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ECR 2018 / C-2687
Focal and diffuse hyperintense hepatic lesions on unenhanced T1-weighted MR images: a pictorial essay
Congress: ECR 2018
Poster No.: C-2687
Type: Educational Exhibit
Keywords: Parasites, Metabolic disorders, Haemangioma, Contrast agent-intravenous, Chemoembolisation, Biopsy, MR, Liver, Anatomy, Abdomen
Authors: L. Mammino1, D. C. Caltabiano1, V. Costanzo1, M. Coronella1, G. Mazzone2, P. V. Foti1, P. Milone1, A. Basile1, S. Palmucci1; 1Catania/IT, 2Sant'agata Li Battiati (CT)/IT

Findings and procedure details

According to their histopathology liver lesions can be distinguished in benign and malignant.


Benign liver lesions


Diffuse pathologies:

  • Diffuse hepatic steatosis (Fig. 1): due to overload of triglycerides within the hepatocytes; may be distinguished an alcoholic- and nonalcoholic-disease. Since it is a benign lesion, there are no mass effect/infiltration of liver vessels and no contrast-enhanced areas of inhomogeneities. Out-of-phase T1w-images show loss of signal.


  • Wilson’s disease:  an autosomal recessive disease that is characterized by increased intestinal copper uptake due to abnormal caeruloplasmin metabolism and subsequent deposition of copper and damage to various organs. Hepatic manifestations include fatty changes, cirrhosis and sometimes fulminant hepatic necrosis. Perihepatic fat layer and normal caudate lobe are typical features of Wilson's disease. In the context of cirrhotic liver parenchyma, multiple nodular lesions may be observed: T2-weighted images show hypointense signal and hyperintense on T1-weighted images, according to copper deposit paramagnetic effect. However, paramagnetic effect may be masked by high level of T1 signal of liver in advanced cirrhotic stages [13].

Focal pathologies:


  • Focal hepatic steatosis (Fig. 2 - Fig. 3): may mimic a hepatic malignant lesion. Typical locations are adjacent to the falciform ligament, gallbladder fossa and liver hilum. It presents the same benign signs of diffuse pattern.
  • Complicated cyst (Fig. 4):  cysts are normally hypointense in T1 weighted images and hyperintense in T2; they may show high T1 signal because of hemorrhage or suppuration.
  • Hematoma: due to liver traumas or coagulation disorders, blood deposit is hyperintense in T1w images. Anamnesis, lesion morphology and the use of contrast medium are usually enough to raise a correct diagnosis.
  • Regenerative hyperplastic nodules (Fig. 5): generally related to chronic liver injury such as: alteration of tissue perfusion (portal hypertension or Budd-Chiari syndrome), toxic injury (alcohol) or viruses (HBV, HCV). These nodules are usually hypointense on T2 and T2* w images, and have variable T1 signal intensity. When they contain lipids they may show high T1 signal and signal loss in out-of-phase GRE images. Nodules present post-contrast enhancement similar to the adjacent liver both in arterial and hepatocellular phase [14].
  • Hepatic Adenoma: generally arises in young women exposed to long-term oral contraceptive therapy. According to their histopathology [15] liver adenomas may be classified in: 
  1. HNF1-alfa mutated (Fig. 6 - Fig. 7): associated with fat-content multiple adenomas.
  2.   Beta-catenin mutated: associated with glycogen metabolism alteration, abuse of anabolic steroids and higher probability of malignant degeneration.
  3. Inflammatory adenoma: the most common hepatic adenoma, usually hyperintense on T2w images. "Atoll sign" may be manifest.
  4. Unclassified adenoma: no mutations identifiable, no inflammation.

Hepatic adenoma are in 59-77% of cases fat-containing, showing usually signal loss in out-of-phase images. Intralesional hemorrhage or sinusoid dilatation may be other causes of T1 hyperintensity.

  • Atypical focal nodular hyperplasia (Fig. 8): represents a hyperplastic process of liver parenchyma that shows an abnormal microarchitecture pattern. Typical FNH  shows a central scar with radial arrangement of fibrous septa. Atypical lesions lack the central scar and may show T1 hyperintensity, which is related to copper accumulations due to bile duct obstruction, sinusoidal dilatation, hemorrhage (less frequent than in adenomas) or fat deposition (very uncommon) [10,16].
  • Lipoma (Fig. 9): very rare tumor consisting of mature adipose tissue. It shows T1 hyperintensity, india ink sign in out-of-phase images and signal loss in T1 fat-sat image [17].
  • Angiomyolipoma (Fig. 10): rare tumor formed by fatty cells, smooth muscle and blood vessels, that is associated with tuberous sclerosis. Contrast images show prolonged enhancement due to nonfatty components and sometimes an enlarged central vessel.


Malignant liver lesions


  • HCC (Fig. 11): generally hypointense on T1w-images and hyperintense on T2w-images. T1 hyperintensity may be present in 31-61% of tumors smaller than 3 cm due to intralesional presence of fat, copper, glycogen or proteins. Fat content is considered an important sign of transformation of premalignant lesion to HCC. Large tumors may show T1 high dishomogeneous signal because of hemorrhage or necrotic debris [18]. After chemoembolization the presence of lipiodol within the mass reduces T1 relaxation time resulting in hyperintensity. Radiofrequency ablation, also induces coagulative necrosis that causes T1 hyperintensity (Fig. 12)


  • Metastasis: normally are hypointense on T1w images and hyperintense in T2w- images. T1 high signal is related to hemorrhagic metastasis (Fig. 13), mucinous carcinoma’s metastasis or melanoma metastasis [19].


  • Liposarcoma: very rare malignant mesenchymal tumor. Fat content depends on grade of differentiation: low grade lesion has a high T1w images signal reflecting high fat content and shows contrast enhancement or local invasion evidence; high grade lesion shows low T1w signal because of the absence of fat and similar characteristics to other sarcomas. Most liver localizations of liposarcomas are indeed metastases of retroperitoneal or extremity liposarcomas [4,20].  


Rare entities


Very uncommon lesions may appear hyperintense on T1 w images such as: adrenal rest tumor of the liver, focal intrahepatic extramedullary hematopoiesis, cystic teratoma, pseudolipoma of the Glisson’s capsule, xanthomatous lesions in Langheran’s cell histiocytosis and perihepatic endometriosis (Fig. 14)[12].

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