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o s te r T e m p la te ro m w w w .m a n c h e s te .a c .u k /p h o to g ra p h ic s Age (months) Congenital Hyperinsulinism of Infancy (CHI) is a potentially lethal condition of profound hypoglycaemia caused by unregulated insulin release in the neonatal period and early infancy. CHI mainly arises due to mutations in ATPsensitive K-channel genes (ABCC8 and KCNJ11) which can manifest in all islets cells – diffuse CHI (CHI-D), or can be localised to a focal lesion, focal CHI (CHI-F). Increased rates of cell proliferation have been reported in the CHI-D and this may be liked to ABCC8 and KCNJ11 defects. Here, we examined the proliferative index (PI) of islet cells in CHI-D patients and compared this with focal CHI (CHI-F), which is caused by loss of cell cycle repression in β-cells specifically within the focal domain. We also examined islet PI in patient tissues with severe CHI unrelated to defects in ABCC8 and KCNJ11, atypical CHI (CHI-A). Background

Islet cell proliferation is inappropriately maintained in the pancreas of children with congenital hyperinsulinism in infancy