Relationship between hepatocellular injury and transfusional iron overload prior to and during iron chelation with desferrioxamine: a study in adult patients with acquired anemias

Abstract

The role of iron overload as cause of liver dysfunction has never been studied in detail in patients without concomitant hepatotropic infections who receive multiple transfusions. We therefore investigated the relationship between the extent of hepatocellular injury as reflected by serum levels of aminotransferases (

Comparison of the Prophylactic Effect of Silymarin and Deferoxamine on Iron Overload-Induced Hepatotoxicity in Rat

“…The protective effect of silymarin is associated with its antioxidant properties, as it possibly acts as a free radical scavenger, lipid peroxidation inhibitor, and preservation of the activity of total serum antioxidants [17]. The prophylactic effect of silymarin and deferoxamine on iron overload-induced nephrotoxicity in rats was evaluated by our research team.…”

Iron-overload in long-term survivors of hematopoietic transplantation

“…Therefore, in the absence of data from liver biopsy, it appears that clinically significant iron overload does not occur until serum ferritin levels are greater than 1000 mg/dL. 9 Few studies report the clinical significance of iron overload in transplant survivors. However, Butt et al 5 reported on serum iron parameters in 32 long-term survivors of acute myelogenous leukemia (allogeneic ¼ 6, autologus ¼ 10, chemotherapy ¼ 16).…”

“…8 At 1 year post transplant, when inflammatory stress has largely subsided, most patients have a serum ferritin of o1000 mg/dL and no clinical evidence of iron-overload; serum ferritin in these patients declines slowly with time. 9 In another group of patients, however, issues such as viral hepatitis (25-50% incidence in some series) and GVHD affect both liver function tests and serum ferritin, 3,4 and confound the diagnosis of clinically significant iron overload. Jensen et al, 9 identified liver iron concentrations of 300-350 mM/g as a critical level above which hepatocelluar injury, as reflected by aminotransferase elevation, was likely to occur.…”

“…9 In another group of patients, however, issues such as viral hepatitis (25-50% incidence in some series) and GVHD affect both liver function tests and serum ferritin, 3,4 and confound the diagnosis of clinically significant iron overload. Jensen et al, 9 identified liver iron concentrations of 300-350 mM/g as a critical level above which hepatocelluar injury, as reflected by aminotransferase elevation, was likely to occur. Both increased urinary iron excretion (415 mg/24 h) and serum ferritin 41000 mg/dL (R 2 ¼ 0.55, Po0.0001) correlated with alanine aminotransferase elevation and high liver iron.…”

“…6,7 Apart from its harmful effects on organ function (liver, heart, endocrine organs), iron overload can also result in worsening of viral hepatitis and its response to therapy, worsening of hepatic GVHD, and increased risk of opportunistic infections (Yersinia enterocolitica, Vibrio vulnificans, Listeria monocytogenes, Aspergillosis and Mucormycoses). 4,6,[8][9][10] Hyperferritinemia is a common late effect of hematopoietic transplantation. 3 Although serum ferritin level does not correctly reflect body iron stores in all clinical circumstances, the combination of elevated ferritin with elevated transferrin saturation accurately identifies patients with increased body iron stores.…”