Background: Congenital heart disease (CHD) is the most common cause of major congenital anomalies. Malnutrition is a constant phenomenon among children with congenital heart disease, irrespective of the nature of the cardiac defect and the presence or not of cyanosis. Many factors may influence growth failure in C.H.D. like feeding disorders, inadequate caloric intake and endocrine factors.
Objectives: The aim of this work was to evaluate insulin like growth factor 1 in children with congenital heart diseases as possible cause of growth affection.
Patients and Methods: After obtaining the approval of the Al-Azhar University Ethical Committee, A cross-sectional study was conducted on sixty children (32 males and 28 females). The study was carried out in Al-Azhar University Hospitals (AL- Hussein &Sayed Galal Hospitals), during the period from January 2017 to May 2019. All patients gave their written informed consents prior to their inclusion in the study. Sixty children divided into 3 groups (control, cyanotic & acyanotic). A blood sample was taken from each participant with the aim of assessment of IGF1. Also Echocardiography, Chest x ray, Electrocardiography had done, Anthropometric measures & Oxygen saturation were measured.
Results: we found highly statistical significant (p-value < 0.001) decrease in the level of IGF1 between studied groups. There was no statistical significant difference (p1-value = 0.15) between cyanotic group and acyanotic group. Highly statistical significant difference (p2-value < 0.001) between cyanotic group and control group. Highly statistical significant (p3-value < 0.001) decrease between acyanotic group and control group. Also we found Highly statistical significant difference (p-value < 0.001) between studied groups as regard weight, B.M.I, SD weight for length and height (p-value=0.001).
Conclusion: We determined that IGF1 was low in children with congenital heart diseases. It was lower in malnourished more than well nourished, and was also lower in cyanotic more than acyanotic. As when caloric restriction is present, mammals synthesize less IGF-1 and its synthesis in the liver is refractory to GH stimulation