Background/purpose: The proto-oncogene c-kit encodes a receptor tyrosine kinase C-KIT. W/Wv mice, which are devoid of C-KIT+ mast cells as a result of mutations in the c-kit gene, develop spontaneous gastric ulceration or perforation after day 7 of life at a high frequency, whereas normal litter mates do not. The authors hypothesized that a lack of C-KIT+ mast cells may be implicated in the development of idiopathic gastric perforation (GP) in neonates.
Methods: Postmortem gastric wall specimens were taken from neonates who died of GP (idiopathic, n = 6; secondary, n = 4), and other causes (controls, n = 6). Specimens were taken at random from various sites in the stomach and labeled with antibody to C-KIT. The number of C-KIT+ mast cells from five random fields per specimen were compared under light microscopy (200x).
Results: Overall, the number of C-KIT+ mast cells was significantly lower in gastric wall specimens from cases of idiopathic GP when compared with controls or cases of secondary GP irrespective of the sites of sampling (P<.01, analysis of variance test) with the distribution of cells being uniform and unique for each stomach.
Conclusion: A lack of C-KIT+ mast cells may underlie the development of idiopathic GP in neonates.