Growth hormone deficiency natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]
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
- Increased risk of recurrent illnesses when compared to their counterparts
- Fractures of the lumbar spine are somewhat lower in patients with adult-onset GH deficiency[1]
- The degree of osteopenia appears to correlate directly with the degree of GH deficiency[2]
- Cardiovascular complications:
- Dyslipidemia[3]
- Increased inflammatory markers (ESR)[4]
- Increased biochemical markers of endothelial dysfunction[5]
- High coronary calcium scores (a marker of subclinical atherosclerosis)
- 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.[6]
Prognosis
- Recombinant DNA–derived growth hormone has significantly improved the prognosis of growth hormone deficiency.[7]
- If initiated early, children with growth hormone deficiency tend to achieve normal height potential.
Childhood
- In the first year of treatment, the growth rate may increase from half as fast as other children are growing to twice as fast.
- Growth typically slows in the following years but remains above normal.
- As a result, the treated child may grow into the normal height range. Excess adipose tissue may be reduced.
- The SOCS2 polymorphism is a genetic marker that could identify among GH-treated patients who are predisposed to have less favorable outcomes.[8]
Adulthood
- GH treatment can improve symptoms such as lack of energy and can improve bone density.
- Muscle mass may increase with decreased adipose tissue.[9]
- Adults with hypopituitarism have been shown to have a reduced life expectancy and a cardiovascular mortality rate more than normal.[6]
- Treatment has not improved mortality even after improved blood lipid levels.[10]
- Rates of fractures have not been shown to improve, although, bone density improve with treatment.
References
- ↑ Kužma M, Binkley N, Bednárová A, Killinger Z, Vaňuga P, Payer J (2016). "TRABECULAR BONE SCORE CHANGE DIFFERS WITH REGARD TO 25(OH)D LEVELS IN PATIENTS TREATED FOR ADULT-ONSET GROWTH HORMONE DEFICIENCY". Endocr Pract. 22 (8): 951–8. doi:10.4158/EP151183.OR. PMID 27042750.
- ↑ Mazziotti G, Doga M, Frara S, Maffezzoni F, Porcelli T, Cerri L; et al. (2016). "Incidence of morphometric vertebral fractures in adult patients with growth hormone deficiency". Endocrine. 52 (1): 103–10. doi:10.1007/s12020-015-0738-z. PMID 26433736.
- ↑ B. A. Bengtsson, R. Abs, H. Bennmarker, J. P. Monson, U. Feldt-Rasmussen, E. Hernberg-Stahl, B. Westberg, P. Wilton & C. Wuster (1999). "The effects of treatment and the individual responsiveness to growth hormone (GH) replacement therapy in 665 GH-deficient adults. KIMS Study Group and the KIMS International Board". The Journal of clinical endocrinology and metabolism. 84 (11): 3929–3935. doi:10.1210/jcem.84.11.6088. PMID 10566630. Unknown parameter
|month=ignored (help) - ↑ B. A. Bengtsson, R. Abs, H. Bennmarker, J. P. Monson, U. Feldt-Rasmussen, E. Hernberg-Stahl, B. Westberg, P. Wilton & C. Wuster (1999). "The effects of treatment and the individual responsiveness to growth hormone (GH) replacement therapy in 665 GH-deficient adults. KIMS Study Group and the KIMS International Board". The Journal of clinical endocrinology and metabolism. 84 (11): 3929–3935. doi:10.1210/jcem.84.11.6088. PMID 10566630. Unknown parameter
|month=ignored (help) - ↑ T. A. Elhadd, T. A. Abdu, J. Oxtoby, G. Kennedy, M. McLaren, R. Neary, J. J. Belch & R. N. Clayton (2001). "Biochemical and biophysical markers of endothelial dysfunction in adults with hypopituitarism and severe GH deficiency". The Journal of clinical endocrinology and metabolism. 86 (9): 4223–4232. doi:10.1210/jcem.86.9.7813. PMID 11549653. Unknown parameter
|month=ignored (help) - ↑ 6.0 6.1 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.