الفهرس 
Material and methodsOnly 14 pages are availabe for public view
 |  | from | 275 |  |  |
| | | from | 275 | | |
Abstract
In our study we investigated the serum growth hormone
releasing hormone (GHRH) and growth hormone levels after a
mixed meal. The degree of metabolic control was assessed
by measuring the glycosylated haemoglobin Ale. Growth
parameters including weight, height and weight by stature
were measured as a centile according to the age.
In our work 56 children were included:
- 20 healthy controls (10 males and 10 females).
- 36 100M children (12 males and 24 females).
Both groups were sUbjected to:
- Full history and thorough clinical examination
- Urine analysis: sugar - acetone - albumin.
- Complete blood picture and sedimentation rate.
- Kidney function tests: blood urea & serum creatinine.
- Fundus examination.
- X-ray chest.
Serum GHRH and GH levesl were measured using
radioimmunoassay.
217
our results showed:
* A non significant difference between both patients and
controls regarding GHRH (P > 0.05).
* A significant increase in s. G.H. in diabetic patients as
compared to the control.
* A highly significant increase in glycOsylated haemoglobin
(HbA1C) in diabetic patient as compared to the control
(P < 0.001).
* A non significant difference between diabetic patient
group and control groUP regarding growth parameters.
Recently an argument has been held around the role of
the hypothalamic pituitary axis.
GHRH
GHRH outside
secreting pancreatic tumours causing acromegallY has been
identified. Many researchers has postulated the release of
GHRH from the upper GIT and pancreas espe,ciallY after a
mixed meal. So, we wanted to find out whether there is any
difference between diabetic patient group and control
normal groUP,
but we
could not find a significant
difference.
plays a significant, if any, role in the regulation of the
metabolic control in diabetic children.
so, it seems unlikelY that circulating GHRH
218
The significant increase in serum G.H. concentrations
in diabetic patients when compared with the control groUP,
with the following explanation:
* Insulin like growth factor I (IGF-I) decrease causes an
increase in G.H. level as a compensatory mechanism by
the pituitary.
* A failure of the pituitary to be suppressed in response
to hyperglycaemia implies a possible second abnormality.
It is probablY more likely that gluCose acts indirectlY
by stimulating hypothalamic somatostatin secretion.
Another explanation is that althOUgh the blood gluCoSe
levels are high, the intracellular gluCOse
concentrations are decreased i.e. ”starvation in the
midst of plenty”. These intracellular hypothalamic
nuclei (which secrete GHRH and somatostatin) will
stimulate the pituitary G.H. secreting cells.
Regarding growth parameters, there was a non
significant difference between both groUPs. 100M children
who are now on two daily doses of insulin can maintain
their growth well without a significant influence on the
achieved growth. There was a non significant correlation
with glycosylated haemoglobin Ale i.e. degree of metabolic
control.