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

1994 ◽  
Vol 40 (4) ◽  
pp. 65-81
Author(s):  
М. Bengt-Ake Bengtsson

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.

2006 ◽  
Vol 16 ◽  
pp. S50-S51
Author(s):  
Maria Koltowska-Haggstrom ◽  
Hugo Fideleff ◽  
Pascale Abrams ◽  
Hugo Boquete ◽  
Ulla Feldt-Rasmussen ◽  
...  

2021 ◽  
Vol 96 (5) ◽  
pp. 400-407
Author(s):  
Jung Hee Kim

Adult growth hormone (GH) deficiency is associated with insulin resistance, elevated cardiovascular risk profile, increased fat mass, reduced muscle mass, skeletal fragility, and impaired quality of life. GH replacement therapy improves body composition, exercise capacity, skeletal health, cardiovascular outcomes, and quality of life, while reducing mortality. Prior to initiation of GH replacement therapy, it is essential to diagnose GH deficiency via a GH stimulation test in adults suspicious of such deficiency. Therapy should be started using (individualized) low dose of GH, followed by titration to the normal range of insulin-like growth factor-1. Clinical improvements should be monitored and side effects should be minimized.


Pituitary ◽  
2020 ◽  
Author(s):  
Isabela Peixoto Biscotto ◽  
Valéria Aparecida Costa Hong ◽  
Rafael Loch Batista ◽  
Berenice Bilharinho Mendonca ◽  
Ivo Jorge Prado Arnhold ◽  
...  

1999 ◽  
Vol 51 (2) ◽  
pp. 173-179 ◽  
Author(s):  
Emanuel R. Christ ◽  
Michael H. Cummings ◽  
Peter J. Lumb ◽  
Martin A. Crook ◽  
Peter H. Sönksen ◽  
...  

2017 ◽  
Vol 13 (27) ◽  
pp. 19
Author(s):  
Nestan Bostoganashvili ◽  
Elene Giorgadze ◽  
Shota Janjgava ◽  
Marine Lomidze

Introduction: Recently, Growth hormone deficiency (GHD) has become one of the reasons of significant metabolic and psychological morbidity in children and adults. The aim of our study was to find out the impact of GH replacement therapy on lipid profile in Georgian patients with GHD, which was caused by surgical resection. Design: Double Blind placebo controlled study for 12 months and an open study for another 12 months. Patients and Methods: 20 Georgian adults, aged 40.75±2.2 years (mean ± SE, range 20.5-60), with adult onset GH deficiency were enrolled in the study. The patients were selected from the basis of National Institute of Endocrinology. We set the inclusive and exclusive criteria to study these patients, who needed the growth hormone replacement therapy. We collected standardized information about central and peripheral hormones, metabolic activity and physical features. Results: after 12 months of GH replacement, there was no significant improvement of lipid profile in the GH deficient patients. After 24 months of the treatment, the study showed the upward trend of Triglycerides, Total cholesterol and HDL-CH, and a decrease of LDL-CH. Conclusion: The response of lipid profile to the 12 and 24 months of GH replacement in patients with GH deficiency was disappointing. The results significantly differ from the ones, provided by the European Endocrine societies. Thus, longer-term studies are required, in order to investigate accurately the whole lipid profile among our patients for the following years.


2004 ◽  
pp. 153-159 ◽  
Author(s):  
A Golgeli ◽  
F Tanriverdi ◽  
C Suer ◽  
C Gokce ◽  
C Ozesmi ◽  
...  

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.


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