ECE2015 Eposter Presentations Pituitary: clinical (121 abstracts)
1Department of Zoology, Pir Mehr Ali Shah Arid Agriculture University Rawalpindi, Rawalpindi, Pakistan; 2The Childrens Hospital Pakistan Institute of Medical Sciences (PIMS), Islamabad, Pakistan; 3Shifa International Hospital, Islamabad, Pakistan.
In GH deficiency (GHD), which is a medical condition caused by problems in the pituitary gland, the body does not produce sufficient amount of GH, resulting in short stature in children. The treatment of GHD short children with exogenous GH increases linear growth velocity (LGV). The present study determined the effect of exogenous GH treatment on LGV, the dose(s) of exogenous GH that effectively impacts LGV and the stage(s) of puberty at which the effect of exogenous GH treatment on LGV is more pronounced. Blood samples, height, weight, and LGV of forty (20 boys and 20 girls) GHD short children were obtained, plasma was separated and plasma concentrations of GH and IGF1 were determined using specific assay systems. Data were analysed using Students t-test and ANOVA. The GHD short children, diagnosed on the basis of low plasma GH, IGF1 and lower responses to stimulation tests, were given varying doses of GH (0.021.7 mg/day for 1242 months) administered intramuscularly at different ages (518 years) and stages (pre-, early, mid, and late) of pubertal development. GH replacement therapy caused greater increases in LGV at higher doses at pre- and early puberty in both female and male patients as compared to GH treatment at mid and late puberty. The plasma concentrations of GH and IGF1 increased significantly in all patients as compared to those found prior to GH treatment, which indicates that increases in LGV is secondary to augmentation in IGF1 secretion. In conclusion, the present study demonstrates that patients of GHD grow at a greater rate at higher doses of GH. The current investigation also shows that GH therapy caused higher increases in LGV at pre- and early puberty in both girls and boys through its effects on IGF1.