Distribution of liver haemosiderin iron in 187 patients with various types of hepatic diseases

Abstract

The purpose of this study was to evaluate the distribution of haemosiderin iron in various regions of the liver (central, intermediary and peripheral hepatocytes, Kupffer cells, portal macrophages and bile duct epithelial cells) in 174 patients with different hepatic diseases (alcoholic cirrhosis (n=49), alcoholic steatosis (n=60), non‐alcoholic cirrhosis (n=16), acute hepatitis (n=20), clinically overt untreated hereditary haemochromatosis (n=3), miscellaneous disorders (n = 26)), and in 13 subjects with a normal liver biopsy. Furthermore, the relationship between liver haemosiderin iron, biochemical iron status markers and biochemical liver tests was investigated. In haemochromatosis iron was consistently present in all examined regions of the liver, and in 43% of patients with alcoholic liver disease haemosiderin was present in at least one region of the liver lobule. In 65% of patients with acute hepatitis, haemosiderin was present in macrophages and Kupffer cells. In other hepatic diseases and in normal livers, haemosiderin was rarely seen. Regression analyses showed a correlation between iron status markers in most patients, except in those with high serum aspartate aminotransferase levels. In conclusion, haemosiderin iron is distributed in a typical pattern in haemochromatosis, alcoholic liver disease and acute hepatitis. Both histochemical liver iron and serum ferritin are of value as indirect markers of liver iron stores in patients with moderate hepatocellular damage.

Clinical significance of serum ferritin in patients with systemic sclerosis

“…The SF in the blood circulation was cleared by hepatocytes, 17 and the ability to deal with SF decreased when the liver was injured, resulting in an increase in serum SF. In addition, the increase in SF was caused by the release of SF into the blood because of the degeneration or necrosis of some hepatocytes, and the increase in SF was positively correlated with the degree of hepatocyte damage 18 . Therefore, we believe that the increase in SF in patients with SSc may be related to liver injury.…”

“…In addition, the increase in SF was caused by the release of SF into the blood because of the degeneration or necrosis of some hepatocytes, and the increase in SF was positively correlated with the degree of hepatocyte damage. 18 Therefore, we believe that the increase in SF in patients with SSc may be related to liver injury.…”

Hemosiderin deposits in chronic graft‐vs.‐host disease related myopathy

“…Hemosiderosis, which resembles primary hemochromatosis, usually involves mainly the liver and spleen but also may occur in the pancreas, heart and joints. Typical features of hemosiderosis are high serum ferritin, low transferrin and deposits of hemosiderin, a ferroprotein complex found mainly in the reticuloendothelial system (27–29).…”