Patterns of Catch-Up Growth
Caroline C. de Wit, MD1, Theo C. J. Sas, MD, PhD2,3, Jan M. Wit, MD, PhD4, and Wayne S. Cutfield, MD, PhD1
F
rom embryogenesis to young adulthood, growth rate
declines dramatically. This deceleration in growth
velocity is most extreme in infancy with a more subtle
slowing in growth velocity through mid-childhood, interrup-
ted by the pubertal growth spurt, after which the growth rate
gradually declines to zero.1 While in the first years of life the
length of healthy infants can cross the percentiles toward
their genetic target height (TH) SDS, height tends to remain
within a narrow “channel” on the growth charts between
3 years and the onset of puberty, close to the same percentile
or SDS position. The tendency to keep to this narrow and
predictable track of growth is called “canalization.”2 An
SDS change of >0.25/year is rarely seen in longitudinal
growth studies on normal children.3
A large variety of growth-retarding illnesses, including
hypothyroidism, celiac disease (CD), malnutrition, Cushing
syndrome or chronic steroid treatment, and growth hormone
(GH) deficiency, can lead to a slowing in growth with a
downward deviation from the standard growth curve. After
release from these growth-inhibiting conditions, exaggerated
acceleration in linear growth can occur. In 1963, Prader et al4
and Tanner5 introduced the term “catch-up growth” to
describe this period of rapid linear growth in children that
followed a period of growth inhibition, leading toward their
original growth channel. The term catch-up growth is also
used for the growth acceleration seen in 85% of infants
born small for gestational age (SGA),6 although in these cases
there is usually no information about the foregoing down-
ward deviation.
The term catch-up growth is mostly used for height.
Catch-up growth has been defined as “a height velocity above
the statistical limits of normality for age or maturity during
a defined period of time, following a transient period of
growth inhibition; the effect of catch-up growth is to take
the child towards his/her pre-retardation growth curve.”7
Even though this definition would imply that for a proper
assessment of catch-up growth the full growth trajectory
has to be evaluated (up to adult height), only few studies
on catch-up growth have included all parts of this trajectory
(the phases of growth inhibition, growth acceleration, growth
maintenance, and puberty and the achieved adult height in
comparison with the genetic growth potential). Furthermore,
several alternative definitions of catch-up growth have been
used, for example (in children born SGA) reaching an SDS
of > 2 for the reference population8 or a cut-off of a change
CD Celiac disease
GH Growth hormone
SGA Small for gestational age
TH Target height
of >0.67 SDS in the first year.9 Data on the growth curve after
the initial phase of catch-up growth and on the adult height
corrected for mid-parental height (TH) are often lacking,
presumably because of the difficulties in obtaining frequent
growth data over long periods of time. In only a few studies,
for example in GH deficiency,10,11 hypothyroidism,12,13 and
CD,14 have data on the complete pattern of catch-up growth
including data on adult height been described.
Catch-up growth also occurs for other growth parame-
ters, such as body weight, body composition, head circum-
ference, and body segments (sitting height and leg length).
For example, catch-up growth observed in the early stages
after treatment of CD is generally characterized by an ini-
tial weight increase before height catches up, thus an initial
rise of body mass index.14 A mismatch between catch-up
growth in height and in abdominal fat is seen in babies
born preterm or SGA, in which there is greater increase
in adiposity than height, which has been associated with
a higher risk of cardiovascular disease.15
Parameters of Catch-Up Growth
We have previously argued16 that the first year height velocity
is not suitable as the sole parameter for catch-up growth,
because it is highly variable, lacks precision, and incompletely
depicts catch-up growth.17 In addition, the average height
velocity for age is highly dependent on the height percentile
of the child. For example, if height is to stay on 3rd percentile,
a height velocity at approximately the 25th percentile is
needed.16 Furthermore, from a series of height velocities
one cannot get a good impression of the position of the
patient’s height versus the population’s reference charts.
A better parameter of catch-up growth, particularly when
assessed over the full trajectory, is height SDS and its change
over time.16 There is no agreed cut-off criterion for catch-up
growth, and we suggest that a sustained increase in height
SDS toward the height SDS before the start of growth
retardation would suffice as definition. One would expect
that the size and speed of the height SDS change during the
first years of catch-up growth depend on the distance
between height SDS and TH SDS, as well as on age. In fact,
this has been observed for GH deficiency.18
From the 1The Liggins Institute, University of Auckland, Auckland, New Zealand;
2
Department of Pediatrics, Albert Schweitzer Hospital, Dordrecht, The Netherlands;
3
Department of Pediatrics, Erasmus Medical Centre, Rotterdam, The Netherlands;
and 4Department of Pediatrics, Leiden University Medical Center, Leiden, The
Netherlands
The authors declare no conflicts of interest.
0022-3476/$ - see front matter. Copyright ª 2013 Mosby Inc.
All rights reserved. http://dx.doi.org/10.1016/j.jpeds.2012.10.014
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Potential Mechanisms of Catch-Up Growth
We have previously discussed the 2 main hypotheses that
have been proposed to explain catch-up growth: the neuro-
endocrine hypothesis and the growth plate hypothesis.7 The
neuroendocrine hypothesis was proposed by Tanner in
1963 and is based on the classical endocrine concept of
central steering of processes.5 Tanner suggested that a
mechanism—possibly located in the hypothalamus—is able
to compare the size of the body with the individual’s expected
size for that age. This was called a “time tally.” If a mismatch
is recognized, the body is encouraged to continue growing at
a faster-than-normal rate. When the mismatch becomes less
distinct, the growth velocity will decrease.5 So far, no exper-
imental evidence for this hypothesis has been collected.
The growth plate hypothesis is based on an old concept pro-
posed by Osborne and Mendel in 1914, who showed that pro-
longed nutritional deprivation in the rat was followed by
growth at an age well beyond the normal growth period of
the species. They suggested that age is not the limiting factor
for growth but that growth is limited by the intrinsic capacity
for growth of the tissue itself.19 After further work in this area
by Williams,20 a study in rabbits by Baron et al21 gave this hy-
pothesis its present shape by suggesting that the mechanism
for catch-up growth is intrinsic to the growth plate. They pro-
posed that catch-up growth arises from a delay in normal
growth plate senescence. During normal growth plate senes-
cence, the proliferative rate of the growth plate chondrocytes
diminishes with each successive stem cell cycle. Thus, growth
plate senescence is not a function of time per se but rather
a function of the cumulative number of divisions the stem cells
have undergone. After cessation of suppression of prolifera-
tion, in Baron et al’s experiments by glucocorticoids or hypo-
thyroidism, the cumulative number of stem cell divisions is
lower than expected. After the suppression of proliferation,
the cells therefore begin to proliferate at a faster rate than
the nonexposed cells, leading to local catch-up growth.21
None of the 2 hypotheses gives a fully satisfactory explana-
tion for the mechanism of catch-up growth in humans. The
neuroendocrine hypothesis lacks experimental support, and
the growth plate hypothesis can only explain one specific
type of catch-up growth.22
Published Patterns of Catch-Up Growth
In 2 seminal articles,23,24 Tanner distinguished 3 different
growth patterns that potentially lead to the same (normal)
adult height. In the first pattern (A), the cessation of the
growth restriction is followed by an increased height velocity
(up to 4 times the mean velocity for chronologic age), which
fully eliminates the growth deficit. When the original growth
curve is achieved, height velocity returns to normal. In the
second pattern (B), the growth-restricted child grows slightly
faster than normal for age but at a normal velocity for bone
age, resulting in a longer growth period and a normal adult
height. The third pattern (C) shows a growth velocity at
the average level for chronologic age but with delayed bone
416
Vol. 162, No. 2
maturation, resulting in growth that goes on for longer
than usual. As noted by Tanner and by ourselves, type C
formally cannot be considered catch-up growth, because by
definition “velocity” should be above normal for age,16,24
and we do not discuss this further.
Type A catch-up growth is seen as the classic example of
catch-up growth and has been reported for several children,
such as in some of the cases in the first reports of Prader et al4
and Tanner.25 This pattern can be seen in some infants and
young children after growth restriction due to CD when
a gluten-free diet is introduced,14 in the majority of young
children with hypothyroidism after treatment with levothyr-
oxine,13 and in many children with GH deficiency who are
receiving GH treatment. Children with CD show on average
a type B catch-up growth, with a height velocity that is
consistent with height age and bone age,22 conforming to
the hypothesis of delayed senescence.21,26 Another example
of type B catch-up growth was given in a report on 2 men
with hypopituitarism, in whom GH treatment was started
at age 22.7 and 24.3 years at a bone age of 13-14 years. At
ages 27.9 and 29.1 years, respectively, they had gained 22
and 21 cm in height, and their growth velocity was normal
for their bone age.27
An Intermediate Type of Catch-Up Growth
(Type AB)
We noticed that some catch-up growth curves of children
with CD,14,22,28 hypothyroidism,13,29 GH deficiency,11 and
preterm born children30,31 showed a catch-up growth pattern
inconsistent with the classic types described by Tanner. In-
stead, they showed an increased growth velocity in the first
years of treatment, followed by a stabilization of height
SDS about half of the initial height SDS and genetic TH for
a number of years, and a delayed pubertal growth spurt, after
which they finally reached an adult height that was close to
TH (or lower). If this pattern was arbitrarily defined as a fail-
ure to catch up toward the target range (TH 1 SD) within 3
years and further growth toward adult height of >1 SD, it was
observed in 4 of 11 children (aged 1.2-10.1 years) with
primary hypothyroidism and 2 of 8 children with GH defi-
ciency (aged 0.4-9.3 years) (J.W., unpublished analysis of
data reported by Ranke et al13 and Sas et al11). For illustrative
purposes, we show the growth curve of a boy with GH
deficiency, who participated in a dose-response study,11 in
comparison with the theoretical curves for type A and B
catch-up growth (Figure 1). This type of catch-up growth
is intermediate between types A and B. We suggest calling
this form “catch-up growth type AB,” which is
characterized by an initial faster growth than normal for
bone age, which then passes into a phase of stable height
SDS, which remains below TH SDS, until the delayed
puberty causes an increase of height SDS toward TH SDS.
It is unclear why in some children catch-up growth is
abrogated halfway and in others it continues until TH SDS
is reached. We speculate that if the underlying disease re-
mains active (eg, inadequately treated CD), treatment is
de Wit et al
February 2013 COMMENTARY

Figure 1. Growth curve of a boy with GH deficiency, treated with GH, compared with the A and B types of catch-up growth
according to Tanner (interrupted lines). The boy grew at 2 SDS in the first 2 years, followed by a downward deviation to 4.1
SDS. At 6.6 years, GH treatment was started (0.7 mg/m2 body surface area/d, at 1 m2 equivalent to 25 mg/kg body weight/d) and,
in the first years of treatment, height SDS gradually increased to 2.4, followed by a stabilization at that height SDS until 17 years
of age. Although the onset of puberty (13.2 years) was still within the normal range, the tempo of puberty was slow, and adult
height was 173 cm ( 1.5 SDS), close to TH ( 1.3 SDS).32

nonphysiologic or inadequately dosed (eg, suboptimal dose
or poor adherence to GH treatment in children with GH
deficiency) or chondrocyte maturation has been adversely
affected (by previous exposure to corticoids or sex steroids),
type AB may be more likely to occur. In some cases, type AB
may also be a manifestation of underlying constitutional de-
lay of growth and puberty or of superimposed illness.
Phases of Growth of Children with Catch-Up
Growth
Ideally, for each child with an acquired growth disorder who
shows catch-up growth, information on his or her growth
curve should be available for the whole trajectory. In a com-
plete dataset, various phases of growth can be distinguished:
(1) the period of normal growth before the onset of the disease
(initial growth); (2) poor growth during the disease (growth
retardation); (3) the rapid phase of growth acceleration; (4)
the maintenance phase; (5) growth in adolescence; and (6)
adult height.
To assess whether catch-up growth is complete in an indi-
vidual child, one can follow 2 approaches. First, adult height
can be compared with the preillness growth curve, and catch-
up growth can be considered complete if adult height SDS is
close to the original height SDS. Second, adult height can be
compared with TH, and at an individual level catch-up
Patterns of Catch-Up Growth
growth can be considered complete if adult height is within
a range of TH 1.632 or 1.3.13,16 At a group level, complete
catch-up growth is defined by a mean adult height not statis-
tically different from mean TH.
The multiphase approach would imply that there is not
one single marker of catch-up but rather a pattern composed
of several elements. In the following paragraphs, we discuss
what is known about these phases in different conditions
where catch-up growth has been described.
Phases of Catch-Up Growth in Several
Disorders
Hypothyroidism
In theory, hypothyroidism is the best human model for
catch-up growth because it is free of growth constraints asso-
ciated with chronic disease. However, acquired primary hy-
pothyroidism, usually due to Hashimoto thyroiditis, occurs
mainly in older children and adolescents, so that catch-up
growth is often concurring with the pubertal growth spurt.
The growth retardation observed in hypothyroidism appears
to be a direct effect of thyroxine deficiency on skeletal growth,
but a secondary reduction of GH secretion and circulating
insulin-like growth factor-1 may also play a role.33
Once thyroxine replacement therapy is commenced, a
period of catch-up growth starts. In most young children,
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type A catch-up growth is observed, but some children show
a growth pattern more consistent with type AB.13 Because of
the unavailability of data on bone age at start of treatment, we
cannot rigorously exclude type B catch-up growth in these
children. However, growth in the first year is so rapid in
some children that it is likely greater than expected for
bone age. Even after a prolonged period of growth retarda-
tion, a very high growth velocity can be observed.29 In older
children and adolescents, catch-up growth coincides with pu-
bertal development, which is probably the main reason that
on average catch-up growth is not complete.12,29,34
There are very few data on catch-up growth after a long pe-
riod of thyroxine deficiency in infants born with congenital
hypothyroidism, because these children are usually detected
very early through congenital hypothyroidism screening.
We reported on a 14-year-old patient who had been hypothy-
roid from birth29 and showed an extremely fast catch-up
growth for 5 years, but in this patient pubertal development
occurred at the same time and is presumably responsible for
the short adult height. In such cases, administration of a go-
nadotropin-releasing hormone analog in early puberty may
improve adult height outcome.35,36
CD
In affluent countries, CD is one of the most prevalent causes of
reversible growth retardation.37 The pathophysiology of
growth retardation in CD has not been fully elucidated. It is
generally assumed that nutritional deficiency due to gastroin-
testinal malabsorption and inflammation plays a major role,
but cytokines from the diseased gastrointestinal tract may
also be involved. In a retrospective study on the effect of a glu-
ten-free diet, we found several patients who showed a clear
type A pattern of catch-up growth and average height SDS in-
creased to 0 SDS, suggestive of complete catch-up growth.14
However, in a later prospective study we showed that in the
first years the average catch-up growth is concordant with
type B.22,28 It is unclear whether a suboptimal catch-up
growth is primarily seen in patients who are less adherent to
the gluten-free diet. In the first 6-12 months after initiation
of the gluten-free diet, weight increases to the predicted weight
percentile, followed by an increase of length or height SDS.14
Besides CD, there are several other conditions that cause
undernutrition and subsequent growth inhibition. Often,
malnutrition is accompanied by other factors influencing
growth including suboptimal hygiene, vitamin deficiency,
and unfavorable psychosocial conditions, so that it is difficult
to assess catch-up growth. In a rare case of malnutrition in an
adolescent with intestinal protein loss secondary to constric-
tive pericarditis, surgical treatment led to resolution of the
protein loss and impressive catch-up growth, resulting in
a normal adult height.16
GH Deficiency
The growth of children with GH deficiency can be greatly
improved by GH replacement therapy, but in this condition
there is no certainty that physiologic conditions have been
fully restored. Studies on the growth response of children
418
Vol. 162, No. 2
with GH deficiency have shown that the pattern and com-
pleteness of catch-up growth depend on the dose chosen
and several other predictive variables.38 Of 8 children youn-
ger than 10 years on a relatively low GH dosage of 0.7 mg/m2/
d (equivalent to 25 mg/kg/d) 4 showed type A catch-up
growth. Two of the remaining children showed type AB
catch-up growth resulting in an adult height close to TH
(Figure 1), and 2 showed a partial catch-up growth and an
adult height below the target range. For the 7 children aged
1-10 years, we calculated mean (SD) height SDS for
chronologic age in the first 4 years of GH treatment, as well
as height SDS for adjusted age based on initial bone age.
The significant positive slope in the first 2 years indicates
that the average pattern of catch-up growth is not
consistent with type B (Figure 2). On the double dose, all
children showed type A catch-up growth (J.W. and T.S.,
unpublished analysis of data from Sas et al11).
It should be noted that even if adult height is in the pop-
ulation range, and close to TH, this can be the result of
relatively long legs and a short trunk, a consequence of
delayed spontaneous or induced puberty. These abnormal
body proportions have been documented several times and
have recently been illustrated by the growth curves of identi-
cal twins, one of whom had panhypopituitarism.39
In a review of several studies,40 as well as in a study of
a large database, adult height SDS of children with GH
A
2
Height SDS for CA
0
-2
-4
-6
0 1 2 3 4
Years of GH treatment
B
2
Height SDS for adjusted age
0
-2
-4
0 1 2 3 4
-6
Years of GH treatment
Figure 2. Height SDS for A, chronological age (CA) and B,
adjusted for initial bone age after institution of GH therapy (0.7
mg/m2 body surface/d) in 7 children with GH deficiency aged
1-10 years. Height SDS for adjusted age significantly in-
creased in the first year (P < .001) and second year (P = .014).
In the third and fourth years, no further increase was observed
(P = .401 and .618, respectively). Data derived from Sas
et al.11
de Wit et al
February 2013
deficiency who were treated with GH was substantially lower
than the population mean.41 It is likely that this is mainly
caused by suboptimal GH doses because the Swedish cohort
in this study (using a GH regimen of 0.23 mg/kg/wk)
reached an adult height close to TH.10 An additional reason
for incomplete catch-up growth may be noncompliance,
which appears more frequent that previously expected.42
Cushing Syndrome
In an initial report on catch-up growth by Prader et al4 and
a later article on the follow-up of several patients43 by Prader,
the authors described a girl who had an adrenal tumor result-
ing in Cushing syndrome. After surgical removal of the tu-
mor, an impressive, although incomplete, type A catch-up
growth was observed.43 A report on 10 children with Cushing
disease showed an increase in height velocity shortly after
treatment, but adult height was 1.3 SDS.44 It appears likely
that catch-up growth is incomplete because of a combination
of factors, such as irreversible effects on growth plates,7 adre-
nal androgen excess (and hence estrogen excess), and, subse-
quently, after pituitary surgery, hypopituitarism.
As far as we know, there are no reports on catch-up growth
after discontinuation of exogenous glucocorticoid adminis-
tration.
SGA and Prematurity
SGA is the common proxy parameter of intrauterine growth
restriction. There are multiple known causes of SGA, but in
many cases its cause remains unknown. It is well documented
that 80%-85% of children born with SGA increase their
height SDS above the lower limit of normal in the first year
of life,6,45-48 whereas the remaining children stay below the
3rd percentile.
The usual pattern of children born SGA who catch up is
that they show increased growth velocity in the first 2-3 years,
followed by a stable height SDS in childhood (usually some-
what lower than TH SDS), a normal age at onset of puberty,
and an adult height below TH.6,45-47 There are insufficient
data to determine if the pattern of catch-up growth is type
B or AB, but catch-up growth is usually incomplete.
Similarly to term infants born SGA, most preterm born in-
fants show catch-up growth in weight and length and head
circumference after initial postnatal growth failure.31,48-51 If
catch-up growth occurs, it generally starts early in the first
months of life and is often achieved within the first years
of life.31,48,49 In a representative study, catch-up growth in
height before the age of 3 years occurred in 81% of extremely
low birth weight infants, and catch-up growth in weight and
head circumference was found in 79% and 81%, respectively.
This resulted in an overall achieved catch-up growth for all 3
parameters in 65%.48 However, late catch-up growth of
preterm subjects, by many investigators also labeled as posi-
tive percentile crossing, has been described throughout
childhood50 and even in adolescence.52-55 Various studies
show that on average catch-up growth was not complete.
Like children born SGA, there are no data to determine the
type of catch-up growth.
Patterns of Catch-Up Growth
COMMENTARY
In a cohort of preterm and/or very low birth weight infants
followed until young adulthood,15 the average adult height
SDS was 0.55 and 0.60 for males and females, respec-
tively, but body mass index SDS was 0.10 and 0.17 and
waist circumference SDS was +0.24 for males and +0.73 for
females, indicating that catch-up growth did not run in
parallel for different measurements and may contribute to
a less favorable cardiovascular disease risk profile.15
Discussion
After the cessation or appropriate treatment of a postnatal
insult or illness leading to slow growth, catch-up growth is
expected. Besides the classic type A catch-up growth and
the slower type B, we suggest the existence of an
intermediate-type AB characterized by an initial period of
fast growth followed by a stable height SDS below TH SDS.
Although type catch-up growth is seen in most children
treated for primary hypothyroidism and classic GH deficiency
and type B in CD and possibly infants born SGA, we observed
type AB in some children with primary hypothyroidism, as
well as children with GH deficiency who are treated with
relatively low doses of GH. We suggest that, in reports on
catch-up growth, all phases of the growth curve up to adult
height should be described in the context of parental
heights. n
The authors thank Dr S.M.P.F de Muinck Keizer-Schrama (Erasmus
MC, Rotterdam, The Netherlands) for allowing us to use the data on
the cases with GH deficiency.
Submitted for publication May 30, 2012; last revision received Sep 6, 2012;
accepted Oct 4, 2012.
Reprint requests: Jan M. Wit, MD, PhD, Department of Pediatrics, J6S, Leiden
University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
E-mail: j.m.wit@lumc.nl
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