In this study, we studied pathologically confirmed FNH-like lesions in 13 patients with alcoholic cirrhosis. The radiological features of FNH-like lesions included hypervascularity despite small lesions, lack of “corona-like” enhancement in the late phase on CT during hepatic angiography (CTHA), high-intensity on T1WI, slightly high- or iso-intensity on T2WI, no signal decrease in out-of-phase images, and complete SPIO uptake or incomplete/partial uptake of gadoxetic acid. There have been several recent reports of FNH-like lesions in cirrhotic livers [1–6]. Although there remains no established definition for an FNH-like lesion/nodule, FNH is known to develop in normal livers. Accordingly, FNH–like lesions refer to similar nodules observed in patients with chronic liver disease [7]. These lesions have been extensively reported in alcoholic liver disease [8, 9]. Most of these hyperplastic lesions are highly vascular and relatively small-sized; additionally, they are difficult to differentiate from HCC lesions, especially early-stage HCC lesions [7–9]. We included 13 patients with alcoholic liver disease and hyperplastic liver lesions who were negative for hepatitis virus markers. Here, we discuss the imaging findings with respect to reported imaging characteristics of such lesions [10–14].
In our cases, except for a normal hepatic background and absence of a central scar, the pathological findings were consistent with those of FNH; accordingly, the patients were diagnosed with FNH-like lesions based on the original text in the WHO classification (version 5) [15]. There has been no previous report on the radiographic findings of FNH-like lesions based on our exact definition since there remains no established definition. However, considering the similarities of the histopathology and imaging findings with those of FNH, it is highly likely that FNH–like lesions have been previously described as atypical FNH based on imaging findings. Approximately 80% of FNH cases are reported to be atypical on imaging [16]. Typical FNH on plain CT is characterized by hypo- to iso-attenuation, with homogeneous attenuation in early-phase contrast enhancement and isoattenuation with the surrounding liver from the PVP to the equilibrium phase. On MRI, these lesions present as iso- to moderately hypointense on T1WIs, iso- to somewhat hyperintense on T2WIs, and iso- to somewhat hyperintense or ring-like hyperintense in the hepatocyte phase after gadoxetic acid-enhanced MR imaging [10–14, 17]. The central scar is hypointense on plain CT and early-phase contrast enhancement CT, with delayed enhancement into the equilibrium phase. Additionally, the central scar is hypointense on T1WIs and hyperintense on T2WIs; further, the region, including the surrounding area, has low uptake of gadoxetic acid during the hepatocyte phase. However, a central scar is only observed in approximately 50% of cases [18].
Single-level dynamic CTHA has indicated that blood flows from a dilated feeding artery inside the central scar; moreover, blood within the lesion directly flows into the hepatic vein via the fibrous septum and dilated veins at the margin of the lesion [19]. Grazioli et al. [17] did not report the imaging characteristics of six nodules with hypointense enhancement; therefore, it remains unclear whether there was a complete lack of enhancement. Notably, the enhancement was relatively lower than that of the surrounding liver; moreover, the heterogeneity was similar to that in our cases; however, their nodules exhibited overall hypointense enhancement. In addition, similar to our cases, the nodule lacked a central scar. Furthermore, although there is heterogeneity in the signal intensity in the hepatocyte phase of typical FNH, which ranges from iso- to hyperintense enhancement, the mechanisms underlying these findings remain unclear. Moreover, the cause of the relatively low enhancement in the uptake area within the nodule remains unclear.
This study has several limitations. First, this retrospective study had inevitable selection bias. Additionally, all patients with FNH-like lesions were pathologically confirmed using fine-needle biopsy specimens rather than surgical specimens. Finally, there was no standard follow-up imaging of the FNH-like lesions; further, we did not describe the frequency of this phenomenon. Further large-scale multicenter studies using surgical specimens are warranted.
In conclusion, the radiological features of FNH-like lesions in patients with chronic alcoholic liver disease are as follows: (1) small lesion (approximately < 1.5 cm); (2) high signal intensity on T1WIs; (3) no chemical shift effect (no signal intensity decrease on opposed phase); (4) uptake of SPIO or gadoxetic acid; and (5) hypervascularity despite the small-sized lesion. Pathologically, FNH-like lesions present a high number of unpaired arteries and sinusoidal capillarization, which may mimic HCC. It is important to identify differential radiological, pathological, and clinical findings between FNH-like nodules and HCC.