Clinical_Rounds_in_Endocrinology_Volume_II_-_Pediatric_Endocrinology

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  1. What is “catch-up” growth?


“Catch-up” growth is defined as accelerated height velocity above statistical
limits for the corresponding age and gender during a particular time interval,
following a transient period of growth inhibition. “Catch-up” growth helps the
child to attain pre-retardation growth curve. The exact mechanisms implicated
in “catch-up” growth are not well explicited, but two hypotheses have been
proposed: “neuroendocrine” hypothesis and “growth plate” hypothesis. The
neuroendocrine hypothesis proposes that there is a set point in the brain for an
individual’s growth termed as “sizo-stat,” and this allows the “catch-up” growth
after a period of growth inhibition to achieve the age specified “preset” height
of an individual. However, it was refuted later. The “growth plate” hypothesis
reveals that during the period of growth inhibition, there is a slowing of chon-
drocyte senescence, followed by increased chondrocyte growth and prolifera-
tion during subsequent “catch-up” growth.


  1. Can “catch-up” growth occur despite decreased height velocity?


A unique type of “catch-up” growth is described in patients with precocious
puberty who are on therapy with gonadotropin-releasing hormone (GnRH) ago-
nists. In children with precocious puberty, height age is more than chronologi-
cal age but lesser than bone age. On treatment with GnRH agonist, the height
velocity actually decreases, but this is without advancement in bone age thereby
“height age catches up with bone age,” allowing them to attain the target height.
This is an example of “catch-up growth with decreased height velocity.”


  1. What is “catch down” growth?


The “catch down” growth is defined as deceleration in height velocity below
statistical limits for the corresponding age and gender during a particular time
interval. The term is commonly used to describe the growth pattern during ini-
tial period of life in children with FSS and CDGP, who rapidly crosses centile
downward during first 3 years of age. The exact cause for this phenomenon is
unknown; however, it is attributed to transient and subnormal functioning of
GHRH–GH–IGF1 axis (“lazy pituitary syndrome”).


  1. What are skeletal dysplasias?


Skeletal dysplasias (osteochondrodysplasias) are heterogeneous group of inherited
disorders which are characterized by intrinsic abnormality of chondro- osteogenesis.
Skeletal dysplasias are commonly classified on the basis of site of involvement as
epiphyseal, metaphyseal, diaphyseal, or spondylo (spine) dysplasia. These disor-
ders may be associated with short stature and/or short arm/thighs (rhizomelia),
short forearm/legs (mesomelia), or generalized shortening of the entire limb
(micromelia/phocomelia). Achondroplasia is the prototype of skeletal dysplasia
and is characterized by disproportionate short stature with rhizomelia (shoulder to
elbow length < elbow to metacarpal length) and metaphyseal dysplasia. Children
with achondroplasia are born with normal birth length but experience progressive
decline in growth velocity by 1–2 years of age, and the final adult height is severely

1 Disorders of Growth and Development: Clinical Perspectives
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