Growth Failure Workup

  • Author: Stephen Kemp, MD, PhD; Chief Editor: Bruce Buehler, MD   more...
 
Updated: Apr 13, 2012
 

Laboratory Studies

  • Thyroxine (T4) and thyroid-stimulating hormone (TSH): T4 and TSH levels are important to rule out hypothyroidism and to screen for panhypopituitarism as a cause for short stature and growth failure.
  • Serum electrolytes: A low bicarbonate level may indicate renal tubular acidosis, which can result in growth failure. Electrolyte levels out of the reference range may indicate renal failure. Hypokalemic alkalosis may indicate Bartter syndrome.
  • CBC count and sedimentation rate: These tests may be helpful if inflammatory bowel disease is suspected.
  • IGF-1 and IGFBP-3: Both IGF-1 and the binding protein IGFBP-3 are growth hormone (GH) dependent. Low values suggest growth hormone deficiency. However, they are also sensitive to other factors such as nutritional state, so a low value alone is not diagnostic of growth hormone deficiency.
  • Karyotype: Girls with otherwise unexplained short stature should have karyotype determined to rule out Turner syndrome. Although Turner syndrome is diagnosed in many girls from signs present on physical examination, some girls with Turner syndrome have short stature as the only recognizable feature. In particular, girls with mosaic karyotypes or karyotypes with isochromosomes tend to exhibit fewer signs specific to Turner syndrome.
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Imaging Studies

  • MRI of the head: Patients who are diagnosed with growth hormone deficiency should undergo MRI of the head to rule out a brain tumor, such as a craniopharyngioma. As many as 10% of children diagnosed with a craniopharyngioma present with growth failure as the only sign. Also, approximately 15% of patients with growth hormone deficiency have an abnormality of the pituitary gland, such as an ectopic bright spot, an empty sella, or a small sella. Discovery of one of these conditions aids diagnosis of growth hormone deficiency and significantly increases the probability that such a patient requires lifelong growth hormone replacement.
  • Bone age determination: A radiograph of the left wrist can be compared with standards to provide an estimation of skeletal maturation. Bone age also provides a determination of growth potential (predicted adult stature may be estimated from the tables of Bayley and Pinneau).
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Other Tests

  • Growth hormone response to insulin has been considered the most reliable test for growth hormone deficiency. For recognition of the diagnosis of growth hormone deficiency, many insurance companies require documenting a failure to demonstrate a growth hormone response (with a growth hormone level >10 ng/mL) to 2 provocative stimuli. Provocative stimuli include insulin-induced hypoglycemia, arginine, levodopa (L-dopa), clonidine, and glucagon.
  • Over time, the potential growth hormone supply has increased, and the peak growth hormone level considered "adequate" has increased to 10 ng/mL. In true (or classic) growth hormone deficiency, the peak growth hormone response to provocative stimuli is probably less than 5 ng/mL. Children who have classic growth hormone deficiency robustly respond to relatively small doses of growth hormone (especially during the early part of treatment), particularly in terms of growth velocity. However, many patients who have peaks in the 5-10 ng/mL range in response to growth hormone provocative agents may also respond well to growth hormone therapy.[6] In fact, no great difference in terms of response to GH is noted between this group and those whose growth hormone provocative tests are read as adequate (ie, a growth hormone peak >10 ng/mL). This latter category has been called idiopathic short stature.
  • Because of these issues, in 2003, the US Food and Drug Administration (FDA) approved growth hormone therapy for especially short children (height >2.25 standard deviations below the mean) who are not growth hormone deficient and thus fall into the category of idiopathic short stature. Also, because growth hormone testing with provocative agents uses a cut-off peak growth hormone level of 10 ng/mL, some practitioners have avoided these growth hormone provocative tests. However, the author believes that recognizing children who are severely growth hormone deficient (classic growth hormone deficiency) is valuable because these children may be more at risk for other pituitary hormone deficiencies and are much more likely to need lifelong growth hormone replacement.
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Contributor Information and Disclosures
Author

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Neslihan Gungor, MD  Instructor, Department of Pediatrics, Section of Endocrinology, Children's Hospital of Pittsburgh and University of Pittsburgh

Neslihan Gungor, MD is a member of the following medical societies: American Academy of Pediatrics and American Association of Clinical Endocrinologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Thomas A Wilson, MD  Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London)  Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Merrily P M Poth, MD  Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences

Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Bruce Buehler, MD  Professor, Department of Pediatrics and Genetics, Director RSA, University of Nebraska Medical Center

Bruce Buehler, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Pediatrics, American Association on Mental Retardation, American College of Medical Genetics, American College of Physician Executives, American Medical Association, and Nebraska Medical Association

Disclosure: Nothing to disclose.

References

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  3. Lacey KA, Parkin JM. Causes of short stature. A community study of children in Newcastle upon Tyne. Lancet. Jan 12 1974;1(7846):42-5. [Medline].

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  6. Richmond E, Rogol AD. Current indications for growth hormone therapy for children and adolescents. Endocr Dev. 2010;18:92-108. [Medline].

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  10. Hintz RL. Growth hormone treatment of idiopathic short stature. Horm Res. 1996;46(4-5):208-14. [Medline].

  11. Hintz RL. Disorders of growth. In: Brunwald E, Fauci AS, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill Medical Publishing Division; 1994.

  12. Horner JM, Thorsson AV, Hintz RL. Growth deceleration patterns in children with constitutional short stature: an aid to diagnosis. Pediatrics. Oct 1978;62(4):529-34. [Medline].

  13. Kojima M, Hosoda H, Date Y. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. Dec 9 1999;402(6762):656-60. [Medline].

  14. Kojima M, Hosoda H, Matsuo H. Ghrelin: discovery of the natural endogenous ligand for the growth hormone secretagogue receptor. Trends Endocrinol Metab. Apr 2001;12(3):118-22. [Medline].

  15. Stabler B, Clopper RR, Siegel PT, et al. Academic achievement and psychological adjustment in short children. The National Cooperative Growth Study. J Dev Behav Pediatr. Feb 1994;15(1):1-6. [Medline].

  16. Stabler B, Siegel PT, Clopper RR, et al. Behavior change after growth hormone treatment of children with short stature. J Pediatr. Sep 1998;133(3):366-73. [Medline].

  17. Tanner JM. Fetus into Man: Physical Growth from Conception to Maturity. Cambridge, Mass: Harvard University Press; 1990.

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  19. Zemel B. The recognition and treatment of growth disorders - a 50-year retrospective. Ann Hum Biol. Sep-Oct 2009;36(5):496-510. [Medline].

 
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Growth failure in length and weight with a normal head circumference in an infant with growth hormone deficiency.
 
 
 
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