growth hormone

1. GROWTH HORMONE : ITS DEFICIENCY
AND EXCESS
Chair person Dr Sumit Kumar Chakraborty
(Associate Prof. DM Endocrinology, Dept. of General Medicine, NRSMCH)
Presenter Dr Soumyasil Das(2nd Yr. PGT)

2. GROWTH HORMONE
Hyper-secretion
• 1. Gigantism
• 2. Acromegaly
• 3. Acromegalic-gigantism
Hypo-secretion
• 1. Dwarfism
• 2. Acromicria (GHD in Adults)
• 3. Simmonds disease (pan-hypo-
pituitarism)

3. ffa
IGF-I
(somatomedinC)
the most important
IGF in postnatal
growth, is produced
in the liver,
chondrocytes,
kidneys, muscles,
pituitary gland, and
GIT.

4. CAUSES
• Due to tumor of acidophil cell in
pars distalis(somatotroph tumor)
of the anterior pituitary.
• Other causes of increased and
unregulated GH production,
include
1. increased GH-releasing hormone (GHRH)
from hypothalamic tumours;
2. ectopic GHRH from nonendocrine
tumours; and
3. ectopic GH secretion by nonendocrine
tumours.----all very rare
usually seen in the lung or pancreas,
occasionally in the duodenum as a
neuroendocrine carcinoma.

5. PRIMARY PITUITARY GH EXCESS
Pituitary Adenomas
• In most individuals  benign pituitary
tumour composed of somatotrophs
(GH-secreting cells) or
mammosomatotrophs (GH-secreting
and prolactin-secreting cells) in the form
of a pituitary microadenoma (< 1 cm)
or macroadenoma (>1 cm).
• Well-demarcated.
• Rarely spreads outside the sella, invading
the sphenoid bone, optic nerves, and
brain.(paediatric patients than in adults.)
Gs-alpha (Gsa) mutation
• 20% of patients with gigantism have
McCune-Albright syndrome and pituitary
hyperplasia or adenomas.
• Activating mutations of the stimulatory
Gsa protein have been found in the
pituitary lesions in McCune-Albright
syndrome.
• G proteins play an important role in post
ligand signal transduction by stimulating
adenyl cyclase, resulting in an
accumulation of cyclic adenosine
monophosphate (cAMP) and subsequent
gene transcription.

6. PRIMARY PITUITARY GH EXCESS
• Abnormality at Carney loci on
chromosomes 2 and 17
• The Carney complex, is
characterized by myxomas,
endocrine tumours, and spotty
pigmentation,
• is transmitted as an autosomal
dominant trait.
• About 8% have GH-producing
pituitary adenomas.
• Gene  2p16 and 17q22-24.
• Germline mutations in PRKAR1A.

7. SECONDARY GH EXCESS
GHRH excess
• Activating mutation in hypothalamic
GHRH neurons.
• Excess GHRH secretion may be due to an
intracranial or ectopic tumour.
• Intracranial gangliocytomas
• Ectopic GHRH-secreting tumours have
included carcinoid, pancreatic islet-cell,
and bronchial neoplasms.
• Prolonged secretion of GHRH leads to
pituitary hyperplasia, with or without
adenomatous transformation.
Disruption of somatostatin tone
• Tumor infiltration into
somatostatinergic pathways are
hypothesized to be the basis for
GH excess in rare incidents of
gigantism associated with
neurofibromatosis and optic
glioma or astrocytoma.

8. HYPER-SECRETION OF GROWTH HORMONE
Gigantism
• May begin at any age before
epiphyseal fusion.
• Extremely rare.(approx 100
reported cases to date.)
• Presentation is usually dramatic
because of close monitoring of
growth in children
Acromegaly
• After the fusion of epiphysis with
shaft of bone.
• More common.
• mean age of onset  third decade
• mean age at diagnosis for
acromegaly is 40 years in males and
45 years in females.
• Delay of 5-15 years for the diagnosis
from the time of onset.

9. GIGANTISM
 Standing height >+ 2 SD above the mean
for the person's sex, age, and Tanner stage
(ie, height Z score >+2 SD).
 Disorder characterised by excess growth
of the body.
 Due to excessive action of insulin like
growth factor I (IGF-I)
 Subjects look like a giant and with average
height of about 7-8 feet

10. HISTORY
Gigantism
• Presentation is usually dramatic
because of close monitoring of
growth in children
• Few soft tissue effects
• Longitudinal acceleration of linear
growth is the cardinal feature
• Tumour mass may cause headaches,
visual changes due to optic nerve
compression, and hypopituitarism
• Hyperprolactinemia is common
because mammosomatotrophs are
the most common type of GH-
secreting cells involved in childhood
gigantism
Acromegaly
• insidious onset
• Symptoms due to
local mass
effects of an
intracranial
tumour
due to excess
of GH/IGF-I

11. SYMPTOMS OF ACROMEGALY
local mass effects of an intracranial
tumor
• Headaches and visual field defects
are the most common symptoms
• Tumor damage to the pituitary
stalk may
causehyperprolactinemia
• Damage to normal pituitary tissue
Bitemporal Hemianopia
Headache
ACTH,LH, FSH,TSH
Hypothyroidism, amenorrhoea, Addison's
Ds, Infertility

12. SYMPTOMS OF ACROMEGALY
Due to excess of IGF1/GH
• Soft tissue swelling and enlargement of
extremities
• Increase in ring and/or shoe size
• Coarsening of facial features,
• Prognathism, Macroglossia
• diabetes mellitus, hypertension, and
cardiovascular disease
• Hyperphosphatemia, hyper-calcuria,
and hypertriglyceridemia
• Colonic polyps and adenocarcinoma of
the colon
• Congestive heart failure, due to
uncontrolled hypertension or to an
intrinsic form of cardiomyopathy
attributable to excess GH/IGF-I
• OSA
• Hyperhidrosis, Arthritis

13. Radiological features of acromegaly
Hell pad sign
>21mm (male)
>18mm (female)
lateral view of a pituitary
adenoma.
expanded sella turcica
(between the orbit on the left
and the radio-dense mastoid
on the right).

15. ACROMEGALIC FACE
WITH ITS FEATURES
Doughy-feeling skin over the face and
extremities.
Deepening of creases on the forehead
and nasolabial folds
Thick and oedematous eyelids
Enlargement of the lower lip and nose
(the nose takes on a triangular
configuration)
Cutis verticis gyrata (i.e. furrows
resembling gyri of the brain):
Acromegaly may be first evident as cutis
verticis gyrata.
Hypertrichosis (found in approximately
one half of acromegaly patients): Unlike
virializing disorders, hypertrichosis of
acromegaly does not affect the beard
area
Oily skin (acne is not common)
Hyperpigmentation (40% of patients)

16. MEASUREMENT OF GH AND IGF1
Growth Hormone
• 100gm of glucose given to patient
• Measure serum GH after 1 hr
• <5ng/ml >10ng/ml
Normal ACROMEGALY
IGF-I
• most reliable biochemical
indicator of acromegaly
• not only in diagnosis, but also in
monitoring the efficacy of therapy
• Starvation, obesity, and diabetes
mellitus decrease IGF-I
concentration, while pregnancy
increases
5-10do other tests

17. a = Visual field compromise is absolute
indication for surgery.
b = Primary medical therapy can be
considered if there is no visual field deficit
and there is no possibility of surgical cure
because of cavernous sinus involvement.
c = Reconsider surgery to debulk tumour to
improve response to medical therapy, to
reduce medical comorbidities, or to comply
with patient preference.
d = Consider a dopamine agonist (DA) in the
setting of modest disease.
e = Consider radiotherapy (RT) in patients
with residual tumour after surgery. This
decision is based on several factors, including
age, reproductive status, pituitary function,
and patient preference regarding long-term
medical therapy.
f = Addition of a DA in the setting of modest
disease.
GH = growth hormone;
GHAnt = growth hormone antagonist;
IGF-1 = insulin like growth factor-I;
SSA = somatostatin analogue.

18. TREATMENT IS NOT ABSOLUTE BUT INDIVIDUALIZED
• For most patients with acromegaly, surgical removal of the pituitary
gland tumour should be considered the primary treatment.
• For pituitary adenomas, trans sphenoidal surgery is usually
considered the first line of treatment, followed by medical therapy for
residual disease.
• ‘R’adiation treatment usually is reserved for ‘R’ecalcitrant cases.
• Cure, or adequate control, will be said when there is a glucose-
suppressed GH concentration is less than 1ng/mL, as determined by
radioimmunoassay (1 mcg/L by IRMA), and normalization of IGF-I
concentration.

19. NEED FOR MEDICAL
THERAPY
Remove or shrink the pituitary
mass
Restore GH secretory patterns to
normal
Restore serum total IGF-I and IGF
binding protein 3 (IGFBP-3) levels
to normal
Retain normal pituitary secretion
of other hormones
Prevent recurrence of disease
 Somatostatin analogues
Octreotide, Lanreotide, Pasireotide
 Dopamine receptor agonist
Bromocriptine, Cabergoline
 GH-receptor antagonists
Pegvisomant (Somavert)

20. SOMATOSTATIN ANALOGUE(OCTREOTIDE)
• Binds to the SSTR subtypes II and V
• suppresses the serum GH level to
less than 2.5 mcg/L in 65% of
patients.
• normalizes circulating IGF-I levels in
70% of patients.
• inhibits the secretion of GH, insulin,
and glucagon.
• Octreotide also inhibits prolactin
release by means of vasoactive
intestinal peptide (VIP) ̶ and
thyrotropin-releasing hormone
(TRH) ̶ mediated secretion of
prolactin.
• Gallbladder problems (>60%):
Decreased gallbladder
contractility, gallstones,
cholecystitis, cholestatic hepatitis
• Dysglycemia (25%)
• Hypothyroidism (25%)
• Bradycardia (25%)
• Bioavailability: SC, 100%; IM,
60%
• CAT-B in pregnancy

21. IF SYMPTOMS UNCONTROLLED
AND GH > 2.5 NG/ML OR IGF-I
ELEVATED, INCREASE DOSE TO 30
MG IM EVERY 4 WEEKS; IF
SYMPTOMS PERSIST, INCREASE TO
40 MG IM
• Solution 50-500mcg SC TDS
for 2 weeks
• Suspension(depot) 20 mg IM
(gluteal) every 4 weeks for 3 months
• If GH < 1 ng/mL if GH <2.5ng/ml
and IGF-1 normal and IGF-1 norm
decrease to 10mg maintain at 20mg
every 4 weeks every 4 weeks
Monitor IGF-1 levels every 2
weeks to guide titration; goal: GH
levels <1 ng/mL or IGF-1 levels
<1.9 units/mL (men) and <2.2
units/mL (women)
Monitor IGF-1 or GH levels every
6 months when GH and IGF-1
stabilises to target value
Octreotide regime

22. DOPAMINE RECEPTOR D2 AGONIST (MAINLY AS
ADJUVANT)
Bromocriptine
• Reduces GH level to less than 5
ng/mL in only 20% of patients
with acromegaly
• Normalizing IGF-I in only 10%
• Shrinkage in tumour size also
occurs, fewer than 20%
Cabergoline
• reducing GH level in 46%
• normalizing IGF-I in only 33%
somewhat more
effective

23. GH-RECEPTOR ANTAGONIST PEGVISOMANT
(SOMAVERT)
• GH-receptor antagonist
• Normalization of IGF-I levels occurs in as many as 90% of patients treated daily
with this drug for 3 months
• Titrate by 5 mg increments q4-6Wks according to IGF-1 levels
• No more than 30 mg/day maintenance
• Baseline LFT>3 times ULN before starting Do not use pegvisomant
• LFTs During Treatment ≥3 but <5 times ULN continue monitor LFTs qWk
• ≥5 times ULN Discontinue pegvisomant
Load: 40 mg SC
Maintenance:
10 mg SC OD

24. KEEPING IT SIMPLE
Consider surgery
first
If not possible
Start with
OCTREOTIDE
If GH>1 or IGF-1Octreotide+ D2A
Partial biochemical
response
No response i.e.
GH>1 or IGF-1
Pegvisomant
alone
Octreotide
+
pegvisomant
IGF-1
IGF-1
RT

25. CONDITIONS ASSOCIATED WITH GIGANTISM
• Multiple endocrine neoplasia (MEN) type I
• McCune-Albright syndrome
• Neurofibromatosis
• Tuberous sclerosis
• Carney complex

26. HYPO SECRETION OF GROWTH HORMONE
• Dwarfism
• Acromicria
• Simmonds disease

27. DWARFISM/SHORT
STATURE
Short stature is defined as height
<3rd centile or <2 SDs below the
median
for that age and sex according to
the population standard.
Little people go to school, go to
work, drive cars, marry, and raise
children, just like their average-
size peers.

28. WHAT CAUSES
SHORT STATURE?
• Most are caused by genetic changes i.e.
mutation in the egg or sperm.
• other include metabolic or hormonal
disorders in infancy or childhood,
• Chromosomal abnormalities, Turner,
Noonan, Prader-Willi
• pituitary gland disorders (which
influence growth and metabolism),
• absorptive problems (when the body
can't absorb nutrients adequately), and
• kidney disease.
More than 300 well-
described conditions are
known to cause short
stature in a child
So please don’t think
that that there is GH
deficiency when you see
a dwarf.

29. TYPES OF SHORT STATURE
Proportionate short stature
• meaning a person's arms, legs,
and trunk are all shortened but
remain in proportion to overall
body size.
Disproportionate short stature
• meaning the limbs and the trunk
are not of the same proportion as
those of typically-statured people.

30. DISPROPORTIONATE SHORT STATURE
Short trunk short Short limb short
• Spondyloepiphyseal dysplasia,
• Mucolipidosis,
• Mucopolysaccharidosis
• Caries spine,
• Hemivertebrae.
• Achondroplasia (most common),
• Hypo-chondroplasia,
• Chondrodysplasia punctata,
• Chondroectodermal dysplasia,
• Diastrophic dysplasia,
• Metaphyseal chondrodysplasia,
• Osteogenesis imperfecta,
• Refractory rickets
Mainly Genetic Causes

31. DISPROPORTIONATE SHORT STATURE
Short trunk short Short limb short
Spondyloepiphyseal
dysplasia Achondroplasia

33. PROPORTIONATE SHORT STATURE
Normal Variants
• Familial Short Stature
• Constitutional delay in growth
and puberty.
Pathological
• Intrauterine growth restriction (placental,
infections or teratogen)
• • Genetic disorders (chromosomal and metabolic
disorders). Down’s, Turner, Noonan, Prader-Willi
• • Under nutrition
• • Chronic systemic illness
• • Psychosocial short stature (emotional
deprivation)
• • Endocrine causes
• – Growth hormone deficiency/insensitivity
• – Hypothyroidism
• – Juvenile diabetes mellitus
• – Cushing’s syndrome
• – Pseudo hypoparathyroidism
• – Precocious/delayed puberty.

34. ADD A SLIDE
TITLE - 6
Sex Both equally affected More common in boys
Length at birth Normal Normal (starts falling < 5
centile in first 3yrs of life)
Family history Short stature Delayed puberty
Parents stature Short (one or both) Average
Height velocity Normal Normal
Puberty Normal Delayed
Bone age (BA) and
chronological age (CA) BA = CA > height age CA > BA = height age
Final height Short Normal
Familial short stature Constitutional delay

35. LETS COMPARE THE TWO IN A GRAPH
Children with constitutional growth
delay (CGD),
retarded linear growth within the first 3
years of life.
linear growth velocity and weight gain
slows since 3-6 months of age,
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.

36. HOW TO EVALUATE A CASE OF SHORT STATURE
Initial evaluation of short stature should include
• history and physical examination,
• accurate growth assessment,
• calculation of the growth velocity,
• mid parental height, and
• radiography to evaluate bone age(should be done in all children)

37. CLUES TO AETIOLOGY OF SHORT STATURE
FROM HISTORY
History
• Delay in puberty in parents
• Low birth weight
• Neonatal jaundice, hypoglycaemia
and micro-penis
• Dietary intake, greasy stool
diarrhoea
• Lethargy, constipation, wt gain
• Polyuria
• Social history
Aetiology
• Constitutional delay
• SGA
• GH deficiency/ Hypo-thyroidism
• Undernutrition
malabsorption
• Hypothyroidism
• CRF, RTA
• Psycho-social dwarfism

38. CLUES TO ETIOLOGY SHORT STATURE FROM
EXAMINATION
Examination findings
• Disproportion
• Dysmorphism
• Hypertension
• Goitre, coarse skin
• Central obesity, striae
Aetiology
• Skeletal dysplasia, rickets
• Congenital syndromes
• Chronic renal failure
• Hypothyroidism
• Cushing’s syndrome

39. ASSESSMENT OF
GROWTH RATE
• Birth to 12 months 23 to 27 cm
• 12 months to 2 year 10 to 14 cm
• 2 to 3 years 8 cm
• 3 to 5 years 7 cm
• 5 years to puberty 5 to 6 cm
• Puberty
Girls: 8 to 12 cm
Boys: 10 to 14 cm
Because children grow in spurts,
two measurements at least 3-6
months apart, and preferably6-12
months apart, are needed to
accurately determine growth
velocity.
Measure ht always at the same
time of day to prevent diurnal
variation.
Variation from this normal
pattern of growth may be a sign of
pathologic conditions.

40. MID-PARENTAL HT
• Mean of parents height
(father’s ht + mother’s ht)/2
+6.5cm -6.5cm
Boy’s ht Girl’s ht
Calculation of the sex-adjusted
mid-parental height, also termed
the "target height," helps to
evaluate a child's genetic potential
to achieve his/her target ht in
adulthood.
The target height is plotted on the
growth chart and
if the child is falling within the
target height, the cause could be
genetic or constitutional.
Otherwise, it is considered
abnormal
+/-10cm +/-10cm

41. BONE AGE (SHOULD BE DONE IN ALL CHILDREN WITH SHORT
STATURE.)
• Bone age should be compared with
chronologic age to narrow the
differential diagnosis of short
stature.
• Children with normal variations of
growth may have advanced or
delayed bone age,
• Bone age is delayed compared to
CA (BA<CA) in almost all causes of
pathological short stature.

42. BONE AGE
• Greulich and Pyle atlas
• Tanner Whitehouse-20score
points(gold standard)
X-ray of left hand and wrist (AP
view) containing the distal end of
both radius n ulna along with all
the fingers.
Helps to determine the prognosis
of therapy and also when to
terminate the therapy
To Determine the predicted height

43. Maturation is proximal to distal
Fusion is distal to proximal

46. Height <2SD mean for age & sex
Growth vel <5cm/yr
Or <2SD mid parental ht
GI or Endocrine
symptoms
Yes No
Coeliac Ds,
IBD, Hypo-thyroidsm, yes no
Cortisol excess
Yes No
Is patient dysmorphic
Proportionate
evaluate for genetic
syndrome like
TURNER,DOWNS,NOO
NAN, PRADER-WILLI
Assess Growth vel,
Projected Ht, Wt, BA
Growth vel>5cm/yr
+
Delayed BA
Growth vel>5cm/yr
+
Normal BA
+
Projected Ht consistent
with mid-parental ht
Growth vel<5cm/yr
Delayed BA
Normal or Increased Wt
Constitutional
delay of growth &
puberty
Familial
short
stature
Endocrine
issues,
Chronic
illness
Evaluate
for
chondro-
dystrophy

47. INVESTIGATIONS TO GET THE CAUSE OF SHORT
Level 1
• Complete hemogram with ESR
• Bone age
• Urinalysis (microscopy, pH,
osmolality)
• Stool (parasites, steatorrhea, occult
blood)
• Blood (renal function test, Ca, PO4,
ALP, venous gas, FBS, albumin,
transaminases).
Level 2
• Serum thyroxine, thyroid-
stimulating hormone (TSH)
• Karyotype to rule out Turner’s
syndrome in girls
If above investigations are normal and height
between - 2 to - 3 SD,
then observe height velocity for 6–12 months.
If height < 3 SD, proceed to level 3
investigations

48. LEVEL 3 INVESTIGATIONS
• Celiac serology (anti-endomyseal or anti-tissue transglutaminase
antibodies)
• Duodenal biopsy
• Growth hormone stimulation test with glucagon or insulin and
serum IGF-1 levels.

49. CLUE TO GET IDEA OF REASON FOR SHORT
STATURE
• Complete blood count
• Comprehensive metabolic panel
• ESR, C-reactive protein
• Follicle-stimulating hormone
karyotyping
• Insulin like growth factor 1
• Thyroid profile
• Tissue transglutaminase and total
immunoglobulin A
• Urinalysis
• Anaemia
• Hepatic and renal diseases
• Inflammatory bowel disease
• Turner syndrome
• Growth hormone deficiency
• Hypothyroidism
• Celiac disease
• CRF, RTA

50. REMEMBER
Bone age of a child with endocrine
diseases will progressively fall
behind chronologic age,
Hence, calculating bone age every
12 months might be useful to
differentiate constitutional delay
of growth from endocrine
diseases.
familial short
stature or idiopathic
short stature have
BA=CA
constitutional delay
of growth and
puberty or
endocrine disorders
BA<CA
Endocrine disorders, growth hormone deficiency,
hypothyroidism, glucocorticoid excess,  normal
to increased weight,
Systemic disease decreased height and
weight

51. REASONS FOR SHORT STATURE(INDIAN SCENE)
1. protein energy malnutrition (PEM)
2. chronic systemic disease(tuberculosis, bronchiectasis, cirrhosis)
3. Chronic anaemia
4. skeletal disorders
5. constitutional short stature
6. endocrine disorders
7. intrauterine growth retardation
8. chromosomal disorders
9. miscellaneous
mainly GHD & Hypo thyroidsm

52. GROWTH HORMONE DEFICIENCY
• rare disorder
 Congenital, resulting from genetic mutations or from structural defects in the brain.
 Acquired later  trauma, infection, radiation therapy, or tumour growth within the brain,
drugs(steroids for asthma, AEDs)
 Idiopathic
Childhood-onset GHD
may be all three:
congenital, acquired,
or idiopathic.
Adult-onset GHD is most often is
acquired from a pituitary tumor
or trauma to the brain but may
also be idiopathic.

53. HYPO-SECRETION OF GROWTH HORMONE
• Dwarfism
• Acromicria = GHD in adults
• Simmonds disease = Pan Hypo-pituitarism = pituitary cachexia

54. CHILDHOOD GHD
Pudgy and cherubic appearance
because
height is usually more affected than
weight and
with a characteristic distribution of
fat in the face and abdomen.

55. CLINICAL FEATURES
Children
• growth retardation, short stature, and
maturation delays reflected by BA<CA
• normal size at birth
• H/O hypo-glycaemic episode during the new
born period
• Males may have a small penis (micro penis)
female patients do not have abnormalities of
genital development
• delayed rates of development of facial bones,
• slow tooth eruption,
• delayed lengthening of long bones,
• fine hair, and poor nail growth.
• truncal obesity,
• a high pitched voice, and
• delayed closure of the sutures of the skull,
causing delayed closure of the fontanelles.
• cleft palate or single central incisor
Adults
• reduced energy levels, anxiety,
and/or depression
• altered body composition, increase in
fat mass, especially abdominal and
visceral, reduced muscle strength,
• osteoporosis
• lipid abnormalities such as increased
LDL cholesterol, & TAG
• insulin resistance, and
• impaired cardiac function.

56. DIAGNOSIS
GH useless, because GH is intermittently
secreted in brief nocturnal pulses (of 10-15
minutes during deep sleep)
IGF-1 and IGF-2
Testing is very important in
determining whether the child
with growth retardation does
indeed have growth hormone
deficiency.
vary with the patient's
age, nutritional status,
and sexual maturation.
In children younger than
8 years, serum IGF-1
levels may be
indistinguishable from
levels measured in
children with GHD.
vary less than
IGF-1 levels do
at a given age;
however, serum
IGF-2 is less GH
dependent than
IGF-1.
superior to measuring the free IGF-1
concentration vary less with nutritional status than free
IGF-1.
even in young children, typically more than 500 mg/mL;
therefore, the detection of low levels is feasible.
IGFBP-3

57. MRI/X-RAY SKULL
Before rhGH therapy is started,
patients with GHD should
undergo MRI of the brain to
exclude the possibility of an
organic lesion.

58. TREATMENT
• Outcome is best if started before 4yrs
• Monitor every 3 months
• A/e Pseudotumor cerebri do
fundoscopy
• Height, weight estimation
• Bone age
• Correct other pituitary hormones, IBD
• maintain an IGF-1 value in the upper
quartile for the child's age and sex.
• Titrate dose as per weight
0.175-0.75 mg/kg/wk
Dividing the weekly dose into 6 or
7 daily doses is more effective
than 3 doses given in alternate
days.
100% bioavailability in SC
Increase in growth velocity
(averaging 10-11 cm/y during 1st
yr of therapy)”catch up growth”
Subsequently slows down over
next yrs  “waning effect”
Recombinant Human
Growth Hormone (rhGH)

59. FDA APPROVED INDICATIONS FOR THE
ADMINISTRATION OF RHGH IN CHILDREN
• Growth failure associated with GHD
• Chronic renal failure
• Turner syndrome
• Prader-Willi syndrome
• SGA with failure to catch up in first 2 yrs.
• Idiopathic short stature
• SHOX gene deficiency
• Noonan syndrome

60. FEATURES ALL S/O GHD BUT WE FOUND EXCESS GH
• It means GH is there but it cannot act at its site of action.
• This is known as GH insensitivity syndrome or
Primary IGF-1 deficiency syndrome
Laron Syndrome
Due to abnormal growth hormone secretagogue receptors in liver

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