A 60-year-old woman was admitted to a local hospital for an acute abdominal pain on 18 February 2009. On CT scan, a large subcapsular haematoma was discovered. There was no haemorrhagic shock. She was admitted to our digestive intensive care unit.
This overweight patient (body mass index 29) was treated for hypertension for a short period of time when she was 16 years old and then since 1994. She was also treated for high cholesterol level (past 10 years) and hypertriglyceridaemia (past 4 years). There was a family history of heart diseases (her mother, the father and brother of the mother; her brother had died at a young age of heart infarcts or arterial hypertension).
She smoked 1 pack of cigarettes/day (for 42 years) and took contraceptive pills for 20 years. She was menopaused at the age of 45 with a substitutive hormonal treatment until 2000.
In 2005 she had an MRI showing at least three FNH (), one located in the right lobe (58 mm), and two (40 and 30 mm) located in the left lobe, as well as liver steatosis. The three nodules had characteristic MRI pattern of FNH with strong arterial enhancement and typical central scar in particular.
Figure 1 2005 MRI showing typical FNHs. (A) Phase opposed T1 image showing nodules in segments VII (58 mm) and II (40 mm), appearing hyperintense in a steatotic liver. (B) Fat suppressed T2W scan showing both hyperintense lesions, with a high signal intensity (more ...)
On the last MRI (2009) there was another tumour with strong arguments for a hepatocellular carcinoma (HCC) (data not shown) with an intrahepatic rupture () and subcapsular haematoma. The three FNH were still present () with a significant shrinkage (segment VII: 41 mm vs 58 mm diameter in 2005, segment II: 21 mm vs 40 mm, segment II (data not shown): 16 mm vs 30 mm). Furthermore in 2009, MRI features of the segment VII lesion had changed and were no more typical of FNH. This lesion was in particular heterogenous in T2W with an atypical hypointense central scar and did not exhibit the characteristic strong arterial enhancement after gadolinium-contrast injection. In the portal venous and delayed gadolinium-enhanced sequences, the lesion showed progressive enhancement suggestive of fibrous component.
Figure 2 2009 MRI. (A) Fat-suppressed T2W image shows a large subcapsular haematoma and shrinkage of the segment VII FNH (41 mm) which appears heterogenous with atypical hypointense central scar (arrow). (B) Gadolinium-enhanced fat-suppressed T1W sequence (arterial (more ...)
The patient underwent a right hepatectomy and a segment II tumorectomy on 26 February 2009. The follow-up was uneventful except for a parietal abcess.
The resected liver portion had a weight of 2000 g. In the right lobe, the large subcapsular hematoma (15 × 10 cm) was in contact with a subcapsular multinodular necrotico haemorrhagic poorly limited tumour (). This tumour was a grade 3–4 Edmonson HCC (data not shown).
(A,B) Fresh resected specimen. (A) Cut section of the haematoma and part of the hepatocellular carcinoma (HCC); (B) cut section of the shrunked FNH; the haematoma is also visible (right).
Nearby the HCC, there was another whitish/brown, hard tumour (4 × 3 cm) (). At the microscopic level, part of the tumour was a recognisable FNH, with hepatocytes nodules surrounded by fibrotic bands, inflammatory infiltrate and mild ductular reaction ( and ), and with a typical GS immunostaining (). The other part of the tumour was more fibrotic ( and ), with numerous arteries exhibiting extremely thick walls and a very narrow lumen (). In this area devoid of hepatocytes, glutamine synthetase staining was negative (), and there was no ductular reaction (). In segment II, there was a typical FNH () with large steatotic areas (data not shown) and the characteristic GS staining (). The non-tumoral liver was steatosic (80%) (data not shown).
The FNH is made of two parts: the fibrotic pink part in the middle limited by the dotted line and the peripheral part corresponding to a more classical aspect of FNH. The fibrotic parts contain mainly arteries (arrows).
The fibrotic zone (upper part) is devoid of glutamine synthetase (GS) staining, compared to the rest of the FNH.
There is no cytokeratin 7 (CK7) staining in the fibrotic area (upper part) compared to its periphery.
In the fibrotic area, there are many arteries with thick wall and narrow lumen. SMA, smooth muscle antibody.
No ductular reaction was observed in the area devoid of hepatocytes and with numerous arteries.
Figure 9 Cut section of segment three FNH (seen in the upper right corner). Glutamine synthetase (GS) well delineates the nodule. Compared to GS localisation in the non-tumoral liver, restricted to a few hepatocytes rows around hepatic veins, in FNH the staining (more ...)