1: Typical HCC nodule in the cirrhotic liver in CT/MRI and histopathology.
Male; 56 y; follow up in HCV cirrhosis.
CT contrast medium: lesion > 2 cm; global contrast enhancement in arterial phases (wash in); wash out in following phases; capsule enhancement (Fig.1).
MRI is more sensitive and is performed to exclude other lesion.
The sequence after contrast medium confirms the contrast enhancement behavior of the lesion as CT image (Fig 2).
The lesion appears mild hyperintense in T2w fat-sat and in DWI (high density cellularity).
No loss of signal in out phase,
due to absence of fat (Fig.3).
Radiologic diagnosis is HCC.
The patient is candidate for surgery.
Resection specimen of hepatic lesion:gross appearance of capsulated nodular lesion,
in the background of cirrhotic parenchyma (Fig.
In microscopic image (silver stain) the hepatocellular architecture is distorted; multiple nodular hepatic cell plates,
surrounded by fibrous septa,
typical findings of cirrhosis (Fig.
EE stain on lesion show a nodular hypercellular lesion with capsula, different from surrounding cirrhotic parenchyma (Fig.
Magnification of the lesion: pseudoglandolar aspect; the reticulin fibers show thickening of the hepatic cell plates which appear as two or three cell thick plates instead of the usual 1 cell thick plate.
Areas of reticular loss are presents (Fig.
Immunohistochemistry CD34 show unpaired arteries and sinusoidal capillarization (Fig.
Microscopic vascular invasion implies impossibility to liver transplant (Fig.
Pathological diagnosis: hepatocellular carcinoma with vascular invasion.
Male; 80 y; aspecific liver disease; occasional US detection of a lesion on the left lobe.
MRI: left lobe is replaced by a large mass.
This shows inhomogeneous signal (Fig.
A few restriction areas are present; mild loss of signal because of small amount of fat (Fig.
After administration of gadolinium,
no significative contrast enhancement.
After 20 minutes the lesion appears hyperintense,
except for a few hypointense areas (Fig.
Radiologic suspect is atypical HCC on cirrhosis liver.
In microscopical image distorted architecture with multiple nodular formation.
Microscopical features: no portal spaces are present; few mithosis are observed,
still these features do not allow a straightforward diagnosis (G1?) (Fig.
Silver stain: loss of reticular and increased cellular density with monomorphic pattern.
CD 34: sinusoidal capillarization (Fig.
Due to the small amount of specimen,
to support diagnosis,
immunohistochemistry is performed.
Lesion is proven to be malignant (Fig.
Left lobectomy is performed (Fig.
steatotic and peliotic features are demonstrated on the surgical specimen (Fig.
Pathological diagnosis:Well- differentiated hepatocellular.
chronic liver disease.
MRI: The lesion > 2 cm; contrast enhancement in arterial phases; mild wash out in following phases; capsule enhancement.
Inhomogenously hypointense in the hepatobiliary phase (Fig.
Radiologic suspect is a malignant lesion.
After biopsie:Regular hepatocites,
no portal space.
Absence of atypia.
Reticulin structures are maintained (Fig.
Vascular remodeling is present (Fig 20).
The positive to rhodanin stain demonstrates the presence of copper.
The pathologic suspect is Focal Nodular Hyperplasia.
Dysmorphic proliferation of biliar ducts in the external portion of lesion.
Glutamine synthetase normally stains a thin rim of hepatocytes around the central veins.
staining in focal nodular hyperplasias will show an irregular typical “maplike” pattern (Fig.
Pathological diagnosis:Focal Nodular Hyperplasia.
Patient male; 66 y; alcoholic liver disease.
Suspect HCC nodule.
CT show mild hypodense lesion in basal with contrast enhancement in arterial phase and fade in venous phase (Fig.
Radiological suspect is HCC for new onset and for the underlyng disease.
Liver resection was performed (Fig.
In specimen typical features of cirrhosis was present (Fig.
Intralesion Masson Stain is positive for the presence of many amount of collagene.
Furthermore presence of lymphocites,
in absence of hepatocites (Fig.
The vascular spaces are clearly identified by immunohistochemistry for the endothelial marker CD34 (Fig.
Pathological diagnosis: sclerotic haemangiomas.