Eosinophilia can depend on many diseases, such as neoplastic diseases, parasitic infestations, allergic reactions, and hypereosinophilic syndromes. Some parasitic infestations manifest as focal lesions in the hepatic parenchyma via penetration or hematogenous migration of the parasite to the liver7
. Lymphoma, leukemia, and carcinoma may be associated with eosinophilia. However, these patients have a primary tumor mass. Eosinophilia may resolve following extraction of the primary mass8
. Neither a parasitic infestation nor a primary tumor mass was found in our patients.
The hypereosinophilic syndrome is a spectrum of disorders characterized by marked eosinophilic leukocytosis without organ dysfunction and with no known cause. Liver involvement may be present, and hepatomegaly and abnormal results on liver tests are present in 40% to 90% of patients with the disorder1,2,5. Men constitute approximately 85% of the patients with the hypereosinophilic syndrome, which occurs primarily in middle age. The most frequent complaints are weight loss, dry cough, and weakness, although symptoms and signs vary. WBC counts generally range from 10 000 to 100.000/mm3, and peripheral eosinophil percentages are 30%-70% in the majority of patients1,2,9. Because our first patient had eosinophilia, minimally abnormal results on his liver function tests, no allergic reactions, and his complaints were nonspecific, we thought that he might have the hypereosinophilic syndrome.
There are reports of pathologic changes from eosinophil-related hepatic damage on CT and US4-6,10. The most common pathologic findings are severe infiltration by eosinophils in the periportal area, eosinophilic abscess, and hepatocellular necrosis. The first patient had foci of hepatocellular necrosis, fibrosis, severe infiltration of the periportal area by eosinophils and mononuclear leukocytes, and inflammatory changes to produce an abscess.
In the hypereosinophilic syndrome, findings on US are hepatomegaly, diffuse, coarse parenchymal echogenicity without focal mass; or multiple, hypoechoic, isoechoic, or hyperechoic focal nodular lesions in the liver. The margins of lesions may be ill-defined or well-defined5,6. In our first case, there was diffuse hyperechogenicity of the liver without any focal mass on US. The left liver lobe showed hypoechoic patchy areas with poorly defined margins. In the second case, the lesion margins were well-defined on US. In previous reports, abdominal CT images have demonstrated oval or round, hypodense lesions, particularly in areas adjacent to the portal veins. These lesions were well-defined or ill-defined, with an average diameter of 2 cm (range, 1-4 cm). Most lesions were visible during the portal venous phase more so than during the hepatic arterial phase. During the equilibrium phase, some lesions showed contrast enhancement and disappeared5,6,11. Similarly, in our first patient, there were multiple hypodense lesions with relatively poorly defined margins during the portal phase. Some of this patients lesions during the equilibrium phase showed minimal contrast enhancement. Contrast enhancement of lesions during the equilibrium phase was more pronounced in our second patient. According to previous reports, the isodense appearance results from the fact that contrast material diffuses more easily into small, hypodense lesions6. As reported earlier, we found that CT, as compared with US, demonstrated a greater number of lesions, of greater sizes, with more clearly defined margins. Kim and associates reported that CT images obtained 2 to 6 months after the start of corticosteroid or antihistamine therapy showed a nearly normal appearance of the liver5. The percentage of eosinophils in peripheral blood has been associated with the number of lesions6. In the second patient in this report, we did not apply a specific therapy because the patients eosinophil count was normal and the number of lesions decreased after 2.5 months and we believed that the lesions might have arisen from eosinophilia-related hepatic damage.
If the CT and US findings of eosinophil-related liver necrosis are nonspecific, it may be difficult to differentiate them from metastatic lesions. There have been reports in the literature of some imaging findings that can help differentiate these lesions from metastatic hepatic lesionsspecifically, that focal hepatic lesions in the portal or hepatic vein might be indicative of benign parenchymal lesions. However, malignant neoplasms are rarely observed in these vessels without mass effect6,12 Unfortunately, these lesions were not distinguished from metastatic lesions by us on the basis of the above knowledge.
In summary, if a patient has eosinophilia in the peripheral blood, eosinophil-related liver involvement and liver necrosis should be considered. CT images provide a greater degree of information than does US about eosinophil-related liver involvement. Additionally, the number of lesions in the liver is correlated with the amount of eosinophils in the peripheral blood. Therefore, follow-up CT is important in this patient population. To differentiate these lesions from metastatic lesions on CT images, a liver biopsy and a control CT should be performed.