33-year-old patient with no past history of interest, diagnosed with ileal Crohn's disease in early 2005. He had been treated with claversal 500 mg/8 h and azathioprine at a dose of 150 mg/day since December 2005 for corticodependence. He was also being treated with quarterly oral iron, monthly intramuscular vitamin B12 and folic acid two days a week. Since then the patient was asymptomatic. In January 2007, an increase in cholestasis enzymes over time was observed, and it was decided to extend the study on an outpatient basis and withdraw azathioprine.
Physical examination: Blood pressure: 100/60 mm/sec; Pulse: 70 bpm; Temperature: 36oC; Weight: 80 kg; Height: 180 cm; Good general condition. Conscious and oriented. Cardiopulmonary auscultation normal. Abdomen soft, depressible, not painful, no masses or megaliths. Lower extremities without alterations.
Given the persistence of cholestasis, the following tests were performed:
Blood tests. Blood count and coagulation normal. Platelets: 108,000/ml. Liver profile: Transaminases normal. FA: 248U/L. GGT: 390U/L. Ferric profile and autoimmunity negative. Hepatitis B and C virus serology negative.
Abdominal ultrasound. Liver diffusely increased in size, with smooth contour and diffusely coarse, heterogeneous and hyperechogenic parenchyma, without occupational lesions. Mild splenomegaly. Calibre and permeability of the portal portal normal. Rest of structures without alterations.
Abdominal MRI. Liver diffusely increased in size, smooth capsular contour and homogeneous parenchyma in mid-level T1 sequences, in T2 sequences appears hypointense, with diffuse patchy areas, slightly hyperintense, without occupational lesions. Slight splenomegaly. Rest of structures without alterations.
Gastroscopy. In the lower third of the oesophagus 3 small varicose cords were observed, which disappeared with insufflation.
Given the persistence of dissociated cholestasis despite the withdrawal of azathioprine, it was decided to perform a liver biopsy in which a preserved general architecture was observed. Some portal spaces are widened with incomplete porto-portal bridging. Isolated centrolobulillary veins. No cholestasis or haemosiderosis. No macrophages. PAS diastase positive. Some portal spaces have a slight infiltrate of round cells that does not overflow the limiting plate. The irregular hepatocyte trabeculae show a regenerative and pavement-like pattern in some areas. There are frequent binucleated cells, vascular structures and dilated sinusoidal areas with a peliotic pattern. There is an irregular reticulin framework with areas of collapse. The histology described above is compatible with nodular regenerative hyperplasia.

The subsequent evolution, both analytical and portal hypertension data, was good with normal analytical normality and disappearance of the oesophageal varices.