Constitutional Growth Delay 

Updated: Jan 08, 2019
Author: Pamela A Clark, MD; Chief Editor: Sasigarn A Bowden, MD 


Practice Essentials

Children with constitutional growth delay (CGD), the most common cause of short stature and pubertal delay,[1] typically have retarded linear growth within the first 3 years of life. In this variant of normal growth, linear growth velocity and weight gain slows beginning as young as age 3-6 months, resulting in downward crossing of growth percentiles, which often continues until age 2-3 years. At that time, growth resumes at a normal rate, and these children grow either along the lower growth percentiles or beneath the curve but parallel to it for the remainder of the prepubertal years.

See the image below.

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

At the expected time of puberty, the height of children with constitutional growth delay begins to drift further from the growth curve because of delay in the onset of the pubertal growth spurt. Catch-up growth, onset of puberty, and pubertal growth spurt occur later than average, resulting in normal adult stature and sexual development.

However, a report by Rohani et al on males with constitutional growth delay—mean age 15.2 years at presentation and 20 years at study’s end—found that the majority of patients attained neither their target height nor their predicted adult height. The mean final or near-final height reached by the subjects was 165.7 cm, compared with a predicted adult height of 170.7 cm and a target height of 171.8 cm.[2]

Although constitutional growth delay is a variant of normal growth rather than a disorder, delays in growth and sexual development may contribute to psychological difficulties, warranting treatment for some individuals. Studies have suggested that referral bias is largely responsible for the impression that normal short stature per se is a cause of psychosocial problems; nonreferred children with short stature do not differ from those with more normal stature in school performance or socialization.


Constitutional growth delay is a global delay in development that affects every organ system. Delays in growth and sexual development are quantified by skeletal age, which is determined from bone age radiographic studies of the left hand and wrist. Growth and development are appropriate for an individual's biologic age (skeletal age) rather than for their chronologic age. Timing and tempo of growth and development are delayed in accordance with the biologic state of maturity. Constitutional growth delay may be inherited as an autosomal dominant, recessive, or X-linked trait.[3]


US frequency

Approximately 15% of patients with short stature referred for endocrinologic evaluation have constitutional growth delay. Individuals with constitutional growth delay and familial short stature represent another 23%. The frequency of constitutional growth delay may be underestimated because individuals with milder delays and those who are not psychologically stressed may not be seen by subspecialists. In a study of 555 (out of 80,000) schoolchildren below the third percentile in height for age with growth rates below normal (< 5 cm/y), twice as many boys as girls were affected. Constitutional growth delay was found in 28% of boys and 24% of girls, and another 18% of boys and 16% of girls had familial short stature in combination with constitutional growth delay.


No racial bias has been identified.


Although the epidemiologic data indicate that all variants of normal growth are twice as common in boys as in girls, referrals for short stature reflect an even more divergent sex ratio. This likely reflects greater concern about males who are shorter than their peers or who have delayed sexual development.


Patterns of growth consistent with constitutional growth delay occur in infants as young as 3-6 months. However, individuals often do not seek medical attention until puberty, when lack of sexual development becomes a concern and discrepancy in height from peers is magnified by the delay in pubertal growth spurt.




Individuals with constitutional growth delay (CGD) are usually of normal size at birth. Deceleration in both height and weight velocity typically occurs within the first 3-6 months of life. This shift downward is similar to that observed in infants experiencing normal lag-down growth but tends to be more severe and prolonged. Individual variation is substantial; however, most children resume a normal growth velocity by age 2-3 years. During childhood, these individuals grow along or parallel to the lower percentiles of the growth curve.

Indeed, looking at height changes from birth to age 5 years, a study by Rothermel et al found that in children with either constitutional growth delay or familial short stature, there was a greater decrease in the height standard deviation score (SDS) in the first 2 years of life than between ages 2 and 5 years, while in children with idiopathic growth hormone deficiency, there was a steady decrease in height SDS during the first 5 years of life.[4]

Skeletal age, which is estimated from radiographic studies of the left hand and wrist, is usually delayed in constitutional growth delay (typically 2-4 y by late childhood) and is most consistent with the child's height age (age for which a child's height is at the 50th percentile) rather than the child’s chronologic age.

Because the timing of the onset of puberty, pubertal growth spurt, and epiphyseal fusion are determined by a child's skeletal age (biologic age), children with constitutional growth delay are often referred to as "late bloomers."

At the usual age for puberty, these children continue to grow at a prepubertal rate appropriate for their biologic stage of development. Natural slowing of linear growth just before onset of puberty may be exaggerated, emphasizing the difference in size from peers who are accelerating in growth. The timing of the pubertal growth spurt is delayed, and the spurt may be prolonged with a lower peak height velocity. In patients with both constitutional growth delay and familial short stature, the degree of growth retardation may appear more severe, but the adult height is appropriate for the genetic background.


Physical examination findings in patients with constitutional growth delay are essentially normal, with the exception of immature appearance for age. Body proportions may reflect the delay in growth. During childhood, the upper-to-lower body ratio may be greater than normal, reflecting more infantile proportions. In adults, the ratio is often reduced (ie, < 1 in whites, < 0.9 in blacks) as a result of the longer period of leg (long bone) growth.[5]


Constitutional growth delay is thought to be inherited from multiple genes from both parents. The strong role of heredity is reflected in the 60-90% likelihood of this growth pattern in a family member of the same or opposite sex. A delay in the reactivation of the hypothalamic-pituitary pulse generator results in a later onset of puberty.[5, 6]





Laboratory Studies

Constitutional growth delay (CGD) in children with slow growth or delayed puberty is a diagnosis of exclusion. Evaluation excludes hormonal deficiencies, occult systemic illness, or syndromes associated with growth impairment as potential underlying causes.

Hormonal evaluation

Thyroid function

Thyroxine (T4) and thyroid-stimulating hormone (TSH) levels are within the reference range in patients with constitutional growth delay.

GH production

Random growth hormone (GH) values are of little use because of the pulsatile fashion in which GH is secreted by the pituitary. Rather, levels of insulinlike growth factor-1 (IGF-1) and its major binding protein (IGFBP-3) are measured. They are a reliable reflection of GH production if malnutrition is not a concern. IGF-1 and IGFBP-3 levels are sex and age specific; they should be interpreted using skeletal age (see Radiography) rather than chronologic age. GH production is normal for bone age (biologic age) in constitutional growth delay but may appear decreased if interpreted in the context of chronologic age because of the natural increment in GH production with advancing age and pubertal stage. GH provocative testing may also yield falsely low values in some prepubertal individuals with constitutional growth delay unless they are primed with sex steroids (ie, testosterone, estrogen).[7]

Gonadotropin (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) secretion

LH and FSH are helpful only if the skeletal maturation is advanced to the stage consistent with puberty (ie, at least age 10 y in girls and age 12 y in boys). Low levels of these hormones are expected in young children and adolescents with younger skeletal age. This is defined as physiologic hypogonadotropic hypogonadism.[8] Extremely elevated LH and FSH levels are indicative of gonadal dysfunction (ie, pathologic hypergonadotropic hypogonadism) and convey a poor prognosis for spontaneous pubertal development and future sexual function. Such levels are found in patients with Turner syndrome and in patients with Kallmann syndrome (see below) and gonadal damage from chemotherapy and irradiation.


A study by Rohayem et al indicated that inhibin B and anti-Müllerian hormone (AMH) are useful in differentiating between boys with prepubertal constitutional delay of growth and puberty and those with hypogonadotropic hypogonadism. The study found that the former had higher levels of inhibin B and AMH than did the latter.[9]

A retrospective study by Varimo et al suggested that in prepubertal boys, testicular volume, gonadotropin-releasing hormone–induced LH level, and basal inhibin B level are the best markers for differentiating constitutional delay of growth and puberty from congenital hypogonadotropic hypogonadism.[10]

Routine laboratory studies

Abnormal routine laboratory study findings may suggest the presence of diseases such as inflammatory bowel disease, renal tubular acidosis, occult malignancy, infections, and autoimmune disorders. Routine screening to rule out occult systemic disease as a cause for growth impairment or pubertal delay includes the following tests:

  • CBC count with differential

  • Chemistries including renal and hepatic indices

  • Erythrocyte sedimentation rate

  • Urinalysis

Genetic evaluation

If syndromes are suspected based on physical examination findings or family history, a karyotype or referral for genetic evaluation may be indicated. Syndromes that may mimic constitutional growth delay include, but are not limited to, the following:

  • Turner syndrome (females) - Short stature and gonadal failure; abnormality of X chromosome

  • Noonan syndrome - Turner phenotype but normal karyotype; often with abnormalities of pubertal development

  • Kallmann syndrome - Hyposmia or anosmia and hypogonadotropic hypogonadism

  • Russell-Silver syndrome - Marked growth retardation of prenatal onset

Imaging Studies


A radiographic study of the left hand and wrist to assess skeletal maturation is critical in diagnosing constitutional growth delay. Typically, the bone age begins to lag behind chronologic age during early childhood and is delayed in adolescence by an average of 2-4 years. Because the timing of puberty, the pubertal growth spurt, and epiphyseal fusion are dependent on biologic age (skeletal maturation) rather than chronologic age, all of these events are delayed in accordance with bone age. Lateral skull radiographs are rarely obtained because they are only helpful in the context of intracranial calcifications, such as those associated with craniopharyngiomas.


MRI of the pituitary gland is indicated if pituitary dysfunction is found upon hormonal evaluation or when physical symptoms (eg, visual changes, severe headaches) are present in the context of growth failure or pubertal delay.



Medical Care

Medical care in constitutional growth delay (CGD) is aimed at obtaining several careful growth measurements at frequent intervals, often every 6 months. These measurements are used to calculate linear height velocities and establish a trajectory on the growth curve. Medical treatment of this variation of normal growth is not necessary but may be initiated in adolescents experiencing psychosocial distress (see Medication).


No special dietary requirements are necessary, although a balanced diet with adequate calories and calcium intake is recommended to support normal growth and bone development.


No restrictions on activity are necessary. However, adolescents with constitutional growth delay who participate in contact sports must realize their limitations in competition with larger, stronger peers. Adolescents who wish to participate in weight lifting or resistance-training activities should use lower weights with greater repetitions to avoid undue stress on immature growth plates.



Medication Summary

Because constitutional growth delay (CGD) is not a disorder but rather a variation of normal growth, medical treatment is not necessary. However, short courses of sex hormones are an option for those patients experiencing psychological distress because of their delay in growth and development. In males, androgens can be used to accelerate linear growth and onset of pubertal changes. When used appropriately, no detrimental effects on adult height are evident. Therapy does not increase adult stature.

A retrospective study by Giri et al indicated that in adolescent boys with constitutional delay of growth and puberty, height velocity is improved 1 year after treatment with intramuscular testosterone, although, as stated above, final predicted height is not affected by the therapy. The investigators found that at 1 year posttherapy, treated patients had a mean height velocity of 8.4 cm/year, compared with 6.1 cm/year in untreated patients.[11]

A study by Chioma et al indicated that transdermal testosterone gel and intramuscular testosterone are each effective in increasing height velocity in boys with constitutional delay of growth and puberty (as observed after 6 months). However, untreated patients were found to have a greater increase in testicular volume.[12]

Alternatives to testosterone being investigated for boys with low predicted adult stature include oxandrolone, a weaker anabolic steroid than testosterone, and aromatase inhibitors.[13] The latter are used to decrease estrogen-stimulated epiphyseal fusion, resulting in a longer period of growth.[14, 15] Guidelines have been established for children in whom growth hormone (GH) therapy is indicated.[5, 16, 17]

Anabolic steroids

Class Summary

These agents promote growth and sexual maturation.

Testosterone (Delatestryl, Depo-Testosterone)

The depot preparation of testosterone is available as enanthate or cypionate salt. It is available in a multiuse vial for intramuscular injection. Transdermal preparations are available and have been used successfully in this context, although no established protocols are available.



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.[18]

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.


Questions & Answers


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