Severe Hemosiderosis Post Allogeneic Bone Marrow Transplantation

Abstract

Abnormal liver function persisting late after allogeneic BMT is usually attributed to chronic GvHD, viral hepatitis or drug toxicity. We describe a patient who had negative hepatitis serology, was on no hepatotoxic medication, had no evidence of GvHD but had abnormal liver function 15 months post MBT. She was diagnosed as having grade IV hemosiderosis of the liver. Her total red cell support had only been 52 units. We therefore postulate that in a proportion of patients receiving allogeneic BMT impaired intestinal iron absorption may be an important cause of hemosiderosis.

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

“…Generalized hemosiderosis is frequently described in cGVHD after SCT (24–26). Its causes include prior transfusion of red blood cell concentrates and presumably an impaired intestinal iron absorption in cGVHD.…”

Iron overload in bone marrow transplant recipients

“…However, in this study, no correlation was found between the total number of transfused red cell units and tissue iron content, suggesting that other factors, including dyserythropoiesis leading to increased intestinal iron absorption, are also important. 6,23 It should be noted that 8/10 patients in this series had received 50 or fewer red cell units since diagnosis of their hematologic disease. This level of transfusion is much lower than the 100-150 units of blood generally considered necessary for iron-induced tissue damage.…”

“…Iron overload may be a cause of persistent hepatic dysfunction after marrow transplantation, 6,8 possibly due to a combination of acute toxic effects with free radical formation and lipid peroxidation of membranes, 25,26 the effects of intracellular iron accumulation. 27 Patients with hepatic iron overload, particularly if they are also immunocompromised, are at increased risk of a variety of opportunistic infections wich such organisms as Yersinia enterocolitica, 28 Listeria monocytogenes, 29 mucormycosis 30 and non-cholera vibrio species.…”

“…4,5 However, there are limited data on objective quantitation of liver iron content after marrow transplantation for hematologic malignancy. Furthermore, the consequences of excess tissue iron in non-thalassemic patients who survive marrow transplantation have not been clearly defined, although a role in both short-and long-term hepatic dysfunction [5][6][7][8] appears likely. The aims of this study were to examine the degree of hepatic iron overload in patients receiving bone marrow transplantation for hematologic malignancy and to evaluate a new method of morphometric analysis of marrow iron content as a means of estimating hepatic iron stores in these patients.…”

Genomic screening and complications of hematopoietic stem cell transplantation: has the time come?

“…[82][83][84][85][86][87][88][89] Iron present in excess amounts or in reactive forms is a potent pro-oxidant and probably a radiosensitizing agent, because it can rapidly generate highly toxic free radicals in vivo ( Figure 5). 8,[90][91][92] Iron overload is common in this population due to red cell transfusion and/ or dyserythropoiesis.…”