Study of insulin-like growth factor-1 (IGF-1) and platelet-derived endothelialcell growth factor (PDEGF) expression in children with infantile hypertrophic pyloric stenosis.
Janusz Jabłoński, Renata Gawrońska, Aleksandra Gawłowska, Józef Kobos, Ewa Andrzejewska
Med Sci Monit 2006; 12(1): CR27-30
Background: The pathogenesis of infantile hypertrophic pyloric stenosis(IHPS) is not fully understood. Hypertrophy of the pyloric muscle is probably regulated by growth factors.Recent studies reported an increase in the local synthesis of insulin-like growth factor-1 (IGF-1). Thereare no reports concerning platelet-derived endothelial cell growth factor (PDEGF) playing an importantrole in the pathological angiogenesis. The aim of this study was to analyze the expressions of IGF-1and PDEGF by immunohistochemistry (IHC) in the muscularis propria of the pyloric muscle in children withIHPS. Material/Methods: Twenty-two muscle biopsies were obtained at the time of pyloromyotomy. The controlgroup consisted of seven children. Specimens were evaluated by routine histopathological methods andby immunohistochemistry using monoclonal mouse anti-PDEGF or -IGF-1 antibodies. Cells showing positivereaction were counted in five random 200x high-power fields. Values were expressed as the mean +/-SDof the real expression area of the analyzed marker to the total analyzed area. Results: In children withIHPS the average area of PDEGF expression was 62+/-52.5, whereas in the control group it was 15+/-12.1.The average area of IGF-1 expression was 1037+/-491.9) in study group and 259+/-221.44 in the controls.Statistically significant differences were found. Conclusions: These results show a local increase inthe expressions of IGF-1 and PDEGF in the muscularis propria of the pyloric muscle in children with IHPS,which may have implications to the pathogenesis of the disease.
Keywords: Biopsy, Animals, Child, Humans, Immunohistochemistry, Infant, Insulin-Like Growth Factor I - metabolism, Pyloric Stenosis, Hypertrophic - surgery, Pylorus - surgery, Random Allocation, Thymidine Phosphorylase - metabolism