Jp. Lu et K. Hayashi, SELECTIVE IRON DEPOSITION IN PANCREATIC-ISLET B-CELLS OF TRANSFUSIONAL IRON-OVERLOADED AUTOPSY CASES, Pathology international, 44(3), 1994, pp. 194-199
Pancreatic islets of 36 autopsy cases with transfusional iron-overload
were examined. Immunohistochemical and histochemical stainings were u
sed to clarify the relationship between blood transfusion and iron dep
osition in the islet. Disease of the lymphohemopoietic system (leukemi
a, lymphoma, aplastic anemia) or liver (carcinoma and/or cirrhosis) ac
counted for 86.1% of the patients' main diagnosis. Sixteen of them had
slight hemosiderin deposition (Group 1), twenty cases had severe hemo
siderin 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 +/- 3.6, 17.5 +/- 12.2 L for Groups 1 and
2, respectively. The plasma glucose was 137.8 +/- 54.4 and 170.6 +/-
108.4mg/dL, respectively. Four cases in Group 1 and 14 cases in Group
2 had glycosuria. The number of islet cells with hemosiderin increased
with the enlargement of transfusion volume (r = 0.664, P < 0.001). Pl
asma glucose also related with the percentage of hemosiderin positive
islet cell (r = 0.386, P < 0.025). In severely iron-overloaded 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 mellit
us of the patients.