Hypereosinophilic Syndrome with Hepatic Involvement in a Young Child

Hypereosinophilic syndrome, whose etiology is unknown, involves the infiltration of various organs by a large number of eosinophils. The sites of involvement are the heart, skin, lung, liver, nervous system, and gastrointestinal tract. The disorder occurs mostly in middle-aged men and is characterized by striking peripheral eosinophilia. There have been few reports of hypereosinophilic syndrome in patients younger than 15 years and the disease also shows a predilection for males. We report a case of hypereosinophilic syndrome with hepatic involvement in a 17-month-old girl, and correlate the imaging features with the pathologic findings.

Nodular Regenerative Hyperplasia of the Liver in an Infant: Case Report

Nodular regenerative hyperplasia (NRH) of the liver is an uncommon disease entity, especially in the pediatricage group. A few cases have been reported in the radiologic literature, but follow-up imaging studies are rare. We describe a case of NRH, diagnosed by ultrasound-guided needle biopsy, in a seven-month-old infant with cri-du-chat syndrome. Initial ultrasound revealed several small hypoechogenic nodules in the liver, but CT and MR failed to demonstrate their presence. Two follow-up sonographic examinations were performed 7 and 20 months later, revealing increases in the size and number of the nodules.

Atrophy of the Left Hepatic Lobe Caused by a Biliary Tract Disease

PURPOSE: To study the CT patterns of left lobar atrophy, including pathologic and hemodynamic features, incases of primary biliary disease. MATERIALS AND METHODS: CT findings of left hepatic lobar and segmental atrophyin 26 patients with histologically or radiologically-proven underlying bile-duct disease were reviewed. Seventeen cases were oriental cholangiohepatitis (OCH) with left intrahepatic stones and nine were cholangiocarcinomainvolving the hilar or left hepatic bile duct. The distribution and appearance of atrophy and adjacent lobarhypertrophy were studied. CT scans were examined for the presence of stenosis or obstruction of the left portalvein, and the enhancing pattern of lobar atrophy was analysed. In patients who had undergone left lobectomy, themechanism of lobar atrophy was correlated with radiographic and pathologic features. RESULTS: All patients showedbile duct dilatation localized to atrophic left hepatic segments. In cholangiocarcinoma, the distribution ofatrophy was characteristically lobar, in contrast to segmental distribution in OCH. Compensatory hypertrophy wasmore common in OCH and particularly involved the caudate lobe. Organic and functional occlusion of the left portalvein was a cause of atrophy, even in OCH. Periportal fibrosis and inflammation were the main pathological featureof atrophy. On spiral CT scan, delayed enhancement of atrophic liver parenchyma was the characteristic feature. CONCLUSION: Lobar or segmental left hepatic lobe atrophy is seen in bile duct disease caused by OCH orcholangiocarcinoma. This finding suggests that the disease process is advanced, and that there is obstruction ornarrowing of the left portal vein, associated with periportal fibrosis and inflammation.