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Constitutional Growth Delay Follow-up

  • Author: Pamela A Clark, MD; Chief Editor: Stephen Kemp, MD, PhD  more...
Updated: Nov 19, 2015

Further Outpatient Care

Periodic evaluation of height, weight, and stage of sexual development should be performed in children and adolescents with constitutional growth delay (CGD). Plotting of growth parameters on standard growth charts, calculation of growth velocities, and documentation of Tanner stages for genital or breast and pubic hair development should be included.

In addition to the above, adolescent males undergoing testosterone therapy should have an early morning testosterone level obtained a day or so before an injection is due when therapy may need to be discontinued. If the adolescent's endogenous testosterone level is 150 mg/dL or greater, therapy can be stopped and pubertal development can be expected to proceed normally.


Inpatient & Outpatient Medications

Medication therapy is with testosterone enanthate or cypionate (optional for males).



Short-term complications of constitutional growth delay are primarily limited to psychosocial issues resulting from differences in stature and sexual development from peer groups. As infants, delay in bone age may also manifest as delays in motor skills and control of bowel or bladder function as a result of immature muscular development.

Long-term consequences of constitutional growth delay are now recognized and may include height at the lower end of the reference range for an individual's family and osteopenia. The height deficit at the onset of puberty, shorter period between the onset of puberty and the adolescent growth spurt, and lower peak height velocity can contribute to a slightly lower adult height. Data on bone density are more conflicting. Osteopenia during adulthood is a concern because of the potential for reduced bone accrual during adolescence. Bone mineralization increases most in girls aged 11-14 years and in boys aged 14-17 years. More than half of adult bone calcium accumulates during this pubertal period. Delays in circulating sex steroids and resultant increases in growth hormone concentrations may lead to permanent deficiencies in bone mass. Some studies show that, although decreases in total bone that may be related to reduced limb bone mass and size may be present, volumetric density is normal.



Most children with constitutional growth delay attain a normal adult height; however, stature tends to be at the lower end of the reference range for that individual's family because of the lower peak height velocity during the pubertal growth spurt. This observation may also reflect a bias in the individuals studied (more significantly delayed children referred to endocrinologists). Adult height is in contrast to individuals with idiopathic short stature (ISS), in whom stature and growth rate are likely to result in a low adult height (< 61 in for males or < 57 in for females).

Predictions for adult height can be obtained through the use of tables designed to take into consideration current height and skeletal maturation. The Bayley-Pinneau tables are most commonly used to offer predictions for adult stature from a bone age in children aged 6-7 years and older. Different tables are available for normal, early, and late maturers because differences in the tempo of puberty and peak height velocity influence growth potential. Patients and parents should be aware that these predictions are estimates that become more accurate with advancing skeletal maturation.

Constitutional growth delay is not associated with increased mortality because it is a variant of normal growth rather than a disease. However, in some affected individuals, it can be associated with significant psychological stress, resulting in poor self-image and social withdrawal. Researchers have also found that individuals with constitutional growth delay may be at increased risk for reduced bone mass in adulthood because of the delay in sex steroid influence on bone accrual during adolescence.

One compared associations between bone formation markers and resorption and bone mineral density in healthy children and in children with constitutional growth delay. The study concluded that parathyroid hormone was a valuable marker in bone mineralization during puberty and that accelerated bone mineralization was reflected by high serum parathyroid hormone levels during puberty.[10]


Patient Education

Education of patients and their families about normal growth patterns and the role of skeletal age as a predictor of onset and progression of puberty and ultimate height potential are important. Once patients realize that their growth pattern is not pathologic, anxiety is often ameliorated and they are less likely to perceive a need for pharmacologic intervention.

For excellent patient education resources, visit eMedicineHealth's Thyroid and Metabolism Center. Also, see eMedicineHealth's patient education articles Growth Failure in Children, Growth Hormone Deficiency, Growth Hormone Deficiency Medications, and Growth Hormone Deficiency FAQs.

Contributor Information and Disclosures

Pamela A Clark, MD Consulting Staff, McLeod Physician Associates; Consulting Staff, McLeod Pediatric Subspecialists

Pamela A Clark, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

Barry B Bercu, MD Professor, Departments of Pediatrics, Molecular Pharmacology and Physiology, University of South Florida College of Medicine, All Children's Hospital

Barry B Bercu, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Medical Association, American Pediatric Society, Association of Clinical Scientists, Endocrine Society, Florida Medical Association, Pediatric Endocrine Society, Society for Pediatric Research, Southern Society for Pediatric Research, Society for the Study of Reproduction, American Federation for Clinical Research, Pituitary Society

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former 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, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Arlan L Rosenbloom, MD Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida College of Medicine; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology

Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, Florida Chapter of The American Academy of Pediatrics, Florida Pediatric Society, International Society for Pediatric and Adolescent Diabetes

Disclosure: Nothing to disclose.

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Comparison of the growth patterns between idiopathic short stature and constitutional growth delay.
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