Basal metabolic rate in adults with growth hormone deficiency and in patients with acromegaly: relationship with lean body mass, plasma insulin level and leucocyte sodium pump activity

1992 ◽  
Vol 83 (3) ◽  
pp. 325-330 ◽  
Author(s):  
Franco Salomon ◽  
Ross C. Cuneo ◽  
Richard Hesp ◽  
Jenny F. Morris ◽  
Lucilla Poston ◽  
...  

1. The relationship of lean body mass, plasma insulin concentration and leucocyte active sodium transport with basal metabolic rate was investigated in 24 adults with growth hormone deficiency before and after treatment with recombinant human growth hormone and in 10 patients with untreated acromegaly. 2. Based on total-body potassium determined by whole-body 40K counting, patients with acromegaly had increased lean body mass, whereas lack of growth hormone was associated with decreased lean body mass. 3. By indirect calorimetry, patients with acromegaly had increased basal metabolic rates and patients with growth hormone deficiency had decreased values when expressed as percentages of values predicted from the WHO/FAO/UNU equations. Basal metabolic rate expressed in terms of lean body mass was similar in acromegaly and growth hormone deficiency, but was higher than normal in both patient groups. 4. The leucocyte ouabain-sensitive sodium efflux rate constant was decreased in both patients with acromegaly and patients with growth hormone deficiency, and there was no correlation with basal energy expenditure, fasting plasma insulin level or serum growth hormone level. 5. There was no increase in the sodium efflux rate constant in patients with growth hormone deficiency after 1 month on treatment with recombinant human growth hormone. 6. Apparent differences in basal metabolic rate in growth hormone deficiency and acromegaly are due to changes in lean body mass. Both adults with growth hormone deficiency and patients with acromegaly have increased energy expenditure, probably owing to changes in fuel metabolism which are not reflected in the leucocyte sodium pump activity.

1994 ◽  
Vol 87 (2) ◽  
pp. 201-206 ◽  
Author(s):  
F. Salomon ◽  
R. C. Cuneo ◽  
A. M. Umpleby ◽  
P. H. Sönksen

1. Adults with growth hormone deficiency have an abnormal body composition. Alterations in body composition are closely related to substrate concentrations and insulin action. The lack of growth hormone has been associated with increased insulin sensitivity. 2. We investigated the correlations of body composition with fasting insulin levels and substrate concentrations in 24 adults with growth hormone deficiency over a wide range of adiposity (body mass index 18.8-42.3 kg/m2). 3. Lean body mass was measured by total body potassium, computer tomography of the thigh and urinary creatinine excretion. Muscle fibre distribution was evaluated from vastus lateralis biopsies. Fat mass was assessed by skinfold thickness measurements, computer tomography of the thigh, and waist and hip girth. 4. Fasting plasma insulin level increased with fat mass (r = 0.67, P = 0.0004) and with waist girth (r = 0.76, P = 0.0001). Fasting plasma insulin level increased with fasting plasma glucose level (r = 0.53, P = 0.01). Fasting plasma glucose level in turn was positively correlated with lean body mass (r = 0.49, P = 0.01) and with total thigh muscle area (r = 0.54, P = 0.01). There was no correlation between lean body mass and fat mass (r = 0.17, not significant) nor between muscle fibre types and fat mass or fat distribution. Fasting plasma insulin level showed no correlation with any measurement of lean body mass or muscle fibre type. 5. These data demonstrate that the presence of obesity is associated with hyperinsulinaemia as the result of insulin resistance in adults with growth hormone deficiency, which could contribute to the increased cardiovascular mortality in adults with growth hormone deficiency.


2021 ◽  
Vol 12 ◽  
Author(s):  
Regis Coutant ◽  
Jordi Bosch Muñoz ◽  
Cristina Patricia Dumitrescu ◽  
Dirk Schnabel ◽  
Caroline Sert ◽  
...  

ObjectiveThe International Cooperative Growth Study, NutropinAq® European Registry (iNCGS) (NCT00455728) monitored long-term safety and effectiveness of recombinant human growth hormone (rhGH; NutropinAq® [somatropin]) in paediatric growth disorders.MethodsOpen-label, non-interventional, post-marketing surveillance study recruiting children with growth disorders. Endpoints included gain in height standard deviation score (SDS), adult height, and occurrence of adverse events (AEs).Results2792 patients were enrolled. 2082 patients (74.6%) had growth hormone deficiency (GHD), which was isolated idiopathic in 1825 patients (87.7%). Non-GHD diagnoses included Turner syndrome (TS) (n=199), chronic renal insufficiency (CRI) (n=10), other non-GHD (n=498), and missing data for three participants. Improvements from baseline height SDS occurred at all time points to Month 132, and in all subgroups by disease aetiology. At Month 12, mean (95% CI) change in height SDS by aetiology was: idiopathic GHD 0.63 (0.61;0.66), organic GHD 0.71 (0.62;0.80), TS 0.59 (0.53; 0.65), CRI 0.54 (-0.49;1.56), and other non-GHD 0.64 (0.59;0.69). Mean height ( ± SD) at the last visit among the 235 patients with adult or near-adult height recorded was 154.0 cm ( ± 8.0) for girls and 166.7 cm ( ± 8.0) for boys. The most frequent biological and clinical non-serious drug-related AEs were increased insulin-like growth factor concentrations (314 events) and injection site haematoma (99 events). Serious AEs related to rhGH according to investigators were reported (n=30); the most frequent were scoliosis (4 events), epiphysiolysis (3 events), and strabismus (2 events).ConclusionsThere was an improvement in mean height SDS in all aetiology subgroups after rhGH treatment. No new safety concerns were identified.


2020 ◽  
Author(s):  
Magdalena Kobylińska ◽  
Roksana Ewa Malak ◽  
Katarzyna Majewska ◽  
Włodzimierz Samborski ◽  
Andrzej Kędzia

Abstract Background. Growth hormone plays a vital role in the human body. Its deficiency can lead to numerous disorders, including musculoskeletal system defects. Treatment with recombinant human growth hormone (rhGH) in children suffering from growth hormone deficiency (GHD) increases muscle mass and improves bone structure.Aim. The purpose of this study was to evaluate the angle of trunk rotation (ATR) in patients diagnosed with GHD treated with rhGH and to observe the incidence of scoliosis.Material and Methods. The study was conducted among 50 children diagnosed with GHD. The group consisted of 11 girls and 39 boys aged 6-16. The study group included 50 children: 10 children just qualified for rhGH treatment and 40 patients undergoing this treatment, with different therapy duration. ATR was measured using a Bunnell scoliometer on five levels of the spine: cervical 7 / thoracic 1, thoracic 6, thoracic 12 / lumbar 1, lumbar 3, lumbar 5 / sacral 1.Results. The most numerous asymmetries among the examined group were in the thoracolumbar segment and at the thoracic 6 level. Girls had greater asymmetries compared to boys especially at thoraco – lumbar and lumbar 3 level. There were no statistically significant differences in ATR at any level comparing patients before hormonal treatment and patients undergoing rhGH treatment. The age of the beginning of the therapy, the duration of rhGH therapy, and body mass index (BMI) also had no effect on ATR. Sport activities had a positive impact on the results obtained by scoliometer assessment.Conclusions. The angle of trunk rotation is higher in growth hormone-deficient females than in males. Weight, height, BMI, the time of growth hormone therapy beginning and the duration of this therapy do not influence ATR. The more sport activities, the lower value of the angle of trunk rotation, especially in male patients. Obtained results support the thesis, that treatment with recombinant human growth hormone does not increase the incidence of scoliosis.


Author(s):  
Aurora Aragon-Alonso ◽  
Mark Sherlock ◽  
Andrew A. Toogood

It has been known for many years that growth hormone is essential for normal linear growth, but over the past few years, with the advent of recombinant human growth hormone therapy, the importance of growth hormone during adult life has been described in detail. The growth hormone peptide was first isolated from bovine pituitaries in the 1940s (1), but was found to be species specific and inactive in humans. In 1956, growth hormone was extracted from human cadaveric pituitary tissue (2) and a year later was administered to a 13-year-old boy with hypopituitarism, resulting in an increased growth velocity (3). The first report suggesting growth hormone could have beneficial actions in adulthood was published in 1962 in which a 35-year-old woman with hypopituitarism reported increased vigour, ambition, and wellbeing after 2 months treatment with cadaveric growth hormone (4). However, the limited supply of pituitary-derived growth hormone confined its use to the treatment of children with severe growth failure caused by proven growth hormone deficiency (GHD). In 1985, the association of cadaveric growth hormone treatment with Creutzfeldt–Jakob disease led to its withdrawal from use worldwide (5). Since then, all growth hormone in clinical use has been produced using recombinant DNA technology. The first placebo-controlled trials of growth hormone replacement therapy in adults with GHD were published in 1989 (6, 7). These and subsequent studies have led to the recognition of adult GHD as a specific clinical syndrome and the impact of GHD and replacement therapy in adults with GHD has been studied in detail.


2016 ◽  
Vol 175 (6) ◽  
pp. 633-643 ◽  
Author(s):  
Adam Stevens ◽  
Philip Murray ◽  
Jerome Wojcik ◽  
John Raelson ◽  
Ekaterina Koledova ◽  
...  

Objective Single-nucleotide polymorphisms (SNPs) associated with the response to recombinant human growth hormone (r-hGH) have previously been identified in growth hormone deficiency (GHD) and Turner syndrome (TS) children in the PREDICT long-term follow-up (LTFU) study (Nbib699855). Here, we describe the PREDICT validation (VAL) study (Nbib1419249), which aimed to confirm these genetic associations. Design and methods Children with GHD (n = 293) or TS (n = 132) were recruited retrospectively from 29 sites in nine countries. All children had completed 1 year of r-hGH therapy. 48 SNPs previously identified as associated with first year growth response to r-hGH were genotyped. Regression analysis was used to assess the association between genotype and growth response using clinical/auxological variables as covariates. Further analysis was undertaken using random forest classification. Results The children were younger, and the growth response was higher in VAL study. Direct genotype analysis did not replicate what was found in the LTFU study. However, using exploratory regression models with covariates, a consistent relationship with growth response in both VAL and LTFU was shown for four genes – SOS1 and INPPL1 in GHD and ESR1 and PTPN1 in TS. The random forest analysis demonstrated that only clinical covariates were important in the prediction of growth response in mild GHD (>4 to <10 μg/L on GH stimulation test), however, in severe GHD (≤4 μg/L) several SNPs contributed (in IGF2, GRB10, FOS, IGFBP3 and GHRHR). Conclusions The PREDICT validation study supports, in an independent cohort, the association of four of 48 genetic markers with growth response to r-hGH treatment in both pre-pubertal GHD and TS children after controlling for clinical/auxological covariates. However, the contribution of these SNPs in a prediction model of first-year response is not sufficient for routine clinical use.


1993 ◽  
Vol 128 (4) ◽  
pp. 334-338 ◽  
Author(s):  
K Devriendt ◽  
G Massa ◽  
F de Zegher ◽  
M Vanderschueren-Lodeweyckx ◽  
JJ Cassiman ◽  
...  

Serum levels of pregnancy zone protein were measured in children with growth hormone deficiency and in girls with Turner syndrome, before and during treatment with recombinant human growth hormone and in healthy controls. The pregnancy zone protein serum levels in growth hormone deficiency patients before treatment were significantly higher than in controls (median value 2420 μg/l vs 434 μg/l; p≤0.001). In Turner syndrome patients they were within the normal range. The administration of rhGH to both growth hormone deficiency and Turner syndrome patients resulted in a significant decrease in the serum pregnancy zone protein levels by approximately 50%. The addition of 50 ng·kg−1·d −1 ethinylestradiol to the growth hormone treatment in Turner syndrome patients led to an increase in pregnancy zone protein concentrations in four out of five patients. Elevated pregnancy zone protein levels were also found in two children with growth hormone resistance (Laron type dwarfism). In one patient with placental growth hormone deficiency, pregnancy zone protein serum levels during pregnancy were within the normal range. These results suggest that the serum pregnancy zone protein levels are down-regulated by growth hormone.


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