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Endocrine tumors of the pancreas are uncommon. They occur in approximately 1 in 100,000 of the population and represent 1–2% of all pancreatic neoplasms. The tumors show no significant gender predilection and occur at all ages, with a peak incidence between 30 and 60 years. Some may be part of the multiple endocrine neoplasia type 1 (MEN1) and von Hippel-Lindau (VHL) disease. Microadenomatosis represents the presence of multiple small endocrine tumors in the pancreas [1]. Microadenomatosis of the endocrine pancreas is a hallmark of MEN1 syndrome [2, 3]. Interestingly, this condition is rarely described in a non-MEN1 setting [4, 5]. We herein report a unique case of pancreatic microadenomatosis occurring in a nonfamilial VHL disease patient with renal cell carcinoma (RCC). Moreover, genetic analysis for the VHL gene showed a missense mutation at the codon 167 (Arg167Trp, heterozygous) in this case. The type of VHL mutation has been reported to correlate with the clinical manifestations of the disease [6–9], and we also discuss this issue.

Pulmonary injury with leukocyte infiltration is a frequent occurrence in obstructive cholangitis patients. We wished to evaluate the roles of reactive oxygen species and vascular cell adhesion molecule-1 (VCAM-1) in this distant organ failure. Wild type (WT) and transgenic (SODtg) mice overexpressing superoxide dismutase underwent bile duct ligation and transection (BDL). VCAM-1 expression was quantified, and histopathology was assessed for the liver and lung. BDL resulted in increased leukocyte infiltration to the lung at five days in WT mice. VCAM-1 expression significantly increased in WT mouse liver at three days and WT mouse lung at five days. When these same experiments were performed in SODtg mice, these increases in leukocyte infiltration and VCAM-1 expression in lung were significantly attenuated. These data suggest that reactive oxygen species produced in response to BDL may up-regulate VCAM-1 expression in the lung and play an important role in the pathophysiology of this pulmonary injury.

The present study aimed to clarify the endoscopic ultrasonography (EUS) features of nonneoplastic (cholesterol polyps and adenomyomatosis) and neoplastic (adenoma and adenocarcinoma) gallbladder polyps and to evaluate the effectiveness and limitation of EUS in the differential diagnosis of these lesions. We retrospectively compared EUS images with histologic findings in 29 surgical cases with gallbladder polyps with a diameter of 10 to 20 mm. Those cases were indicated for surgery based on the findings of a sessile appearance, a solitary lesion, low echogenicity, and/or a lobulated surface. Six of 10 cholesterol polyps were atypically seen as partially or completely hypoechoic due to predominant proliferation of glandular epithelia. Nine of 10 cholesterol polyps demonstrated an aggregation of hyperechoic spots, which represented multiple granules of cholesterosis. All adenomyomatoses (n = 10) showed multiple microcysts, which corresponded to proliferated Rokitansky-Aschoff sinuses. However, three of nine neoplastic lesions (three adenomas and six adenocarcinomas) showed one of these signs due to concomitant cholesterosis (n = 2) or proliferated Rokitansky-Aschoff sinuses (n = 1). In conclusion, 69% (20/29) of gallbladder polyps larger than 10 mm that were preoperatively suspected of malignancy were nonneoplastic. An aggregation of hyperechoic spots and multiple microcysts are considered to be important predictive factors for cholesterol polyps and adenomyomatosis, respectively. However, we should caution that these findings can also occur in neoplastic polyps when they contain a concomitant nonneoplastic component (cholesterosis or proliferated Rokitansky-Aschoff sinuses).

Pulmonary injury with leukocyte infiltration is a frequent occurrence in obstructive cholangitis patients. We wished to evaluate the roles of reactive oxygen species and vascular cell adhesion molecule-1 (VCAM-1) in this distant organ failure. Wild type (WT) and transgenic (SODtg) mice overexpressing superoxide dismutase underwent bile duct ligation and transection (BDL). VCAM-1 expression was quantified, and histopathology was assessed for the liver and lung. BDL resulted in increased leukocyte infiltration to the lung at five days in WT mice. VCAM-1 expression significantly increased in WT mouse liver at three days and WT mouse lung at five days. When these same experiments were performed in SODtg mice, these increases in leukocyte infiltration and VCAM-1 expression in lung were significantly attenuated. These data suggest that reactive oxygen species produced in response to BDL may up-regulate VCAM-1 expression in the lung and play an important role in the pathophysiology of this pulmonary injury.