Siderotic nodule is a nodular lesion containing iron (hemosiderin) deposition in the liver parenchyma. In cirrhotic liver, regenerative nodules and dysplastic nodules can accumulate iron. Iron is retained via the reticuloendothelial system (Kupffer cells) in the setting of portal hypertension and chronic liver disease. It is the hepatic analog of Gamna-Gandy bodies in the spleen. Shows markedly hypointense signal on T2-weighted and especially GRE sequences on MRI.
Age Range
40-75
Peak Age
55
Gender
Male predominant
Prevalence
Common
In cirrhotic liver, hepatic blood flow is disrupted due to portal hypertension. Preserved portal vascularization and Kupffer cells (reticuloendothelial system) in regenerative nodules continue to accumulate iron (hemosiderin) particles via phagocytosis. Iron deposition is particularly prominent in nodules with preserved portal blood flow — therefore siderotic nodules are typically seen in the setting of LGDN or regenerative nodules. In HGDN and HCC, portal tract architecture is lost and Kupffer cell function decreases → iron is not retained → 'iron-sparing' phenomenon occurs. Iron exhibits superparamagnetic properties and dramatically shortens T2/T2* relaxation.
Much more pronounced hypointensity and blooming on GRE sequences compared to T2-weighted (hypointense area larger than actual nodule size). The superparamagnetic effect of iron particles disrupts local magnetic field homogeneity, dramatically shortening T2* relaxation. This finding is the pathognomonic MR signature of siderotic nodule.
Markedly hypointense signal on T2-weighted sequences. Results from iron deposition shortening T2 relaxation time.
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Multiple nodules demonstrating markedly hypointense signal on T2-weighted sequences are seen in the cirrhotic liver, consistent with siderotic nodules.
Much more pronounced signal loss and blooming artifact on GRE (T2*) sequences compared to T2-weighted. Most sensitive sequence for iron detection.
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Exaggerated hypointense appearance of nodules (blooming artifact) on GRE (T2*) sequences confirms iron deposition.
Isointense or mildly hyperintense signal on T1-weighted. Iron may also cause T1 shortening through paramagnetic effect.
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The nodules show isointense/mildly hyperintense signal on T1-weighted sequences.
No enhancement on arterial phase of contrast-enhanced MRI. Benign iron deposition does not contain neoangiogenesis.
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No significant enhancement is observed in siderotic nodules on contrast-enhanced series.
May appear mildly hyperattenuating to liver parenchyma on unenhanced CT. However, CT is much less sensitive than MR for iron detection.
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Small nodules mildly hyperattenuating to liver parenchyma are seen on unenhanced CT; MRI evaluation is recommended for iron deposition.
Variable uptake on hepatobiliary phase with gadoxetic acid — iron deposition complicates signal assessment. Usually isointense or difficult to interpret.
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Hepatobiliary phase assessment in siderotic nodules is limited due to susceptibility effect of iron deposition.
Criteria
Iron deposition in regenerative nodule. Most common type. Very low malignant potential.
Distinct Features
Usually <10 mm, multiple, and homogeneously hypointense. Size and signal characteristics remain stable over time.
Criteria
Iron deposition in dysplastic nodule. Portal vascularization preserved, Kupffer cells active.
Distinct Features
LGDN features + T2/GRE hypointensity. Development of 'iron-sparing' focus during follow-up indicates hepatocarcinogenesis progression.
Criteria
Diffuse iron deposition throughout the liver in hereditary hemochromatosis or transfusional siderosis. Diffuse rather than focal nodular form.
Distinct Features
Entire liver homogeneously hypointense on T2/GRE. Pancreatic involvement may accompany (hemochromatosis). Splenic involvement favors transfusional siderosis (spleen is spared in hemochromatosis).
Distinguishing Feature
Regenerative nodule without iron may be isointense or mildly hypointense on T2 but does not show marked blooming on GRE. In siderotic nodule, GRE hypointensity is much more pronounced (susceptibility effect).
Distinguishing Feature
HCC is typically 'iron-sparing' — while siderotic surrounding parenchyma/nodules are T2 hypointense, HCC focus does not retain iron and appears relatively T2 hyperintense. HCC shows arterial enhancement and washout; siderotic nodule has no enhancement.
Distinguishing Feature
Calcified granuloma shows punctate calcification on CT — hypointense on T1/T2 on MRI but does not show as marked blooming on GRE as siderotic nodule. CT is superior to MR for detecting calcification; MR is superior to CT for detecting iron.
Distinguishing Feature
Peliosis hepatis contains blood-filled sinusoidal dilation and is T2 hyperintense (not hemosiderin, but fresh blood/lacunae). May be T1 hyperintense if hemorrhage is present. Shows enhancement. T2 hypointensity and lack of enhancement in siderotic nodule are distinguishing.
Urgency
surveillanceManagement
conservativeBiopsy
Not NeededFollow-up
12-monthSiderotic nodules are benign and do not require treatment on their own. However, annual MRI follow-up is recommended due to hepatocarcinogenesis risk in cirrhotic liver. Development of an 'iron-sparing' focus (area not retaining iron within siderotic nodule) during follow-up is an early sign of HCC transformation and requires short-interval follow-up/biopsy. The underlying cause (hemochromatosis, transfusional siderosis) should be investigated and treated.
Benign lesion requiring no treatment. However, as it occurs in cirrhotic liver, it should be followed as part of regular HCC surveillance. Loss of iron content in siderotic nodules (T2 signal increase) is a warning sign for dysplastic transformation.