The increase of iron in the liver could be due:

1. to a genetic hemochromatosis: the iron load is frequently significant with a ratio LIC/age>2. Right now, the diagnosis is done by genetic test and there is no place for MR. The level of overload could be estimated by hperferritinemia, if there is no other associated disease. In genetic hemochromatosis, the iron overload is due to a default of regulation of iron intestinal absorption and then the iron in excess is stored in the liver.
2. to a dysmetabolic hemosiderosis, a frequent disease, combining a slight overheight, glucid or lipid metabolism dysregulation ... Patient are older. A splenic slight overload is frequent.
3. to a chronic hemolysis, repeated blood transfusions (17, 18). In that context, splenic overload is predominant.
4. to a cirrhosis (33) ...

The decrease of liver signal is usually homogeneous. Rarely the liver could be heterogeneous in case of cirrhosis, abnormalities of vascular distribution (35), hematoma after biopsy, underlying heterogeneous liver steatosis or presence of nodules (36).

After 45 yo, the screening for a small hepatocellular carcinoma must be systematic, using 5 mm slice thickness and a T2 weighted sequence (breathhold T2* GRE sequence or respiratory gated T2 FSE.
 

Multifocal HCC easily seen in a hypointense liver

GRE "T1"  TR=120 ms, TE=4 ms, PA=90°	GRE "T1"  TR=120 ms, TE=4 ms, PA=90°

 
 

On the other hand, a decrease of splenic signal is observed in secondary overload, when iron is predominantly stored in the reticuloendothelial system (37). 
 

Decrease of the signal intensity of the spleen

GRE "T2"  TR=120 ms, TE=14 ms, PA=20°

 
Small siderotic nodules in the spleen are observed in case of portal hypertension.