Growth hormone deficiency laboratory findings: Difference between revisions
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==Overview== | ==Overview== | ||
==Laboratory Findings== | ==Laboratory Findings== | ||
=== Neonatal and children evaluation === | |||
==== ''Testing in the neonate'' ==== | |||
A GH level should always be measured | |||
in the presence of neonatal hypoglycemia in the absence of | |||
a metabolic disorder. A random GH measurement in a polyclonal | |||
RIA of less than 20 mg/L would suggest GHD in the | |||
newborn. An IGFBP-3 measurement is of value for the diagnosis | |||
of GHD in infancy. | |||
==== Children evaluation ==== | |||
Criteria to initiate immediate investigation include | |||
1) severe short stature, defined as a height more than 3 sd | |||
below the mean; | |||
2) height more than 1.5 sd below the midparental | |||
height; | |||
3) height more than 2 sd below the mean and | |||
a height velocity over 1 yr more than 1 sd below the mean | |||
for chronological age, or a decrease in height sd of more than | |||
0.5 over 1 yr in children over 2 yr of age; | |||
4) in the absence of short stature, a height velocity more than 2 sd below the | |||
mean over 1 yr or more than 1.5 sd sustained over 2 yr; this | |||
may occur in GHD, presenting in infancy, or in organic | |||
acquired GHD; | |||
5) signs indicative of an intracranial lesion; | |||
7) neonatal symptoms and signs of | |||
GHD. | |||
The evaluation for GHD in a short child, where short stature is defined as a height more than 2 sd below the population mean, should not be initiated until other causes of growth failure, such as hypothyroidism, chronic systemic disease, Turner syndrome, or skeletal disorder, have been considered and appropriately excluded. | |||
GH secretion is pulsatile and its secretion is regulated by two hypothalamic factors; growth hormone releasing hormone and somatostatin.<ref name="pmid20161791">{{cite journal| author=Osterstock G, Escobar P, Mitutsova V, Gouty-Colomer LA, Fontanaud P, Molino F et al.| title=Ghrelin stimulation of growth hormone-releasing hormone neurons is direct in the arcuate nucleus. | journal=PLoS One | year= 2010 | volume= 5 | issue= 2 | pages= e9159 | pmid=20161791 | doi=10.1371/journal.pone.0009159 | pmc=2820089 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20161791 }}</ref> | GH secretion is pulsatile and its secretion is regulated by two hypothalamic factors; growth hormone releasing hormone and somatostatin.<ref name="pmid20161791">{{cite journal| author=Osterstock G, Escobar P, Mitutsova V, Gouty-Colomer LA, Fontanaud P, Molino F et al.| title=Ghrelin stimulation of growth hormone-releasing hormone neurons is direct in the arcuate nucleus. | journal=PLoS One | year= 2010 | volume= 5 | issue= 2 | pages= e9159 | pmid=20161791 | doi=10.1371/journal.pone.0009159 | pmc=2820089 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20161791 }}</ref> | ||
| Line 33: | Line 84: | ||
* In a patient with other pituitary hormone defects or a genetic defect, one test is sufficient to establish the diagnosis.<ref name="pmid18425584">{{cite journal| author=Richmond EJ, Rogol AD| title=Growth hormone deficiency in children. | journal=Pituitary | year= 2008 | volume= 11 | issue= 2 | pages= 115-20 | pmid=18425584 | doi=10.1007/s11102-008-0105-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18425584 }}</ref> | * In a patient with other pituitary hormone defects or a genetic defect, one test is sufficient to establish the diagnosis.<ref name="pmid18425584">{{cite journal| author=Richmond EJ, Rogol AD| title=Growth hormone deficiency in children. | journal=Pituitary | year= 2008 | volume= 11 | issue= 2 | pages= 115-20 | pmid=18425584 | doi=10.1007/s11102-008-0105-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18425584 }}</ref> | ||
* Pharmacologic stimuli include clonidine, glucagon, arginine, and insulin-induced hypoglycemia:<ref name="pmid169508">{{cite journal| author=| title=Stimulation of growth hormone secretion by levodopa-propranolol in children and adolescents. | journal=Pediatrics | year= 1975 | volume= 56 | issue= 2 | pages= 262-6 | pmid=169508 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=169508 }}</ref> | * Pharmacologic stimuli include clonidine, glucagon, arginine, and insulin-induced hypoglycemia:<ref name="pmid169508">{{cite journal| author=| title=Stimulation of growth hormone secretion by levodopa-propranolol in children and adolescents. | journal=Pediatrics | year= 1975 | volume= 56 | issue= 2 | pages= 262-6 | pmid=169508 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=169508 }}</ref> | ||
The interpretation of the test results depends upon age and sex hormone concentrations.Children with constitutional delay of growth and puberty may have low GH results on provocative testing in the absence of true GHD (ie, false-positive results). Administration of sex steroids for a few days prior to the provocative GH testing reduces the chance of a false-positive result, as discussed below. | The interpretation of the test results depends upon age and sex hormone concentrations.Children with constitutional delay of growth and puberty may have low GH results on provocative testing in the absence of true GHD (ie, false-positive results). Administration of sex steroids for a few days prior to the provocative GH testing reduces the chance of a false-positive result, as discussed below. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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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
Laboratory Findings
Neonatal and children evaluation
Testing in the neonate
A GH level should always be measured
in the presence of neonatal hypoglycemia in the absence of
a metabolic disorder. A random GH measurement in a polyclonal
RIA of less than 20 mg/L would suggest GHD in the
newborn. An IGFBP-3 measurement is of value for the diagnosis
of GHD in infancy.
Children evaluation
Criteria to initiate immediate investigation include
1) severe short stature, defined as a height more than 3 sd
below the mean;
2) height more than 1.5 sd below the midparental
height;
3) height more than 2 sd below the mean and
a height velocity over 1 yr more than 1 sd below the mean
for chronological age, or a decrease in height sd of more than
0.5 over 1 yr in children over 2 yr of age;
4) in the absence of short stature, a height velocity more than 2 sd below the
mean over 1 yr or more than 1.5 sd sustained over 2 yr; this
may occur in GHD, presenting in infancy, or in organic
acquired GHD;
5) signs indicative of an intracranial lesion;
7) neonatal symptoms and signs of
GHD.
The evaluation for GHD in a short child, where short stature is defined as a height more than 2 sd below the population mean, should not be initiated until other causes of growth failure, such as hypothyroidism, chronic systemic disease, Turner syndrome, or skeletal disorder, have been considered and appropriately excluded.
GH secretion is pulsatile and its secretion is regulated by two hypothalamic factors; growth hormone releasing hormone and somatostatin.[1]
So, measurement of a random serum GH level alone is not helpful and usually other tests used with it:
- Insulin-like growth factor I (IGF-I)
- Insulin-like growth factor binding protein-3 (IGFBP-3) levels: it is the major serum carrier protein for IGF-I and the most GH dependent.[2]
- Their concentrations often reflect the concentration of secreted GH.[3]They are better tests than GH level because they are stable during the day and not pulsatile.[4]
Limitations
Serum IGF-I levels may be low in conditions other than GHD such as growth hormone insensitivity, hypothyroidism, renal failure, diabetes, and cancer.[5]
Interpretation
- Reduced level of IGF-I and IGFBP-3 with delayed bone age: provocative GH testing is needed. If the growth failure is severe and IGF-I and IGFBP-3 are severely low, there is no need to perform GH stimulation testing.
- Normal IGF-1 and IGFBP-3: no further testing is required.
GH stimulation tests
- It is indicated for most patients suspected to have GHD.
- The results should be interpreted in the context of auxological findings, bone age, and IGF-1 and IGFBP-3 concentrations.
- If the clinical and other laboratory criteria are sufficient to make the diagnosis of GHD, there is no need to perform the test.
- A serum GH concentration of >10 mcg/L, but a cutoff of 7.5 mcg/L is often used for modern assays.
- The stimulation tests are performed after an overnight fast. Serum samples are collected at intervals to capture the peak GH level.
- Two different stimuli should be used for most patients.[6]
- In a patient with other pituitary hormone defects or a genetic defect, one test is sufficient to establish the diagnosis.[7]
- Pharmacologic stimuli include clonidine, glucagon, arginine, and insulin-induced hypoglycemia:[8]
The interpretation of the test results depends upon age and sex hormone concentrations.Children with constitutional delay of growth and puberty may have low GH results on provocative testing in the absence of true GHD (ie, false-positive results). Administration of sex steroids for a few days prior to the provocative GH testing reduces the chance of a false-positive result, as discussed below.
References
- ↑ Osterstock G, Escobar P, Mitutsova V, Gouty-Colomer LA, Fontanaud P, Molino F; et al. (2010). "Ghrelin stimulation of growth hormone-releasing hormone neurons is direct in the arcuate nucleus". PLoS One. 5 (2): e9159. doi:10.1371/journal.pone.0009159. PMC 2820089. PMID 20161791.
- ↑ Baxter RC, Martin JL (1986). "Radioimmunoassay of growth hormone-dependent insulinlike growth factor binding protein in human plasma". J Clin Invest. 78 (6): 1504–12. doi:10.1172/JCI112742. PMC 423906. PMID 2431001.
- ↑ Nunez SB, Municchi G, Barnes KM, Rose SR (1996). "Insulin-like growth factor I (IGF-I) and IGF-binding protein-3 concentrations compared to stimulated and night growth hormone in the evaluation of short children--a clinical research center study". J Clin Endocrinol Metab. 81 (5): 1927–32. doi:10.1210/jcem.81.5.8626859. PMID 8626859.
- ↑ Martha PM, Rogol AD, Veldhuis JD, Kerrigan JR, Goodman DW, Blizzard RM (1989). "Alterations in the pulsatile properties of circulating growth hormone concentrations during puberty in boys". J Clin Endocrinol Metab. 69 (3): 563–70. doi:10.1210/jcem-69-3-563. PMID 2760171.
- ↑ Powell DR, Rosenfeld RG, Baker BK, Liu F, Hintz RL (1986). "Serum somatomedin levels in adults with chronic renal failure: the importance of measuring insulin-like growth factor I (IGF-I) and IGF-II in acid-chromatographed uremic serum". J Clin Endocrinol Metab. 63 (5): 1186–92. doi:10.1210/jcem-63-5-1186. PMID 3760118.
- ↑ Grimberg A, DiVall SA, Polychronakos C, Allen DB, Cohen LE, Quintos JB; et al. (2016). "Guidelines for Growth Hormone and Insulin-Like Growth Factor-I Treatment in Children and Adolescents: Growth Hormone Deficiency, Idiopathic Short Stature, and Primary Insulin-Like Growth Factor-I Deficiency". Horm Res Paediatr. 86 (6): 361–397. doi:10.1159/000452150. PMID 27884013.
- ↑ Richmond EJ, Rogol AD (2008). "Growth hormone deficiency in children". Pituitary. 11 (2): 115–20. doi:10.1007/s11102-008-0105-7. PMID 18425584.
- ↑ "Stimulation of growth hormone secretion by levodopa-propranolol in children and adolescents". Pediatrics. 56 (2): 262–6. 1975. PMID 169508.