Growth hormone deficiency natural history, complications and prognosis: Difference between revisions
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==Overview== | ==Overview== | ||
*If left untreated, may progress to develop | *If left untreated, patients with growth hormone deficiency may progress to develop [[Delayed growth;|delayed postnatal growth]], [[Bone age|delayed bone age]], [[delayed puberty]], infantile fat distribution, and infantile voice. Common complications of growth hormone deficiency include [[osteopenia]], [[dyslipidemia]], [[delayed puberty]], and higher mortality rates than normal subjects. Prognosis is generally good with treatment. GH treatment can improve GH-deficient adults symptoms. Since [[Recombinant DNA|recombinant]] DNA–derived growth hormone became available, most children with growth hormone deficiency reach normal adult stature. | ||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
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* Growth typically slows in subsequent years, but usually remains above normal so that over several years a child who had fallen far behind in his height may grow into the normal height range. Excess [[adipose tissue]] may be reduced. | * Growth typically slows in subsequent years, but usually remains above normal so that over several years a child who had fallen far behind in his height may grow into the normal height range. Excess [[adipose tissue]] may be reduced. | ||
* The SOCS2 polymorphism has an influence on the adult height of children with GHD after long-term GH therapy. The use of these genetic markers could identify among rhGH-treated patients those who are genetically predisposed to have less favorable outcomes.<ref name="pmid24905066">{{cite journal| author=Braz AF, Costalonga EF, Trarbach EB, Scalco RC, Malaquias AC, Guerra-Junior G et al.| title=Genetic predictors of long-term response to growth hormone (GH) therapy in children with GH deficiency and Turner syndrome: the influence of a SOCS2 polymorphism. | journal=J Clin Endocrinol Metab | year= 2014 | volume= 99 | issue= 9 | pages= E1808-13 | pmid=24905066 | doi=10.1210/jc.2014-1744 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24905066 }}</ref> | * The SOCS2 polymorphism has an influence on the adult height of children with GHD after long-term [[Growth hormone|GH]] therapy. The use of these genetic markers could identify among rhGH-treated patients those who are genetically predisposed to have less favorable outcomes.<ref name="pmid24905066">{{cite journal| author=Braz AF, Costalonga EF, Trarbach EB, Scalco RC, Malaquias AC, Guerra-Junior G et al.| title=Genetic predictors of long-term response to growth hormone (GH) therapy in children with GH deficiency and Turner syndrome: the influence of a SOCS2 polymorphism. | journal=J Clin Endocrinol Metab | year= 2014 | volume= 99 | issue= 9 | pages= E1808-13 | pmid=24905066 | doi=10.1210/jc.2014-1744 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24905066 }}</ref> | ||
=== Adulthood === | === Adulthood === | ||
* GH treatment can | * GH treatment can improve GH-deficient adults symptoms, such as enhanced energy and strength, and improved [[bone density]]. Muscle mass may increase at the expense of [[adipose tissue]].<ref name="pmid24485161">{{cite journal| author=Díez JJ, Cordido F| title=[Benefits and risks of growth hormone in adults with growth hormone deficiency]. | journal=Med Clin (Barc) | year= 2014 | volume= 143 | issue= 8 | pages= 354-9 | pmid=24485161 | doi=10.1016/j.medcli.2013.11.026 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24485161 }}</ref> | ||
* Although adults with [[hypopituitarism]] have been shown to have a reduced life expectancy, and a cardiovascular [[mortality rate]] more than double controls<ref name="pmid16597813" />, treatment has not been shown to improve [[Mortality rate|mortality]] even after improved [[Blood lipids|blood lipid]] levels.<ref name="pmid9467546">{{cite journal| author=Carroll PV, Christ ER, Bengtsson BA, Carlsson L, Christiansen JS, Clemmons D et al.| title=Growth hormone deficiency in adulthood and the effects of growth hormone replacement: a review. Growth Hormone Research Society Scientific Committee. | journal=J Clin Endocrinol Metab | year= 1998 | volume= 83 | issue= 2 | pages= 382-95 | pmid=9467546 | doi=10.1210/jcem.83.2.4594 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9467546 }}</ref> | * Although adults with [[hypopituitarism]] have been shown to have a reduced life expectancy, and a cardiovascular [[mortality rate]] more than double controls<ref name="pmid16597813" />, treatment has not been shown to improve [[Mortality rate|mortality]] even after improved [[Blood lipids|blood lipid]] levels.<ref name="pmid9467546">{{cite journal| author=Carroll PV, Christ ER, Bengtsson BA, Carlsson L, Christiansen JS, Clemmons D et al.| title=Growth hormone deficiency in adulthood and the effects of growth hormone replacement: a review. Growth Hormone Research Society Scientific Committee. | journal=J Clin Endocrinol Metab | year= 1998 | volume= 83 | issue= 2 | pages= 382-95 | pmid=9467546 | doi=10.1210/jcem.83.2.4594 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9467546 }}</ref> | ||
* Although measurements of [[bone density]] improve with treatment, rates of fractures have not been shown to improve. | * Although measurements of [[bone density]] improve with treatment, rates of fractures have not been shown to improve. |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
- If left untreated, patients with growth hormone deficiency may progress to develop delayed postnatal growth, delayed bone age, delayed puberty, infantile fat distribution, and infantile voice. Common complications of growth hormone deficiency include osteopenia, dyslipidemia, delayed puberty, and higher mortality rates than normal subjects. Prognosis is generally good with treatment. GH treatment can improve GH-deficient adults symptoms. Since recombinant DNA–derived growth hormone became available, most children with growth hormone deficiency reach normal adult stature.
Natural History, Complications, and Prognosis
Natural History
- The symptoms of growth hormone deficiency usually develop in the first days of life and start with symptoms such as perinatal asphyxia, neonatal hypoglycemia, reduced birth length, and prolonged jaundice especially if associated with ACTH deficiency. If left untreated, patients with growth hormone deficiency may progress to develop delayed postnatal growth, delayed bone age, delayed puberty, infantile fat distribution, and infantile voice.
Complications
- Patients less healthy and less energetic than normal people of the same age.
- Fractures of the lumbar spine are somewhat lower in patients with adult-onset GH deficiency.
- The degree of osteopenia appears to correlate directly with the degree of GH deficiency.
- Cardiovascular complications
- Dyslipidemia[7]
- Increased inflammatory markers (ESR)[8]
- Increase in biochemical markers of endothelial dysfunction[9]
- High coronary calcium scores (a marker of subclinical atherosclerosis)[10]
- Mortality
Patients with growth hormone deficiency have a mortality rate twice that of normal subjects, a difference due to an increased number of cardiovascular events.[1]
Prognosis
- Since recombinant DNA–derived growth hormone became available, most children with growth hormone deficiency reach normal adult stature.[2]
- Initiate growth hormone therapy as early as possible and continue therapy through adolescence to ensure the best chance of achieving height potential.
Childhood
- In the first year of treatment, the rate of growth may increase from half as fast as other children are growing to twice as fast.
- Growth typically slows in subsequent years, but usually remains above normal so that over several years a child who had fallen far behind in his height may grow into the normal height range. Excess adipose tissue may be reduced.
- The SOCS2 polymorphism has an influence on the adult height of children with GHD after long-term GH therapy. The use of these genetic markers could identify among rhGH-treated patients those who are genetically predisposed to have less favorable outcomes.[3]
Adulthood
- GH treatment can improve GH-deficient adults symptoms, such as enhanced energy and strength, and improved bone density. Muscle mass may increase at the expense of adipose tissue.[4]
- Although adults with hypopituitarism have been shown to have a reduced life expectancy, and a cardiovascular mortality rate more than double controls[1], treatment has not been shown to improve mortality even after improved blood lipid levels.[5]
- Although measurements of bone density improve with treatment, rates of fractures have not been shown to improve.
References
- ↑ 1.0 1.1 Prabhakar VK, Shalet SM (2006). "Aetiology, diagnosis, and management of hypopituitarism in adult life". Postgrad Med J. 82 (966): 259–66. doi:10.1136/pgmj.2005.039768. PMC 2585697. PMID 16597813.
- ↑ Rosenfeld RG, Wilson DM, Dollar LA, Bennett A, Hintz RL (1982). "Both human pituitary growth hormone and recombinant DNA-derived human growth hormone cause insulin resistance at a postreceptor site". J Clin Endocrinol Metab. 54 (5): 1033–8. doi:10.1210/jcem-54-5-1033. PMID 7037819.
- ↑ Braz AF, Costalonga EF, Trarbach EB, Scalco RC, Malaquias AC, Guerra-Junior G; et al. (2014). "Genetic predictors of long-term response to growth hormone (GH) therapy in children with GH deficiency and Turner syndrome: the influence of a SOCS2 polymorphism". J Clin Endocrinol Metab. 99 (9): E1808–13. doi:10.1210/jc.2014-1744. PMID 24905066.
- ↑ Díez JJ, Cordido F (2014). "[Benefits and risks of growth hormone in adults with growth hormone deficiency]". Med Clin (Barc). 143 (8): 354–9. doi:10.1016/j.medcli.2013.11.026. PMID 24485161.
- ↑ Carroll PV, Christ ER, Bengtsson BA, Carlsson L, Christiansen JS, Clemmons D; et al. (1998). "Growth hormone deficiency in adulthood and the effects of growth hormone replacement: a review. Growth Hormone Research Society Scientific Committee". J Clin Endocrinol Metab. 83 (2): 382–95. doi:10.1210/jcem.83.2.4594. PMID 9467546.