International Journal of Clinical Case Reports 2015, Vol.5, No. 45, 1-6
3
Table I The average height of patients GHD at diagnosis in both sexes
AUXOLOGY
Boys N :84
Girls N :66
P
Average height X cm ±SD
Extremes
103,3 ±2
(58 – 152)
97,3 ±3
(56 – 140)
DNS
X DS ±SD
Extremes
- 4,7 ±1,8
(- 12,0)
- 4,9 ±2,3
(- 11,8, - 2,8)
DNS
X SDS ±SD
Extremes
- 4,7 ±1,6
(-9,4 ; 0,8)
- 4,9 ±2,3
(-11,9, - 2,8)
DNS
Average Growth rate during the year prior to treatment
X cm / an ±SD(Extremes)
2,7 ±0,5
( 1 – 3,2 )
2,5 ±0,4
( 2 – 3,5 )
DNS
Table II Results on the pubertal growth
Height
B ( n = 84) G ( n = 66)
Average height at puberty
X cm
SDS
XDS
SDS
140,2
1,2
- 3,8
1,3
96,2
2,3
- 4,3
1,4
Pubertal Average Stature Gain
X cm
SDS
14,7
1,2
12,2
1,9
The exact prevalence of this disorder is unknown in
Algeria. In Europe and the United States, it is
variously estimated and varies between 1/4000 and
1/10 000 (August et al., 1990).
When the diagnosis is suspected, it is advisable carry
out a quick and paraclinical exploration and to undertake
substitutive treatment with biosynthetic growth hormone
in order to correct the stature deficit because in the
absence of substitutive hormone, the spontaneous
evolution is a dwarfism with adult final height between -
4 and -7 DS / TC (Job, 1992; Besson et al., 2003).
The main effect of growth hormone treatment is to
stimulate during childhood growth in stature and thus
enable obtaining adult height that is equal to the target
height. In addition to this very important effect, growth
hormone plays a key role in body composition,
carbohydrate and lipid metabolism and bone mass
(Albertsson-wikland, 1999; Abdu, 2001).
A significant improvement in the final height with
biosynthetic growth hormone was found in the literature.
This is correlated in addition to parental height, early
diagnosis, optimization of treatment and height at
onset of puberty. Bernasconi et al. (2000), Blethen et
al. (1993) and Cutfield et al. (1999) have clearly
demonstrated through their large series the correlation
existing between age at start of treatment and the final
height.
The bad results regarding the final height of our
patients are explained by the late age at diagnosis and
getting started hormone substitutive therapy. The
irregular, inadequate and the non repayment of the
treatment that our country knew before the last decade
explain the stature evolution of GH D. These results
are almost those of a spontaneous evolution. The
ignorance of the disease and abnormalities of growth
by many practitioners and the lack of systematic
monitoring of all children by the growth curve explain
the long delay in diagnosis and the start up treatment.
Yet the growth curve reflects the health of the child
and any slowdown or break of the growth rate should
lead to undertake an informed etiological exploration.
In terms of sexual development, pubertal delay is
typically reported in GHD patients especially in boys
(Burns et al., 1981; Coutant and Carel, 2002). This
delay is found in almost all the cases in our study. In
agreement with the literature, it is more important for
boys than for girls. Burns and al (Burns et al., 1981)
found that the age of pubertal development in these
patients was 15.9 years for boys and 12.7 years for
girls. The comparison of pubertal development of
patients in the study with those of the Marshall studies
(Marshall and Tanner, 1970) and those of Maiza (1983)
on Algerian healthy subjects showed that boys have an
average onset puberty and later completion of puberty:
2.4 years (this study) vs. 12 (Marshall) and 12.16
years (Maiza)
16.4 and 19.8 ±2.2 years (this study)
vs. 15.18 years (Marshall) and 16.16 ±1 year (Maiza).
However the course of puberty is normal and
comparable to the results of Marshall (Marshall and
Tanner, 1970; Maiza, 1983).
