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ISSN: 2081-237X
Pediatric Endocrinology Diabetes and Metabolism
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vol. 30

Human growth hormone therapy – in three stages: past, present, and future

Maciej Hilczer
Mieczysław Walczak

  1. Department of Endocrinology and Metabolic Diseases, Polish Mother`s Memorial Hospital – Research Institute, Lodz Poland
  2. Department of Paediatrics, Endocrinology, Diabetology, Metabolic Disorders, and Cardiology of the Developmental Age, Pomeranian Medical University, Szczecin, Poland
Pediatr Endocrinol Diabetes Metab 2024; 30 (2): 49-50
Online publish date: 2024/07/07
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In 1921 Evans and Long reported the presence of growth-promoting substances in the pituitary glands of rats, indicating a close relationship between the pituitary gland and physical growth [1]. Engelbach in 1932 named “GH” (growth hormone) the substance extracted from the bovine pituitary and reported its effectiveness in children [2].
The start of the history of GH treatment was in 1957 when Raben extracted hGH (human growth hormone) from an acetone-preserved human pituitary gland with glacial acetic acid. Raben reported also the world`s first case of pituitary dwarfism treated with hGH in a 17-year-old boy in 1958.
In Poland pituitary extract hGH – the hormone of the first generation was applied in 1964 by Tomasz E. Romer and Irena Lenartowska. The treatment was administered by intramuscular injection at 0.5 IU/kg b.w./week, divided into 2–3 administrations per week.
The qualification to the GH therapy was then the value of GH response in stimulation tests was of ≤ 5 ng/ml. The auxological criteria to the input of GH therapy were stronger than now, i.e. height standard deviation score (SD) of ≤ –2.5 SD in children aged < 10 years, growth rate < 3 cm/year, and bone age of ≤ 75% of the chronological age.
In 1985 multiple cases of Creutzfeldt-Jakob disease (CJD) were reported in the US and United Kingdom in patients treated with pituitary hGH (pit hGH). It was thought that many pituitary glands collected for hGH extraction might have been accidentally contaminated by the pathogen known as a prion, which caused CJD. IN 1985 the decision was made to discontinue phGH therapy [1].
The introduction of recombinant human GH (rhGH) in 1985 ended the phase of pituitary-derived human growth hormone (hGH) and its associated limitations and risks, opening the possibility of widespread clinical use.
The US is already using Somatonorm, a methionyl hGH containing methionine added by generic engineering, and phGH was removed from the market.
Very quickly the third generation of hGH was manufactured – recombinant DNA technology human growth hormone, 22 kDa, 191 amino-acid-long hGH.
The virtually unlimited supply of rhGH led to the expansion of indications for rhGH therapy, now including childhood and adult GH deficiency, Turner syndrome, chronic renal failure, small for gestational age, Prader-Willi syndrome, Noonan syndrome, SHOX deficiency, idiopathic short stature (ISS), achondroplasia, short bowel syndrome, and HIV wasting...

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recombinant growth hormone, IGF-I LAGH

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