Two Years of Growth Hormone (GH) Treatment Increases Bone Mineral Content and Density in Hypopituitary Patients with Adult-Onset GH Deficiency

1996 ◽  
Vol 6 (6) ◽  
pp. 498
Author(s):  
&NA;
1994 ◽  
Vol 131 (1) ◽  
pp. 41-49 ◽  
Author(s):  
Anders Juul ◽  
Søren A Pedersen ◽  
Steen Sørensen ◽  
Kjeld Winkler ◽  
Jens OL Jørgensen ◽  
...  

Juul A, Pedersen SA, Sørensen S, Winkler K, Jørgensen JOL, Christiansen JS, Skakkebæk NE. Growth hormone (GH) treatment increases serum insulin-like growth factor binding protein- bone isoenzyme alkaline phosphatase and forearm bone mineral content in young adults with GH deficiency of childhood onset. Eur J Endocrinol 1994;131:41–9. ISSN 0804–4643 Recent studies have demonstrated that growth hormone (GH)-deficient adults have a markedly decreased bone mineral content compared to healthy adults. However, there are conflicting results regarding the effects of GH treatment on bone mineral content in GH-deficient adults. Therefore, we evaluated the effect of GH treatment on a marker of bone formation (bone alkaline phosphatase), hepatic excretory function and distal forearm bone mineral content in GH-deficient adults. Growth hormone was administered subcutaneously in 21 adults (13 males and 8 females) with GH deficiency of childhood onset for 4 months in a double-blind, placebo-controlled GH trial, while 13 of the patients then received further GH for an additional 14 months. Serum insulin-like growth factor I (IGF-I) increased significantly from 100 to 279 μg/l and IGF binding protein-3 (IGFBP-3) from 1930 to 3355 μg/l after 4 months of GH treatment (p < 0.0001). In addition, the molar ratio between IGF-I and IGFBP-3 increased significantly from 0.22 to 0.33 after GH treatment (p < 0.0001), Bone alkaline phosphatase increased significantly from 38.6 to 92.9 U/l during GH therapy in male patients (p < 0.0001), whereas liver-derived alkaline phosphatase was unaltered by GH. In the females, the increase in bone alkaline phosphatase did not reach statistical significance (19.1 vs 40.0 U/l, p = 0.06). The GH-induced increase in bone alkaline phosphatase correlated significantly with the increase in serum IGFBP-3 (r = 0.46, p = 0.04) but not with the increase in serum IGF-I (p = 0.16). Liver function as assessed by the galactose elimination capacity was within the normal range for healthy adults and did not change after GH treatment. Bone mineral content increased significantly between 7 and 14 months of GH treatment (mean increase in bone mineral content Z score = 0.24 sd/ 7 months), but remained low even after 14 months of GH treatment (Z score = –2.2 ± 0.24 (mean ± sem)). We conclude that GH administration increases serum levels of bone-derived alkaline phosphatase in male patients and has a potentially beneficial impact on bone mineral content in young adults with GH deficiency of childhood onset. Anders Juul, Department of Growth and Reproduction, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark


Endocrinology ◽  
1996 ◽  
Vol 137 (8) ◽  
pp. 3368-3374 ◽  
Author(s):  
J Sandstedt ◽  
J Törnell ◽  
E Norjavaara ◽  
O G Isaksson ◽  
C Ohlsson

2009 ◽  
Vol 10 (9) ◽  
pp. 1352-1358 ◽  
Author(s):  
Harold N. Rosen ◽  
Vicki Chen ◽  
Antonio Cittadini ◽  
Susan L. Greenspan ◽  
Pamela S. Douglas ◽  
...  

2001 ◽  
Vol 24 (4) ◽  
pp. 224-230 ◽  
Author(s):  
Alessandro Sartorio ◽  
S. Ortolani ◽  
E. Galbiati ◽  
G. Conte ◽  
V. Vangeli ◽  
...  

2019 ◽  
Vol 181 (6) ◽  
pp. 629-638 ◽  
Author(s):  
Charlotte Höybye ◽  
Pia Burman ◽  
Ulla Feldt-Rasmussen ◽  
Judith Hey-Hadavi ◽  
Ferah Aydin ◽  
...  

Objective Clinical observations over time of adults with growth hormone (GH) deficiency (GHD) have indicated a shift in patient characteristics at diagnosis. The objective of this study was to compare baseline characteristics of patients diagnosed with adult-onset GHD naive to GH replacement during three study periods (1994–1999 (P1), 2000–2004 (P2), and 2005–2012 (P3)) using the KIMS (Pfizer’s International Metabolic) database. Methods Data were retrieved for a total of 6069 patients with adult-onset GHD from six countries (Belgium, Germany, Netherlands, Spain, Sweden, and UK): P1 (n = 1705), P2 (n = 2397), and P3 (n = 1967). Results The proportions of patients with pituitary/hypothalamic tumors and patients with multiple pituitary hormone deficiencies decreased per entry year period, while the proportions with hypertension and diabetes increased. The lag time from diagnosis of pituitary disease to start of GH treatment decreased by 2.9 years over the entry year periods. IGF-1 increased by 0.1 standard deviation score per entry year period. Maximum GH following various stimulation tests, BMI, and waist circumference increased. The use of radiotherapy, glucocorticoid replacement doses, and the proportion of women >50 years on estrogen replacement therapy decreased. The effects of 1 year of GH replacement were similar over the entry year periods despite changes in the patients’ baseline characteristics. An expected increase in fasting blood glucose was seen after 1 year of GH treatment. Conclusions The degree of confirmed GHD became less pronounced and more patients with co-morbidities and diabetes were considered for GH replacement therapy, possibly reflecting increased knowledge and confidence in GH therapy gained with time.


2002 ◽  
Vol 87 (7) ◽  
pp. 3368-3372 ◽  
Author(s):  
Andrea F. Attanasio ◽  
Simon Howell ◽  
Peter C. Bates ◽  
Paul Frewer ◽  
John Chipman ◽  
...  

If GH therapy of children with GH deficiency (GHD) has been adequate, body composition should be comparable to that of patients who have undergone normal childhood development and become hypopituitary thereafter. To assess this, body composition was determined in 92 patients with childhood onset (CO) GHD, aged 18–30 yr, who had been treated to final height with GH for 8.98 ± 4.30 yr and had stopped treatment 1.57 ± 1.20 yr previously, but who remained GHD (assessed by a GH stimulation test and IGF-I values). These were compared with 35 age-matched GH-naïve hypopituitary patients with adult onset (AO) GHD. Lean body mass, fat mass, and total bone mineral content were assessed by dual energy x-ray absorptiometry and corrected for actual height. CO patients were shorter (CO height, −1.18 ± 1.16 sd score; AO height, −0.38 ± 1.12 sd score; P &lt; 0.001) and had lower body mass index (CO, 23.19 ± 5.76 kg/m2; AO, 28.9 ± 6.27 kg/m2; P &lt; 0.001) than the AO group. Although there were gender differences, within genders CO patients had lower lean body mass, fat mass, and bone mineral content (P &lt; 0.001 in all cases) compared with AO patients. Standard deviation scores for IGF-I (CO female, −9.2 ± 3.1; AO female, −5.2 ± 2.6; CO male, −6.4 ± 2.7; AO male, −3.5 ± 2.3; P &lt; 0.001 within each gender) and IGFBP-3 (CO female, −3.5 ± 2.5; AO female, −1.7 ± 1.5; CO male, −2.8 ± 2.0; AO male, −1.1 ± 1.6; P &lt; 0.001 within each gender) were significantly lower in the CO group. These results suggest that patients with CO GHD who were treated to final height suffer a significant maturational deficit despite GH replacement during childhood.


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