Growth disturbances manifest as abnormal absolute height or
growth velocity.
Short stature is defined as height that is two standard 
deviations below the mean height for age and sex (less than
the 3rd percentile) or more than two standard deviations
below the midparental height.
Growth velocity disorder is defined as an abnormally slow
growth rate, which may manifest as height deceleration
across two major percentile lines on the growth chart.
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
three phases 
after birth: infancy, childhood and pubertal growth 
.1st year 25cm/year 
2-3 year 7.5-13cm/year 
7cm/year at 3-4 year s and 
6cm/year at 5-6 years. It then remains at 4-6cm/year 
until puberty occurs when their growth will slow to about 4 cm/year 
Girls have their peak height velocity at early puberty, 9cm/year
. 
Boys reach their peak height velocity during midpuberty , with growth 
rate 10cm/year
In male skeletal growth till 17years while in female till age of 14 years 
. 
A-Genetic short stature/Familial short stature 
the most common type 
a condition characterized by 
1- height below the third percentile for age, 
2- normal annual growth rate 
3- normal bone age, 
4- family history of short stature, 
5- expected adult height below the third percentile, 
6- normal onset of puberty, 
7- and normal result to findings on physical examination
8- no endocrine abnormalities., 
.


1- No signs or symptoms of systemic disease 
2- Bone age delayed up to 2 to 4 years but consistent with height age (age 
at which individual’s height would plot on the 50th percentile)
3- Period of poorest growth often occurring between the ages of 18 and 
30 months, with steady linear growth thereafter (i.e., normal rate of
growth for bone age)
4- IGF-1 levels tend to be low for chronological age but within the 
normal range for bone age.
5- GH responses to provocative testing tend to be lower than in children 
with a more typical timing of puberty.
6- Parental or sibling history of delayed physical development 
7-Height prediction consistent with family characteristics 
8-delayed puberty with normal eventual height. 
the child is seen once every 3 to 6 months for accurate height 
measurements
and determination of growth velocity. A bone age test may be 
done yearly to assess the
progression of bony maturation. 
In children who are of mid- to late 
pubertal ages (girls >13 years; boys >14 years) but showing 
minimal or no `signs of puberty,
selective use may be made of estrogen or testosterone 
supplementation to initiate puberty,
additional assessment may be indicated 
It is result from fetal, placental, maternal
Could be symmetrical (early) 
Or asymmetrical (late) 

1- turner syndrome Always think of Turner’s in Girls

2- Noonan Syndrome, 
3-RussellSilver, 
4- Williams Syndrome 
5- Down’s .Prader-Willi syndrome,


1-Growth hormone insufficiency is the most type , congenital, acquired
secondary to CNS tumors, radiotherapy for malignancy, meningitis,
histiocytosis, and trauma. head injury or even
common)transient due to psychosocial deprivation) 
2- severe GH presented with micropenis, hypoglycemia, less than 3year
3- Hypothyroidism 
4-Cushing's Syndrome is another cause of short stature. 
The patient is usually obese and short 
Others causes 
1-skeletal dysplasia(achondrplasia) , (Mucopolysaccaridosis). 
2-celaic disease , IBD 
3- CHD 
4- Psychological deprivation 
5- any chronic illness type)SLE) 


Genetic short stature 
Constitutional growth delay 
Combined genetic short stature and constitutional growth
delay
Short stature following small for gestational age 
Dysmorphic syndromes 
Endocrine disorders 
Skeletal dysplasia 
Chronic diseases 
Psychosocial deprivationA 

Accurate serial height measurements documented over time on
a growth chart are key in the evaluation of children and serve
as the foundation for the diagnosis of growth abnormalities.
Height, weight, height velocity 
Height of parents 
Birth weight, gestation 
History of short stature, past medical history 
Family history of puberty, consanguinity, social history, school
performance 
Systemic inquiry 
Examination of dysmorphic features 
Systemic examination 
Pubertal development staging 
Blood test if necessary (CBC, TSH, RFT, LFT) 
Radiological examination if necessary (bone age) 
Endocrine assessment (if indicated) 


A strong clinical suspicion is important in establishing the diagnosis because
laboratory measures of GH sufficiency lack specificity,

Random growth hormone levels are of little value because they are generally low
in the daytime, even in children of average height.
IGF-1 (or somatomedin C) mediates the anabolic effects of growth hormone, and
levels correlate well with growth hormone status. However,IGF-1 can also be low
in non endocrine conditions (e.g., malnutrition, liver disease), and the assays are
somewhat inconsistent from laboratory to laboratory.
IGFBP-3, which is the major binding protein for IGF-1 in serum, is also regulated
by growth hormone. IGFBP-3 levels generally indicate growth hormone status
and are less affected by nutritional factors than IGF-1.
. 
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


Many endocrinologists now use IGF-1 and IGFBP-3 as their initial 
screening tests for growth hormone deficiency, IGF-1 and IGF-BP3 levels
should be matched to normal values for skeletal age rather than
chronological age. Values in the upper part of the normal range for age
effectively exclude GH deficiency.
Definitive diagnosis of GH deficiency traditionally requires demonstration
of absent or low levels of GH in response to stimulation. A variety of
provocative tests have been devised that rapidly increase the level of GH
in normal children. These include administration of insulin, arginine,
clonidine, or glucagon. In chronic GH deficiency, the demonstration of
poor linear growth, delayed skeletal age, and peak levels of GH (<10
ng/mL) in each of 2 provocative tests, are compatible with GH deficiency

The recommended dose of hGH is 0.18–0.3 mg/kg/wk during childhood.
Higher doses have been used during puberty. Recombinant GH is
administered subcutaneously in 6 or 7 divided doses AT night. Maximal
response to GH occurs in the 1st year of treatment
If growth rate drops below the 25th percentile, compliance should be 
evaluated before dose is increased
the Criteria for stopping treatment include a decision by the patient that
he or she is tall enough, a growth rate less than 1 inch/yr and a bone age
>14 yr in girls and >16 yr in boys


Concurrent treatment with GH and a gonadotropin-releasing 
hormone (GnRH) agonist has been used in the hope that
interruption of puberty will delay epiphyseal fusion and
prolong growth.
Recombinant IGF-1 is approved for use in the United States. It is 
given subcutaneously twice a day. The risk of hypoglycemia is
reduced by giving the injections concurrently with a meal or
snack. These conditions include abnormalities of the GH
receptor, as well as severe GH deficiency in patients who have
developed antibodies to administered GH.
GH is currently approved in the United States for treating 
children with growth failure as a result of Turner syndrome,
end-stage renal failure before kidney transplantation, PraderWilli syndrome, intrauterine growth retardation, and idiopathic
short stature.
1-Some patients treated with GH have developed leukemia 
2-pseudotumor cerebri, slipped capital femoral epiphysis, 
gynecomastia, and worsening of scoliosis.
3-Fasting and postprandial insulin levels are 
characteristically low before treatment, and they normalize
during GH replacement. Treatment does not increase risk of
type 1 diabetes, but it may increase the risk of type 2 diabetes.
4-Use of recombinant GH over the past 2 decades has 
eliminated the risk for CK(Creutzfeldt-Jakob ) disease and
reduced the risk of antibody formation during treatment.
. In which of the following conditions is the
bone age consistent with chronologic age (ie,
not delayed)?
A. Acquired hypothyroidism.
B. Constitutional delay of growth and
adolescence.
C. Familial short stature.
D. Glucocorticoid excess.
E. Psychosocial dwarfism