword(s):  
Growth Hormone ◽  
Replacement Therapy ◽  
Blood Lipid ◽  
Hormone Deficiency ◽  
Late Adolescent ◽  
Gh Therapy ◽  
Gh Treatment ◽  
Beneficial Effects ◽  
Gh Replacement ◽  
Adult Growth

The consequences of severe growth hormone deficiency (GHD) in adults and the beneficial effects of GH replacement therapy are clear. However, the majority of children who have a diagnosis of GHD and who are treated with GH do not have permanent GHD and will not require treatment during adulthood. Several issues must be considered in selecting candidates for adult GH treatment and transitioning their care from pediatrics to adult medicine. Counseling about possible lifelong treatment should focus on children with panhypopituitarism and those with severe isolated GHD that is associated with central nervous system abnormalities. When to terminate growth-promoting GH therapy should be guided by balancing the high cost of late-adolescent treatment with the attainment of reasonable statural goals. Retesting for GH secretion is appropriate for all candidates for adult GH therapy; the GH axis can be tested within weeks after the cessation of treatment, but confirming an emerging adult GHD state with body composition, blood lipid, and quality-of-life assessments may require 1 year or more of observation. Selecting patients for lifelong adult GH replacement therapy will present diagnostic, therapeutic, and ethical problems similar to those in treating childhood GHD. The experience and expertise of pediatric endocrinologists in diagnosing and treating GHD should be offered and used in identifying and transitioning appropriate patients to adult GH therapy.

Effects of 5 years of growth hormone (GH) replacement therapy on cardiac parameters and physical performance in adults with GH deficiency

Pituitary ◽  
2009 ◽  
Vol 12 (4) ◽  
pp. 322-329 ◽  
Author(s):  
Maria Claudia Peixoto Cenci ◽  
Débora Vieira Soares ◽  
Luciana Diniz Carneiro Spina ◽  
Rosane Resende de Lima Oliveira Brasil ◽  
Priscila Marise Lobo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Replacement Therapy ◽  
Physical Performance ◽  
Gh Deficiency ◽  
Gh Replacement
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