International Journal of Clinical Case Reports 2015, Vol.5, No. 45, 1-6
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Table III Final herght of patients GHD who completed their puberty in both sexes
Height
B (n = 84)
G (n = 66)
Average target height(cm)
Extremes
168,6 ±1,8
(164,4 – 170,6)
163,7 ±4,7
(156,2 – 166,1)
Average height at the 1
st
consultation
X DS
SDS(Extremes)
- 4,1
0,8
(- 4,77 ; - 3,5)
- 5, 2
1,2
(- 6,3 ; - 4,02)
Growth retardation
Average /Tc at the 1
st
consultation
XDS
SDS(Extremes)
- 3,5
1,02
(- 4,3 ; - 2,9)
- 4,7
1,7
(- 6,3 ; - 3,1)
Average final height
X cm
SDS(Extremes)
153,2
5,3
(148,4 – 157,8)
142,8
5,7
(136,6 – 146,8)
Average final height
X DS
SDS(Extremes)
- 3,4
1,02
(- 4,1 ; - 2,8)
- 3,8
1,06
(- 4,8 ; - 2,9)
Average final height / Tc
XDS
SDS(Extremes)
- 2,1
1,1
(- 2,9 ; - 1,9)
- 3,8
1,03
(- 4,8 ; - 2,8)
Total average stature gain
XDS
SDS(Extremes)
0,7 ±0,7
(0,2 – 1,2)
1,4 ±1,1
(0,3 ; 2,4)
The same observations can be made for the girls.
Average age of patients in the study at the beginning
of puberty was 13.9 ±2.8 years (vs. 11 years (Marshall)
and 11.7 ±1.33 year (Maïza)). The Age at the end of
puberty was 17.4 ±2.8 years (vs. 14.5 (Marshall) and
16.3 years (Maiza)). However, the time of the progress
of puberty: 3, 1 ± 1.1 years was comparable to the
results of Marshall (Marshall and Tanner, 1970) and
Maiza (1983).
As regards the menarche, the average age is significantly
delayed compared to Marshall 15.46 ±2.00 vs. 13.47
± 0.10 years (p <0.005) and Maiza 13.66 (P<0.05)
(Carroll and Christ, 1998), and if we consider the
secular advance of menarche, the noticed delay would
be found even greater.
In fact, regardless of sex, puberty can be performed at
a normal age when the diagnosis of GH is made and
treatment is instituted early; this was found in ten
patients in the study.
On the other hand, it should also be noted that if
puberty is generally carried out normally, a reduction
in the duration of the course of puberty may even
(Bourguignon et al., 1986). This was observed in two
patients in this study. This reduction in the duration of
puberty is linked to the action of growth hormone on
bone maturation. An advance of puberty may also be
(Tobiume et al., 1997; Price and Heidelberg, 1999).
Currently, all authors would agree to say the role of
diagnosis and early treatment with the GHr in the
development of puberty. Indeed, GH plays a key role
in gonadal function by inducing local production of
IGF1 in the ovaries and testes which increases sex
steroids production. The IGF1 promotes ovulation in
females (Daftary and Gore, 2005).
Also, the lack of growth hormone IGF1 includes
disrupting follicular development which could be the
cause of ovarian disease (DOPK) in GHD patients
whose frequency has been reported by some authors
(Kazerr et al., 1990; Morales, 1997; Pienkowski et al.,
2007).
This aspect of DOPK was found in five patients in the
study who showed Spanio menorrheys with multiple
ovarian sub-centimeter follicles in ultrasound.
The finding of DOPK in GH emphasizes the need for
prevention of this complication by early and regular
hormone substitution.
Moreover, it should be noted that the used strategies to
optimize growth stature pubertal failed to consensus.
Whether to increase GH doses in order to mimic the
physiology of the pubertal growth (Blethen, 1997;
Codner, 1997; Carel, 2004), or block puberty using
similar LHRH (Hibi et al., 1989; Balducci et al., 1995;
CASSORLA, 1997). The results are divergent. If
Mauras et al. (1996) demonstrated that tripling the
