Selective iron deposition in pancreatic islet B cells of transfusional iron‐overloaded autopsy cases

Pancreatic islets of 36 autopsy cases with transfusional ironoverload were examined. lmmunohistochemical and histochemical stainings were used to clarify the relationship between blood transfusion and iron deposition in the islet. Disease of the lyrnphohernopoietic system (leukemia, lyrnphorna, aplastic anemia) or liver (carcinoma and/or cirrhosis) accounted for 86.1% of the patients’ main diagnosis. Sixteen of them had slight hernosiderin deposition (Group l), twenty cases had severe hemosiderin deposition (Group 2). Another ten cases were used as controls (Group 3). The cases had a similar age distribution to Group 1 and 2, with neither blood transfusion nor hemosiderin deposition. The volume of blood transfusion was 6.1 2 3.6, 17.5 t 12.2 L for Groups 1 and 2, respectively. The plasma glucose was 137.8 2 54.4 and 170.6 t 108.4 rng/dL, respectively. Four cases in Group 1 and 14 cases in Group 2 had glycosuria. The number of islet cells with hernosiderin increased with the enlargement of transfusion volume (f = 0.664, P c:: 0.001). Plasma glucose also related with the percentage of hernosiderin positive islet cell (r = 0.386, P ‘: 0.025). In severely ironoverloaded cases, hemosiderin was selectively deposited in B cells of the islet. It was concluded that large amounts of blood transfusions for non-congenital disease can induce selective hemosiderin deposition and impairment of pancreatic B cell that may result in hyperglycemia and diabetes rnellitus of the patients.