الفهرس 
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Abstract
One of the hallmarks of isolated growth hormone deficiency (GHD) is the impairment of linear growth. In addition, children with GHD also show changes in body composition mainly consisting in increased adipose tissue with preferential central deposition and accompanying decrease in lean mass (Van der Sluis et al., 2002). Several studies have addressed the metabolic role of GH as it has proven lipolytic effect and a direct influence on carbohydrate metabolism (Del Rinconet al., 2007).
The aim of our work was to assess glucose homeostasis in GH deficient children, assess serum leptin in GH deficient children, and determine the effect of GH replacement on their level after 9 months of therapy.
This study was conducted on 50 children, [30 GHD children (14 males and 16 females) recruited from Nile Health Insurance, whose age ranged from 5-11 years, with mean of 8.39 ± 2.009 years, and 20 healthy controls (14 male and 6 female) recruited from Pediatric Outpatient Clinic, Children’s Hospital Ain Shams University, whose age ranged from 5-10, with mean of 7.73±1.89].
All subjects matching the inclusion criteria were subjected to:
1- Full history taking: lying stress on age, gestational age, birth weight, height of parents.2- Full clinical examination laying stress on:
Systemic examination to exclude other illness. Anthropometric measurements which includes height, height SDS, weight, weight SDS, BMI, BMI SDS according to norms of Cole, (2000).
Tanner pubertal staging according to (Marshall and Tanner, 1969).
3- Laboratory investigations:
Serum levels of fasting blood glucose (FBS), fasting serum insulin, fasting serum leptin were measured.
Our study revealed the following:
Height SDS was significantly lower in the cases than controls.
Fasting blood glucose was significantly higher while serum leptin was significantly lower among cases than controls.
There were non significant differences regarding all clinical data among both sexes.
All laboratory data did not differ among both sexes in studied cases.
All auxological parameters increased significantly after GH therapy among studied cases.
Fasting insulin rose significantly while leptin dropped significantly after GH therapy. Serum leptin did not correlate significantly with any of clinical parameters before and after GH treatment.
Serum leptin did not correlate with any of the glycemic parameters but correlated negatively with GH levels.
Changes in GH was a significant predictor of reduction in serum leptin levels.