K. Thakerngpol et al., LIVER-INJURY DUE TO IRON OVERLOAD IN THALASSEMIA - HISTOPATHOLOGIC AND ULTRASTRUCTURAL STUDIES, BioMetals, 9(2), 1996, pp. 177-183
The livers of 30 cases of thalassemia (19/beta-thal/HbE, seven thal/Hb
H and four beta-thal major) were studied histopathologically and elect
ron microscopically, in an effort to define the morphologic alteration
s due to iron overload. The results of light and electron microscopy w
ere similar in most cases. Iron accumulation and fibrosis were the com
mon features found in these patients, except that thal/HbH exhibited l
esser hepatic damage. The degrees of iron deposition and fibrosis were
found to be higher in splenectomized and cirrhotic than non-splenecto
mized and non-cirrhotic patients. The subcellular changes were swollen
mitochondria, with the presence of an electron dense matrix and ruptu
red mitochondrial membrane. Proliferation of smooth endoplasmic reticu
lum (ER) and dilated rough ER was observed. Increases in lysosomal hem
osiderin in hepatocytes and in Kupffer cells were demonstrated. The po
ssible ways by which the iron compounds or free radicals mediated memb
rane damage are mentioned. The pattern of liver cell damage is similar
to that of viral hepatitis.