Our observation of an ac-cell response to arginine stimulation comparable with that seen in idiopathic diabetes agrees with the observations of Passa et a14 and contrasts with the impaired responses found in patients with transfusional haemosiderosis, suggesting that factors other than iron deposition play a part in the genesis of diabetes associated with IH.In IH, however, there may possibly be a selective destruction of the 5-cell, the high plasma glucagon values thus merely reflecting insulin lack, and it is of interest that McGavran et al,5 in necropsy studies, observed more iron in the n-cells than in the ax-cells.This predisposition of the p-cell .oriron deposition was, how- ever, also noted in transfusional haemosiderosis.Clearly further histological studies using modern techniques are indicated.Hepatic cirrhosis (proved in nine of our cases) may contribute to the diabetes associated with IH, but is unlikely to be the cause of the high glucagon concentrations, since liver function values were abnormal in only two of our cases and there was no evidence of portocaval shunting.These findings add to the accumulating evidence that diabetes in patients with IH is not due solely to islet cell damage by iron.' 2 4 Several factors, including hepatic cirrhosis, genetic influences, or iron deposition, might play a part.Each of these may operate to varying degrees in individual cases.
R E B TagartD. G. BrathertonL. HartleyKarol Sikora