Initially, doses comparable with that used in children were given 0. These studies, however, were associated with a high incidence of side-effects including salt and water retention. Later studies, therefore, used half this dose, which decreased the incidence of side-effects and the presence of supranormal levels of serum IGF-I 4 , 6 , In acromegaly, long term excessive GH levels are associated with an increase in morbidity and mortality, mainly due to cardiovascular disorders 17 , With the development of new, high sensitivity assays to measure the serum GH concentration and by using intensified blood sampling over 24 h, the physiological GH production in adults is lower than had been thought for years and is dependent on age and gender 9 , Most studies used a GH dose based on body weight or body surface.
However, several investigators reported a negative correlation between the physiological GH production and body fat 8 , 9. Therefore, using an rhGH dose based on weight is contradictory. The doses used in this study were derived from the physiological GH production 0.
It is widely used to assess disease activity in acromegaly 19 , 22 , 23 , and it is a good screening measurement of GHD in children IGFBP-3 is secreted by many normal cell types, including osteoblasts, endothelial cells, and fibroblasts The underlying mechanism for the difference in biochemical parameters between GHD acquired at childhood or that acquired as an adult is not clear. However, lower organ mass and, thus, synthetic capacity in childhood-onset GHD are plausible, but if organ mass as such is the most important factor in the synthesis of GH-dependent proteins, one would also expect a parallel decrease in serum IGF-I in childhood-onset GHD, which is not the case.
Finally, it is possible, that the metabolism of IGFBP-3 by proteolytic enzymes is different in these two patient groups, but direct evidence for this is lacking. In healthy controls, GH secretion is subject to exquisite metabolic regulation, including rapid negative feedback regulation by serum IGF-I.
Van den Berg et al. Lieberman et al. They reported a higher incremental response in women without estrogen replacement therapy and concluded that orally administered estrogen inhibits the IGF-I response to GH. The hypothesis of a difference in feedback sensitivity of the hypothalamo-pituitary axis can be rejected based on the results of the present study. In active acromegaly, this ratio is increased, and in the elderly, it is decreased.
In summary, this study demonstrates differences in the biochemical characteristics of childhood-onset and adult-onset GHD. This dose could, therefore, be a starting dose in the treatment of GH-deficient adults. Google Scholar. Clin Endocrinol Oxf. J Clin Endocrinol Metab.
Endocr Rev. N Engl J Med. Endocrinol Metab. Horm Res. Q J Med. Zapf J , Froesch ER. Growth Regul. J Pediatr. Acta Endocrinol Copenh. Horm Metab Res. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation.
Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Subjects and Methods. Janssen , Y. Oxford Academic.
Revision received:. Cite Cite Y. Select Format Select format. Permissions Icon Permissions. Table 1. Baseline characteristics of the patients in the three dose groups.
Open in new tab. Open in new tab Download slide. Table 2. P value. Table 3. IGF-I sd score. IGFBP-3 sd score. Baseline 9. Baseline 5. Google Scholar Crossref. Search ADS. Treatment of adults with growth hormone GH deficiency with recombinant human GH. Google Scholar PubMed. The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency.
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Download all slides. View Metrics. Email alerts Article activity alert. Advance article alerts. New issue alert. Receive exclusive offers and updates from Oxford Academic. Each product is produced by recombinant DNA technology and has a sequence identical to that of human GH. Patients with severe GH deficiency in adulthood are defined as patients with known hypothalamic pituitary abnormality and at least one known deficiency of another pituitary hormone excluding prolactin.
These patients should undergo a single diagnostic test in order to diagnose the presence of GH deficiency. In patients with childhood onset isolated GH deficiency no evidence of hypothalamic pituitary abnormality or cranial irradiation , two diagnostic tests should be recommended, except for those having low IGF-1 a marker of GH response concentrations standard deviation score less than -2 who may be considered for one test.
The initial dose is 0. For the first 2—3 months dosage adjustments are made after monthly assessments of serum levels of IGF-1, and in response to the presence of adverse effects, until a maintenance dose is achieved. The currently used median maintenance dose is 0. GH requirements may decrease with age. Benign intracranial hypertension is a rare complication.
GH treatment is also contraindicated during pregnancy and lactation.
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