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Internal Distribution of Excess Iron and Sources of Serum Ferritin in Patients with Thalassaemia
Author(s) -
Cazzola Mario,
BorgnaPignatti Caterina,
Stefano Piero de,
Bergamaschi Gaetano,
Bongo Ilde G.,
Dezza Laura,
Avato Franco
Publication year - 1983
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1983.tb01494.x
Subject(s) - ferritin , spleen , siderosis , ascorbic acid , medicine , concanavalin a , chemistry , endocrinology , ferrihydrite , hepatitis , pathology , immunology , biochemistry , food science , organic chemistry , adsorption , in vitro
Liver and spleen iron concentrations, serum ferritin level and binding of S‐ferritin to concanavalin A (Con A) were measured in 12 patients with thalassaemia major or intermedia at the time of splenectomy. All these subjects had increased liver iron concentration, most of them had hepatic fibrosis but none of them had histological evidence of chronic hepatitis. No patient had ascorbic acid deficiency. Serum ferritin concentration was increased in all cases, ranging from 266 to 5 504 μg/l. In all but 2 subjects most of the protein did not bind to Con A, thus behaving as tissue ferritin. There were highly significant correlations between serum ferritin concentration, amount of blood transfused and liver iron concentration. On the average, iron concentration in the liver was about 3 times that in the spleen. The findings obtained suggest that in patients with thalassaemia major or intermedia most of the iron is deposited in parenchymal tissues and most of the S‐ferritin derives by leakage from the cytosol of iron‐loaded parenchymal cells. S‐ferritin is a valid index of liver iron overload in thalassaemic patients without complications such as viral hepatitis and/or ascorbic acid deficiency.