Hepatic angiomyolipoma (AML) is known as a rare benign tumor with invasive growth. In the past, some of these tumors were misdiagnosed as hepatocellular carcinomas, because of the similar pattern on imaging studies. Recently, correct diagnoses have been increasing, with the development of HMB-45 immunohistochemical staining, and it appears that the majority of these tumors behave as benign tumors. However, there are not a few cases which have resulted in fatal courses because of recurrence and metastasis of the tumor. The clinical features and signs of the malignant potential of this tumor are unknown; thus, the management and treatment of the tumor are still controversial. Here in this article, we report a case of hepatic AML which showed a size increase of 175% in 1 year, and portal vein thrombosis detected by angiography. During a follow up of 3 years after a curative hepatic lobectomy, no metastasis or recurrence was seen. Review of the literature suggests that portal vein thrombosis could be one of the markers of the malignant potential and transformation of this tumor. Therefore, in this paper, we recommend surgical treatment of hepatic AML in which there is a strong suspicion of portal vein thrombosis.

Nonocclusive mesenteric ischemia (NOMI)

We report on a case of eosinophilic esophagitis in a 33-year-old Japanese woman who visited our hospital with dysphagia and esophageal food impaction in April 2006. She had had the same symptoms in May 2005, and, by endoscopic and histologic examination, she was diagnosed with eosinophilic esophagitis. Biopsy specimens from multiple locations in the esophageal mucosa had shown remarkable infiltration of eosinophils, more than 20 eosinophils per high-power field in squamous mucosa, and she had been treated with Th2 cytokine antagonist and proton pump inhibitor at the time. Her symptoms had not improved, but she had received no further medical treatment. In 2006, upper gastrointestinal endoscopy showed edematous whitish esophageal mucosa, multiple ulcerations with whitish exudates on their surfaces, and white plaques. Biopsy specimens showed the same change as before, and corticosteroid (prednisolone 20 mg/day) was administered orally. After 2 weeks of corticosteroid therapy, her symptom had effectively improved. Endoscopy after 15 weeks of the therapy revealed remarkable improvement, and biopsy specimens from esophageal mucosa revealed the disappearance of the eosinophil infiltrates. We report on a case of eosinophilic esophagitis effectively treated with systemic corticosteroids. Eosinophilic esophagitis has, as yet, no standardized treatment. However, wider recognition of its features on endoscopy may reveal more cases, thereby increasing our understanding of this disease, and will provide new therapeutic possibilities.