Hepatic peliosis

A 16-year-old female patient was referred to the imaging department to perform an abdominal ultrasound due to a 3-year history of intermittent umbilical discharge, which had begun after umbilical piercing. She was otherwise asymptomatic. Apart from oral contraceptive agents, she did not take any other medication.

Besides an infected urachal cyst, the ultrasound revealed a heterogeneous lesion with hyperechoic components in the right hepatic lobe (Figs. 1-2).

Blood tests performed one week later revealed elevation of C-reactive protein (6,49 mg/dL), aspartate aminotransferase (58 U/L), alanine aminotransferase (90 U/L), and alkaline phosphatase (206 U/L).

Magnetic resonance imaging (MRI) revealed a heterogeneous hepatic lesion with ill-defined contours, mainly T1- and T2-hypointense (Figs. 3-4), but with a T2-hyperintense halo, with heterogeneous contrast-enhancement (Fig. 5) and without restricted diffusion. Parenchymal heterogeneity was noted in segment VI on the images obtained 30 seconds after contrast injection, which disappeared in the later phases.

Percutaneous biopsy of the hepatic lesion performed under ultrasound guid­ance led to a histopathologic diagnosis of hepatic peliosis (HP).

The patient was treated for the infected urachal cyst and stopped the contraceptive agents. Subsequent ultrasounds and an abdominal MR performed three years later showed regression of the liver lesion.

HP is a rare benign entity, characterised by variably-sized blood-filled lacunar spaces within the liver. Histologically, it is characterised by cystic dilated sinusoids filled with erythrocytes and bound by cords of liver cells [1]. Peliotic lesions can be multiple or focal [1,2].

HP pathogenesis remains unclear, although some mechanisms have been proposed [3]. HP has been associated with certain medications (including oral contraceptive agents), toxins, chronic wasting diseases, infectious agents (eg.: Bartonella), among others [1,3-7]. It can also be idiopathic [1,4]. In our patient’s case, the HP was most likely associated with the intake of oral contraceptive agents.

HP is frequently asymptomatic [1] and can be identified incidentally on imaging studies performed for other reasons, as occurred in our patient. However, it may present with liver failure, portal hypertension or intraabdominal haemorrhage [1,8-10].

It is often difficult to diagnose HP radiologically, because its imaging features are nonspecific.

On ultrasound, lesions can be hyperechoic in patients with healthy liver, homogeneously hypoechoic in patients with hepatic steatosis, or heterogeneously hypoechoic if complicated by haemorrhage [1,4].

MRI findings of HP depend on the age and status of the blood component [1]. On T2-weighted sequences, peliotic lesions are usually hyperintense to liver parenchyma, with high-signal foci [1,11]. On T1-weighted sequences, peliotic lesions are usually hypointense, although isointense and hyperintense foci can also occur [1,12]. On T1-weighted images after contrast material injection, peliotic lesions usually show contrast-enhancement which is typically centrifugal, but centripetal enhancement pattern can occur [1,13,14].

Our patient’s lesion presented some atypical imaging findings: the ultrasound features were different from the typical HP ultrasonographic findings; it was mainly T2-hypointense with a T2-hyperintense halo and had a heterogeneous contrast-enhancement. However, the liver heterogeneity seen in segment VI on the images obtained 30 seconds after contrast injection, not seen on other sequences, could be due to sinusoidal dilatation, a characteristic of HP.

For HP diagnosis, histopathological confirmation is recommended. However, if clinical and imaging findings suggest HP, percutaneous liver biopsy should be avoided because of the risk of severe bleeding.

HP may regress after resolution of an associated infectious disease or withdrawal of the offending medication/toxin [1], as occurred in our patient. However, a pseudotumoral and haemorrhagic evolution has been described [15]. If left untreated, HP can be fatal [1,10]. Because of its potential complications, if HP lesions do not regress, surgical resection of the involved liver parenchyma should be considered.

Written informed patient consent for publication has been obtained.