Case 335: Hemosiderosis
54 year old woman with myelodysplastic syndrome.
MR: With focal fat in segment 4
MR with gadolinium shows focal fatty replacement adjacent to the falciform ligament in a siderotic liver. There is diffuse decreased signal intensity in the liver and spleen parenchyma in the in-phase, opposed-phase and fat saturated T2w images, representing iron overload.
On the in-phase image the area of focal steatosis is hyperintense, which proves that it is also spared from iron overload, as iron overload is transmitted to the liver mainly through the portal vein. The area of sparing adjacent to the falciform ligament is typically void of portal venous blood supply as it is vascularized solely by arteries and an aberrant splanchnic vein from the distal stomach, pancreas or proximal duodenum, which do not carry iron overloaded blood from the small bowel. The aberrant vein is therefore sparing this area from exposure to iron overload.
On the out-of-phase image the lesion is hypointense, which proves that this part of segment 4 is not only free of iron overload, but over exposed to insulin loaded splanchnic blood, which comes from the pancreas, suggesting that in this patient the aberrant blood supply originates from a pancreatic vein. Increased concentrations of insulin in the liver cause focal areas of fatty replacement, as they cause hepatic steatosis in chronic hyperinsulinemia. The region is isointense to liver parenchyma on fat suppressed T2w and shows no restricted diffusion.
Upon contrast administration, the focal steatotic area is hyperintense relative to liver parenchyma on the arterial phase and becomes isointense to liver parenchyma in the portal venous and equilibrium images. There is no mass effect on the surrounding vessels.