Transcript Slide 1

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Short Stature:
The Long and Short of It
Diagnosis, Etiology, and
Treatment
Jay Cohen, MD, FACE, FAAP, CEC
Medical Director
Endocrine Clinic
Memphis, TN
Activity Evaluation
In order to obtain credit for this activity, please
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evaluation.
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the faculty and are in no way to be considered the
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Communications, or Tercica, Inc. Any disclosures
regarding significant relationships are provided in the
following 2 slides.
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Faculty Disclosures
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Support of Continuing Medical Education and
the ACCME guidelines, it is our policy to inform
participants of any relationships the faculty has
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presentations. The faculty reports the following
relationships:
Faculty Disclosure:
Jay Cohen, MD, FACE, FAAP, CEC
Dr. Cohen has made the following disclosures:
Speakers Bureau, Grants/Research Support:
– Pfizer, Genentech, Eli Lilly, Tercica Inc.
Medical Education Resources, Inc. requires that the
learners in all of its certified activities are informed if
there is any discussion regarding off-label use of a
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Dr. Cohen has disclosed there will be discussion about the
use of products for non-FDA approved or investigational
use.
Educational Objectives
At the end of this educational activity,
participants should be able to:
1. Describe the criteria for the definition of short
stature
2. Discuss the conditions that constitute
idiopathic short stature (ISS)
3. Outline the methodology for determining the
presence of short stature in a young child
4. Review the treatment options for short
stature and when they should be used
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This activity is supported through an
unrestricted educational grant provided by
Tercica, Inc.
Short Stature:
The Long and Short of It
Diagnosis, Etiology, and
Treatment
Jay Cohen, MD, FACE, FAAP, CEC
Medical Director
Endocrine Clinic
Memphis, TN
Short Stature
• Normal variants
– Familial short stature*
– Constitutional delay*
• Pathological
– Primary growth abnormalities
– Secondary growth disorders
– Idiopathic short stature
*Diagnosis of exclusion
Larson P, Williams Textbook of Endocrinology, 10th ed. 2003.
Primary Growth Abnormalities
• Osteochondrodysplasias or skeletal
dysplasia (eg, osteogenesis imperfecta)
• Chromosomal abnormalities
– Turner syndrome
– Prader-Willi syndrome
– Noonan syndrome
– Trisomy 13,18, 21 (eg, Down syndrome)
• Intrauterine growth abnormalities
– Small for gestational age (SGA)
Larson P, Williams Textbook of Endocrinology, 10th ed. 2003.
Secondary Growth Abnormalities
• Malnutrition/nutritional insufficiency
– Food allergies
– Inadequate nutritional intake
• Emotional deprivation
– Psychosocial dwarfism
• Chronic neglect
• Starvation
• Chronic or systemic disease
Larson P, Williams Textbook of Endocrinology, 10th ed. 2003.
Secondary Growth Abnormalities:
Systemic Conditions
• Hematological - anemia
• Cardiovascular - cardiac failure, shunting
• Pulmonary
– Cystic fibrosis (CF), asthma, chronic corticosteroids
usage (prednisone), chronic obstructive pulmonary
disease (COPD), restrictive lung disease
• Gastrointestinal
– Malabsorption, inflammatory bowel disease (IBD), celiac
disease, reflux
• Kidney
– Renal tubular acidosis (RTA), chronic renal failure,
occult renal disease
• Liver - chronic active hepatitis
Larson P, Williams Textbook of Endocrinology, 10th ed. 2003.
Secondary Growth Abnormalities:
Endocrine Disorders
•
•
•
•
•
•
•
•
Hypothyroidism/hyperthyroidism
Cushing’s syndrome
Pseudohypoparathyroidism
Rickets (Vitamin D – rickets resistant)
Chronic hypernatremia (hypothalamic adipsia, diabetes insipidus)
Glucocorticoid imbalances (hypercortisolism)
Poorly controlled diabetes (diabetes mellitus)
IGF deficiency
– Growth hormone deficiency (GHD) – hypothalamic dysfunction,
pituitary GDH
– GH resistance (primary vs secondary GH insensitivity)
– Primary defects of IGF synthesis
– Primary defects of IGF transport and clearance
– IGF insensitivity (IGF-1 receptor defects vs post-receptor defects)
Larson P, Williams Textbook of Endocrinology, 10th ed. 2003.
Idiopathic Short Stature
• Diagnosis of exclusion
• Normal size at birth
• Significantly below average height for age &
gender
– >2 standard deviations below average height
– Corresponds to the shortest 2.3% of children
• Tempo of growth may be slow or normal
• Short stature of unknown origin (idiopathic)
– No evidence of other medical problems, such as:
•
•
•
•
Systemic disease
Malnutrition
Hypothyroidism
Growth hormone deficiency (GHD)
Ranke M. Horm Res. 1996;45:64-66.
Short Stature:
Variations of Normal
• Familial (genetic) short stature
– Short, but appropriate for parental height
• Parallels normal growth rate curves
– Bone age corresponds with chronologic age
– Normal onset of puberty
• Constitutional growth delay (“late bloomers”)
– Parents of average/tall height
– Normal (but short) growth rate, including body
proportions
– Family history of “late bloomers”
• At least one parent had delayed puberty
– Delayed bone age and sexual maturation
Larson P, Williams Textbook of Endocrinology, 10th ed. 2003.
Growth Curves:
Measurement is Key
190
95%
180
50%
170
5%
Stature (cm)
160
150
X
X
X
X
X
140
X
130
X
X
120
X
X
110
X
Pathological
X
100
Constitutional
X
90
80
X
X
X
X
Familial
X
2
4
6
8
10
12
14
16
18
Age (years)
Lifshitz F. Pediatric Endocrinology; 5th ed. 2006.
• Growth curves help
distinguish normal
growth from pathologic
variants of short stature
• Below average height
and weight but
parallels normal curve
– eg, familial short stature
and constitutional
growth delay
Growth Curves:
Points of Interest
•
•
•
Reliability of measurement
Target height or “genetic potential”
Bone age
–
•
Upper/lower (U/L) body ratio and some chromosomal
abnormalities
–
•
•
Skeletal age relative to chronologic age
Abnormal in skeletal dysplasias
Height velocity
Weight to height relationship
–
–
Endocrine disorders: weight percentile is greater than height
percentile (eg, hypothyroidism, growth hormone deficiency)
Systemic disorders: usually lose weight first and are thin by
the time they are short
Farber R, Kerrigan J. Pediatric Annals. 2006;35(12):926-932.
What’s Normal
and When to Worry
• Short and dysmorphic (abnormal U/L body ratio)
– Skeletal dysplasias
• Increased U/L = long bone; Decreased U/L = spine
– Short stature syndromes (eg, Turner, Down, Prader-Willi)
• Short and thin
– Usually systemic disease
• Short with greater than normal weight percentile
– Usually an endocrine disorder (GH, thyroid, cortisol)
• Proportionate with greater than normal weight
percentile
– Congenital growth hormone deficiency (GHD), acquired GHD
(tumors, trauma, post-infectious), hypothyroidism, Cushing
syndrome
Evaluating a Child
with Short Stature
Short Stature
Normal Variants
Familial short stature
Constitutional delay
Pathologic
Disproportionate
Skeletal dysplasia
Rickets
Chromosomal abnormalities
Proportionate
Prenatal
IUGR
Placental disease
Infections
Teratogens
Dysmorphic syndromes
Chromosomal disorders
Postnatal
Endocrine disorders
Psychosocial dwarfism
Malnutrition
Gastrointestinal diseases
Cardiopulmonary diseases
Chronic anemia
Renal disorders
IUGR, Intrauterine growth retardation.
Larson P, Williams Textbook of Endocrinology, 10th ed. 2003.
Clinical Evaluation
for Short Stature
• Detailed history and physical (from head to
toe)
• Including but not limited to:
–
–
–
–
–
–
–
Date of onset
Perinatal birth history
Medical/surgical history
Developmental history
Nutritional history
Family/social history
Parental heights
and pubertal history
–
–
–
–
–
–
–
–
Onset of puberty
Allergies
Sitting height
Limb length
Hypospadius
Absence of goiter
Cleft lip/palate; abnormal palate/teeth
Shortened 4th metacarpal
Clinical Evaluation
for Short Stature (cont.)
• Height velocity
– Growth chart that depicts the child's growth over
time
– Allows comparison of the height or weight to
other children and graphically depicts changes in
growth or growth velocity
• Bone age determination
– Left hand and wrist radiograph to estimate
skeletal maturation
Clinical Evaluation
for Short Stature (cont.)
• Respiratory system
– Chest deformities, chronic lung disease (eg, CF, asthma)
• Cardiovascular system
– Congenital heart disease, hypertension, cardiac failure
• Abdominal evaluation
– Hepatomegaly, splenomegaly, masses, ascites
• Renal system
– Urine output
• Central nervous system
– Visual acuity/visual fields, hydrocephalus, focal signs
Clinical Diagnosis of Short
Stature: Laboratory Testing
• Urinalysis and pH
• Thyroxine (Free T4 and TSH)
– Hypothyroidism should be excluded
• Comprehensive metabolic profile (CMP)
– Low bicarbonate level may indicate renal tubular acidosis
– Abnormal electrolytes (Ca, K) may indicate renal failure, liver
function tests
• CBC and sedimentation rate (anemia, leukopenia, etc.)
– May be helpful if inflammatory bowel disease is suspected
• IGF-1 and IGFBP-3
– Both IGF-1 and IGFBP-3 are GH-dependent
– Low values of IGF-1 and IGFBP-3 suggest GHD
– IGFs are sensitive to other factors such as nutritional state and
chronic systemic disease so a low value alone is not diagnostic
Consideration of
Additional Laboratory Testing
•
•
•
•
•
Prolactin
Chromosome analysis
FSH/LH levels
Celiac panel
Total IgA
Growth Hormone Pathway
Hypothalamus
Somatostatin –
GHRH +
Anterior pituitary
GH
Liver
IGF-1
Somatostatin
Cartilage & bone growth
Muscle & other organs:
• Protein synthesis &
growth
(GH levels and effects are
most pronounced during puberty)
Adipose Tissue (lipolysis)
Most Tissues
 glucose utilization
 blood glucose
Growth Hormone
Deficiency (GHD)
• Inadequate secretion of growth hormone
• May result from disruption of the GH axis in the
higher brain, hypothalamus, or pituitary
• Most instances of GHD are idiopathic
• Organic
– Congenital malformations of hypothalamus and
pituitary
– Brain tumors, especially craniopharyngioma
– CNS surgery, head trauma and radiation
– Chronic inflammation
• Genetic GHD
GH-IGF Axis
Hypothalamus
GH receptor
GHRH
GH
GHBP
Signal
Transduction
Pituitary
Liver
IGF-I
Type I IGF receptor
Growth
plate
GROWTH
ALS, acid-labile subunit.
IGFBP-3
ALS
Other IGFBPs
GH-IGF Axis:
GH Deficiency
Hypothalamus
GH receptor
GHRH
GH
GHBP
Signal
Transduction
Pituitary
Liver
IGF-I
Type I IGF receptor
Growth
plate
GROWTH
ALS, acid-labile subunit.
IGFBP-3
ALS
Other IGFBPs
What GHD Looks Like
• GHD subject is 18 cm
shorter than her sister,
despite being one and a
half years older
Image obtained online and available at: www.schoolscience.co.uk. Accessed 07-17-07.
Prevalence of GHD
• According to Utah Growth Study, 2.5% of the population is
short
– Largest population-based survey of growth in children
– Assessed height & growth velocity in ~115,000 American
children
– Among 555 children with short stature (height below the third
percentile) and poor growth rate (growth velocity <5 cm
annually), only 5% had an endocrine disorder
– 48% of children with GHD or Turner syndrome (TS) had
been undiagnosed or untreated
• An endocrine disorder (eg, GHD) is often suspected as the
major cause of short stature
– This study confirms that most (95%) children with poor
growth (velocity <5 cm/y) do not have an endocrine disorder
Lindsay R, et al. J Pediatr. Jul 1994;125(1):29-35.
Growth Hormone Therapy
• Generally, highly effective in children with
unequivocal GH deficiency
• Responsiveness to GH in most other
approved indications is highly variable and
not always predictable
• Thus, GH therapy has clear utility but also
has limitations
New Treatment
Perspectives on ISS
• Despite efficacy data, a considerable amount of variability
in response to GH remains, even within the same
diagnostic category, such as GHD
• Some children with ISS have shown little or no benefit of
therapy suggesting that GH therapy is suboptimal in some
patients
• A range of growth response to GH therapy exists including
GH responsiveness, GH unresponsiveness, GH
insensitivity
• Current data suggests that up to 25-50% of children with
ISS may have primary IGF-1 deficiency (based on normal
GH secretion and low IGF-1 levels)
Rosenthal S, et al. Pediatr Endocrinol Rev. May 2007;4(Suppl. 2):S252-S271.
What Is a
Poor Response to GH?
Height Velocity (cm/yr)
Height velocity data for 8442 males with IGHD during first year in NCGS
24
22
20
18
16
14
12
10
8
6
4
2
0
Mean HV + 1 SD
Mean HV
Mean HV – 1 SD
2
3
4
5
6
7
8
9
10 11 12 13 14 15 16 17
Age at Baseline
Rosenfeld R, et al. Growth Hormone Research Society/IGF Society Meeting. 2006.
What Is a
Poor Response to GH? (cont.)
Height velocity data for females with IGHD, including mean -2 SD and
mean pre-treatment height velocity
Height Velocity (cm/yr)
16
14
12
10
Mean HV + 1 SD
8
Mean HV
6
Mean HV – 1 SD
4
Mean HV – 2 SD
Mean Pretreatment HV
2
0
2
3
4
5
6
7
8
9
10 11 12 13 14 15 16 17
Age at Baseline
Rosenfeld R, et al. Growth Hormone Research Society/IGF Society Meeting. 2006.
Insulin-like
Growth Factor-1 (IGF-1)
• IGF-1 is normally secreted in
response to stimulation by
growth hormone
• IGF-1 stimulates multiple
processes leading to growth
including
• glucose uptake
• glycogen and protein
synthesis
• amino acid transport
Adopted from Felix F. Vajdos, et al. 2001.
Role of IGF-1
• Growth hormone - a naturally occurring hormone
– One of its major functions, among other actions, is to
promote production of IGF-1
• IGF-1 is normally secreted in response to stimulation
by growth hormone
• IGF-1 is usually necessary for normal growth and
metabolism, and stimulates multiple processes
including:
– Glucose uptake
– Glycogen and protein synthesis
– Amino acid transport
• Deficiency of, or resistance to, growth hormone can
cause IGFD, which can lead to short stature in children
IGF-I Measurements in the
Diagnosis of Short Stature
Significance of basal IGF-I measurements in the diagnostics of
short stature in children
600
GHD
500
400
95th
300
50th
200
5th
95th
300
50th
200
5th
100
0
0
5
10
15
20
(Percentile)
400
100
0
Non-GHD
500
(Percentile)
IGF-I (µg/L)
IGF-I (µg/L)
600
0
Age (Years)
• Virtually all GHD are secondary IGFD
• 50% of the non-GHD are also Primary IGFD
Ranke M, et al. J Clin Endocrinol Metab. 2000;85:4212-4218.
5
10
15
Age (Years)
20
Measuring IGF-1 and IGF-BP3
Levels to Assess for GHD
• IGF-I and IGFBP-3 more than 2 standard
deviations below the mean for age and gender
strongly suggest GH insufficiency
• Low IGF-1: GHD or GH resistant
• GH levels are measured
• If GH levels are high, GH resistance is likely
• However, low levels of GH may not distinguish GHD
from GH resistance
– Under these circumstances, provocative (stimulation)
tests of growth hormone secretion may be indicated
Farber R, Kerrigan J. Pediatric Annals. 2006;35(12):926-932.
Growth Hormone Provocative
(Stimulation) Testing
• A number of provocative agents can be used to test for GHD
including arginine, clonidine, glucagon, insulin, and L-dopa
• GH response to insulin is the most reliable test for GHD
– Great care should be exercised in using insulin or
glucagon in young children
• Before accepting a GHD diagnosis, many insurance
companies require a documented failure to demonstrate a
GH response after presentation of 2 provocative stimuli
• However, provocative testing often has limitations:
– Poor assay standardization among laboratories
– Results may conflict with other growth data
– No bimodal distribution of response
GH Research Society. J Clin Endocrinol Metabol. 2000;85(11):3990-3993; Owens G. Am J
Manag Care. 2000;6(15 Suppl):S839–S852.
Magnetic Resonance Imaging (MRI)
of the Brain and Pituitary Gland
• Cranial imaging may be appropriate
in patients found to be GHD and
– IGF-1 levels are low or
– IGFBP-3 levels and GH stimulation
tests are low
• Rule out brain tumor (eg,
craniopharyngioma) or other
etiologies
• Approximately 15% of patients with
GHD have an abnormality of the
pituitary gland (eg, ectopic bright
spot, empty or small sella)
Scott R, Hedley-Whyte E. N Eng J Med. 2002;347(20):1604-1611.
Growth Axis:
The Primary Pathway
Growth Hormone
Receptor Activation
Growth Hormone
Secretion
Post-Receptor
GH Signaling
IGF-1 Gene
Expression
IGF-1 Secretion
Endocrine IGF-1
Growth
Short Stature Due to Primary
IGF-1 Deficiency
Growth Hormone
Receptor
Growth Hormone
Secretion
Primary
IGFD
Post-Receptor
GH Signaling
IGF-1 Gene
Expression
GHD
(Secondary
IGFD)
IGF-1 Deficiency
Short Stature
Insulin-like Growth Factor-1
(IGF-1) Deficiency
• Primary Insulin-like Growth Factor-1 Deficiency
(IGFD) refers to IGFD caused by resistance to
growth hormone
• Short stature due to Primary IGFD
– Height standard deviation score ≤–2.0 and
– Basal IGF-1 standard deviation score ≤–2.0 and
– Normal or elevated growth hormone
• Resistant to the effects of growth hormone
• Restoring IGF-1 levels to normal may be an
appropriate treatment option
Height (cm, in)
IGF-1 Deficiency: Short Stature
but Normal Growth Rate
x
x
x
xx
x
x x
x
x x
x
x
Hwa V, et al. J Clin Endocrinol Metab. 2005;90:4260-4266.
Untreated severe
Primary IGFD
Distribution of First Year
Change in Height
Pre-pubetal IGHD & ISS Patients
Percent of patients
IGHD
ISS
-1
0
2
1
Year 1 change in height SDS
3
• Median first year
changes in height were
+0.77 SDS in IGHD and
+0.60 SDS in non-GHD
ISS patients
• 24% of IGHD patients
and 13% of ISS patients
had a first-year change
in height SDS between
year 1 and 2
Rosenthal S, et al. Pediatr Endocrinol Rev. May 2007;4(Suppl. 2):S252-S271.
Synergistic Effect of Growth Hormone
and IGF-1 in Mouse Postnatal Growth
17 %
34 %
14 %
69 %
35 %
W:
G:
I:
D:
Wild-type (100% of normal body weight)
GHR KO (52% of normal body weight)
IGF-I KO (30% of normal body weight)
IGF-I & GHR KO (17% of normal body weight)
GHR, growth hormone receptor; KO, knock-out.
Lupu F, et al. Dev Biol. 2001;229(1):141-162.
Non GH or IGF
GH KO alone
IGF-I KO
GH + IGF-I KO
Treatment Algorithm: Severe
Primary IGFD (Height <-3 SDS)
Short Stature
Height <-3 SD
GHST
-3< Height <-2.25 SD
Height >-2.25 SD
Reassess in 6-12
months, as indicated
GHST
GH <10 ng/mL
GHD
MRI, molecular studies
GH Rx
GH <10 ng/mL
GHD
MRI, molecular studies
GH Rx
GH >10 ng/mL
GH >10 ng/mL
ISS
IGF-I >-3SD
ISS
Consider GH Rx
Consider GH Rx
IGF-I <-3 SD
Primary IGFD
Consider molecular studies
Consider no Rx
Consider IGF-I Rx
Consider GH Rx
Consider No Rx
Rosenthal S, et al. Pediatr Endocrinol Rev. May 2007;4(Suppl. 2):S252-S271.
Treatment Algorithm:
Primary IGFD
Short Stature
Poor linear growth
Delayed puberty
Absence of family history
Height <–2.25 SD
Height >–2.25 SD
GHST
Reassess in 6-12
months, as indicated
GH <10 ng/mL
GHD
MRI, molecular studies
GH Rx
IGF-I <–2.5 SD
Primary IGFD
GH >10 ng/mL
ISS
Consider molecular studies
Consider GH Rx
Consider IGF–I Rx
Consider GH Rx
Consider no Rx
Consider No Rx
Mecasermin: Recombinant-human
Insulin-like Growth Factor-1
• FDA-approved for long-term
treatment for growth failure
in children with severe
primary IGF-1 deficiency or
GH gene deletions who
have developed neutralizing
antibodies
• Patients undergoing at least
one year of mecasermin
treatment demonstrated
statistically significant
improvements in growth
Increlex™ Prescribing Information (Mecasermin, Tercica, N=71).
Mecasermin Improves Height
• In clinical trials, height
velocity increased the
first year, on average to
8.0 cm/year from a
baseline of 2.8 cm/year
(P<0.0001)
• In Years 2 through 6,
height velocity was
sustained at
approximately 5
cm/year (P<0.005)
Increlex™ Prescribing Information (Mecasermin, Tercica, N=71).
Important Considerations
with Mecasermin Therapy
• Mecasermin is not a substitute for GH treatment
• Primary IGFD patients cannot be expected to
respond adequately to exogenous GH treatment
• Mecasermin should not be used for growth
promotion in patients with
– closed epiphyses
– active or suspected neoplasia
– allergies to mecasermin (IGF-1)
Increlex™ Prescribing Information (Mecasermin, Tercica, N=71).
Adverse Events with
Mecasermin Treatment
• Hypoglycemia
– Highest frequency occurred in the first month of treatment and is
more frequent in younger children
• Tonsillar hypertrophy was noted in 11 (15%) subjects in the
first 1 to 2 years of therapy with lesser tonsillar growth in
subsequent years
• Intracranial hypertension occurred in 3 subjects
– Events resolved without interruption of treatment in 2 patients
and the other patient discontinued and resumed later at a lower
dose without recurrence
• Lipohypertrophy at injection sites noted in 24 subjects (32%)
– Resolved when injections were properly rotated
Increlex™ Prescribing Information (Mecasermin, Tercica, N=71).
Short Stature: Summary
• Short stature can be promptly recognized with accurate
measurements of growth and critical analysis of growth
data
• Appropriate evaluation for poor growth and endocrine
consultation are crucial prior to electing therapy
• An individualized approach to children with short stature
should be practiced, taking into consideration factors such
as psychosocial concerns and must exclude alternative
etiologies of poor growth prior to consideration of therapy
• Recent advances in the field have resulted in several
successful treatment options, including GH and mecaserim
Appendix
Supplemental Slides
Helpful Hints with Reimbursement:
GH Stimulation Test Coding Sheet
• 99211 Limited office visit
• 99354 Prolonged attendance, 1st hour (face-to face)
• 99355 Prolonged attendance each additional 30 minutes
physician (face-to face) x 4
– Bill this code 4 times
• 99358 Prolonged attendance, 1st hour physician not
face-to-face (then 99359)
– Use this instead of 99354, 99355 if no MD present
• 36415 Venipuncture
• 32912 Injection, sodium chloride
• 31820 Injection, insulin up to 100 units
Cohen, J. Personal communication.
Helpful Hints with Reimbursement:
GH Stimulation Test Coding Sheet
• 33490 Arginine
• 80428 Growth hormone stimulation panel
– Growth hormone – 83003 x 4
• 80435 Growth hormone deficiency panel
– Glucose – 82947 x 5; growth hormone – 83003 x 5
• 80434 Insulin tolerance panel
– Cortisol – 82533 x 5; glucose – 82947 x 5
• 82533 Cortisol – each additional
• 82948 Glucometer – each additional
• 83003 Growth hormone – each additional
Cohen, J. Personal communication.
Unique Educational
Opportunity!!!
• Join your colleagues in a live Q&A/Discussion
with a leading pediatric endocrinology expert
• Share your challenging cases
• Discuss current treatment strategies
• Register Online Today at
www.plexuscomm.com/shortstature
Thank You
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If you have any questions, please contact
[email protected].
Thank You!!!
Jay Cohen, MD, FACE, FAAP,
CEC